<?xml version="1.0" encoding="UTF-8" standalone="no" ?><xml><records><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87209</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ozer,M.</style></author><author><style face="normal" font="default"> Buyuktiryaki,B.</style></author><author><style face="normal" font="default"> Sahiner,U.M.</style></author><author><style face="normal" font="default"> Teksam,O.</style></author><author><style face="normal" font="default"> Karaatmaca,B.</style></author><author><style face="normal" font="default"> Soyer,O.</style></author><author><style face="normal" font="default"> Sekerel,B.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Hacettepe University, Faculty of Medicine, Department of Pediatrics, Ankara, Turkey</style></auth-address><titles><title><style face="normal" font="default">Repeated doses of salbutamol and aeroallergen sensitisation both increased salbutamol-induced hypoxia in children and adolescents with acute asthma</style></title><secondary-title><style face="normal" font="default">Acta Paediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Acta Paediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">AIM: We aimed to identify the frequency, magnitude and risk factors of salbutamol-induced hypoxia in children with acute asthma. METHODS: This study was conducted at Hacettepe University on children who presented to the paediatric allergy clinic or the paediatric emergency room with acute asthma between July 2014 and June 2015. Vital signs, pulse oximeter defined oxygen saturation and modified pulmonary index scores were evaluated before and after the first, second and third doses of nebulised salbutamol and repeated one and 10 days later. RESULTS: We included 304 patients (65.7% male) from median age of 5.3 years (range 1-18 years). Salbutamol-induced hypoxia was detected in 14.7%, 3.9% and 1.3%, respectively, after the first, second and third doses of salbutamol. The risk factors for hypoxia were younger age and a higher modified pulmonary index score, but the risk factors for salbutamol-induced hypoxia were the number of salbutamol doses given in the last six hours and the presence of aeroallergen sensitisation. The maximum decrease in oxygen saturation after salbutamol was %5. CONCLUSION: Although bronchodilators are the first-line treatment for acute asthma, they caused modest hypoxemia, especially at repeated doses and, or, in patients with aeroallergen sensitisation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1651-2227 (Electronic)IS - 0803-5253 (Linking)LA - engPT - Journal ArticleCO - Turkey -</style></notes><work-type><style face="normal" font="default">10.1111/apa.14202</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29284188">PM:29284188</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Paediatr\20180102-OzerM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Paediatr\20180102-OzerM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Ozer M</style></custom2><misc3><style face="normal" font="default">10.1111/apa.14202</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87210</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Martinez-Giron,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Protozoal Respiratory Pathology Research Unit, INCLINICA Foundation, Calvo Sotelo, 16, 33007 Oviedo, Spain.</style></auth-address><titles><title><style face="normal" font="default">Flagellated protozoa detected in Dermatophagoides by light microscopy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">House dust mites (HDM) are arthropods of medical importance due to their relationship with allergic diseases. House dust provides a detrital habitat for these organisms, in which human skin scales are a primary food source. For digestion, wall gut cells elaborate potent proteases. Nevertheless, the observation of flagellated protozoa in intestinal extracts of HDM by light microscopy might contribute to digestive processes in mites, opening a new avenue of research regarding the ecological interactions between mites and these microorganisms in the utilisation of such substrates, as well as with regard to allergic diseases</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.05.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29279261">PM:29279261</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-MartinezGironR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-MartinezGironR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171224, Martinez-Giron R</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.05.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87211</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yan,A.</style></author><author><style face="normal" font="default"> Luo,G.</style></author><author><style face="normal" font="default"> Zhou,Z.</style></author><author><style face="normal" font="default"> Hang,W.</style></author><author><style face="normal" font="default"> Qin,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Ophthalmology, Yi Chang Hospital of Traditional Chinese Medicine, Yi Chang, China</style></auth-address><titles><title><style face="normal" font="default">Tear osteopontin level and its relationship with local Th1/Th2/Th17/Treg cytokines in children with allergic conjunctivitis</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergic conjunctivitis (AC) is one of the most common allergic ocular diseases worldwide. Osteopontin (OPN), as a recently described Th2 inflammation related protein, may play a role in the pathogenesis of AC. The aim of this study was to identify the expression of OPN in children with AC. METHODS: Eighty AC children (seasonal and perennial AC) and twenty controls were enrolled in this study. Serum and tears of different time points (during and out of the pollen season) were collected and used for enzyme-linked immunosorbent assay (ELISA) of OPN and T-help cell related cytokines, respectively. The relationship between serum and tears OPN and Th1/2/17Treg related cytokines as well as disease severity were analysed. RESULTS: Our results showed that expression of tear OPN protein by perennial AC patients increased significantly compared with controls or seasonal AC patients out of the pollen season. Tear OPN expression was positively related to local Th2/17 cytokines and negatively related to IL-10 and TGF-beta expression. The tear OPN expression was also significantly related to disease severity. CONCLUSION: Tear OPN reflects the local clinical status of ocular allergy and might play an important pathophysiological role in local Th2/17/Treg inflammation in children with AC</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.05.00</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29279263">PM:29279263</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-YanA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-YanA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171224, Yan A</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.05.00</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87212</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Navarrete-Rodriguez,E.M.</style></author><author><style face="normal" font="default"> Rios-Villalobos,L.A.</style></author><author><style face="normal" font="default"> Alcocer-Arreguin,C.R.</style></author><author><style face="normal" font="default"> Del-Rio-Navarro,B.E.</style></author><author><style face="normal" font="default"> Del Rio-Chivardi,J.M.</style></author><author><style face="normal" font="default"> Saucedo-Ramirez,O.J.</style></author><author><style face="normal" font="default"> Sienra-Monge,J.J.L.</style></author><author><style face="normal" font="default"> Frias,R.V.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy and Clinical Immunology, Hospital Infantil de Mexico Federico Gomez, Ciudad de Mexico, Mexico</style></auth-address><titles><title><style face="normal" font="default">Cross-over clinical trial for evaluating the safety of camel's milk intake in patients who are allergic to cow's milk protein</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Cow's milk protein allergy (CMPA) affects between 0.6 and 0.9% of the general population, and its treatment implies the total elimination of the intake of this protein. Camel's milk has been suggested as an alternative for patients over one year of age who suffer from CMPA due to the difference in the amino acid sequence from that of cow's milk. The objective of this study was to evaluate the safety and tolerability of camel's milk in children with CMPA. METHODS: Crossed clinical trial for the use of camel's milk vs. amino acid formula, carried out at the Dr. Federico Gomez Children's Hospital of Mexico (HIMFG) on patients between one and 18 years of age with diagnosed CMPA confirmed through double-blind, placebo-controlled food challenges (DBPCFCs). Only those whose allergies were confirmed were randomly placed into two groups: those to be administered camel's milk and those to be administered the amino-acid formula for two weeks, followed by a six-week wash-out period, and then a group crossing for a further two weeks. RESULTS: 49 patients with suspected CMPA were included in the study; the diagnosis was confirmed through DBPCFCs in 15 patients, who were those who participated in the study. After having been administered camel's milk, none of the patients presented adverse effects. CONCLUSIONS AND CLINICAL RELEVANCE: Camel's milk is safe and tolerable in patients above one year of age with CMPA and can be considered as a good alternative given the benefit of its taste compared to other formulas</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Mexico -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.06.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29223706">PM:29223706</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171207-NavarreteRodriguezEM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171207-NavarreteRodriguezEM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Navarrete-Rodriguez EM</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.06.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87213</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Antunes,L.</style></author><author><style face="normal" font="default"> Duarte de Souza,A.P.</style></author><author><style face="normal" font="default"> de Araujo,P.D.</style></author><author><style face="normal" font="default"> Pinto,L.A.</style></author><author><style face="normal" font="default"> Jones,M.H.</style></author><author><style face="normal" font="default"> Stein,R.T.</style></author><author><style face="normal" font="default"> Pitrez,P.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of Clinical and Experimental Immunology, Pontificia Universidade Catolica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil</style></auth-address><titles><title><style face="normal" font="default">iNKT cells are increased in children with severe therapy-resistant asthma</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Invariant natural killer T (iNKT) cells play complex functions in the immune system, releasing both Th1 and Th2 cytokines. The role of iNKT cells in human asthma is still controversial and never described in severe therapy-resistant asthma in children. The objective of this work was to analyse iNKT frequency in peripheral blood of children with severe therapy-resistant asthma (STRA), compared to children with milder asthma and healthy controls. METHODS: Children with asthma (n=136) (non-severe and STRA) from a referral centre and healthy controls (n=40) were recruited. Peripheral blood mononuclear cells were isolated, stained with anti-CD3 and anti-iNKT (Valpha24Jalpha18), and analysed through flow cytometry. Atopic status was defined by measuring specific IgE in serum. Airway inflammation was assessed by induced sputum. RESULTS: Children with asthma presented an increased frequency of CD3(+)iNKT(+) cells (median 0.38% IQR 0.18-1.9), compared to healthy controls (median 0.26% IQR 0.10-0.43) (p=0.025). Children with STRA also showed an increased frequency of iNKT cells (1.5% IQR 1.05-2.73) compared to healthy controls and non-severe asthmatic children (0.35% IQR 0.15-1.6; p=0.002). The frequency of iNKT cells was not different between atopic and non-atopic children. In addition, iNKT cells were not associated with any inflammatory pattern of induced sputum studied. CONCLUSION: Our data suggests that iNKT cells play a role in paediatric asthma, which is also associated with the severity of disease, but independent of the atopic status</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.05.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29279262">PM:29279262</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-AntunesL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-AntunesL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171224, Antunes L</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.05.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87215</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pitrez,P.M.</style></author><author><style face="normal" font="default"> Stein,R.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Infant Center, Institute of Biomedical Research, Pontificia Universidade Catolica do Rio Grande do Sul (PUCRS), Av. Ipiranga, 6690/2(o) andar, CEP: 90.610-000, Porto Alegre/RS, Brazil.</style></auth-address><titles><title><style face="normal" font="default">Low dose treatment of mice with bacterial extract (OM-85) for attenuation of experimental atopic asthma in mice - Reply</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - LetterCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.06.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29289436">PM:29289436</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171228-PitrezPM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171228-PitrezPM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Pitrez PM</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.06.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87216</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sanchez-Borges,M.</style></author><author><style face="normal" font="default"> Gonzalez-Aveledo,L.</style></author><author><style face="normal" font="default"> Capriles-Hulett,A.</style></author><author><style face="normal" font="default"> Caballero-Fonseca,F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy and Clinical Immunology Department, Centro Medico Docente La Trinidad, Caracas, Venezuela</style></auth-address><titles><title><style face="normal" font="default">Scabies, crusted (Norwegian) scabies and the diagnosis of mite sensitisation</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Scabies is observed with relatively high frequency in Allergy and Dermatology clinics in developing countries where poor sanitary conditions are prevalent and increasingly in some areas of the world with increased immigrant populations. Since the immunological response to scabies mites includes the production of IgE class antibodies to Sarcoptes scabiei allergens which cross-react with Dermatophagoides major allergens Der p 1 and Der p 2, positive immediate-type skin tests to house dust mite extracts should be interpreted cautiously. Additionally, scabies should be included routinely in the differential diagnosis of itchy rashes in patients living in those areas</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Venezuela -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.05.006</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29279260">PM:29279260</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-SanchezBorgesM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171224-SanchezBorgesM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171224, Sanchez-Borges M</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.05.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87220</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kuperstock,J.E.</style></author><author><style face="normal" font="default"> Pritchard,N.</style></author><author><style face="normal" font="default"> Horny,M.</style></author><author><style face="normal" font="default"> Xiao,C.C.</style></author><author><style face="normal" font="default"> Brook,C.</style></author><author><style face="normal" font="default"> Platt,M.P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Inhalant allergen sensitization is an independent risk factor for the development of angioedema</style></title><secondary-title><style face="normal" font="default">Am J Otolaryngol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Am J Otolaryngol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Angioedema</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Inhalant allergen</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword><keyword><style face="normal" font="default"> Type I hypersensitivity</style></keyword><keyword><style face="normal" font="default"> etiology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0196-0709</style></isbn><abstract><style face="normal" font="default">Background/objective The etiology and risk factors for angioedema remain poorly understood with causative triggers often going undiagnosed despite repeated reactions. The purpose of this study was to determine the relationship between inhalant allergen sensitization and angioedema. Methods A retrospective review of patients who had in vitro inhalant allergy testing from 2006 to 2010 was performed. Patients with a diagnosis of angioedema who underwent inhalant allergy testing were identified. Analyses for co-morbidities, class of sensitization, seasonal timing of angioedema, and concurrent use of known hypertensive medications that can cause angioedema were performed. Results There were 1000 patients who underwent inhalant allergy testing and qualified for the study. 37/1000 had at least one episode of angioedema and of these patients, 34 had positive inhalant sensitization testing results. Multivariate regression models showed overall sensitization status, seasonal allergen and epidermal/mite sensitization as independent risk factors (p &amp;lt; 0.001, p = 0.005, p = 0.025 respectively) when controlling for ACE inhibitor use and other covariates. Tree, and epidermal/mite sensitizations were independent risk factors for angioedema in mono-sensitized subject analysis (p = 0.028, p = 0.029, respectively). Conclusion Both seasonal and perennial allergen sensitizations are independent risk factors for the development of angioedema. In patients with angioedema and an unknown trigger, inhalant allergen sensitization should be considered as a potential contributing factor to the development of angioedema</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.amjoto.2017.12.013</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29329856">PM:29329856</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Am J Otolaryngol\20171227-KuperstockJE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Am J Otolaryngol\20171227-KuperstockJE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Kuperstock JE</style></custom2><misc3><style face="normal" font="default">10.1016/j.amjoto.2017.12.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87221</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Peixoto,S.</style></author><author><style face="normal" font="default"> Soares,J.</style></author><author><style face="normal" font="default"> Monteiro,T.</style></author><author><style face="normal" font="default"> Carvalho,M.</style></author><author><style face="normal" font="default"> Santos,M.</style></author><author><style face="normal" font="default"> Simoes,C.</style></author><author><style face="normal" font="default"> Quaresma,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Departamento de Pediatria, Centro Hospitalar de Tras-os-Montes e Alto Douro (CHTMAD), Vila Real, Portugal.</style></auth-address><titles><title><style face="normal" font="default">[Evaluation of sensitization to Der p 1 and Der p 2 in a pediatric population of the North of Portugal]</style></title><secondary-title><style face="normal" font="default">An Pediatr (Barc)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">An Pediatr (Barc)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">INTRODUCTION: In Portugal, data on the role of Der p 1 and Der p 2 in patients with house dust mite (HDM) allergy are scarce. Allergen-specific immunotherapy (sIT) is the only treatment that improves symptoms, reduces the need for pharmacological therapy and modifies the natural history of the disease. With this study, the authors aim to understand the local epidemiology and to clarify if the molecular assay of major allergens is advantageous in deciding and/or modifying the decision to initiate sIT in children with clinical indication which are sensitized to Dermatophagoides pteronyssinus. METHODS: Retrospective study with analysis of patients with asthma and/or rhinitis. STUDY PERIOD: January/2013-December/2016. INCLUSION CRITERIA: 1) positive prick-test to Dermatophagoides pteronyssinus; and 2) clinically relevant disease under treatment. Assay Der p 1 and Der p 2 values >/=0.35 kUA/L were considered positive. Statistical significance was set at P&lt;.05. RESULTS: The clinical files of 279 patients. Mean ages 9.55 years (min.4-max.17). Asthma was present in 199 children (71.3%) and rhinitis in 245 (87.8%). Der p 1 and Der p 2 was &lt;0.35kUA/L in 29 (10,4%) patients. The value of Der p 1/Der p 2 correlated with the size of the prick-test papule, the value of the eosinophils and the total IgE. CONCLUSIONS: Der p 1 and Der p 2 are dominant allergens in our population and there may be benefits in determining these molecular allergen levels in patients with a positive prick-test and a clinical indication for sIT prior to a decision of initiating sIT or not</style></abstract><notes><style face="normal" font="default">IS - 1695-9531 (Electronic)IS - 1695-4033 (Linking)LA - spaPT - English AbstractPT - Journal ArticleCO - Portugal -</style></notes><work-type><style face="normal" font="default">10.1016/j.anpedi.2017.10.014</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29290503">PM:29290503</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\An Pediatr (Barc)\20171224-PeixotoS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\An Pediatr (Barc)\20171224-PeixotoS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171224, Peixoto S</style></custom2><misc3><style face="normal" font="default">10.1016/j.anpedi.2017.10.014</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87228</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Reshetnikova,I.</style></author><author><style face="normal" font="default"> Khaiboullina,S.</style></author><author><style face="normal" font="default"> Agafonova,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Capabilities of Molecular-Based Allergen Diagnostics in Atopic Diseases</style></title><secondary-title><style face="normal" font="default">BioNanoSci</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">BioNanoSci</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">2191-1649</style></isbn><abstract><style face="normal" font="default">One hundred thirty-one assays were performed to determine the level of specific IgE to major molecular components of the birch pollen</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇörBet v 1, timothy grass pollen</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇörPhl p1, rPhl p 5b, and house dust mites</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇönDer p1, rDer p2 as well as to the minor components of birch pollen</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇörBet v 2, rBet v 4, timothy grass pollen</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇörPhl p7, rPhl p 12, and house dust mites rDer p10 in patients with asthma (N</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë=</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë66) and allergic rhinitis (N</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë=</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë65). It is well established that sensitization to major and minor allergens facilitates the selection of an allergen for the allergen-specific immunotherapy (ASIT). According to the concept of molecular-based allergen diagnostics, the ASIT efficacy is expected to be high when Igðò to major components are present and antibodies to minor components are absent. When elevated Igðò levels to major and minor ASIT proteins are present, a moderate ASIT efficacy is expected</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Russia -</style></notes><work-type><style face="normal" font="default">10.1007/s12668-017-0491-2</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s12668-017-0491-2</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BioNanoSci\20171229-ReshetnikovaI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BioNanoSci\20171229-ReshetnikovaI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171229, Reshetnikova I</style></custom2><misc3><style face="normal" font="default">10.1007/s12668-017-0491-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87229</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ishida,M.</style></author><author><style face="normal" font="default"> Sasaki,T.</style></author><author><style face="normal" font="default"> Nishi,K.</style></author><author><style face="normal" font="default"> Tamamoto,T.</style></author><author><style face="normal" font="default"> Sugahara,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Graduate School of Agriculture , Ehime University , Matsuyama , Japan</style></auth-address><titles><title><style face="normal" font="default">Suppressive effect of ethanol extract from mango (Mangifera indica L.) peel on IgE production in vitro and in vivo</style></title><secondary-title><style face="normal" font="default">Biosci Biotechnol Biochem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biosci Biotechnol Biochem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword></keywords><dates><year Day="3" Month="1" Year="2018">2018/1/3</year></dates><abstract><style face="normal" font="default">Immunoglobulin E (IgE) is involved in the onset of allergic reaction, and the suppression of IgE production leads to alleviation of allergic symptoms. We found that mango peel ethanol extract (MPE) significantly suppresses IgE production by human myeloma cell line U266 cells, suggesting that MPE has an anti-allergic effect by inhibiting the production of IgE. Although mangiferin is contained in mango, which suppresses IgE production by U266 cells, it was not contained in MPE. We investigated the suppressive effect of MPE in 2,4-dinitrofluorobenzene (DNFB)-induced allergic contact dermatitis model mice. The elevation of serum IgE level was significantly suppressed by oral administration of MPE. Intake of MPE also suppressed the expression level of IL-4 in the DNFB-challenged ears, suggesting that MPE suppresses the IL-4-mediated maturation into IgE-producing cells. Our findings indicate that MPE has a potential to alleviate the increase in serum IgE level that is feature of type I allergy</style></abstract><notes><style face="normal" font="default">IS - 1347-6947 (Electronic)IS - 0916-8451 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1080/09168451.2017.1412250</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29297259">PM:29297259</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180103, Ishida M</style></custom2><misc3><style face="normal" font="default">10.1080/09168451.2017.1412250</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87231</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lin,K.</style></author><author><style face="normal" font="default"> Rasheed,A.</style></author><author><style face="normal" font="default"> Lin,S.</style></author><author><style face="normal" font="default"> Gerolemou,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Internal Medicine Department, The Brooklyn Hospital Center, Brooklyn, New York, USA</style></auth-address><titles><title><style face="normal" font="default">Catamenial anaphylaxis: a woman under monthly progesterone curse</style></title><secondary-title><style face="normal" font="default">BMJ Case Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMJ Case Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Angioedema</style></keyword><keyword><style face="normal" font="default"> complications</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">Catamenial or cyclical anaphylaxis is a complex clinical syndrome with poorly reported incidence and prevalence in the literature review. The underlying mechanism is still a myth although a few proposed hypotheses are stated. Early recognition of these symptoms will bring optimal treatment and prevent unnecessary intubation and complications. Here, we present a 48-year-old woman without significant medical and family history with recurrent angioedema in the setting of catamenial anaphylaxis or cyclical anaphylaxis in the setting of progesterone hypersensitivity</style></abstract><notes><style face="normal" font="default">IS - 1757-790X (Electronic)IS - 1757-790X (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1136/bcr-2017-222047</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29301800">PM:29301800</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMJ Case Rep\20171209-LinK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMJ Case Rep\20171209-LinK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171209, Lin K</style></custom2><misc3><style face="normal" font="default">10.1136/bcr-2017-222047</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87233</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jeon,Y.J.</style></author><author><style face="normal" font="default"> Lim,J.H.</style></author><author><style face="normal" font="default"> An,S.</style></author><author><style face="normal" font="default"> Jo,A.</style></author><author><style face="normal" font="default"> Han,D.H.</style></author><author><style face="normal" font="default"> Won,T.B.</style></author><author><style face="normal" font="default"> Kim,D.Y.</style></author><author><style face="normal" font="default"> Rhee,C.S.</style></author><author><style face="normal" font="default"> Kim,H.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Seoul National University Hospital, Seoul, Korea</style></auth-address><titles><title><style face="normal" font="default">Type III interferons are critical host factors that determine susceptibility to Influenza A viral infection in allergic nasal mucosa</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergic respiratory conditions have been associated with increased susceptibility to viral infection due to impaired interferon (IFN)-related immune responses but the mechanisms for reinforcement of mucosal immunity against viral infection in allergic diseases are largely unknown. OBJECTIVES: To determine whether IFN induction would be impaired in allergic nasal mucosa and to identify if higher loads of influenza A virus (IAV) in allergic nasal mucosa could be controlled with IFN treatment. METHODS: IAV mRNA, viral titers and IFN expression were compared in IAV-infected normal human nasal epithelial (NHNE, N=10) and allergic rhinitis nasal epithelial (ARNE, N=10) cells. We used in vivo model of allergic rhinitis (BALB/C mouse, N=10) and human nasal mucosa from healthy volunteers (N=72) and allergic rhinitis patients (N=29) to assess the induction of IFNs after IAV infection. RESULTS: IAV mRNA levels and viral titers were significantly higher in ARNE compared with NHNE cells. IFN-beta and -lambdas were induced in NHNE and ARNE cells up to 3 days after IAV infection. Interestingly, induction of IFN-lambdas mRNA levels and the amount of secreted proteins were considerably lower in ARNE cells. The mean IFN-lambdas mRNA level was also significantly lower in the nasal mucosa of AR patients and we found that recombinant IFN-lambda treatment attenuated viral mRNA levels and viral titers in IAV-infected ARNE cells. In vivo AR mouse were exhibited higher viral load after IAV infection but intranasal inoculation of IFN-lambda completely decreased IAV protein expression and viral titer in nasal mucosa of IAV-infected AR mouse. CONCLUSION: Higher susceptibility of the allergic nasal mucosa to IAV may depend on impairment of type III IFN induction, and type III IFN is a key mechanistic link between higher viral loads and control of IAV infection in allergic nasal mucosa. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13082</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288502">PM:29288502</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-JeonYJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-JeonYJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Jeon YJ</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13082</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87234</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Masuda,C.</style></author><author><style face="normal" font="default"> Miyasaka,T.</style></author><author><style face="normal" font="default"> Kawakami,K.</style></author><author><style face="normal" font="default"> Inokuchi,J.I.</style></author><author><style face="normal" font="default"> Kawano,T.</style></author><author><style face="normal" font="default"> Dobashi-Okuyama,K.</style></author><author><style face="normal" font="default"> Takahashi,T.</style></author><author><style face="normal" font="default"> Takayanagi,M.</style></author><author><style face="normal" font="default"> Ohno,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pathophysiology, Department of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University, Sendai, Japan</style></auth-address><titles><title><style face="normal" font="default">Sex-based differences in CD103(+) dendritic cells promote female-predominant Th2 cytokine production during allergic asthma</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Gender disparities in adult patients with asthma regarding its prevalence and severity are mainly due to enhanced type 2 T-helper (Th2) cytokine production in female patients compared to that in male patients. However, the pathways mediating this effect remain unclear. OBJECTIVE: We aimed to determine the roles of two major subsets of dendritic cells (DCs) in females, specifically those displaying CD11b or CD103, during enhanced Th2-priming after allergen exposure, using an ovalbumin-induced asthma mouse model. METHODS: Sex-based differences in the number of DCs at inflamed sites, co-stimulatory molecule expression on DCs, and the ability of DCs to differentiate naive CD4(+) T cells into Th2 population were evaluated after allergen exposure in asthmatic mice. In addition, we assessed the role of 17beta-estradiol in CD103(+) DC function during Th2-priming in vitro. RESULTS: The number of CD11b(high) DCs and CD103(+) DCs in the lung and bronchial lymph node (BLN) were increased to a greater extent in female mice than in male mice at 16 to 20 hours after ovalbumin (OVA) inhalation. In BLNs, CD86 and I-A/I-E expression levels and antigen uptake ability in CD103(+) DCs, but not in CD11b(high) DCs, were greater in female mice than in male mice. Furthermore, CD4(+) T cells cultured with CD103(+) DCs from female mice produced higher levels of interleukin (IL)-4, IL-5, and IL-13, compared with CD4(+) T cells cultured with CD103(+) DCs from male mice. The 17beta-estradiol oriented-enhancement of CD86 expression on CD103(+) DCs after allergen exposure induced the enhanced IL-5 production from CD4(+) T cells. CONCLUSIONS &amp; CLINICAL RELEVANCE: These findings suggest that with regards to asthma, enhanced Th2 cytokine production in females might be attributed to 17beta-estradiol-mediated Th2-oriented CD103(+) DCs in the BLN. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13081</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288569">PM:29288569</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-MasudaC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-MasudaC.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-MasudaC.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-MasudaC.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20171228, Masuda C</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13081</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87235</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Reier-Nilsen,T.</style></author><author><style face="normal" font="default"> Michelsen,M.M.</style></author><author><style face="normal" font="default"> Lodrup Carlsen,K.C.</style></author><author><style face="normal" font="default"> Carlsen,K.H.</style></author><author><style face="normal" font="default"> Mowinckel,P.</style></author><author><style face="normal" font="default"> Nygaard,U.C.</style></author><author><style face="normal" font="default"> Namork,E.</style></author><author><style face="normal" font="default"> Borres,M.P.</style></author><author><style face="normal" font="default"> Haland,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Paediatric and Adolescent Medicine, Oslo University Hospital, Oslo, Norway</style></auth-address><titles><title><style face="normal" font="default">Predicting reactivity threshold in children with anaphylaxis to peanut</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Peanut allergy necessitates dietary restrictions, preferably individualised by determining reactivity threshold through an oral food challenge (OFC). However, risk of systemic reactions often precludes OFC in children with severe peanut allergy. OBJECTIVE: We aimed to determine if clinical and/or immunological characteristics were associated with reactivity threshold in children with anaphylaxis to peanut and secondarily, to investigate if these characteristics were associated with severity of the allergic reaction during OFC. METHODS: A double-blind placebo controlled food challenge (DBPCFC) with peanut was performed in 96 5-15-year-old children with a history of severe allergic reactions to peanut and/or sensitisation to peanut (skin prick test (SPT) >/= 3 mm or specific immunoglobulin E (s-IgE) >/= 0.35 kUA/L). Investigations preceding the DBPCFC included a structured interview, SPT, lung function measurements, serological immunology assessment (IgE, IgG and IgG(4)), basophil activation test (BAT) and conjunctival allergen provocation test (CAPT). International standards were used to define anaphylaxis and grade the allergic reaction during OFC. RESULTS: During DBPCFC, all 96 children (median age 9.3, range 5.1, 15.2) reacted with anaphylaxis (moderate objective symptoms from at least two organ systems). Basophil activation (CD63+ basophils >/= 15%), peanut SPT and the ratio of peanut s-IgE/total IgE were significantly associated to reactivity threshold and lowest observed adverse events level (LOAEL) (all p &lt; 0.04). Basophil activation best predicted very low threshold level (&lt; 3 mg of peanut protein), with an optimal cut-off of 75.8% giving a 93.5% negative predictive value. None of the characteristics were significantly associated with the severity of allergic reaction. CONCLUSION AND CLINICAL RELEVANCE: In children with anaphylaxis to peanut, basophil activation, peanut SPT and the ratio of peanut s-IgE/total Ig-E were associated with reactivity threshold and LOAEL, but not with allergy reaction severity. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Norway -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13078</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29284183">PM:29284183</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-ReierNilsenT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171228-ReierNilsenT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Reier-Nilsen T</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13078</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87243</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gay,M.</style></author><author><style face="normal" font="default"> Bao,M.</style></author><author><style face="normal" font="default"> MacKenzie,K.</style></author><author><style face="normal" font="default"> Pascual,S.</style></author><author><style face="normal" font="default"> Buchmann,K.</style></author><author><style face="normal" font="default"> Bourgau,O.</style></author><author><style face="normal" font="default"> Couvreur,C.</style></author><author><style face="normal" font="default"> Mattiucci,S.</style></author><author><style face="normal" font="default"> Paoletti,M.</style></author><author><style face="normal" font="default"> Hastie,L.C.</style></author><author><style face="normal" font="default"> Levsen,A.</style></author><author><style face="normal" font="default"> Pierce,G.J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Infection levels and species diversity of ascaridoid nematodes in Atlantic cod, Gadus morhua, are correlated with geographic area and fish size</style></title><secondary-title><style face="normal" font="default">Fish Res</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Fish Res</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anisakis</style></keyword><keyword><style face="normal" font="default"> Distribution in fillets</style></keyword><keyword><style face="normal" font="default"> Hysterothylacium</style></keyword><keyword><style face="normal" font="default"> Molecular identification</style></keyword><keyword><style face="normal" font="default"> Seafood safety</style></keyword><keyword><style face="normal" font="default"> Zoonotic nematodes</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0165-7836</style></isbn><abstract><style face="normal" font="default">Atlantic cod (Gadus morhua) is among the most important commercial fish species on the world market. Its infection by ascaridoid nematodes has long been known, Pseudoterranova even being named cod worm. In the present study, 755 individuals were sampled in the Barents, Baltic and North Seas during 2012</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô2014. Prevalences for Anisakis in whole fish and in fillets in the different fishing areas varied from 16 to 100% and from 12 to 90% respectively. Abundance was also greatly influenced by the sampling area. Generalized additive model results indicate higher numbers of Anisakis in the North Sea, even after the larger body size was accounted for. Numbers and prevalence of Anisakis were positively related to fish length or weight. The prevalence of parasites in whole fish and in fillets was also influenced by the season, with the spring displaying a peak for the prevalence in whole fish and, at the same time, a drop for the prevalence in fillets. Whereas 46% of cod had Anisakis larvae in their fillets, the majority (39%) had parasites mainly in the ventral part of the fillet and only 12% had parasites in their dorsal part. This observation is of importance for the processing of the fish. Indeed, the trimming of the ventral part of the cod fillet would allow the almost total elimination of ascaridoids except for cod from the Baltic Sea where there was no difference between the dorsal and the ventral part. The presence of other ascaridoid genera was also noticeable in some areas. For Pseudoterranova, the highest prevalence (45%) in whole fish was observed in the Northern North Sea, whereas the other areas had prevalences between 3 and 16%. Contracaecum was present in every commercial size cod sampled in the Baltic Sea with an intensity of up to 96 worms but no Contracaecum was isolated from the Central North Sea. Non-zoonotic Hysterothylacium was absent from the Baltic Sea but with a prevalence of 83% in the Barents and the Northern North Sea. A subsample of worms was identified with genetic-molecular tools and assigned to the species A. simplex (s.s.), A. pegreffii, P. decipiens (s.s.), P. krabbei, C. osculatum and H. aduncum. In addition to high prevalence and abundance values, the cod sampled in this study presented a diversity of ascaridoid nematodes with a majority of fish displaying a co-infection. Out of 295 whole infected fish, 269 were co-infected by at least 2 genera</style></abstract><notes><style face="normal" font="default">LA - ENGCO - France -CO - Denmark -CO - United Kingdom -CO - Spain -CO - Italy -CO - Norway -CO - Portugal -</style></notes><work-type><style face="normal" font="default">10.1016/j.fishres.2017.06.006</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.fishres.2017.06.006</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Fish Res\20170626-GayM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Fish Res\20170626-GayM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170626, Gay M</style></custom2><misc3><style face="normal" font="default">10.1016/j.fishres.2017.06.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87248</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Verdes,A.</style></author><author><style face="normal" font="default"> Simpson,D.</style></author><author><style face="normal" font="default"> Holford,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Belfer Research Center-Hunter College, and The Graduate Center, Program in Biology, Chemistry and Biochemistry, The City University of New York; New York, NY 10021</style></auth-address><titles><title><style face="normal" font="default">Are fireworms venomous? Evidence for the convergent evolution of toxin homologs in three species of fireworms (Annelida, Amphinomidae)</style></title><secondary-title><style face="normal" font="default">Genome Biol Evol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Genome Biol Evol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> Prediction</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Amphinomids, more commonly known as fireworms, are a basal lineage of marine annelids characterized by the presence of defensive dorsal calcareous chaetae, which break off upon contact. It has long been hypothesized that amphinomids are venomous and use the chaetae to inject a toxic substance. However, studies investigating fireworm venom from a morphological or molecular perspective are scarce and no venom gland has been identified to date, nor any toxin characterized at the molecular level. To investigate this question, we analyzed the transcriptomes of three species of fireworms-Eurythoe complanata, Hermodice carunculata and Paramphinome jeffreysii-following a venomics approach to identify putative venom compounds. Our venomics pipeline involved de novo transcriptome assembly, open reading frame and signal sequence prediction, followed by three different homology search strategies: BLAST, HMMER sequence and HMMER domain. Following this pipeline, we identified 34 clusters of orthologous genes, representing 13 known toxin classes that have been repeatedly recruited into animal venoms. Specifically, the three species share a similar toxin profile with C-type lectins, peptidases, metalloproteinases, spider toxins and CAP proteins found among the most highly expressed toxin homologs. Despite their great diversity, the putative toxins identified are predominantly involved in three major biological processes: hemostasis, inflammatory response and allergic reactions, all of which are commonly disrupted after fireworm stings. While the putative fireworm toxins identified here need to be further validated, our results strongly suggest that fireworms are venomous animals that use a complex mixture of toxins for defense against predators</style></abstract><notes><style face="normal" font="default">IS - 1759-6653 (Electronic)IS - 1759-6653 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Spain -</style></notes><work-type><style face="normal" font="default">10.1093/gbe/evx279</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29293976">PM:29293976</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Genome Biol Evol\20171223-VerdesA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Genome Biol Evol\20171223-VerdesA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Verdes A</style></custom2><misc3><style face="normal" font="default">10.1093/gbe/evx279</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87251</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,I.S.</style></author><author><style face="normal" font="default"> Cho,D.H.</style></author><author><style face="normal" font="default"> Kim,K.S.</style></author><author><style face="normal" font="default"> Kim,K.H.</style></author><author><style face="normal" font="default"> Park,J.</style></author><author><style face="normal" font="default"> Kim,Y.</style></author><author><style face="normal" font="default"> Jung,J.H.</style></author><author><style face="normal" font="default"> Kim,K.</style></author><author><style face="normal" font="default"> Jung,H.J.</style></author><author><style face="normal" font="default"> Jang,H.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">College of Korean Medicine , Kyung Hee University , Seoul , Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Anti-inflammatory effects of embelin in A549 cells and human asthmatic airway epithelial tissues</style></title><secondary-title><style face="normal" font="default">Immunopharmacol Immunotoxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunopharmacol Immunotoxicol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">OBJECTIVE: Allergic asthma is the most common type in asthma, which is defined as a chronic inflammatory disease of the lung. In this study, we investigated whether embelin (Emb), the major component of Ardisia japonica BL. (AJB), exhibits anti-inflammatory effects on allergic asthma via inhibition of NF-kappaB activity using A549 cells and asthmatic airway epithelial tissues. METHODS: Inflammation was induced in A549 cells, a human airway epithelial cell line, by IL-1beta (10 ng/ml) treatment for 4 h. The effects of Emb on NF-kappaB activity and COX-2 protein expression in inflamed airway epithelial cells and human asthmatic airway epithelial tissues were analyzed via western blot. The secretion levels of NF-kappaB-mediated cytokines/chemokines, including IL-4, 6, 9, 13, TNF-alpha and eotaxin, were measured by a multiplex assay. RESULTS: Emb significantly blocked NF-kappaB activity in IL-1beta-treated A549 cells and human asthmatic airway epithelial tissues. COX-2 expression was also reduced in both IL-1beta-treated A549 cells and asthmatic tissues Emb application. Emb significantly reduced the secretion of IL-4, IL-6 and eotaxin in human asthmatic airway epithelial tissues by inhibiting activity of NF-kappaB. CONCLUSIONS: The results of this study suggest that Emb may be used as an anti-inflammatory agent via inhibition of NF-kappaB and related cytokines</style></abstract><notes><style face="normal" font="default">IS - 1532-2513 (Electronic)IS - 0892-3973 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1080/08923973.2017.1414836</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29299941">PM:29299941</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunopharmacol Immunotoxicol\20180104-LeeIS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunopharmacol Immunotoxicol\20180104-LeeIS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Lee IS</style></custom2><misc3><style face="normal" font="default">10.1080/08923973.2017.1414836</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87257</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kulis,M.D.</style></author><author><style face="normal" font="default"> Patil,S.U.</style></author><author><style face="normal" font="default"> Wambre,E.</style></author><author><style face="normal" font="default"> Vickery,B.P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, University of North Carolina, Chapel Hill NC</style></auth-address><titles><title><style face="normal" font="default">Immune Mechanisms of Oral Immunotherapy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Oral immunotherapy (OIT) has reproducibly demonstrated successful desensitization in food-allergic subjects completing clinical trials and, in some studies, sustained unresponsiveness. These clinical outcomes have been associated with characteristic modifications in the allergen-specific immune response, but a detailed synthesis of OIT's mechanisms of action is lacking. In this Rostrum, we review the current evidence regarding the human immune response to OIT, explore possible mechanisms, and identify knowledge gaps for future research</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.12.979</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288078">PM:29288078</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171226-KulisMD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171226-KulisMD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171226, Kulis MD</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.12.979</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87258</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,Y.</style></author><author><style face="normal" font="default"> Liu,B.</style></author><author><style face="normal" font="default"> Harmacek,L.</style></author><author><style face="normal" font="default"> Long,Z.</style></author><author><style face="normal" font="default"> Liang,J.</style></author><author><style face="normal" font="default"> Lukin,K.</style></author><author><style face="normal" font="default"> Leach,S.M.</style></author><author><style face="normal" font="default"> O'Connor,B.</style></author><author><style face="normal" font="default"> Gerber,A.N.</style></author><author><style face="normal" font="default"> Hagman,J.</style></author><author><style face="normal" font="default"> Roers,A.</style></author><author><style face="normal" font="default"> Finkelman,F.D.</style></author><author><style face="normal" font="default"> Huang,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biomedical Research, National Jewish Health, Denver, CO, USA</style></auth-address><titles><title><style face="normal" font="default">The transcription factors GATA2 and MITF regulate Hdc gene expression in mast cells and are required for IgE/mast cell-mediated anaphylaxis</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Histamine is a critical mediator of IgE/mast cell-mediated anaphylaxis. Histamine is synthesized by decarboxylating the amino acid histidine, a reaction catalyzed by the Hdc-gene encoded enzyme histidine decarboxylase. However, regulation of the Hdc gene in mast cells is poorly understood. OBJECTIVE: We sought to investigate the in vivo regulation of IgE/mast cell mediated anaphylaxis by transcription factors GATA2 and MITF and the mechanisms by which GATA2 and MITF regulate Hdc gene expression in mouse and human mast cells. METHODS: mice deficient in the transcription factors Gata2, Ahr, Ahrr, or Bhlhe40 were assessed for anaphylactic reactions. Chromatin immunoprecipitation sequencing analysis identified putative Hdc enhancers. Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene. The shRNA knock down approach was used to determine the role of MITF in regulating mouse and human HDC gene expression. RESULTS: Connective tissue mast cell (CTMC)-specific Gata2 deficient mice failed to develop IgE/mast cell-mediated anaphylaxis. GATA2 induced the expression of Mitf, Ahr, Ahrr and Bhlhe40 in mast cells. MITF, but not AHR, AHRR or BHLHE40, was required for anaphylaxis. MITF bound to an enhancer located 8.8 kb upstream of the transcription start site of the Hdc gene and directed enhancer activity. MITF overexpression largely restored Hdc gene expression in the Gata2 deficient-mast cells. In human mast cell line LAD2, MITF was required for the HDC gene expression and histamine synthesis. CONCLUSION: The transcription factors GATA2 and MITF regulate Hdc gene expression in mast cells and are required for IgE/mast cell-mediated anaphylaxis</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -CO - China -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.043</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29277702">PM:29277702</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171222-LiY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171222-LiY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Li Y</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.043</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87259</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">McCleary,N.</style></author><author><style face="normal" font="default"> Nwaru,B.I.</style></author><author><style face="normal" font="default"> Nurmatov,U.B.</style></author><author><style face="normal" font="default"> Critchley,H.</style></author><author><style face="normal" font="default"> Sheikh,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Asthma UK Centre for Applied Research, Centre for Medical Informatics, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, UK; Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, Canada. Electronic address: nmccleary@ohri.caAsthma UK Centre for Applied Research, Centre for Medical Informatics, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, UK; Krefting Research Centre, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden; Wallenberg Centre for Molecular and Translational Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, SwedenAsthma UK Centre for Applied Research, Centre for Medical Informatics, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, UK; Division of Population Medicine, School of Medicine, Cardiff University, Cardiff, UKMedical Research Council Centre for Reproductive Health, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UKAsthma UK Centre for Applied Research, Centre for Medical Informatics, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, UK</style></auth-address><titles><title><style face="normal" font="default">Endogenous and exogenous sex steroid hormones in asthma and allergy in females: a systematic review and meta-analysis</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword></keywords><dates><year Day="2" Month="1" Year="2018">2018/1/2</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Canada -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.034</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29305316">PM:29305316</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180102-McClearyN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180102-McClearyN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, McCleary N</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.034</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87260</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,X.Y.</style></author><author><style face="normal" font="default"> Yang,K.Y.</style></author><author><style face="normal" font="default"> Wang,M.Q.</style></author><author><style face="normal" font="default"> Kwok,J.S.</style></author><author><style face="normal" font="default"> Zeng,X.</style></author><author><style face="normal" font="default"> Yang,Z.</style></author><author><style face="normal" font="default"> Xiao,X.J.</style></author><author><style face="normal" font="default"> Lau,C.P.</style></author><author><style face="normal" font="default"> Li,Y.</style></author><author><style face="normal" font="default"> Huang,Z.M.</style></author><author><style face="normal" font="default"> Ba,J.G.</style></author><author><style face="normal" font="default"> Yim,A.K.</style></author><author><style face="normal" font="default"> Ouyang,C.Y.</style></author><author><style face="normal" font="default"> Ngai,S.M.</style></author><author><style face="normal" font="default"> Chan,T.F.</style></author><author><style face="normal" font="default"> Leung,E.L.</style></author><author><style face="normal" font="default"> Liu,L.</style></author><author><style face="normal" font="default"> Liu,Z.G.</style></author><author><style face="normal" font="default"> Tsui,S.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, School of Medicine, Shenzhen University, China</style></auth-address><titles><title><style face="normal" font="default">High-quality assembly of Dermatophagoides pteronyssinus genome and transcriptome reveals a wide range of novel allergens</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword></keywords><dates><year Day="2" Month="1" Year="2018">2018/1/2</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - China -CO - Hong Kong -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.038</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29305317">PM:29305317</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180102-LiuXY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180102-LiuXY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Liu XY</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.038</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87262</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lambrecht,B.N.</style></author></authors></contributors><auth-address><style face="normal" font="default">VIB Center for Inflammation Research, Ghent University, Ghent, Belgium</style></auth-address><titles><title><style face="normal" font="default">FcRn is mother's milk to allergen tolerance</style></title><secondary-title><style face="normal" font="default">J Exp Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Exp Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">In this issue Ohsaki et al. (https://doi.org/10.1084/jem.20171163) explain how breastfeeding can prevent the onset of food allergies in offspring by instructing T reg formation via neonatal Fc receptor (FcRn)-mediated transfer and uptake of allergen-containing IgG immune complexes (Ig-ICs) by gut dendritic cells (DCs)</style></abstract><notes><style face="normal" font="default">IS - 1540-9538 (Electronic)IS - 0022-1007 (Linking)LA - engPT - Journal ArticleCO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1084/jem.20172022.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29196507">PM:29196507</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Exp Med\20180102-LambrechtBN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Exp Med\20180102-LambrechtBN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Lambrecht BN</style></custom2><misc3><style face="normal" font="default">10.1084/jem.20172022.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87264</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yamaga,K.</style></author><author><style face="normal" font="default"> Murota,H.</style></author><author><style face="normal" font="default"> Tamura,A.</style></author><author><style face="normal" font="default"> Miyata,H.</style></author><author><style face="normal" font="default"> Ohmi,M.</style></author><author><style face="normal" font="default"> Kikuta,J.</style></author><author><style face="normal" font="default"> Ishii,M.</style></author><author><style face="normal" font="default"> Tsukita,S.</style></author><author><style face="normal" font="default"> Katayama,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Course of Integrated Medicine, Graduate School of Medicine, Osaka University, Osaka 5650871, Japan</style></auth-address><titles><title><style face="normal" font="default">Claudin-3 loss causes leakage of sweat from the sweat gland to contribute to the pathogenesis of atopic dermatitis</style></title><secondary-title><style face="normal" font="default">J Invest Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Invest Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">The transfer of sweat to the skin surface without leakage is important for the homeostatic regulation of skin and is impaired in atopic dermatitis (AD). Although the precise composition of the leakage barrier remains obscure, there is a large contribution from claudins, the major components of tight junctions. In humans, claudin-1, -3, and -15 are expressed on sweat ducts, and claudin-3 and -10 are expressed on secretory coils. Although only two claudins are expressed in murine sweat glands, we found that the expression of claudin-3 is conserved. AD lesional skin had decreased claudin-3 expression in sweat glands, which was accompanied by sweat leakage. This critical role in water barrier function was confirmed in Cldn3(-/-) and Cldn3(+/-) mice and those with experimentally decreased claudin-3. Our results reveal the crucial role of claudin-3 in preventing sweat gland leakage and suggest that the pathogenesis of dermatoses accompanied by hypohidrosis involves abnormally decreased claudin-3</style></abstract><notes><style face="normal" font="default">IS - 1523-1747 (Electronic)IS - 0022-202X (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.jid.2017.11.040</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29277540">PM:29277540</url></web-urls><pdf-urls><url ppv-ref="no">h-murota@derma.med.osaka-u.ac.jp</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171222, Yamaga K</style></custom2><misc3><style face="normal" font="default">10.1016/j.jid.2017.11.040</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87265</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mazur,M.</style></author><author><style face="normal" font="default"> Olczak,J.</style></author><author><style face="normal" font="default"> Olejniczak,S.</style></author><author><style face="normal" font="default"> Koralewski,R.</style></author><author><style face="normal" font="default"> Czestkowski,W.</style></author><author><style face="normal" font="default"> Jedrzejczak,A.</style></author><author><style face="normal" font="default"> Golab,J.</style></author><author><style face="normal" font="default"> Dzwonek,K.</style></author><author><style face="normal" font="default"> Dymek,B.</style></author><author><style face="normal" font="default"> Sklepkiewicz,P.L.</style></author><author><style face="normal" font="default"> Zagozdzon,A.</style></author><author><style face="normal" font="default"> Noonan,T.</style></author><author><style face="normal" font="default"> Mahboubi,K.</style></author><author><style face="normal" font="default"> Conway,B.</style></author><author><style face="normal" font="default"> Sheeler,R.</style></author><author><style face="normal" font="default"> Beckett,P.</style></author><author><style face="normal" font="default"> Hungerford,W.M.</style></author><author><style face="normal" font="default"> Podjarny,A.D.</style></author><author><style face="normal" font="default"> Mitschler,A.</style></author><author><style face="normal" font="default"> Cousido-Siah,A.</style></author><author><style face="normal" font="default"> Fadel,F.</style></author><author><style face="normal" font="default"> Golebiowski,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Targeting Acidic Mammalian Chitinase is Effective in Animal Model of Asthma</style></title><secondary-title><style face="normal" font="default">J Med Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Med Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">This article highlights our work toward the identification of a potent, selective, and in vivo efficacious acidic mammalian chitinase (AMCase) inhibitor. Rational design, guided by X-ray analysis of several inhibitors bound to human chitotriosidase (hCHIT1) led to the identification of compound 7f as a highly potent, AMCase inhibitor (IC50 values of 14 and 19 nM against human and mouse enzyme, respectively) and selective (>150x against mCHIT1) with very good PK properties. This compound dosed once daily at 30 mg/kg p.o. showed significant anti-inflammatory efficacy in HDM-induced allergic airway inflammation, reducing inflammatory cell influx in the BALF and total IgE concentration in plasma, which correlated with decrease of chitinolytic activity. Therapeutic efficacy of compound 7f in the clinically relevant aeroallergen-induced acute asthma model in mice provides a rationale for developing AMCase inhibitor for the treatment of asthma</style></abstract><notes><style face="normal" font="default">IS - 1520-4804 (Electronic)IS - 0022-2623 (Linking)LA - engPT - Journal ArticleCO - Poland -CO - United States -CO - France -</style></notes><work-type><style face="normal" font="default">10.1021/acs.jmedchem.7b01051</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29283260">PM:29283260</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Med Chem\20171228-MazurM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Med Chem\20171228-MazurM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Mazur M</style></custom2><misc3><style face="normal" font="default">10.1021/acs.jmedchem.7b01051</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87266</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Incorvaia,C.</style></author><author><style face="normal" font="default"> Gritti,B.L.</style></author><author><style face="normal" font="default"> Ridolo,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Cardiac/Pulmonary Rehabilitation, ASST Pini/CTO , Milan , Italy</style></auth-address><titles><title><style face="normal" font="default">The economic advantage of allergen immunotherapy over drug treatment in respiratory allergy</style></title><secondary-title><style face="normal" font="default">J Med Econ</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Med Econ</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="3" Month="1" Year="2018">2018/1/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1941-837X (Electronic)IS - 1369-6998 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1080/13696998.2018.1423567</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29295630">PM:29295630</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Med Econ\20180103-IncorvaiaC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Med Econ\20180103-IncorvaiaC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Incorvaia C</style></custom2><misc3><style face="normal" font="default">10.1080/13696998.2018.1423567</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87268</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,Y.</style></author><author><style face="normal" font="default"> Feng,Y.</style></author><author><style face="normal" font="default"> Li,L.</style></author><author><style face="normal" font="default"> Ye,X.</style></author><author><style face="normal" font="default"> Wang,J.</style></author><author><style face="normal" font="default"> Wang,Q.</style></author><author><style face="normal" font="default"> Li,P.</style></author><author><style face="normal" font="default"> Li,N.</style></author><author><style face="normal" font="default"> Zheng,X.</style></author><author><style face="normal" font="default"> Gao,X.</style></author><author><style face="normal" font="default"> Li,C.</style></author><author><style face="normal" font="default"> Li,F.</style></author><author><style face="normal" font="default"> Sun,B.</style></author><author><style face="normal" font="default"> Lai,K.</style></author><author><style face="normal" font="default"> Su,Z.</style></author><author><style face="normal" font="default"> Zhong,N.</style></author><author><style face="normal" font="default"> Chen,L.</style></author><author><style face="normal" font="default"> Feng,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China</style></auth-address><titles><title><style face="normal" font="default">Immunization with an adenovirus-vectored TB vaccine containing Ag85A-Mtb32 effectively alleviates allergic asthma</style></title><secondary-title><style face="normal" font="default">J Mol Med (Berl)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Mol Med (Berl)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">Current treatments for allergic asthma primarily ameliorate symptoms rather than inhibit disease progression. Regulating the excessive T helper type 2 (Th2) responses may prevent asthma exacerbation. In this study, we investigated the protective effects of Ad5-gsgAM, an adenovirus vector carrying two mycobacterial antigens Ag85A and Mtb32, against allergic asthma. Using an ovalbumin (OVA)-induced asthmatic mouse model, we found that Ad5-gsgAM elicited much more Th1-biased CD4(+)T and CD8(+)T cells than bacillus Calmette-Guerin (BCG). After OVA challenge, Ad5-gsgAM-immunized mice showed significantly lowered airway inflammation in comparison with mice immunized with or without BCG. Total serum immunoglobulin E and pulmonary inducible-nitric-oxide-synthase were efficiently reduced. The cytokine profiles in bronchial-alveolar-lavage-fluids (BALFs) were also modulated, as evidenced by the increased level of interferon-gamma (IFN-gamma) and the decreased level of interleukin (IL)-4, IL-5, and IL-13. Anti-inflammatory cytokine IL-10 was sharply increased, whereas pro-inflammatory cytokine IL-33 was significantly decreased. Importantly, exogenous IL-33 abrogated the protective effects of Ad5-gsgAM, revealing that the suppression of IL-33/ST2 axis substantially contributed to protection against allergic inflammation. Moreover, regulatory T cells were essential for regulating aberrant Th2 responses as well as IL-33/ST2 axis. These results suggested that modulating the IL-33/ST2 axis via adenovirus-vectored mycobacterial antigen vaccination may provide clinical benefits in allergic inflammatory airways disease. KEY MESSAGES: *Ad5-gsgAM elicits Th1 responses and suppresses Th2-mediated allergic asthma in mice. *Ad5-gsgAM inhibits IL-33/ST2 axis by reducing IL-33 secretion but not ILC2 recruiting. *Treg is essential for modulating Th2 responses and IL-33/ST2 axis by Ad5-gsgAM</style></abstract><notes><style face="normal" font="default">IS - 1432-1440 (Electronic)IS - 0946-2716 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s00109-017-1614-5</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29302700">PM:29302700</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Mol Med (Berl)\20180104-ZhangY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Mol Med (Berl)\20180104-ZhangY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Zhang Y</style></custom2><misc3><style face="normal" font="default">10.1007/s00109-017-1614-5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87279</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yon,D.K.</style></author><author><style face="normal" font="default"> Ha,E.K.</style></author><author><style face="normal" font="default"> Lee,S.Y.</style></author><author><style face="normal" font="default"> Kim,W.K.</style></author><author><style face="normal" font="default"> Park,Y.M.</style></author><author><style face="normal" font="default"> Kim,J.</style></author><author><style face="normal" font="default"> Ahn,K.</style></author><author><style face="normal" font="default"> Hahm,M.I.</style></author><author><style face="normal" font="default"> Chae,Y.</style></author><author><style face="normal" font="default"> Lee,K.J.</style></author><author><style face="normal" font="default"> Kwon,H.J.</style></author><author><style face="normal" font="default"> Han,M.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, CHA Bundang Medical Center CHA University School of Medicine, Seongnam, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Hepatitis B immunogenicity after a primary vaccination course associated with childhood asthma, allergic rhinitis, and allergen sensitization</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">There have been significant advances in our understanding of the immunology of allergic diseases in recent years. Most recent studies emphasize the importance of downregulation of Th1 and Th2 responses by regulatory T cells (Tregs), which is mediated by anti-inflammatory cytokines such as IL-10, rather than an imbalance of Th1 and Th2 responses.(1, 2) Many immuno-epidemiological studies on the relationships of allergic diseases with infections or vaccines have focused on the immunological backgrounds of the study subjects.(1, 2) However, few large-scale immuno-epidemiological studies have focused on the host effect of individuals, with consideration of the presence of immune and allergic diseases. We investigated nationwide epidemiologic study on Korean children who received a 3-dose primary vaccination course against hepatitis B to assess the relationship of hepatitis B immunogenicity with the prevalence of different allergic diseases. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - LetterCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12850</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29266497">PM:29266497</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171221-YonDK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171221-YonDK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Yon DK</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12850</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87280</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sakaguchi,K.</style></author><author><style face="normal" font="default"> Koyanagi,A.</style></author><author><style face="normal" font="default"> Kamachi,F.</style></author><author><style face="normal" font="default"> Harauma,A.</style></author><author><style face="normal" font="default"> Chiba,A.</style></author><author><style face="normal" font="default"> Hisata,K.</style></author><author><style face="normal" font="default"> Moriguchi,T.</style></author><author><style face="normal" font="default"> Shimizu,T.</style></author><author><style face="normal" font="default"> Miyake,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics and Adolescent Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, Japan</style></auth-address><titles><title><style face="normal" font="default">Breastfeeding regulates development of immune system through TGF-beta in mice pups</style></title><secondary-title><style face="normal" font="default">Pediatr Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Breast milk contains important nutrients and immunoregulatory factors that are essential for newborn infants. Recently, epidemiological studies suggested that breastfeeding prevents a wide range of infectious diseases and lowers the incidence of infant allergic diseases. METHODS: To examine the effects of breast milk in immunological development in infancy, we established an artificial rearing system for hand-feeding mice and compared mouse pups fed with either breast milk or milk substitute. All mice were sacrificed at 14 days of age and immune cell populations in the thymus, spleen, and small intestine were examined using flow cytometry. RESULTS: The number of thymocytes was higher whereas that of total immune cells of peripheral lymphoid tissues was lower in mice fed breast milk than in those fed milk substitute. In peripheral lymphoid tissues, the frequency of B cells was higher and the frequencies of CD8(+) T cells, macrophages, dendritic cells, and granulocytes were significantly lower in breast milk-fed mice. The similar alteration in immune cells of thymus and peripheral lymphoid tissues as seen in milk substitute-fed mice was observed in pups reared by mother mice treated with anti-TGF-beta mAb. CONCLUSIONS: These results suggested that breast milk regulates the differentiation and expansion of innate and adaptive immune cells partly due to TGF-beta. Our findings may provide the new concept that TGF-beta in breast milk is involved in a new therapeutic strategy for innate immune system-mediated infant diseases. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1442-200X (Electronic)IS - 1328-8067 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/ped.13507</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29290091">PM:29290091</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Int\20171231-SakaguchiK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Int\20171231-SakaguchiK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171231, Sakaguchi K</style></custom2><misc3><style face="normal" font="default">10.1111/ped.13507</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87286</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Iliopoulou,A.</style></author><author><style face="normal" font="default"> Petrodimopoulou,M.</style></author><author><style face="normal" font="default"> Konstantakopoulou,M.</style></author><author><style face="normal" font="default"> Pasioti,M.</style></author><author><style face="normal" font="default"> Papadopoulou,A.</style></author><author><style face="normal" font="default"> Mikos,N.</style></author><author><style face="normal" font="default"> Kompoti,E.</style></author><author><style face="normal" font="default"> Korakianitis,I.</style></author><author><style face="normal" font="default"> Kontogianni,M.</style></author><author><style face="normal" font="default"> Pitsios,C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Profilin sensitization and its clinical relevance to a population of atopic adults in Greece</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> Cross-reaction</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Oral allergy syndrome</style></keyword><keyword><style face="normal" font="default"> Peach</style></keyword><keyword><style face="normal" font="default"> Profiline</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">Background Profilin is a panallergen often responsible for cross-reactivity between pollen and plant foods. Oral allergy syndrome (OAS) consists a clinical expression of this cross-reaction, in some profilin-sensitized patients. The aim of this study was to determine the prevalence of sensitization to profilin in Greece and to examine the correlation of profilin-sensitization with OAS. Methods Two hundred and sixty-four atopic adults were included in the study, with at least one positive SPT to airborne and/or food allergens. Sensitization to profilin was examined with the use of purified date palm profilin Pho d 2. SPT with our standard battery of commercial extracts and an additional panel with profilin-containing foods and pollen were conducted. Results Twenty-nine of our atopic patients (11%) resulted positive to profilin and 79 (29.9%) patients referred symptoms of OAS. Patients with OAS reported peach, walnut, kiwi, banana and hazelnut, as the commonest plant foods causing OAS. OAS was correlated to positive SPT to apple, peach pulp (showing the highest correlation), and other plant foods. No statistically significant correlation was found between sensitization to profilin and OAS. A significant trend of profilin-sensitization was found in patients with allergic rhinitis, but not in asthmatics. Conclusion Our results show a low prevalence of sensitization to profilin, in Greece. The in vivo sensitization to profilin's extract was not correlated to OAS and it is probable that another culprit panallergen is the cause for many OAS cases in our country</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Greece -CO - Cyprus -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.11.001</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.11.001</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\20171226-IliopoulouA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\20171226-IliopoulouA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171226, Iliopoulou A</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.11.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87292</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Diver,S.</style></author><author><style face="normal" font="default"> Brightling,C.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Infection, Immunity and Inflammation, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK</style></auth-address><titles><title><style face="normal" font="default">Big asthma data: getting bigger and more beautiful?</style></title><secondary-title><style face="normal" font="default">Thorax</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Thorax</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1468-3296 (Electronic)IS - 0040-6376 (Linking)LA - engPT - EditorialCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1136/thoraxjnl-2017-211148</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288213">PM:29288213</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Thorax\20171229-DiverS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Thorax\20171229-DiverS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171229, Diver S</style></custom2><misc3><style face="normal" font="default">10.1136/thoraxjnl-2017-211148</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87293</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,X.</style></author><author><style face="normal" font="default"> Huang,L.</style></author><author><style face="normal" font="default"> Wang,N.</style></author><author><style face="normal" font="default"> Yi,H.</style></author><author><style face="normal" font="default"> Wang,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Life Science, College of Environment and Resource, Shanxi University, Taiyuan 030006, China</style></auth-address><titles><title><style face="normal" font="default">Sulfur dioxide exposure enhances Th2 inflammatory responses via activating STAT6 pathway in asthmatic mice</style></title><secondary-title><style face="normal" font="default">Toxicol Lett</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Toxicol Lett</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Sulfur dioxide (SO2) is one of potential risk factors for induction and/or exacerbation of asthma, but the underlying mechanisms are not well understood. In this study, we investigate the role of SO2 in asthma using a classical asthmatic model with allergic airway inflammation by treating C57BL/6 mice with ovalbumin (OVA) and/or 10mg/m(3) SO2. Our results showed that SO2 exposure alone induced slight pathological changes but did not significantly increase inflammatory cell counts, pro-inflammatory cytokine expression, and mucus production in the airway of mice, whereas SO2 exposure in OVA-induced asthmatic mice caused marked pulmonary pathological changes and significantly increased the counts of eosinophil-rich leukocytes compared with OVA alone asthmatic mice. The expression of MUC5AC, TNF-alpha, Th2 cytokines (IL-4, IL-5, and IL-13) and STAT6 was further up-regulated in OVA plus SO2 treated mice compared with OVA alone treated mice. In addition, exposure to SO2 alone markedly elevated STAT6 mRNA levels and hydrogen peroxide (H2O2) content in the lung. These findings suggest that SO2 amplifies Th2 inflammatory responses in OVA-induced asthmatic mice by activating STAT6, which can further induce Th2 cytokine expression. Induction of STAT6 expression might be an important mechanism underlying the increased risk for asthma after environmental exposure</style></abstract><notes><style face="normal" font="default">IS - 1879-3169 (Electronic)IS - 0378-4274 (Linking)LA - engPT - Journal ArticleCO - China -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.toxlet.2017.12.020</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288730">PM:29288730</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Toxicol Lett\20171227-LiX.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Toxicol Lett\20171227-LiX.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Li X</style></custom2><misc3><style face="normal" font="default">10.1016/j.toxlet.2017.12.020</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87302</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tang,L.X.</style></author><author><style face="normal" font="default"> Yang,X.J.</style></author><author><style face="normal" font="default"> Wang,P.P.</style></author><author><style face="normal" font="default"> Ge,W.T.</style></author><author><style face="normal" font="default"> Zhang,J.</style></author><author><style face="normal" font="default"> Guo,Y.L.</style></author><author><style face="normal" font="default"> Lu,J.</style></author><author><style face="normal" font="default"> Tai,J.</style></author><author><style face="normal" font="default"> Zhang,Y.M.</style></author><author><style face="normal" font="default"> Ni,X.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology-Head and Neck Surgery, Beijing Children's Hospital, Capital Medical University, Beijing 100045, China</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of sublingual immunotherapy with Dermatophagoides farinae drops in pre-school and school-age children with allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: The safety and efficacy of sublingual immunotherapy (SLIT) have been confirmed by many studies. However, in China, the research on efficacy and safety in young and older children with allergic rhinitis (AR) is still rare. OBJECTIVE: The aim of this retrospective study is to evaluate the efficacy and safety of SLIT with Dermatophagoides farinae drops in pre-school and school-age children with AR. METHODS: A total of 282 subjects aged 2-13 years with AR received a two-year course of sublingual immunotherapy along with pharmacotherapy. According to the age, patients were defined as the pre-school group (2-6 years old, n=116) and school-age group (7-13 years old, n=166). Total nasal rhinitis symptom scores (TNSS), visual analogue score (VAS) and total medication scores (TMS) were evaluated at four time points: baseline, after SLIT for half a year, one year and two years. The adverse events (AEs) were evaluated at each visit. RESULTS: After two-year SLIT, the four rhinitis symptom scores, TNSS, VAS and TMS scores were significantly lower than baseline (all P&lt;0.05). The comparison of efficacy between one and two-year duration showed no significant difference in global clinical outcomes (all P>0.05). In addition, there were no significant differences between the pre-school and school-age group in TNSS (all P>0.05), VAS (all P>0.05) and TMS scores (P>0.05) after SLIT for half a year, one year and two years. No severe systemic AEs were reported. CONCLUSION: SLIT with D. farinae drops is clinically effective and safe in pre-school and school-age patients with house dust mites (HDMs)-induced AR</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.022</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331618">PM:29331618</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180113-TangLX.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180113-TangLX.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Tang LX</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.022</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87303</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Armentia,A.</style></author><author><style face="normal" font="default"> Martin-Armentia,S.</style></author><author><style face="normal" font="default"> Martin-Armentia,B.</style></author><author><style face="normal" font="default"> Santos-Fernandez,J.</style></author><author><style face="normal" font="default"> Alvarez,R.</style></author><author><style face="normal" font="default"> Madrigal,B.</style></author><author><style face="normal" font="default"> Fernandez-Gonzalez,D.</style></author><author><style face="normal" font="default"> Gayoso,S.</style></author><author><style face="normal" font="default"> Gayoso,M.J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Is eosinophilic esophagitis an equivalent of pollen allergic asthma? Analysis of biopsies and therapy guided by component resolved diagnosis</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Biopsy</style></keyword><keyword><style face="normal" font="default"> Component-resolved diagnosis</style></keyword><keyword><style face="normal" font="default"> Eosinophilic esophagitis</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Peach</style></keyword><keyword><style face="normal" font="default"> Pollen tube</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0301-0546</style></isbn><abstract><style face="normal" font="default">Background Eosinophilic esophagitis (EoE) is characterized by esophageal dysfunction and, histologically, by eosinophilic inflammation. There is not a clear etiologic treatment. Biopsies analysis using plant histology methods may show callose and pollen tubes in the esophageal mucosa. Component-resolved diagnosis (CRD) with microarrays could detect possible allergens involved and indicate an elimination diet and allergen immunotherapy (AIT). Methods One hundred and twenty-nine patients with EoE were tested for environmental and food allergens. CRD, histological and botanical analysis were performed. Clinical scores and endoscopic biopsy were performed every six months for three years. Fifty healthy patients, 50 asthmatics due to pollen, and 53 celiac disease patients were included as comparison groups. CRD-directed AIT was administered in 91 EoE patients and elimination diet in 140 patients (87 EoE and all 53 CD patients). Results CRD detected allergen hypersensitivity in 87.6% of patients with EoE. The predominant allergens were grass group 1 (55%), lipid transfer proteins (LTP) of peach and mugwort, hazelnuts and walnuts. Callose from pollen tubes was found in 65.6% of biopsies. After CRD-guided elimination diet and/or AIT, 101 (78.3%) EoE patients showed significant clinical improvement (p &amp;lt; 0.017) and 97 (75.2%) were discharged (negative biopsy, no symptoms, no medication) without relapse. AIT-treated patients had better outcomes (odds ratio 177.3, 95% CI 16.2</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô1939.0). Conclusion CRD-directed AIT and/or elimination diet was efficient in treating EoE patients and was well tolerated</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.11.001</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.aller.2017.11.001</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180113-ArmentiaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180113-ArmentiaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Armentia A</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.11.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87304</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lv,J.</style></author><author><style face="normal" font="default"> Xiong,Y.</style></author><author><style face="normal" font="default"> Li,W.</style></author><author><style face="normal" font="default"> Cui,X.</style></author><author><style face="normal" font="default"> Cheng,X.</style></author><author><style face="normal" font="default"> Leng,Q.</style></author><author><style face="normal" font="default"> He,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immunology and State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, People's Republic of China</style></auth-address><titles><title><style face="normal" font="default">IL-37 inhibits IL-4/IL-13-induced CCL11 production and lung eosinophilia in murine allergic asthma</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: IL-37 is emerging as an anti-inflammatory cytokine, particularly in innate inflammation. However, the role of IL-37 in Th2-mediated allergic lung inflammation remains uncertain. We sought to determine the role and the underlying mechanisms of IL-37 in the development of house dust mites (HDM)-induced murine asthma model. METHODS: We examined the effect of IL-37 administration during the sensitization or challenge phase on Th2-mediated allergic asthma induced by inhaled HDM. Cellular source of CCL11 and distribution of IL-37 receptors, IL-18Ralpha and IL-1R8, were determined in HDM-exposed lungs. Finally, we examined the effect of IL-37 on CCL11 production and STAT6 activation in different primary lung structural cell types upon IL-4/IL-13 stimulation. RESULTS: IL-37 had no effect on HDM sensitization, but when administrated during the challenge phase, significantly attenuated pulmonary eosinophilia, CCL11 production and airway hyper-reactivity (AHR). Interestingly, IL-37 treatment had no significant effects on lung infiltrating T cells and Th2 cytokine production. Intranasal co-administration of CCL11 reversed the inhibiting effect of IL-37 on HDM-induced pulmonary eosinophilia and AHR. Furthermore, we demonstrated that CCL11 was primarily expressed by fibroblasts and airway smooth muscle cells (AMSC), while IL-37 receptors by tracheobronchial epithelial cells (TEC). In vitro study showed that IL-37 inhibited IL-4/IL-13-induced STAT6 activation and CCL11 production by fibroblasts and AMSC, which was dependent on its direct action on TEC. Moreover, cell-contact was required for the inhibitory effect of IL-37-treated TEC. CONCLUSIONS: IL-37 attenuates HDM-induced asthma, possibly by inhibiting IL-4/IL-13-induced CCL11 production by fibroblasts and AMSC via its direct act on TEC. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1111/all.13395</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319845">PM:29319845</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-LvJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-LvJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Lv J</style></custom2><misc3><style face="normal" font="default">10.1111/all.13395</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87305</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hesse,L.</style></author><author><style face="normal" font="default"> van Ieperen,N.</style></author><author><style face="normal" font="default"> Habraken,C.</style></author><author><style face="normal" font="default"> Petersen,A.H.</style></author><author><style face="normal" font="default"> Korn,S.</style></author><author><style face="normal" font="default"> Smilda,T.</style></author><author><style face="normal" font="default"> Goedewaagen,B.</style></author><author><style face="normal" font="default"> Ruiters,M.H.</style></author><author><style face="normal" font="default"> van der Graaf,A.C.</style></author><author><style face="normal" font="default"> Nawijn,M.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Experimental Pulmonary and Inflammatory Research (EXPIRE), Department of Pathology, Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">Subcutaneous immunotherapy with purified Der p1 and 2 suppresses type-2 immunity in a murine asthma model</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">Allergen-specific immunotherapy can induce long-term suppression of allergic symptoms, reduce medication use and prevent exacerbations of allergic rhinitis and asthma. Current treatment is based on crude allergen extracts, which contain immunostimulatory components such as beta-glucans, chitins and endotoxin. Use of purified or recombinant allergens might therefore increase efficacy of treatment. Here, we test application of purified natural group 1 and 2 allergens from Dermatophagoides pteronyssinus (Der p) for subcutaneous immunotherapy (SCIT) treatment in a house dust mite (HDM) driven mouse model of allergic asthma. HDM-sensitized mice received SCIT with crude HDM extract, a mixture of purified Der p1 and 2 (DerP1/2), or placebo. Upon challenges, we measured specific immunoglobulin responses, allergen-induced ear swelling (ESR), airway hyperresponsiveness (AHR) and inflammation in broncho-alveolar lavage fluid (BAL) and lung tissue. ESR measurement shows suppression of early allergic response in HDM- and DerP1/2-SCIT treated mice. Both HDM-SCIT and DerP1/2-SCIT are able to suppress AHR and eosinophilic inflammation. In contrast, only DerP1/2-SCIT is able to significantly suppress type-2 cytokines in lung tissue and BAL fluid. Moreover, DerP1/2-SCIT treatment is uniquely able suppress CCL20 and showed a trend towards suppression of IL-33, CCL17 and eotaxin levels in lung tissue. Taken together, these data show that purified DerP1/2-SCIT is able to not only suppress AHR and inflammation, but also has superior activity towards suppression of Th2 cells and HDM-induced activation of lung structural cells including airway epithelium. We postulate that treatment with purified natural major allergens derived from HDM will likely increase clinical efficacy of SCIT. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1111/all.13382</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29318623">PM:29318623</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-HesseL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-HesseL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Hesse L</style></custom2><misc3><style face="normal" font="default">10.1111/all.13382</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87306</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kawasaki,A.</style></author><author><style face="normal" font="default"> Ito,N.</style></author><author><style face="normal" font="default"> Murai,H.</style></author><author><style face="normal" font="default"> Yasutomi,M.</style></author><author><style face="normal" font="default"> Naiki,H.</style></author><author><style face="normal" font="default"> Ohshima,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Faculty of Medical Sciences, University of Fukui</style></auth-address><titles><title><style face="normal" font="default">Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, thereby causing IgE-mediated food allergies. OBJECTIVE: We examined whether skin barrier impairment following epicutaneous sensitization exacerbates food allergies. METHODS: BALB/c mice were epicutaneously sensitized by repeated application of ovalbumin (OVA) to MC903-pretreated ear skin for 48 hours weekly and then intragastrically challenged with OVA. After the first oral challenge, the skin barrier was disrupted with topical application of MC903 or by tape-stripping. Mice were monitored for changes in body temperature and the occurrence of diarrhea after undergoing the second oral challenge. Serum levels of mouse mast cell protease-1 (mmcp1) and OVA-specific IgE, IgG1, IgG2a antibodies and OVA-specific IgA levels in intestinal lavage fluid were measured by ELISA. Tissue accumulation of eosinophils was determined histologically. RESULTS: Epicutaneously sensitized mice developed anaphylaxis after intragastric challenge, as evidenced by diarrhea, decreased body temperature and increased serum mmcp1 levels. Skin barrier disruption by MC903 treatment or tape-stripping exacerbated allergic reactions induced by oral challenge. MC903 treatment increased serum baseline and post-challenge mmcp1 levels. Topical pretreatment with dexamethasone alleviated allergic reactions that were exacerbated by MC903-treatement. CONCLUSION: Even after eliminating exposure to the antigen, inflammation from skin barrier disruption can exacerbate the severity of food allergy symptoms. Serum baseline mmcp1 levels might be an effective marker for predicting the severity of antigen-induced allergic symptoms. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/all.13404</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319896">PM:29319896</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-KawasakiA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-KawasakiA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Kawasaki A</style></custom2><misc3><style face="normal" font="default">10.1111/all.13404</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87307</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Soria,I.</style></author><author><style face="normal" font="default"> Lopez-Relano,J.</style></author><author><style face="normal" font="default"> Vinuela,M.</style></author><author><style face="normal" font="default"> Tudela,J.I.</style></author><author><style face="normal" font="default"> Angelina,A.</style></author><author><style face="normal" font="default"> Benito-Villalvilla,C.</style></author><author><style face="normal" font="default"> Diez-Rivero,C.M.</style></author><author><style face="normal" font="default"> Cases,B.</style></author><author><style face="normal" font="default"> Manzano,A.I.</style></author><author><style face="normal" font="default"> Fernandez-Caldas,E.</style></author><author><style face="normal" font="default"> Casanovas,M.</style></author><author><style face="normal" font="default"> Palomares,O.</style></author><author><style face="normal" font="default"> Subiza,J.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Inmunotek, Alcala de Henares, Spain</style></auth-address><titles><title><style face="normal" font="default">Oral myeloid cells uptake allergoids coupled to mannan driving Th1/Treg responses upon sublingual delivery in mice</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Polymerized allergoids coupled to nonoxidized mannan (PM-allergoids) may represent novel vaccines targeting dendritic cells (DCs). PM-allergoids are better captured by DCs than native allergens and favor Th1/Treg cell responses upon subcutaneous injection. Herein we have studied in mice the in vivo immunogenicity of PM-allergoids administered sublingually in comparison to native allergens. METHODS: Three immunization protocols (4-8 weeks long) were used in Balb/c mice. Serum antibody levels were tested by ELISA. Cell responses (proliferation, cytokines and Tregs) were assayed by flow cytometry in spleen and lymph nodes (LNs). Allergen uptake was measured by flow cytometry in myeloid sublingual cells. RESULTS: A quick antibody response and higher IgG2a/IgE ratio was observed with PM-allergoids. Moreover, stronger specific proliferative responses were seen in both submandibular LNs and spleen cells assayed in vitro. This was accompanied by a higher IFNgamma/IL-4 ratio with a quick IL-10 production by submandibular LN cells. An increase of CD4(+) CD25(high) FOXP3(+) Treg cells was detected in LNs and spleen of mice treated with PM-allergoids. These allergoids were better captured than native allergens by antigen presenting (CD45(+) MHC-II(+) ) cells obtained from the sublingual mucosa, including DCs (CD11b(+) ) and macrophages (CD64(+) ). Importantly, all the differential effects induced by PM-allergoids were abolished when using oxidized instead of nonoxidized PM-allergoids. CONCLUSION: Our results demonstrate for the first time that PM-allergoids administered through the sublingual route promote the generation of Th1 and FOXP3(+) Treg cells in a greater extent than native allergens by mechanisms that might well involve their better uptake by oral antigen presenting cells. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1111/all.13396</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319882">PM:29319882</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-SoriaI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-SoriaI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Soria I</style></custom2><misc3><style face="normal" font="default">10.1111/all.13396</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87308</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,X.Y.</style></author><author><style face="normal" font="default"> Ma,T.T.</style></author><author><style face="normal" font="default"> Wang,X.Y.</style></author><author><style face="normal" font="default"> Zhuang,Y.</style></author><author><style face="normal" font="default"> Wang,X.D.</style></author><author><style face="normal" font="default"> Ning,H.Y.</style></author><author><style face="normal" font="default"> Shi,H.Y.</style></author><author><style face="normal" font="default"> Yu,R.L.</style></author><author><style face="normal" font="default"> Yan,D.</style></author><author><style face="normal" font="default"> Huang,H.D.</style></author><author><style face="normal" font="default"> Bai,Y.F.</style></author><author><style face="normal" font="default"> Shan,G.L.</style></author><author><style face="normal" font="default"> Zhang,B.</style></author><author><style face="normal" font="default"> Song,Q.K.</style></author><author><style face="normal" font="default"> Zhang,Y.F.</style></author><author><style face="normal" font="default"> Zhang,T.J.</style></author><author><style face="normal" font="default"> Jia,D.Z.</style></author><author><style face="normal" font="default"> Liu,X.L.</style></author><author><style face="normal" font="default"> Kang,Z.X.</style></author><author><style face="normal" font="default"> Yan,W.J.</style></author><author><style face="normal" font="default"> Yang,B.T.</style></author><author><style face="normal" font="default"> Bao,X.Z.</style></author><author><style face="normal" font="default"> Sun,S.H.</style></author><author><style face="normal" font="default"> Zhang,F.F.</style></author><author><style face="normal" font="default"> Yu,W.H.</style></author><author><style face="normal" font="default"> Bai,C.L.</style></author><author><style face="normal" font="default"> Wei,T.</style></author><author><style face="normal" font="default"> Yang,T.</style></author><author><style face="normal" font="default"> Ma,T.Q.</style></author><author><style face="normal" font="default"> Wu,X.B.</style></author><author><style face="normal" font="default"> Liu,J.G.</style></author><author><style face="normal" font="default"> Du,H.</style></author><author><style face="normal" font="default"> Zhang,L.</style></author><author><style face="normal" font="default"> Yan,Y.</style></author><author><style face="normal" font="default"> Wang,D.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy, Beijing Shijitan Hospital, Capital Medical University</style></auth-address><titles><title><style face="normal" font="default">Prevalence of pollen-induced allergic rhinitis with high pollen exposure in grasslands of northern China</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: The aim of this study was to investigate the prevalence of epidemiologic and physician-diagnosed pollen-induced AR (PiAR) in the grasslands of northern China, and to study the impact of the intensity and time of pollen exposure on PiAR prevalence. METHODS: A multistage, clustered and proportionately stratified random sampling with a field-interviewer administrated survey study was performed together with skin prick tests (SPT) and measurements of the daily pollen count. RESULTS: A total of 6043 subjects completed the study; with a proportion of 32.4% epidemiologic AR and 18.5% PiAR. The prevalence was higher in males than females (19.6% vs 17.4%, P=0.024) but no difference between the two major residential and ethnic groups (Han and Mongolian) was observed. Subjects from urban areas showed higher prevalence of PiAR than rural areas (23.1% vs 14.0%, P&lt;0.001). Most PiAR patients were sensitized to two or more pollens (79.4%) with artemisia, chenopodium, and humulus scandens being the most common pollen types; which were similarly found as the top three sensitizing pollen allergens by SPT. There were significant regional differences in the prevalence of epidemiologic AR (from 18.6% to 52.9%) and PiAR (from 10.5% to 31.4%) among the six areas investigated. PiAR symptoms were positively associated with pollen counts, temperature and precipitation (P&lt;0.05), but negatively with wind speed and pressure P&lt;0.05). CONCLUSION: PiAR prevalence in the investigated region is extremely high due to high seasonal pollen exposure, which was influenced by local environmental and climate conditions. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - China -CO - Singapore -</style></notes><work-type><style face="normal" font="default">10.1111/all.13388</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29322523">PM:29322523</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-WangXY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-WangXY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Wang XY</style></custom2><misc3><style face="normal" font="default">10.1111/all.13388</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87309</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mosges,R.</style></author><author><style face="normal" font="default"> Koch,A.F.</style></author><author><style face="normal" font="default"> Raskopf,E.</style></author><author><style face="normal" font="default"> Singh,J.</style></author><author><style face="normal" font="default"> Shah-Hosseini,K.</style></author><author><style face="normal" font="default"> Hauswald,B.</style></author><author><style face="normal" font="default"> Yarin,Y.</style></author><author><style face="normal" font="default"> Corazza,F.</style></author><author><style face="normal" font="default"> Haazen,L.</style></author><author><style face="normal" font="default"> Pirotton,S.</style></author><author><style face="normal" font="default"> Allekotte,S.</style></author><author><style face="normal" font="default"> Zadoyan,G.</style></author><author><style face="normal" font="default"> Legon,T.</style></author><author><style face="normal" font="default"> Durham,S.R.</style></author><author><style face="normal" font="default"> Shamji,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Medical Statistics, Informatics and Epidemiology (IMSIE), Faculty of Medicine, University of Cologne, Cologne, Germany</style></auth-address><titles><title><style face="normal" font="default">Lolium perenne peptide immunotherapy is well tolerated and elicits a protective B-cell response in seasonal allergic rhinitis patients</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Systemic allergic reactions are a risk for allergen immunotherapy that utilizes intact allergen preparations. We evaluated the safety, efficacy and immune mechanisms of short-course treatment with adjuvant-free Lolium perenne peptides (LPP) following a 6-week dose-escalation protocol. METHODS: In a prospective, dose-escalation study, 61 grass pollen-allergic patients received 2 subcutaneous injections of LPP once weekly for 6 weeks. Safety was assessed evaluating local reactions, systemic reactions and adverse events. The clinical effect of LPP was determined by reactivity to the conjunctival provocation test (CPT). Specific IgE, IgG4, and blocking antibodies were measured at baseline (V1), during (V6) and after treatment (V8). RESULTS: No fatality, serious adverse event or epinephrine use was reported. Mean wheal diameters after injections were &lt;0.6 cm and mean redness diameters &lt;2.5 cm, independent of dose. Transient and mostly mild adverse events were reported in 33 patients. Two patients experienced a grade I and 4 patients a grade II reaction (AWMF classification). At V8, 69.8% of patients became non-reactive to CPT. sIgG4 levels were higher at V6 (8.1-fold, P&lt;0.001) and V8 (12.2-fold, P&lt;0.001) than at V1. The sIgE:sIgG4 ratio decreased at V6 (-54.6%, P&lt;0.001) and V8 (-71.6%, P&lt;0.001) compared to V1. The absolute decrease in IgE-facilitated allergen binding was 18% (P&lt;0.001) at V6 and 25% (P&lt;0.001) at V8. CONCLUSION: Increasing doses of subcutaneous LPP appeared safe, substantially diminished reactivity to CPT and induced blocking antibodies as early as 4 weeks after treatment initiation. The benefit/risk balance of LPP immunotherapy remains to be further evaluated in large studies. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Belgium -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/all.13392</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29322510">PM:29322510</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-MosgesR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-MosgesR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Mosges R</style></custom2><misc3><style face="normal" font="default">10.1111/all.13392</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87310</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Smaldini,P.L.</style></author><author><style face="normal" font="default"> Trejo,F.</style></author><author><style face="normal" font="default"> Cohen,J.L.</style></author><author><style face="normal" font="default"> Piaggio,E.</style></author><author><style face="normal" font="default"> Docena,G.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Instituto de Estudios Inmunologicos y Fisiopatologicos (IIFP), CONICET y Universidad Nacional de La Plata, La Plata</style></auth-address><titles><title><style face="normal" font="default">Systemic IL-2/anti-IL-2Ab complex combined with sublingual immunotherapy suppresses experimental food allergy in mice through induction of mucosal regulatory T cells</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">Therapeutic tolerance restoration has been proven to modify food allergy in patients and animal models and although sublingual immunotherapy (SLIT) has showed promise, combined therapy may be necessary to achieve a strong and long-term tolerance. In this work, we combined SLIT with systemic administration of IL-2 associated with an anti-IL-2 monoclonal antibody (IL-2/anti-IL-2Ab complex or IL-2C) to reverse the IgE-mediated experimental allergy. Balb/c mice were sensitized with cholera toxin and milk proteins and orally challenged with allergen to elicit hypersensitivity reactions. Then, allergic mice were treated with a sublingual administration of very low amounts of milk proteins combined with intraperitoneal injection of low doses of IL-2C. The animals were next re-exposed to allergens and mucosal as well as systemic immunological parameters were assessed in vivo and in vitro. The treatment reduced serum specific IgE, IL-5 secretion by spleen cells and increased IL-10 and TGF-beta in the lamina propria of buccal and duodenal mucosae. We found an augmented frequency of IL-10-secreting CD4(+) CD25(+) Foxp3(+) regulatory T cells (Treg) in the submaxilar lymph nodes and buccal lamina propria. Tregs were sorted, characterized and adoptively transferred to naive mice, which were subsequently sensitized. No allergy was experienced in these mice and we encouragingly discovered a faster and more efficient tolerance induction with the combined therapy compared with SLIT. In conclusion, the combination of two therapeutic strategies rendered Treg-mediated tolerance more efficient compared to individual treatments and reversed the established IgE-mediated food allergy. This approach highlights the ability of IL-2C to expand Tregs, and it may represent a promising disease-modifying therapy for managing food allergy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Argentina -CO - France -</style></notes><work-type><style face="normal" font="default">10.1111/all.13402</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319881">PM:29319881</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-SmaldiniPL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-SmaldiniPL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Smaldini PL</style></custom2><misc3><style face="normal" font="default">10.1111/all.13402</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87311</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Greenhawt,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Section of Allergy and Immunology, Children's Hospital Colorado, University of Colorado School of Medicine</style></auth-address><titles><title><style face="normal" font="default">With tree nut sensitization, take the current when it serves, or lose our ventures</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">Tree nut allergy affects approximately 1.4-2.3%, depending on the study methodology, patient age, and region in which the study was conducted.(1,2) Tree nut allergy can be severe, and tends to persist throughout life.(1,3) Tree nut is not a singular allergen like the other allergens-we use the term "tree nut" to refer to these items, but in essence it can refer to one nut, eight nuts, or per the US Food and Drug Agency classification, on the order of 19 items.(1,4) Older, more conservative practice is to treat one nut as "all nuts", and instruct avoidance of all tree nuts where there is a clinical allergy proven to just one. This is often supported by high rates of co-sensitization, which is high among tree nuts because of structural similarity, and fueled concerns of cross-contamination, proper identification, or labeling confusion.(1,5) This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/all.13383</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319877">PM:29319877</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-GreenhawtM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-GreenhawtM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Greenhawt M</style></custom2><misc3><style face="normal" font="default">10.1111/all.13383</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87312</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Agache,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy and Clinical Immunology, Transylvania University of Brasov, 500112, Brasov, Romania</style></auth-address><titles><title><style face="normal" font="default">EAACI Guidelines on Allergen Immunotherapy - Out With the Old and In With the New</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">Occurring in both developed and developing countries and across all ethnic groups and ages allergic diseases represent a global health problem. During the last few decades, there has been an increase in the prevalence of allergic diseases and it has been predicted that by 2025 half of the entire EU population will be affected [1]. The three major management strategies are avoidance, symptom control by pharmacotherapy and allergen immunotherapy (AIT). By contrast with symptom control by pharmacotherapy AIT aims to modify the immune system via tolerance induction [2] and is potentially able to alter the course of allergic diseases [3]. The potential preventive effect of AIT is currently being explored for pollen [4]. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - EditorialCO - Romania -</style></notes><work-type><style face="normal" font="default">10.1111/all.13393</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319886">PM:29319886</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-AgacheI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-AgacheI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Agache I</style></custom2><misc3><style face="normal" font="default">10.1111/all.13393</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87313</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Akbarshahi,H.</style></author><author><style face="normal" font="default"> Menzel,M.</style></author><author><style face="normal" font="default"> Ramu,S.</style></author><author><style face="normal" font="default"> Mahmutovic,P.I.</style></author><author><style face="normal" font="default"> Bjermer,L.</style></author><author><style face="normal" font="default"> Uller,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Unit of Respiratory Immunopharmacology, Dept. Experimental Medical Science, Lund University, Lund, Sweden</style></auth-address><titles><title><style face="normal" font="default">House dust mite impairs antiviral response in asthma exacerbation models through its effects on TLR3</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Impaired antiviral interferon expression may be involved in asthma exacerbations commonly caused by rhinovirus infections. Allergy is a known risk factor for viral-induced asthma exacerbation, but little is known whether allergens may affect interferon responses. OBJECTIVE: Our hypothesis is that house dust mite (HDM) impairs viral stimulus-induced antiviral signalling. METHODS: Experimental asthma exacerbations were produced in vitro in human bronchial epithelial cells (HBECs) and in mice by using sequential challenges with HDM and a viral infection mimic, Poly(I:C). We examined rhinovirus pattern recognition receptors (PRRs) signalling pathways and potential mechanisms of impaired interferon response. RESULTS: HBECs and mice exposed to HDM prior to Poly(I:C) exhibited a reduced antiviral response compared to Poly(I:C) alone, including reduced IFN-beta, IFN-lambda, TLR3, RIG-I, MDA5, IRF-3 and IRF-7. Heat-inactivation of HDM partially restored the TLR3-induced interferon response in vitro and in vivo. Our HBEC-data further showed that HDM directly affects TLR3 signalling by targeting the receptor glycosylation level. CONCLUSIONS: Direct effects of allergens such as HDM on PRRs can present as potential mechanism for defective antiviral airway responses. Accordingly, therapeutic measures targeting inhibitory effects of allergens on antiviral PRRs may find use as a strategy to boost antiviral response and ameliorate exacerbations in asthmatic patients. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1111/all.13378</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319193">PM:29319193</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-AkbarshahiH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-AkbarshahiH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Akbarshahi H</style></custom2><misc3><style face="normal" font="default">10.1111/all.13378</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87314</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Altrichter,S.</style></author><author><style face="normal" font="default"> Hawro,T.</style></author><author><style face="normal" font="default"> Liedtke,M.</style></author><author><style face="normal" font="default"> Holtappels,G.</style></author><author><style face="normal" font="default"> Bachert,C.</style></author><author><style face="normal" font="default"> Skov,P.S.</style></author><author><style face="normal" font="default"> Maurer,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Charite - Universitatsmedizin Berlin, Department of Dermatology and Allergology, Berlin, Germany</style></auth-address><titles><title><style face="normal" font="default">In chronic spontaneous urticaria, IgE against staphylococcal enterotoxins is common and functional</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Angioedema</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: Chronic spontaneous urticaria (CSU) is a frequent disorder with recurrent itchy wheals and/or angioedema. Despite the known effectiveness of omalizumab therapy, the relevant IgE antigens are largely unknown. Recently, increased rates of elevated levels of IgE towards Staphylococcus aureus enterotoxins (SEs) were described in CSU. AIM: To assess the prevalence and functional relevance of IgE to SEs in CSU. METHOD: We investigated serum levels of IgE against SEs in 49 CSU patients and in 15 CSU patients additional specific IgE to SE components and basophil histamine release (BHR). Sera of15 healthy controls (HCs) served as control group. RESULTS: 25 (51%) of the CSU patients had detectable levels of SE-IgE as compared to 5 (33%) of HCs. Specific IgE to one of the SEs, Staphylococcus enterotoxin B (SEB), was present in 5 (33%) of 15 randomly selected CSU patients vs 3 (20%) of HC. Total IgE serum levels in CSU patients were significantly correlated with SE-IgE (r = 0.52, p&lt;0.001) and SEB-IgE (r = 0.54, p = 0.04) serum concentrations. Interestingly, SEB-IgE levels were strongly correlated with disease activity (UASday) in CSU patients (r=0.657, p=0.01). Furthermore, BHR in response to SEB was significantly higher in basophils loaded with the serum of CSU patients compared to HC (p&lt;0.05) and was clinically correlated with duration of disease (r >0.51, p &lt;0.05). DISCUSSION: IgE against SEs may contribute to the pathogenesis of CSU in a subpopulation of patients Its role and relevance in the pathophysiology of CSU needs to be further analysed. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Belgium -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1111/all.13381</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29315616">PM:29315616</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180109-AltrichterS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180109-AltrichterS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180109, Altrichter S</style></custom2><misc3><style face="normal" font="default">10.1111/all.13381</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87315</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Castan,L.</style></author><author><style face="normal" font="default"> Cheminant,M.A.</style></author><author><style face="normal" font="default"> Colas,L.</style></author><author><style face="normal" font="default"> Brouard,S.</style></author><author><style face="normal" font="default"> Magnan,A.</style></author><author><style face="normal" font="default"> Bouchaud,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">INRA, UR1268, BIA, Nantes, France</style></auth-address><titles><title><style face="normal" font="default">Food allergen-sensitized CCR9(+) lymphocytes enhance airways allergic inflammation in mice</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: The mechanisms of the atopic march, characterized by a natural progression from food and cutaneous allergies to rhinitis and asthma, are still unknown. However, as several organs can be involved, chemokines and their receptors might be implicated in this process and may be instrumental factors. OBJECTIVES: We hypothesized that the T-cell gut-homing receptor CCR9 could be implicated in the evolution of allergic diseases. METHODS: We characterized the immune response and the role of CCR9 in a murine model combining food allergy to wheat gliadin and a model of acute airways inflammation in response to house dust mite. RESULTS: Compared with solely asthmatic-like mice, we demonstrated that the aggravation of pulmonary symptoms in consecutive food and respiratory allergies, characterized by an increase in pulmonary resistance and a higher Th17/ Treg ratio, was abrogated in CCR9 knock-out mice. Moreover, transfer of food-allergic CD4+ T cells from wild-type but not from CCR9-/- aggravated airways inflammation demonstrating that CCR9 is involved in food allergy-enhanced allergic airway inflammation to unrelated allergens. CONCLUSION: Taken together, our results demonstrated a crucial role of the T-cell homing receptor CCR9 in this model and validated its potential for use in the development of therapeutic strategies for allergic diseases. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1111/all.13386</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29315632">PM:29315632</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180109-CastanL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180109-CastanL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180109, Castan L</style></custom2><misc3><style face="normal" font="default">10.1111/all.13386</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87316</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Clausen,M.</style></author><author><style face="normal" font="default"> Jonasson,K.</style></author><author><style face="normal" font="default"> Keil,T.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author><author><style face="normal" font="default"> Sigurdardottir,S.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Children's Hospital, Landspitali University Hospital, Reykjavik, Iceland</style></auth-address><titles><title><style face="normal" font="default">Fish oil in infancy protects against food allergy in Iceland - results from a birth cohort study</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Consumption of oily fish or fish oil during pregnancy, lactation, and infancy has been linked to a reduction in the development of allergic diseases in childhood. METHODS: In an observational study, Icelandic children (n = 1304) were prospectively followed from birth to 2.5 years with detailed questionnaires administered at birth and at one and two years of age, including questions about fish oil supplementation. Children with suspected food allergy were invited for physical examinations, allergic sensitization tests, and a double-blind, placebo-controlled food challenge if the allergy testing or clinical history indicated food allergy. The study investigated the development of sensitization to food and confirmed food allergy according to age and frequency of postnatal fish oil supplementation using proportional hazards modelling. RESULTS: The incidence of diagnosed food sensitization was significantly lower in children who received regular fish oil supplementation (relative risk 0.51, 95% confidence interval 0.32-0.82). The incidence of challenge-confirmed food allergy was also reduced, although not statistically significantly (0.57, 0.30-1.12). Children who began to receive fish oil in their first half year of life were significantly more protected than those who began later (p = 0.045 for sensitization, p = 0.018 for allergy). Indicators of allergy severity decreased with increased fish oil consumption (p = 0.013). Adjusting for parent education and allergic family history did not change the results. CONCLUSION: Postnatal fish oil consumption is associated with decreased food sensitization and food allergies in infants and may provide an intervention strategy for allergy prevention. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Iceland -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13385</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29318622">PM:29318622</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-ClausenM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-ClausenM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Clausen M</style></custom2><misc3><style face="normal" font="default">10.1111/all.13385</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87317</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Curin,M.</style></author><author><style face="normal" font="default"> Garmatiuk,T.</style></author><author><style face="normal" font="default"> Resch-Marat,Y.</style></author><author><style face="normal" font="default"> Chen,K.W.</style></author><author><style face="normal" font="default"> Hofer,G.</style></author><author><style face="normal" font="default"> Fauland,K.</style></author><author><style face="normal" font="default"> Keller,W.</style></author><author><style face="normal" font="default"> Hemmer,W.</style></author><author><style face="normal" font="default"> Vrtala,S.</style></author><author><style face="normal" font="default"> Focke-Tejkl,M.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Immunopathology, Department of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna</style></auth-address><titles><title><style face="normal" font="default">Similar localization of conformational IgE epitopes on the house dust mite allergens Der p 5 and Der p 21 despite limited IgE-cross-reactivity</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rabbits</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Due to high IgE recognition frequency and high allergenic activity, Der p 5 and Der p 21 are clinically important house dust mite (HDM) allergens. The objective of this study was to characterise the immunodominant IgE epitopes of Der p 5 and Der p 21 responsible for their high allergenic activity. METHODS: A panel of 12 overlapping peptides spanning the Der p 5 and Der p 21 sequence were synthesized to search for sequential IgE epitopes by direct testing for allergic patients ' IgE reactivity. Peptide-specific antibodies raised in rabbits were used in inhibition studies for localizing conformational IgE epitopes which were visualized on the surfaces of the allergen structures by molecular modelling. IgE cross-reactivity between the allergens was studied by IgE inhibition studies. RESULTS: Immunodominant IgE epitopes defined by allergic patients' IgE on Der p 5 and Der p 21 were primarily of the conformational, discontinuous type including N- and C-terminal portions of the protein. They could be located on each allergen on one area with similar localization but despite similar structure of the allergens no relevant IgE cross-reactivity could be detected. CONCLUSION: Our study shows that Der p 5 and Der p 21 contain a major conformational IgE epitope-containing area located on similar portions of their structure but they lack relevant IgE cross-reactivity. These data are important for the development of modern allergy vaccines based on defined molecules for allergen-specific immunotherapy of HDM allergy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1111/all.13398</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319884">PM:29319884</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-CurinM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-CurinM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Curin M</style></custom2><misc3><style face="normal" font="default">10.1111/all.13398</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87318</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Apostolovic,D.</style></author><author><style face="normal" font="default"> Da Silva,R.R.</style></author><author><style face="normal" font="default"> Thomas,P.</style></author><author><style face="normal" font="default"> Starkhammar,M.</style></author><author><style face="normal" font="default"> Hamsten,C.</style></author><author><style face="normal" font="default"> van Hage,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine Solna, Immunology and Allergy Unit, Karolinska Institutet and University Hospital, Stockholm, Sweden</style></auth-address><titles><title><style face="normal" font="default">Immunoprofile of alpha-Gal- and B-antigen-specific responses differentiate red meat allergic patients from healthy individuals</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: The Galactose-alpha-1,3-galactose (alpha-Gal) epitope is involved in red meat allergy. As alpha-Gal is structurally similar to the blood group B antigen, we explored the relationship between the immune responses to alpha-Gal- and the B-antigen in red meat allergic patients compared to healthy A/O or B blood donors. METHODS: Sera from 51 red meat allergic patients IgE positive to alpha-Gal and 102 healthy blood donors (51 blood group A/O; 51 blood group B), were included. alpha-Gal and B-antigen specific IgE (ImmunoCAP) and IgG/IgG1-4 (ELISA) responses were determined. Basophil activation tests were performed. RESULTS: Fifteen healthy donors were IgE positive to alpha-Gal, of which 3 had blood group B. The allergic patients had significantly higher alpha-Gal IgE levels compared to the healthy donors. The majority of the allergic patients, but none of the healthy donors, had IgE against the B-antigen. Inhibition studies revealed cross-reactivity between alpha-Gal and the B-antigen. The biological activity of the B-antigen was confirmed by basophil activation tests. Anti-alpha-Gal IgG1 and IgG4 levels were significantly higher in the patients compared to the healthy donors. Moreover, the IgG response to the B-antigen was comparable between the allergic patients and healthy A/O donors. CONCLUSION: Red meat allergic patients showed significantly higher alpha-Gal IgE, IgG1 and IgG4 levels, reflecting a Th2 response, compared to healthy blood donors. Blood group B donors had significantly reduced antibody responses to alpha-Gal, due to similarities with the B-antigen, resulting in a lower risk of sensitization to alpha-Gal and development of red meat allergy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1111/all.13400</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319188">PM:29319188</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-ApostolovicD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-ApostolovicD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Apostolovic D</style></custom2><misc3><style face="normal" font="default">10.1111/all.13400</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87319</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Barbarot,S.</style></author><author><style face="normal" font="default"> Auziere,S.</style></author><author><style face="normal" font="default"> Gadkari,A.</style></author><author><style face="normal" font="default"> Girolomoni,G.</style></author><author><style face="normal" font="default"> Puig,L.</style></author><author><style face="normal" font="default"> Simpson,E.L.</style></author><author><style face="normal" font="default"> Margolis,D.J.</style></author><author><style face="normal" font="default"> de Bruin-Weller,M.</style></author><author><style face="normal" font="default"> Eckert,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Service de Dermatologie, Centre Hospitalier Universitaire de Nantes, Nantes, FranceSanofi, Chilly-Mazarin, France</style></auth-address><titles><title><style face="normal" font="default">Epidemiology of atopic dermatitis in adults: results from an international survey</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: There are gaps in our knowledge of the prevalence of adult atopic dermatitis (AD). OBJECTIVE: To estimate prevalence of AD in adults and by disease severity. METHODS: This international, cross-sectional, web-based survey was performed in the United States, Canada, France, Germany, Italy, Spain, United Kingdom, and Japan. Adult members of online respondent panels were sent a questionnaire for AD identification and severity assessment; demographic quotas ensured population representativeness for each country. A diagnosis of AD required subjects to be positive on the modified UK Working Party/ISAAC criteria and self-report of ever having an AD diagnosis by a physician. The proportion of subjects with AD who reported being treated for their condition was determined and also used to estimate prevalence. Severity scales were Patient-Oriented SCORAD, Patient Oriented Eczema Measure, and Patient Global Assessment. RESULTS: Among participants by region, the point prevalence of adult AD in the overall/treated populations was 4.9%/3.9% in the US, 3.5%/2.6% in Canada, 4.4%/3.5% in EU, and 2.1%/1.5% in Japan. The prevalence was generally lower for males vs females, and decreased with age. Regional variability was observed within countries. Severity varied by scale and region; however, regardless of the scale or region, proportion of subjects reporting severe disease was lower than mild or moderate disease. CONCLUSIONS: Prevalence of adult AD ranged from 2.1% to 4.9% across countries. Severe AD represented a small proportion of the overall AD population regardless of measure or region. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - France -CO - United States -CO - Italy -CO - Spain -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1111/all.13401</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319189">PM:29319189</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-BarbarotS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-BarbarotS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Barbarot S</style></custom2><misc3><style face="normal" font="default">10.1111/all.13401</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87320</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Erbas,B.</style></author><author><style face="normal" font="default"> Jazayeri,M.</style></author><author><style face="normal" font="default"> Lambert,K.A.</style></author><author><style face="normal" font="default"> Katelaris,C.H.</style></author><author><style face="normal" font="default"> Prendergast,L.A.</style></author><author><style face="normal" font="default"> Tham,R.</style></author><author><style face="normal" font="default"> Parrodi,M.J.</style></author><author><style face="normal" font="default"> Davies,J.</style></author><author><style face="normal" font="default"> Newbigin,E.</style></author><author><style face="normal" font="default"> Abramson,M.J.</style></author><author><style face="normal" font="default"> Dharmage,S.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Psychology and Public Health, La Trobe University, Bundoora, Victoria, Australia</style></auth-address><titles><title><style face="normal" font="default">Outdoor pollen is a trigger of child and adolescent asthma ED presentations: a systematic review and meta-analysis</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Aged</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: In the context of increased asthma exacerbations associated with climatic changes such as thunderstorm asthma, interest in establishing the link between pollen exposure and asthma hospital admissions has intensified. Here, we systematically reviewed and performed a meta-analysis of studies on pollen and ED attendance. METHODS: A search for studies with appropriate search strategy in Medline, Embase, Web of Science and CINAHL was conducted. Each study was assessed for quality and risk of bias. The available evidence was summarised both qualitatively and meta-analysed using random effects models when moderate heterogeneity was observed. RESULTS: Fourteen studies were included. The pollen taxa investigated differed between studies, allowing meta-analysis only of the effect of grass pollen. A statistically significant increase in the percentage change in the mean number of asthma ED presentations (MPC) (pooled results from three studies) was observed for an increase in 10 grass pollen grains per cubic meter of exposure 1.88% (95%CI = 0.94%, 2.82%). Time series studies showed positive correlations between pollen concentrations and ED presentations. Age stratified studies found strongest associations in children aged 5 to 17 years old. CONCLUSION: Exposure to ambient grass pollen is an important trigger for childhood asthma exacerbations requiring ED attendance. As pollen exposure is increasingly a problem especially in relation to thunderstorm asthma, studies with uniform measures of pollen and similar analytical methods are necessary to fully understand its impact on human health. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1111/all.13407</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331087">PM:29331087</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180113-ErbasB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180113-ErbasB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Erbas B</style></custom2><misc3><style face="normal" font="default">10.1111/all.13407</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87321</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dubois,A.E.J.</style></author><author><style face="normal" font="default"> Turner,P.J.</style></author><author><style face="normal" font="default"> Hourihane,J.</style></author><author><style face="normal" font="default"> Ballmer-Weber,B.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author><author><style face="normal" font="default"> Chun-Han,C.</style></author><author><style face="normal" font="default"> Gowland,M.H.</style></author><author><style face="normal" font="default"> O'Hagan,S.</style></author><author><style face="normal" font="default"> Regent,L.</style></author><author><style face="normal" font="default"> Remington,B.</style></author><author><style face="normal" font="default"> Schnadt,S.</style></author><author><style face="normal" font="default"> Stroheker,T.</style></author><author><style face="normal" font="default"> Crevel,R.W.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">University Medical Centre Groningen, NLNestle, CHUnilever, UK</style></auth-address><titles><title><style face="normal" font="default">How does dose impact on the severity of food-induced allergic reactions, and can this improve risk assessment for allergenic foods?</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">Quantitative risk assessment for food allergens has made considerable progress in recent years, yet acceptability of its outcomes remains stymied because of the limited extent to which it has been possible to incorporate severity as a variable. Reaction severity, particularly following accidental exposure, depends on multiple factors, related to the allergen, the host and any treatments which might be administered. Some of these factors are plausibly still unknown. Quantitative risk assessment shows that limiting exposure through control of dose reduces the rates of reactions in allergic populations, but its impact on the relative frequency of severe reactions at different doses is unclear. Food challenge studies suggest that the relationship between dose of allergenic food and reaction severity is complex even under relatively controlled conditions. Because of these complexities, epidemiological studies provide very limited insight into this aspect of the dose-response relationship. Emerging data from single-dose challenges suggest that graded food challenges may overestimate the rate of severe reactions. It may be necessary to generate new data (such as those from single dose-challenges) to reliably identify the effect of dose on severity for use in quantitative risk assessment. Success will reduce uncertainty in the susceptible population and improve consumer choice. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Netherlands -CO - United Kingdom -CO - Ireland -CO - Germany -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/all.13405</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331070">PM:29331070</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180113-DuboisAE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180113-DuboisAE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Dubois AE</style></custom2><misc3><style face="normal" font="default">10.1111/all.13405</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87322</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gadermaier,E.</style></author><author><style face="normal" font="default"> Marth,K.</style></author><author><style face="normal" font="default"> Lupinek,C.</style></author><author><style face="normal" font="default"> Campana,R.</style></author><author><style face="normal" font="default"> Hofer,G.</style></author><author><style face="normal" font="default"> Blatt,K.</style></author><author><style face="normal" font="default"> Smiljkovic,D.</style></author><author><style face="normal" font="default"> Roder,U.</style></author><author><style face="normal" font="default"> Focke-Tejkl,M.</style></author><author><style face="normal" font="default"> Vrtala,S.</style></author><author><style face="normal" font="default"> Keller,W.</style></author><author><style face="normal" font="default"> Valent,P.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author><author><style face="normal" font="default"> Flicker,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Immunopathology, Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna General Hospital, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Isolation of a high affinity Bet v 1-specific IgG-derived ScFv from a subject vaccinated with hypoallergenic Bet v 1 fragments</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: Recombinant hypoallergenic allergen derivatives have been used in clinical immunotherapy studies and clinical efficacy seems to be related to the induction of blocking IgG antibodies recognizing the wild type allergens. However, so far no treatment-induced IgG antibodies have been characterized. OBJECTIVE: To clone, express and characterize IgG antibodies induced by vaccination with two hypoallergenic recombinant fragments of the major birch pollen allergen, Bet v 1 in a non-allergic subject. METHODS: A phage-displayed combinatorial single chain fragment (ScFv) library was constructed from blood of the immunized subject and screened for Bet v 1-reactive antibody fragments. ScFvs were tested for specificity and cross-reactivity to native Bet v 1 and related pollen and food allergens and epitope mapping was performed. Germline ancestor genes of the antibody were analyzed with the ImMunoGeneTics (IMGT) database. The affinity to Bet v 1 and cross-reactive allergens was determined by surface plasmon resonance measurements. The ability to inhibit patients' IgE binding to ELISA plate-bound allergens and allergen-induced basophil activation was assessed. RESULTS: A combinatorial ScFv library was obtained from the vaccinated donor after three injections with the Bet v 1 fragments. Despite being almost in germline configuration, ScFv (clone H3-1) reacted with high affinity to native Bet v 1 and homologous allergens, inhibited allergic patients' polyclonal IgE binding to Bet v 1 and partially suppressed allergen-induced basophil activation. CONCLUSION: Immunization with unfolded hypoallergenic allergen derivatives induces high affinity antibodies even in non-allergic subjects which recognize the folded wild-type allergens and inhibit polyclonal IgE binding of allergic patients. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13394</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29315611">PM:29315611</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180109-GadermaierE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180109-GadermaierE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170109, Gadermaier E</style></custom2><misc3><style face="normal" font="default">10.1111/all.13394</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87323</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Simon,H.U.</style></author><author><style face="normal" font="default"> Bieber,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Pharmacology, University of Bern, SwitzerlandDepartment of Dermatology and Allergy, University of Bonn, Germany</style></auth-address><titles><title><style face="normal" font="default">Allergy - Committed to Progress in Allergy and Immunology</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">After more than 8 years, our terms as Co-Editors-in-Chief have now reached an end. We are thankful for having had the privilege to serve the community in this position. We think that we have reached our original goal of increasing the overall quality of the journal (1). The science which is reported every month in Allergy is of high quality and wide interest, largely contributing to the development of the fields of Allergy and Immunology. The impact of the journal is high, as reflected by its present impact factor of 7.36. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Switzerland -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13412</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29330864">PM:29330864</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180113-SimonHU.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180113-SimonHU.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Simon HU</style></custom2><misc3><style face="normal" font="default">10.1111/all.13412</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87324</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Muraro,A.</style></author><author><style face="normal" font="default"> Fernandez-Rivas,M.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author><author><style face="normal" font="default"> Cardona,V.</style></author><author><style face="normal" font="default"> Clark,A.</style></author><author><style face="normal" font="default"> Eller,E.</style></author><author><style face="normal" font="default"> Hourihane,J.O.</style></author><author><style face="normal" font="default"> Jutel,M.</style></author><author><style face="normal" font="default"> Sheikh,A.</style></author><author><style face="normal" font="default"> Agache,I.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author><author><style face="normal" font="default"> Angier,L.</style></author><author><style face="normal" font="default"> Ballmer-Weber,B.</style></author><author><style face="normal" font="default"> Bilo,M.B.</style></author><author><style face="normal" font="default"> Bindslev-Jensen,C.</style></author><author><style face="normal" font="default"> Camargo,C.A.,Jr.</style></author><author><style face="normal" font="default"> Cianferoni,A.</style></author><author><style face="normal" font="default"> DunnGalvin,A.</style></author><author><style face="normal" font="default"> EIgenmann,P.A.</style></author><author><style face="normal" font="default"> Halken,S.</style></author><author><style face="normal" font="default"> Hoffmann-Sommergruber,K.</style></author><author><style face="normal" font="default"> Lau,S.</style></author><author><style face="normal" font="default"> Nilsson,C.</style></author><author><style face="normal" font="default"> Poulsen,L.K.</style></author><author><style face="normal" font="default"> Rueff,F.</style></author><author><style face="normal" font="default"> Spergel,J.</style></author><author><style face="normal" font="default"> Sturm,G.</style></author><author><style face="normal" font="default"> Timmermans,F.</style></author><author><style face="normal" font="default"> Torres,M.J.</style></author><author><style face="normal" font="default"> Turner,P.</style></author><author><style face="normal" font="default"> van Ree,R.</style></author><author><style face="normal" font="default"> Wickman,M.</style></author><author><style face="normal" font="default"> Worm,M.</style></author><author><style face="normal" font="default"> Clare Mills,E.N.</style></author><author><style face="normal" font="default"> Roberts,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Food Allergy Referral Centre Veneto Region, Department of Women and Child Health, Padua General University Hospital, Italy</style></auth-address><titles><title><style face="normal" font="default">The urgent need for a harmonized severity scoring system for acute allergic reactions</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">The accurate assessment and communication of the severity of acute allergic reactions is important to patients, clinicians, researchers, the food industry, public health and regulatory authorities. Severity has different meanings to different stakeholders with patients and clinicians rating the significance of particular symptoms very differently. Many severity scoring systems have been generated, most focusing on the severity of reactions following exposure to a limited group of allergens. They are heterogeneous in format, none has used an accepted developmental approach and none has been validated. Their wide range of outcome formats has led to difficulties with interpretation and application. Therefore there is a persisting need for an appropriately developed and validated severity scoring system for allergic reactions that works across the range of allergenic triggers and addresses the needs of different stakeholder groups. We propose a novel approach to develop and then validate a harmonized scoring system for acute allergic reactions, based on a data-driven method that is informed by clinical and patient experience and other stakeholders' perspectives. We envisage two formats: (i) a numerical score giving a continuum from mild to severe reactions that is clinically meaningful and is useful for allergy healthcare professionals and researchers; and (ii) a three grade based ordinal format that is simple enough to be used and understood by other professionals and patients. Testing of reliability and validity of the new approach in a range of settings and populations will allow eventual implementation of a standardized scoring system in clinical studies and routine practice. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Italy -CO - Spain -CO - Germany -CO - United Kingdom -CO - Denmark -CO - Ireland -CO - Poland -CO - Romania -CO - Switzerland -CO - Austria -CO - Sweden -CO - Netherlands -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/all.13408</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331045">PM:29331045</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180113-MuraroA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180113-MuraroA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Muraro A</style></custom2><misc3><style face="normal" font="default">10.1111/all.13408</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87325</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Siroux,V.</style></author><author><style face="normal" font="default"> Ballardini,N.</style></author><author><style face="normal" font="default"> Soler,M.</style></author><author><style face="normal" font="default"> Lupinek,C.</style></author><author><style face="normal" font="default"> Boudier,A.</style></author><author><style face="normal" font="default"> Pin,I.</style></author><author><style face="normal" font="default"> Just,J.</style></author><author><style face="normal" font="default"> Nadif,R.</style></author><author><style face="normal" font="default"> Anto,J.M.</style></author><author><style face="normal" font="default"> Melen,E.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author><author><style face="normal" font="default"> Wickman,M.</style></author><author><style face="normal" font="default"> Bousquet,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">University Grenoble Alpes, Inserm, CNRS, IAB, 38000, Grenoble, France</style></auth-address><titles><title><style face="normal" font="default">The asthma-rhinitis multimorbidity is associated with IgE polysensitization in adolescents and adults</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Adult</style></keyword><keyword><style face="normal" font="default"> Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: Children with multimorbid asthma and rhinitis show IgE polysensitization to several allergen sources. This association remain poorly studied in adolescents and adults using defined allergen molecules. We investigated IgE sensitization patterns towards a broad panel of aeroallergen components in adults and adolescents with a focus on individuals with asthma and rhinitis multimorbidity. METHODS: IgE reactivity to 64 microarrayed aeroallergen molecules was determined with the MeDALL-chip in samples from the French EGEA study (n=840, age=40.7+/-17.1) and the Swedish population-based birth cohort BAMSE (n=786, age=16+/-0.26). The age- and sex-adjusted associations between the number of IgE-reactive allergen molecules (>/=0.3 ISU) and the asthma-rhinitis phenotypes were assessed using a negative binomial model. RESULTS: Groups representing four phenotypes were identified: no asthma-no rhinitis (A-R-; 30% in EGEA and 54% in BAMSE), asthma alone (A+R-; 11% and 8%), rhinitis alone (A-R+; 15% and 24%), and asthma-rhinitis (A+R+; 44% and 14%). The numbers of IgE-reactive aeroallergen molecules significantly differed between phenotypes (median in A-R-, A+R-, A-R+ and A+R+: 0, 1, 2 and 7 in EGEA and 0, 0, 3, and 5 in BAMSE). As compared to A-R- subjects, the adjusted ratio of the mean number of IgE-reactive molecules was higher in A+R+ than in A+R- or A-R+ (10.0, 5.4 and 5.0 in EGEA and 7.2, 0.7 and 4.8 in BAMSE). CONCLUSION: The A+R+ phenotype combined the sensitization pattern of both the A-R+ and A+R-phenotypes. This multimorbid polysensitized phenotype seems to be generalizable to various ages and allergenic environments and may be associated with specific mechanisms. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - France -CO - Sweden -CO - United Kingdom -CO - Austria -CO - Spain -</style></notes><work-type><style face="normal" font="default">10.1111/all.13410</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331026">PM:29331026</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180113-SirouxV.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180113-SirouxV.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Siroux V</style></custom2><misc3><style face="normal" font="default">10.1111/all.13410</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87326</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Worm,M.</style></author><author><style face="normal" font="default"> Francuzik,W.</style></author><author><style face="normal" font="default"> Renaudin,J.M.</style></author><author><style face="normal" font="default"> Bilo,M.B.</style></author><author><style face="normal" font="default"> Cardona,V.</style></author><author><style face="normal" font="default"> Hofmeier,K.S.</style></author><author><style face="normal" font="default"> Kohli,A.</style></author><author><style face="normal" font="default"> Bauer,A.</style></author><author><style face="normal" font="default"> Christoff,G.</style></author><author><style face="normal" font="default"> Cichocka-Jarosz,E.</style></author><author><style face="normal" font="default"> Hawranek,T.</style></author><author><style face="normal" font="default"> Hourihane,J.O.</style></author><author><style face="normal" font="default"> Lange,L.</style></author><author><style face="normal" font="default"> Mahler,V.</style></author><author><style face="normal" font="default"> Muraro,A.</style></author><author><style face="normal" font="default"> Papadopoulos,N.G.</style></author><author><style face="normal" font="default"> Pfohler,C.</style></author><author><style face="normal" font="default"> Poziomkowska-Gesicka,I.</style></author><author><style face="normal" font="default"> Rueff,F.</style></author><author><style face="normal" font="default"> Spindler,T.</style></author><author><style face="normal" font="default"> Treudler,R.</style></author><author><style face="normal" font="default"> Fernandez-Rivas,M.</style></author><author><style face="normal" font="default"> Dolle,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Allergology, Charite - Universitatsmedizin Berlin, Chariteplatz 1, 10117, Berlin</style></auth-address><titles><title><style face="normal" font="default">Factors increasing the risk for a severe reaction in anaphylaxis: An analysis of Data from The European Anaphylaxis Registry</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Betablockers</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> Mastocytosis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Registries</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Preventive measures to decrease the frequency and intensity of anaphylactic events are essential to provide optimal care for allergic patients. Aggravating factors may trigger or increase the severity of anaphylaxis and therefore need to be recognized and avoided. OBJECTIVE: To identify and prioritize factors associated with an increased risk of developing severe anaphylaxis. METHODS: Data from the Anaphylaxis Registry (122 centers in 11 European countries) was used in logistic regression models considering existing severity grading systems, elicitors, and symptoms to identify the relative risk of factors on the severity of anaphylaxis. RESULTS: We identified higher age and concomitant mastocytosis (OR: 3.1, CI: 2.6 - 3.7) as the most important predictors for an increased risk of severe anaphylaxis. Vigorous physical exercise (OR: 1.5, CI: 1.3 - 1.7), male sex (OR: 1.2, CI: 1.1 - 1.3), and psychological burden (OR: 1.4, CI: 1.2 - 1.6) were more often associated with severe reactions. Additionally, intake of beta-blockers (OR: 1.9, CI: 1.5 - 2.2) and ACE-I (OR: 1.28, CI: 1.05, 1.51) in temporal proximity to allergen exposition were identified as important factors in logistic regression analysis. CONCLUSION: Our data suggest it may be possible to identify patients who require intensified preventive measures due to their relatively higher risk for severe anaphylaxis by considering endogenous and exogenous factors. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - France -CO - Italy -CO - Spain -CO - Switzerland -CO - Bulgaria -CO - Poland -CO - Austria -CO - Ireland -CO - Greece -</style></notes><work-type><style face="normal" font="default">10.1111/all.13380</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29318637">PM:29318637</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-WormM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-WormM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170110, Worm M</style></custom2><misc3><style face="normal" font="default">10.1111/all.13380</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87327</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Flores,K.J.</style></author><author><style face="normal" font="default"> McCleary,N.</style></author><author><style face="normal" font="default"> Nwaru,B.I.</style></author><author><style face="normal" font="default"> Stoddart,A.</style></author><author><style face="normal" font="default"> Sheikh,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Asthma UK Centre for Applied Research, Centre for Medical Informatics, Usher Institute of Population Health Sciences and Informatics, The University of Edinburgh, UK</style></auth-address><titles><title><style face="normal" font="default">Diagnostic accuracy, risk assessment, and cost-effectiveness of component-resolved diagnostics for food allergy: a systematic review</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Registries</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Component-resolved diagnostics (CRD) are promising tools for diagnosing food allergy, offering the potential to determine specific phenotypes and to develop patient-tailored risk profiles. Nevertheless, the diagnostic accuracy of these tests varies across studies; thus, their clinical utility remains unclear. Therefore, we synthesized the evidence from studies investigating the diagnostic accuracy, risk assessment ability, and cost-effectiveness of CRD for food allergy. METHODS: We systematically searched 10 electronic databases and four clinical trial registries for studies published January 2000-February 2017. The quality of included studies was assessed using QUADAS-2. Due to heterogeneity, we narratively synthesized the evidence. RESULTS: Eleven studies met inclusion criteria, altogether recruiting 1,098 participants. The food allergies investigated were cow's milk, hen's egg, peanut, hazelnut, and shrimp. The components with the highest diagnostic accuracy for each allergen, along with their sensitivity-specificity pairs, were: Bos d 4 for cow's milk (62.0% and 87.5%), Gal d 1 for hen's egg (84.2% and 89.8% for heated egg, and 60.6% and 97.1% for raw egg), Ara h 2 for peanut (80.3% and 95.1%), Cor a 14 for hazelnut (100% and 93.8%), and Lit v 1 for shrimp (82.8% and 56.3%) allergy. CONCLUSION: Selected components of cow's milk, hen's egg, peanut, hazelnut, and shrimp allergen showed high specificity, but lower sensitivity. However, few studies exist for each component, and studies vary widely regarding the cut-off values used, making it challenging to synthesize findings across studies. Further research is needed to determine clinically appropriate cut-off values, risk assessment abilities, and cost-effectiveness of CRD approaches. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United Kingdom -CO - Canada -CO - Sweden -CO - Finland -</style></notes><work-type><style face="normal" font="default">10.1111/all.13399</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319184">PM:29319184</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-FloresKJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-FloresKJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">201801210, Flores KJ</style></custom2><misc3><style face="normal" font="default">10.1111/all.13399</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87328</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Davila,I.</style></author><author><style face="normal" font="default"> Dominguez-Ortega,J.</style></author><author><style face="normal" font="default"> Navarro Pulido,A.M.</style></author><author><style face="normal" font="default"> Alonso,A.</style></author><author><style face="normal" font="default"> Antolin-Amerigo,D.</style></author><author><style face="normal" font="default"> Gonzalez-Mancebo,E.</style></author><author><style face="normal" font="default"> Martin,G.C.</style></author><author><style face="normal" font="default"> Nunez-Acevedo,B.</style></author><author><style face="normal" font="default"> Prior,N.</style></author><author><style face="normal" font="default"> Reche,M.</style></author><author><style face="normal" font="default"> Rosado,A.</style></author><author><style face="normal" font="default"> Ruiz-Hornillos,J.</style></author><author><style face="normal" font="default"> Sanchez,M.C.</style></author><author><style face="normal" font="default"> Torrecillas,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Department, University Hospital of Salamanca, Salamanca, Spain</style></auth-address><titles><title><style face="normal" font="default">Consensus document on dog and cat allergy</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Inhalant allergen</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">The prevalence of sensitisation to dogs and cats varies by country, exposure time and predisposition to atopy. It is estimated that, 26% of European adults coming to the clinic for suspected allergy to inhalant allergens are sensitised to cats and 27% to dogs. This document is intended to be a useful tool for clinicians involved in the management of people with dog or cat allergy. It was prepared from a consensus process based on the RAND/UCLA method. Following a literature review, it proposes various recommendations concerning the diagnosis and treatment of these patients, grounded in evidence and clinical experience. The diagnosis of dog and cat allergy is based on a medical history and physical examination that are consistent with each other, and is confirmed with positive results on specific IgE skin tests. Sometimes, especially in polysensitised patients, molecular diagnosis is strongly recommended. Although the most advisable measure would be to avoid the animal, this is often impossible and associated with a major emotional impact. Furthermore, indirect exposure to allergens occurs in environments in which animals are not present. Immunotherapy is emerging as a potential solution to this problem, although further supporting studies are needed. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1111/all.13391</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29318625">PM:29318625</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-DavilaI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-DavilaI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170110, Davila I</style></custom2><misc3><style face="normal" font="default">10.1111/all.13391</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87329</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fazlollahi,M.</style></author><author><style face="normal" font="default"> Chun,Y.</style></author><author><style face="normal" font="default"> Grishin,A.</style></author><author><style face="normal" font="default"> Wood,R.A.</style></author><author><style face="normal" font="default"> Burks,A.W.</style></author><author><style face="normal" font="default"> Dawson,P.</style></author><author><style face="normal" font="default"> Jones,S.M.</style></author><author><style face="normal" font="default"> Leung,D.Y.M.</style></author><author><style face="normal" font="default"> Sampson,H.A.</style></author><author><style face="normal" font="default"> Sicherer,S.H.</style></author><author><style face="normal" font="default"> Bunyavanich,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Genetics and Genomic Sciences and Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, USA</style></auth-address><titles><title><style face="normal" font="default">Early-life gut microbiome and egg allergy</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> genetics</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Gut microbiota may play a role in egg allergy. We sought to examine the association between early-life gut microbiota and egg allergy. METHODS: We studied 141 children with egg allergy and controls from the multi-center Consortium of Food Allergy Research study. At enrollment (age 3 to 16 months), fecal samples were collected and clinical evaluation, egg specific IgE measurement, and egg skin prick test were performed. Gut microbiome was profiled by 16S rRNA sequencing. Analyses for the primary outcome of egg allergy at enrollment, and the secondary outcomes of egg sensitization at enrollment and resolution of egg allergy by age 8 years, were performed using Quantitative Insights into Microbial Ecology (QIIME), Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt), and Statistical Analysis of Metagenomic Profiles (STAMP). RESULTS: Compared to controls, increased alpha diversity and distinct taxa (PERMANOVA P=5.0x10(-4) ) characterized the early-life gut microbiome of children with egg allergy. Genera from the Lachnospiraceae, Streptococcaceae, and Leuconostocaceae families were differentially abundant in children with egg allergy. Predicted metagenome functional analyses showed differential purine metabolism by the gut microbiota of egg allergic subjects (Kruskal Wallis Padj =0.021). Greater gut microbiome diversity and genera from Lachnospiraceae and Ruminococcaceae were associated with egg sensitization (PERMANOVA P = 5.0x10(-4) ). Among those with egg allergy, there was no association between early-life gut microbiota and egg allergy resolution by age 8 years. CONCLUSION: The distinct early-life gut microbiota in egg allergic and egg-sensitized children identified by our study may point to targets for preventive or therapeutic intervention. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/all.13389</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29318631">PM:29318631</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180110-FazlollahiM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180110-FazlollahiM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170110, Fazlollahi M</style></custom2><misc3><style face="normal" font="default">10.1111/all.13389</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87331</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pascual Perez,A.I.</style></author><author><style face="normal" font="default"> Mendez,S.A.</style></author><author><style face="normal" font="default"> Segarra,C.O.</style></author><author><style face="normal" font="default"> Espin,J.B.</style></author><author><style face="normal" font="default"> Jimenez,T.S.</style></author><author><style face="normal" font="default"> Bousono,G.C.</style></author><author><style face="normal" font="default"> Diaz Martin,J.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Area de Gestion Clinica de Pediatria, Hospital Universitario Central de Asturias, Oviedo, Espana.</style></auth-address><titles><title><style face="normal" font="default">[Attitudes towards cow's milk protein allergy management by spanish gastroenterologist]</style></title><secondary-title><style face="normal" font="default">An Pediatr (Barc)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">An Pediatr (Barc)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Food allergy is an increasing health problem in the developed world. Cow's milk protein is the main cause of food allergy in infants. Without an appropriate diagnostic workup, there is a high risk of both over- and underdiagnosis and therefore, over and undertreatment. The objective of our study was to analyze the variability in cow's milk protein allergy (CMPA) management by pediatric gastroenterologists in Spain. METHODS: A fifty item questionnaire, including open and closed items in a Likert's scale from 0 to 5, was drafted and distributed through the Spanish Society for Pediatric Gastroenterology, Hepatology and Nutrition (SEGHNP) e-mail list. RESULTS: Seventy-three questionnaires were received back out of 321. Only 3 of the items achieved concordance greater than 90%. Thirty-three percent considered oral challenge to be necessary for the diagnosis of CMPA under any circumstance. Twenty-five percent considered that symptom improvement after cow's milk removal was enough for the diagnosis. Oral challenge was performed at home by 83.5% in non-IgE mediated cases. Extensively hydrolyzed casein formulas were the treatment of choice for 69.9%. Soy formulas were the last option. Almost all respondents were aware of the existence of clinical guidelines on CMPA, being European Society of Pediatric Gastroenterology, Hepatology and Nutrition guidelines the most followed (64.4%). Twenty-three percent considered that their knowledge about allergy was inadequate. CONCLUSIONS: Although CMPA is a prevalent condition that pediatric gastroenterologists have been treating for decades, we found a huge variability on its management. There is potential for improvement in this field among pediatric gastroenterologist in the future</style></abstract><notes><style face="normal" font="default">IS - 1695-9531 (Electronic)IS - 1695-4033 (Linking)LA - spaPT - English AbstractPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.anpedi.2017.10.015</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29329877">PM:29329877</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\An Pediatr (Barc)\20180109-PascualPerezAI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\An Pediatr (Barc)\20180109-PascualPerezAI.pdf</url></text-urls><related-urls><url ppv-ref="no">presto - Eng. ed. su ISS</url></related-urls></urls><custom2><style face="normal" font="default">20180109, Pascual Perez AI</style></custom2><misc3><style face="normal" font="default">10.1016/j.anpedi.2017.10.015</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87341</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jha,A.</style></author><author><style face="normal" font="default"> Ryu,M.H.</style></author><author><style face="normal" font="default"> Ojo,O.O.</style></author><author><style face="normal" font="default"> Bews,H.J.</style></author><author><style face="normal" font="default"> Carlson,J.C.</style></author><author><style face="normal" font="default"> Schwartz,J.</style></author><author><style face="normal" font="default"> Basu,S.</style></author><author><style face="normal" font="default"> Wong,C.S.</style></author><author><style face="normal" font="default"> Halayko,A.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Departments of Physiology and Pathophysiology, University of Manitoba, Winnipeg, MB, Canada</style></auth-address><titles><title><style face="normal" font="default">Prophylactic benefits of systemically delivered simvastatin treatment in a house dust mite challenged murine model of allergic asthma</style></title><secondary-title><style face="normal" font="default">Br J Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Pharmacol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND AND PURPOSE: Systemically delivered statins can blunt airway inflammation in ovalbumin-challenged mice; however, in asthma clinical trials the beneficial effects of introducing oral statins are not compelling. We aim to reconcile this discrepancy using a clinically relevant murine model of allergic asthma, and by including a prophylactic study arm. EXPERIMENTAL APPROACH: Adult mice were: 1) challenged with house dust mite (HDM) alone or with subcutaneous (s.c.) simvastatin for two weeks; or 2) also treated with simvastatin for one week prior to HDM challenge. We assayed lung function, inflammatory cell influx and cytokine profile, goblet cell abundance, and simvastatin concentration in serum, lung lavage and tissue. KEY RESULTS: Ultrahigh performance liquid chromatography-tandem mass spectrometry revealed that pharmacologically active simvastatin reached peak serum concentration after 8h, but declined rapidly. Prophylactic treatment doubled peak serum simvastatin and repeated s.c. delivery established stable serum levels, but simvastatin was undetectable in the lungs. Both simvastatin treatment arms suppressed indices of HDM-induced airway inflammation and goblet cell hyperplasia, but this was significantly greater with prophylactic therapy, in particular to inhibit neutrophil and eosinophil influx, and cytokine accumulation. Conversely, neither acute nor prophylactic delivery of simvastatin prevented HDM challenge-induced airway hyperreactivity. CONCLUSION AND IMPLICATIONS: Systemically administered simvastatin accumulates in the blood, but not in lung tissues, and reduces leukocyte influx and associated lung inflammation. Prophylactic therapy has the greatest anti-inflammatory effects, but as observed in human clinical trials, systemic simvastatin therapy does not prevent allergic airway hyperreactivity</style></abstract><notes><style face="normal" font="default">IS - 1476-5381 (Electronic)IS - 0007-1188 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1111/bph.14140</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29318574">PM:29318574</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Pharmacol\20180110-JhaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Pharmacol\20180110-JhaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Jha A</style></custom2><misc3><style face="normal" font="default">10.1111/bph.14140</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87344</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Abuelezz,S.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pharmacology Department, Faculty of Medicine, Ain-Shams University, Abbasia, Cairo, EgyptPharmacology Department, Faculty of Medicine, Ain-Shams University, Abbasia, Cairo, Egypt</style></auth-address><titles><title><style face="normal" font="default">Nebivolol attenuates oxidative stress and inflammation in a guinea pig model of ovalbumin-induced asthma: a possible mechanism for its favorable respiratory effects</style></title><secondary-title><style face="normal" font="default">Can J Physiol Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Can J Physiol Pharmacol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">An experimental model of ovalbumin (OVA) induced asthma was used to assess the effects of nebivolol, the third-generation selective beta1-adrenergic receptor blocker, on airway reactivity, lung inflammation, and oxidative stress markers. The asthma induction protocol was done by OVA sensitization and challenge. Guinea pigs were classified into control, asthmatic, or asthmatic receiving nebivolol either 7.5 or 15 mg.kg(-1).day(-1) orally. At the end of the study respiratory, the anti-inflammatory and antioxidative effects of nebivolol were assessed. The asthmatic group exhibited a significant increase in early and late airway resistance, airway hyperreactivity to histamine, total and absolute leucocytic count, tumor necrosis factor-alpha, and interleukin-6 in bronchoalveolar lavage fluid and lung lipid peroxidation and a significant decrease in superoxide dismutase and glutathione compared to the control group. Additionally, there was a significant decrease in lung endothelial nitric oxide synthase (eNOS) and a significant increase in inducible nitric oxide synthase (iNOS) mRNA expression compared to the control group. The high dose of nebivolol counteracted the increased airway resistance induced by OVA, whereas it had no effect on airway hyperresponsiveness. Moreover, nebivolol exhibited significant anti-inflammatory and antioxidant effects and restored the altered levels of eNOS and iNOS compared to the asthmatic group. Collectively, these results suggest a beneficial effect of nebivolol in asthma</style></abstract><notes><style face="normal" font="default">IS - 1205-7541 (Electronic)IS - 0008-4212 (Linking)LA - engPT - Journal ArticleCO - Egypt -</style></notes><work-type><style face="normal" font="default">10.1139/cjpp-2017-0230</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29319332">PM:29319332</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180110, Abuelezz SA</style></custom2><misc3><style face="normal" font="default">10.1139/cjpp-2017-0230</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87345</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Flanigan,C.</style></author><author><style face="normal" font="default"> Sheikh,A.</style></author><author><style face="normal" font="default"> DunnGalvin,A.</style></author><author><style face="normal" font="default"> Brew,B.K.</style></author><author><style face="normal" font="default"> Almqvist,C.</style></author><author><style face="normal" font="default"> Nwaru,B.I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Asthma UK Centre for Applied Research, Centre for Medical Informatics, Usher Institute of Population Health Sciences and Informatics, The University of Edinburgh, Edinburgh, UKSchool of Health Sciences, University of Tampere, Finland</style></auth-address><titles><title><style face="normal" font="default">Prenatal maternal psychosocial stress and offspring's asthma and allergic disease: a systematic review and meta-analysis</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword><keyword><style face="normal" font="default"> Violence</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: Prenatal maternal stress may influence offspring's atopic risk through sustained cortisol secretion resulting from activation of the hypothalamic-pituitary-axis (HPA), leading to Th2-biased cell differentiation in the fetus. We undertook a systematic review and meta-analysis investigating the relationship between prenatal maternal psychosocial stress and risk of asthma and allergy in the offspring. METHODS: We searched 11 electronic databases from 1960 to 2016, search the grey literature, and contacted experts in the field. Type of stress indicator included mood disorders, anxiety, exposure to violence, bereavement and socio-economic problems occurring during pregnancy, both objectively or subjectively measured. We included all possible asthma and IgE-mediated allergy outcomes. We conducted random-effects meta-analyses to synthesize the data. RESULTS: We identified 9,779 papers of which 30 studies (enrolling >6 million participants) satisfied inclusion criteria. The quality of 25 studies was moderate, four were strong, and one was weak. Maternal exposure to any type of stressors was associated with an increased risk of offspring atopic eczema/dermatitis (OR 1.34, 95%CI 1.22-1.47), allergic rhinitis (OR 1.30, 95%CI 1.04-1.62), wheeze (OR 1.34, 95%CI 1.16-1.54) and asthma (OR 1.15, 95%CI 1.04-1.27). Exposure to anxiety and depression had strongest effect compared to other stressors. Exposure during the third trimester had the greatest impact compared to first and second trimesters. The increased risk was stronger for early-onset and persistent than for late-onset wheeze. Bereavement of a child (HR 1.28, 95%CI 1.10-1.48) or a spouse (HR 1.40, 95%CI 1.03-1.90) increased the risk of offspring asthma. CONCLUSIONS: Exposure to prenatal maternal psychosocial stress was associated with increased risk, albeit modestly, of asthma and allergy in the offspring. The pronounced risk during the third trimester may represent cumulative stress exposure throughout pregnancy rather than trimester-specific effect. Our findings may represent a causal effect or a result of inherent biases in studies, particularly residual confounding. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Ireland -CO - Sweden -CO - Finland -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13091</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331049">PM:29331049</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20180113-FlaniganC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20180113-FlaniganC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Flanigan C</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13091</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87346</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Venkataraman,D.</style></author><author><style face="normal" font="default"> Erlewyn-Lajeunesse,M.</style></author><author><style face="normal" font="default"> Kurukulaaratchy,R.J.</style></author><author><style face="normal" font="default"> Potter,S.</style></author><author><style face="normal" font="default"> Roberts,G.</style></author><author><style face="normal" font="default"> Matthews,S.</style></author><author><style face="normal" font="default"> Arshad,S.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">University Hospitals Southampton NHS Foundation Trust, UK</style></auth-address><titles><title><style face="normal" font="default">Prevalence and longitudinal trends of food allergy during childhood and adolescence: results of the Isle of Wight Birth Cohort study</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="8" Month="1" Year="2018">2018/1/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: The prevalence and time trends of food allergy change during childhood depending on the age of the child and the type of food. OBJECTIVE: To study prevalence and longitudinal trends in food allergy from birth to 18 years in an unselected birth cohort in the Isle of Wight. METHOD: Information on food allergy was collected at ages 1, 2, 4, 10 and 18 years from the Isle of Wight Birth Cohort (n = 1456). Skin prick testing (SPT) was performed at the age of 1 and 2 years in symptomatic children. At 4, 10 and 18 years of age, participants were tested to a panel of food and aero-allergens. Food allergy was diagnosed based on the criteria: symptoms suggestive of a typical IgE mediated reaction and reaction &lt;4 hours following exposure to a known food allergen. McNemar's test was used to determine significance of changes in prevalence over time. RESULTS: The prevalence of food allergy remained relatively constant in early childhood (5.3%, 4.4% and 5.0% at 1, 2 and 4 years respectively), with significant decline at 10 years (2.3%, p&lt;0.001 versus 4 years) followed by significant rise at 18 years (4%, p=0.02 versus 10 years). Cow's milk (1.6-3.5%) and egg (1.1-1.4%) were the most common allergens in the first 10 years with peanut (1%) and tree-nuts (0.5%) becoming more prevalent beyond 10 years. Fruit and wheat allergy were less common at 10 years, and shellfish and kiwi emerged during adolescence. The prevalence of food allergy plus positive SPT were 1.3%, 0.8%, 0.8%, 0.9% and 2.2% at 1, 2, 4, 10 and 18 years respectively. CONCLUSION: Food allergy is highly prevalent in infancy with partial resolution during late childhood. However, a number of children acquire new food allergy during adolescence resulting in a relatively higher prevalence at 18 years. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13088</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29315919">PM:29315919</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20180108-VenkataramanD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20180108-VenkataramanD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180108, Venkataraman D</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13088</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87347</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Blank,S.</style></author><author><style face="normal" font="default"> Bilo,M.B.</style></author><author><style face="normal" font="default"> Ollert,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Center of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, Munich</style></auth-address><titles><title><style face="normal" font="default">Component-resolved diagnostics to direct in venom immunotherapy: important steps towards precision medicine</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Honeybee</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">Stings of Hymenoptera can induce IgE-mediated systemic and even fatal allergic reactions. Venom-specific immunotherapy (VIT) is the only disease-modifying and curative treatment of venom allergy. However, choosing the correct venom for VIT represents a necessary prerequisite for efficient protection against further anaphylactic sting reactions after VIT. In the past, therapeutic decisions based on the measurement of specific IgE (sIgE) levels to whole venom extracts were not always straightforward, especially when the patient was not able to identify the culprit insect. In the last years, the increasing knowledge about the molecular structure and relevance of important venom allergens and their availability as recombinant allergens, devoid of cross-reactive carbohydrate determinants, resulted in the development of an advanced component-resolved diagnostics (CRD) approach in venom allergy. Already to date, CRD has increased the sensitivity of sIgE detection and enabled the discrimination between primary sensitization and cross-reactivity, particularly in patients with sensitization to both honeybee and vespid venom. Hence, CRD in many patients improves the selection of the appropriate immunotherapeutic intervention. Moreover, the detailed knowledge about sensitization profiles on a molecular level might open new options to identify patients who are at increased risk for side effects or not to respond to immunotherapy. Therefore, increasing potential of CRD becomes evident, to direct therapeutic decisions in a personalized and patient-tailored manner. Reviewed here are the state of the art options, recent developments and future perspectives of CRD of Hymenoptera venom allergy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Italy -CO - Luxembourg -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13090</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331065">PM:29331065</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20180113-BlankS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20180113-BlankS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Blank S</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13090</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87348</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dantzer,J.A.</style></author><author><style face="normal" font="default"> Wood,R.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pediatric Allergy and Immunology Department of Pediatrics, John Hopkins University School of Medicine, Baltimore, MDDivision of Pediatric Allergy and Immunology Department of Pediatrics, John Hopkins University School of Medicine, Baltimore, MD</style></auth-address><titles><title><style face="normal" font="default">The Use of Omalizumab in Allergen Immunotherapy</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Inhalant allergen</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="5" Month="1" Year="2018">2018/1/5</year></dates><abstract><style face="normal" font="default">Although omalizumab (anti-IgE) is currently only approved for the treatment of asthma and chronic idiopathic urticaria, it has also been studied as an off-label treatment for numerous allergic conditions, including use as an adjunct to allergen immunotherapy in the treatment of allergic rhinitis, asthma, venom hypersensitivity, and food allergy. We conducted a review of publications involving the use of omalizumab with allergen immunotherapy, by searching PubMed with key search terms of "omalizumab" and "immunotherapy." Omalizumab has been used in combination with inhalant allergen immunotherapy for the treatment of seasonal allergic rhinitis and co-morbid asthma. While there have been no randomized controlled trials evaluating the addition of omalizumab to venom IT, several case reports and small patient series have been published on the use of omalizumab with venom IT. Omalizumab has been used in conjunction with oral immunotherapy for the treatment of milk, peanut, and egg, as well as other foods in multi-allergen protocols. In conclusion, omalizumab used in conjunction with immunotherapy has shown promising results, especially in the reduction of adverse reactions. At this stage, larger, randomized, placebo-controlled trials are needed to better identify those patients who would benefit the most from the addition of omalizumab to immunotherapy, as well as optimal dosing strategies and duration of treatment. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13084</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29315922">PM:29315922</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20180105-DantzerJA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20180105-DantzerJA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180105, Dantzer JA</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13084</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87349</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Venter,C.</style></author><author><style face="normal" font="default"> Groetch,M.</style></author><author><style face="normal" font="default"> Netting,M.</style></author><author><style face="normal" font="default"> Meyer,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Children's Hospital Colorado, University of Colorado, in-FLAME Global Network, Research Group of the Worldwide Universities Network (WUN)Department Paediatrics, Imperial College, London, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">A patient specific approach to developing an exclusion diet to manage food allergy in infants and children</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword></keywords><dates><year Day="8" Month="1" Year="2018">2018/1/8</year></dates><abstract><style face="normal" font="default">Food allergy is becoming increasingly common in infants and young children. This paper set out to explain the different factors that should be taken into account during an individualized allergy consultation: Foods to avoid and degree of avoidance, suitable alternatives, self-management skills, co-and cross-reactive allergens and novel allergens alongside the role of the industry in allergen avoidance, importance of nutritional aspects of the diet and the future directions that nutritional guidance make take. Allergy management advice should be individualized to provide a patient specific approach. Changes in the management of food allergies have in particular occurred in nut, milk and egg allergies over the past few years. There has also been a progressive increase in our understanding of cross-reactivity between different foods and also food and aero-allergens. A patient specific approach of allergen avoidance should consider factors relating to industry and the environment such as food and nutrition literacy, threshold levels, cross contact/contamination and safe eating away from home. Increasing migration and travel has also led to exposure of unfamiliar foods. As understanding improves on individual allergens and threshold levels, food labels and food labeling laws are affected. Allergy specialist dietitians should also keep up to date with the latest information on nutrition, the gut microbiome and the immune system to incorporate nutrition strategies in a dietetic consultation using an evidence-based approach. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13087</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29315948">PM:29315948</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20180108-VenterC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20180108-VenterC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180108, Venter C</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13087</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87350</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pickett,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Toxin Science Limited, Wrexham, LL12 7DT, UK</style></auth-address><titles><title><style face="normal" font="default">Can botulinum toxin cause anaphylaxis after an aesthetic treatment?</style></title><secondary-title><style face="normal" font="default">Clin Exp Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1365-2230 (Electronic)IS - 0307-6938 (Linking)LA - engPT - LetterCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/ced.13342</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29314163">PM:29314163</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Dermatol\20180104-PickettA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Dermatol\20180104-PickettA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Pickett A</style></custom2><misc3><style face="normal" font="default">10.1111/ced.13342</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87352</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Herrmann,I.</style></author><author><style face="normal" font="default"> Gotovina,J.</style></author><author><style face="normal" font="default"> Fazekas-Singer,J.</style></author><author><style face="normal" font="default"> Fischer,M.B.</style></author><author><style face="normal" font="default"> Hufnagl,K.</style></author><author><style face="normal" font="default"> Bianchini,R.</style></author><author><style face="normal" font="default"> Jensen-Jarolim,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Comparative Medicine, The Interuniversity Messerli Research Institute, University of Veterinary Medicine Vienna, Medical University Vienna and University Vienna, Veterinarplatz 1, 1210, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Canine macrophages can like human macrophages be in vitro activated toward the M2a subtype relevant in allergy</style></title><secondary-title><style face="normal" font="default">Dev Comp Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Dev Comp Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">The M2a subtype of macrophages plays an important role in human immunoglobulin E (IgE-mediated allergies) and other Th2 type immune reactions. In contrast, very little is known about these cells in the dog. Here we describe an in-vitro method to activate canine histiocytic DH82cells and primary canine monocyte-derived macrophages (MDMs) toward the M2a macrophages using human cytokines. For a side-by-side comparison, we compared the canine cells to human MDMs, and the human monocytic cell line U937 activated towards M1-and M2a cells on the cellular and molecular level. In analogy to activated human M2a cells, canine M2a, differentiated from both DH82 and MDMs, showed an increase in CD206 surface receptor expression compared to M1. Interestingly, canine M2a, but not M1 derived from MDM, upregulated the high-affinity IgE receptor (FcepsilonRI). Transcription levels of M2a-associated genes (IL10, CCL22, TGFbeta, CD163) showed a diverse pattern between the human and dog species, whereas M1 genes (IDO1, CXCL11, IL6, TNFalpha) were similarly upregulated in canine and human M1-cells (cell lines and MDMs). We suggest that our novel in vitro method will be suitable in comparative allergology studies focussing on macrophages</style></abstract><notes><style face="normal" font="default">IS - 1879-0089 (Electronic)IS - 0145-305X (Linking)LA - engPT - Journal ArticleCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1016/j.dci.2018.01.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29329953">PM:29329953</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Dev Comp Immunol\20180110-HermannI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Dev Comp Immunol\20180110-HermannI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Hermann I</style></custom2><misc3><style face="normal" font="default">10.1016/j.dci.2018.01.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87365</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Huang,B.Z.</style></author><author><style face="normal" font="default"> Le Marchand,L.</style></author><author><style face="normal" font="default"> Haiman,C.A.</style></author><author><style face="normal" font="default"> Monroe,K.R.</style></author><author><style face="normal" font="default"> Wilkens,L.R.</style></author><author><style face="normal" font="default"> Zhang,Z.F.</style></author><author><style face="normal" font="default"> Setiawan,V.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA</style></auth-address><titles><title><style face="normal" font="default">Atopic allergic conditions and pancreatic cancer risk: Results from the Multiethnic Cohort Study</style></title><secondary-title><style face="normal" font="default">Int J Cancer</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Cancer</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">Previous case-control studies have suggested that atopic allergic conditions (AACs) are inversely associated with pancreatic cancer, but this relationship has not been supported in many prospective settings. In this study, we investigated the influence of AACs (asthma, hay fever, or allergy) and the treatment of these conditions on pancreatic cancer risk among participants of the Multiethnic Cohort Study (MEC). AACs and antihistamine use were assessed via a baseline questionnaire when participants joined the MEC in 1993-1996. Risk ratios (RRs) and 95% confidence intervals (CIs) for pancreatic cancer incidence by AACs and antihistamines were calculated using Cox regression, adjusting for age, sex, ethnicity, education, smoking status, family history of pancreatic cancer, body mass index, diabetes, and alcohol intake. We further evaluated associations among subgroups defined by age, sex, ethnicity, follow-up time, and known pancreatic cancer risk factors. During an average 16-year follow-up, 1,455 incident cases of pancreatic cancer were identified among 187,226 white, African American, Latino, Japanese American, and Native Hawaiian men and women. AACs (RR 1.00, 95% CI 0.88-1.12) and antihistamines (RR 0.92, 95% CI 0.78-1.07) were not clearly associated with pancreatic cancer incidence. While these associations were also null for most subgroups, we did observe protective associations of AACs (RR 0.74, 95% CI 0.56-0.98) and antihistamines (RR 0.66, 95% CI 0.45-0.96) among the oldest participants (70+). Our results, in agreement with past prospective studies, suggest that AACs are not associated with pancreatic cancer in general, but the observed protective associations among the oldest age group may warrant future investigation</style></abstract><notes><style face="normal" font="default">IS - 1097-0215 (Electronic)IS - 0020-7136 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/ijc.31241</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29314003">PM:29314003</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Cancer\20180104-HuangBZ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Cancer\20180104-HuangBZ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Huang BZ</style></custom2><misc3><style face="normal" font="default">10.1002/ijc.31241</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87370</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Asai,Y.</style></author><author><style face="normal" font="default"> Eslami,A.</style></author><author><style face="normal" font="default"> van Ginkel,C.D.</style></author><author><style face="normal" font="default"> Akhabir,L.</style></author><author><style face="normal" font="default"> Wan,M.</style></author><author><style face="normal" font="default"> Yin,D.</style></author><author><style face="normal" font="default"> Ellis,G.</style></author><author><style face="normal" font="default"> Ben-Shoshan,M.</style></author><author><style face="normal" font="default"> Marenholz,I.</style></author><author><style face="normal" font="default"> Martino,D.</style></author><author><style face="normal" font="default"> Ferreira,M.A.</style></author><author><style face="normal" font="default"> Allen,K.</style></author><author><style face="normal" font="default"> Mazer,B.</style></author><author><style face="normal" font="default"> de Groot,H.</style></author><author><style face="normal" font="default"> de Jong,N.W.</style></author><author><style face="normal" font="default"> Gerth van Wijk,R.</style></author><author><style face="normal" font="default"> Dubois,A.E.J.</style></author><author><style face="normal" font="default"> Grosche,S.</style></author><author><style face="normal" font="default"> Ashley,S.</style></author><author><style face="normal" font="default"> Ruschendorf,F.</style></author><author><style face="normal" font="default"> Kalb,B.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author><author><style face="normal" font="default"> Nothen,M.M.</style></author><author><style face="normal" font="default"> Lee,Y.A.</style></author><author><style face="normal" font="default"> Chin,R.</style></author><author><style face="normal" font="default"> Cheuk,S.</style></author><author><style face="normal" font="default"> Hoffman,J.</style></author><author><style face="normal" font="default"> Jorgensen,E.</style></author><author><style face="normal" font="default"> Witte,J.S.</style></author><author><style face="normal" font="default"> Melles,R.B.</style></author><author><style face="normal" font="default"> Hong,X.</style></author><author><style face="normal" font="default"> Wang,X.</style></author><author><style face="normal" font="default"> Hui,J.</style></author><author><style face="normal" font="default"> Musk,A.W.B.</style></author><author><style face="normal" font="default"> Hunter,M.</style></author><author><style face="normal" font="default"> James,A.L.</style></author><author><style face="normal" font="default"> Koppelman,G.H.</style></author><author><style face="normal" font="default"> Sandford,A.J.</style></author><author><style face="normal" font="default"> Clarke,A.E.</style></author><author><style face="normal" font="default"> Daley,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Dermatology, Department of Medicine, Queen's University, Kingston ON, Canada and Division of Experimental Medicine, Department of Medicine, McGill University, Montreal, QC, Canada</style></auth-address><titles><title><style face="normal" font="default">Canadian genome-wide association study and meta-analysis confirm HLA as a risk factor for peanut allergy independent of asthma</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="8" Month="1" Year="2018">2018/1/8</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Canada -CO - Germany -CO - Australia -CO - Netherlands -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.047</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29325868">PM:29325868</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180105-AsaiY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180105-AsaiY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180105, Asai Y</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.047</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87371</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kronborg,C.</style></author><author><style face="normal" font="default"> Pumar,M.</style></author><author><style face="normal" font="default"> Gillman,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">The first case of methemoglobinemia associated with omalizumab</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Omalizumab</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.11.037</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.11.037</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180112, Kronborg C</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.11.037</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87373</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Albuhairi,S.</style></author><author><style face="normal" font="default"> Sare,T.</style></author><author><style face="normal" font="default"> Lakin,P.</style></author><author><style face="normal" font="default"> El Khoury,K.</style></author><author><style face="normal" font="default"> Crestani,E.</style></author><author><style face="normal" font="default"> Schneider,L.C.</style></author><author><style face="normal" font="default"> Anzaldi,R.</style></author><author><style face="normal" font="default"> Patterson,A.</style></author><author><style face="normal" font="default"> Rachid,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">Systemic Reactions in Pediatric Patients Receiving Standardized Allergen Subcutaneous Immunotherapy with and without Seasonal Dose-áAdjustment</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword><keyword><style face="normal" font="default"> Systemic reaction</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">The 2003 Joint Task Force on Practice Parameters recommended standardizing allergen subcutaneous immunotherapy (SCIT). Data from longitudinal surveillance survey in North America reported a systemic reaction (SR) rate of 0.1% to 0.2% of injection visits. The rate of SR to standardized SCIT in pediatric patients has not been well evaluated. The objective of this study was to evaluate the rate of SRs to standardized SCIT in pediatric patients aged 5 to 18 years in a single tertiary care center in the United States. A retrospective chart review was conducted in 2 groups: group 1 started SCIT within a period extending from January 2009 to June 2012, whereas group 2 started SCIT within a period extending from January 2013 to June 2016. The protocol was modified in group 2 such that updosing and maintenance doses were adjusted in the spring for tree and grass pollen and in the fall for weed pollen. There were a total of 128 patients in group 1 and 118 patients in group 2. The rate of SR was 0.429% in group 1 and 0.364% in group 2, which was not significant. There was no difference in the severity of SR in the 2 groups with no-fatal or near-fatal SR noted. Asthma was a significant risk factor in the younger age subgroup aged 5 to 11 years. Standardized SCIT appears to be associated with an SR rate of 0.429% to 0.364% of visits in pediatric patients. Protocol modification did not lead to a significant drop in SR. Larger multicenter studies are required to further evaluate the rate of SRs from standardized SCIT</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.11.040</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.11.040</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180112, Albuhairi S</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.11.040</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87374</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lind,C.</style></author><author><style face="normal" font="default"> Skaarup,S.H.</style></author><author><style face="normal" font="default"> Lorentz,A.</style></author><author><style face="normal" font="default"> Hoffmann,H.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Diseases and Allergy, Aarhus University Hospital, Denmark</style></auth-address><titles><title><style face="normal" font="default">Basophil testing with CD63 in pollen sensitised patients is independent of the circadian clock</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Denmark -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.048</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29330012">PM:29330012</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180109-LindC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180109-LindC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180109, Lind C</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.048</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87378</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Noh,G.</style></author><author><style face="normal" font="default"> Kang,S.H.</style></author><author><style face="normal" font="default"> Lee,K.</style></author><author><style face="normal" font="default"> Kim,W.J.</style></author><author><style face="normal" font="default"> Han,C.W.</style></author><author><style face="normal" font="default"> Choi,I.B.</style></author><author><style face="normal" font="default"> Ha,C.W.</style></author><author><style face="normal" font="default"> Noh,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Rush Immunotherapy Using IFN-Gamma for Aspirin in Acute Coronary Syndrome: Case Report</style></title><secondary-title><style face="normal" font="default">J Allergy Ther</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Allergy Ther</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">complications</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Aspirin plays a key role in the secondary prevention of atherothrombotic events and thrombotic complications after stent implantation and aspirin sensitivity is a limitation for the implantation of bare-metal and drug-eluting coronary stents. Several desensitization protocols have been described. In this report, desensitization by introducing IFN-gamma as an immunomodulatory adjuvant was successful for the patients who required early invasive management and the prompt administration of aspirin but failed the classical desensitization by showing allergic symptoms and signs during desensitization.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Korea -CO - United States -</style></notes><work-type><style face="normal" font="default">10.4172/2155-6121.1000269</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.4172/2155-6121.1000269</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Ther\20171127-NohG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Ther\20171127-NohG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171127, Noh G</style></custom2><misc3><style face="normal" font="default">10.4172/2155-6121.1000269</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87379</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kitani,T.</style></author><author><style face="normal" font="default"> Maruyama,S.</style></author><author><style face="normal" font="default"> Aoishi,K.</style></author><author><style face="normal" font="default"> Nishida,N.</style></author><author><style face="normal" font="default"> Ogawa,H.</style></author><author><style face="normal" font="default"> Abe,Y.</style></author><author><style face="normal" font="default"> Hayashi,Y.</style></author><author><style face="normal" font="default"> Yamashita,M.</style></author><author><style face="normal" font="default"> Hato,N.</style></author></authors></contributors><titles><title><style face="normal" font="default">Suppressive Effect of a Thioamide-Related Compound SH-2251 on a Murine Allergic Rhinitis Model</style></title><secondary-title><style face="normal" font="default">J Allergy Ther</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Allergy Ther</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Background: SH-2251 inhibits IL-5 production and type2 airway inflammation in a murine bronchial asthma model. However, the therapeutic effect of SH-2251 on allergic rhinitis (AR) has not been tested. We investigated whether or not SH-2251 could improve the nasal symptoms and inflammation in the nasal mucosa of a murine model of AR.Methods: AR was induced via intraperitoneal injection of ovalbumin (OVA) followed by daily intranasal challenge with OVA. SH-2251 (10 mg/kg) or vehicle (DMSO+Tween80) was administered orally once a day in the same period as the nasal challenge. Nasal symptoms were evaluated by counting the number of sneezing and nasal rubbing events on days 14, 17, 21, 28 and 35. On day 35, the levels of Il4, Il5, Il13, Ifn? and Il1rl1 mRNA in the nasal mucosa were examined. The histological findings were examined on day 36.Results: The numbers of sneezing and nasal rubbing events were significantly decreased by the administration of SH-2251. Both eosinophil infiltration and the hickness of the nasal mucosa were improved in the SH-2251- administered mice compared that in vehicle-treated control mice. The mRNA expression of Il5, Il13 and Il1rl1 in the nasal mucosa was significantly decreased in the SH-2251-treated group compared to the vehicle group.Conclusion: These results suggest that SH-2251 may be a new therapeutic candidate for AR. In addition, SH-2251 might improve the pathogenesis of type2 chronic inflammation by targeting the IL-33 signaling via the inhibition of Il1rl1 expression.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Japan -</style></notes><work-type><style face="normal" font="default">10.4172/2155-6121.1000267</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.4172/2155-6121.1000267</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Ther\20171023-KitaniT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Ther\20171023-KitaniT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171023, Kitani T</style></custom2><misc3><style face="normal" font="default">10.4172/2155-6121.1000267</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87380</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Porchetta,A.</style></author><author><style face="normal" font="default"> Ippodrino,R.</style></author><author><style face="normal" font="default"> Marini,B.</style></author><author><style face="normal" font="default"> Caruso,A.</style></author><author><style face="normal" font="default"> Caccuri,F.</style></author><author><style face="normal" font="default"> Ricci,F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Chemistry, University of Rome , Tor Vergata, Via della Ricerca Scientifica, 00133 Rome, Italy</style></auth-address><titles><title><style face="normal" font="default">Programmable Nucleic Acid Nanoswitches for the Rapid, Single-Step Detection of Antibodies in Bodily Fluids</style></title><secondary-title><style face="normal" font="default">J Am Chem Soc</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Chem Soc</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">Antibody detection plays a pivotal role in the diagnosis of pathogens and monitoring the success of vaccine immunization. However, current serology techniques require multiple, time-consuming washing and incubation steps, which limit their applicability in point-of-care (POC) diagnostics and high-throughput assays. We developed here a nucleic acid nanoswitch platform able to instantaneously measure immunoglobulins of type G and E (IgG and IgE) levels directly in blood serum and other bodily fluids. The system couples the advantages of target-binding induced colocalization and nucleic acid conformational-change nanoswitches. Due to the modular nature of the recognition platform, the method can potentially be applied to the detection of any antibody for which an antigen can be conjugated to a nucleic acid strand. In this work we show the sensitive, fast and cost-effective detection of four different antibodies and demonstrate the possible use of this approach for the monitoring of antibody levels in HIV+ patients immunized with AT20 therapeutic vaccine</style></abstract><notes><style face="normal" font="default">IS - 1520-5126 (Electronic)IS - 0002-7863 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1021/jacs.7b09347</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29313682">PM:29313682</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Chem Soc\20180109-PorchettaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Chem Soc\20180109-PorchettaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180109, Porchetta A</style></custom2><misc3><style face="normal" font="default">10.1021/jacs.7b09347</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87381</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Alissafi,T.</style></author><author><style face="normal" font="default"> Kourepini,E.</style></author><author><style face="normal" font="default"> Simoes,D.C.M.</style></author><author><style face="normal" font="default"> Paschalidis,N.</style></author><author><style face="normal" font="default"> Aggelakopoulou,M.</style></author><author><style face="normal" font="default"> Sparwasser,T.</style></author><author><style face="normal" font="default"> Boon,L.</style></author><author><style face="normal" font="default"> Hammad,H.</style></author><author><style face="normal" font="default"> Lambrecht,B.N.</style></author><author><style face="normal" font="default"> Panoutsakopoulou,V.</style></author></authors></contributors><auth-address><style face="normal" font="default">Cellular Immunology Laboratory, Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece</style></auth-address><titles><title><style face="normal" font="default">Osteopontin Promotes Protective Antigenic Tolerance against Experimental Allergic Airway Disease</style></title><secondary-title><style face="normal" font="default">J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="12" Month="1" Year="2018">2018/1/12</year></dates><abstract><style face="normal" font="default">In the context of inflammation, osteopontin (Opn) is known to promote effector responses, facilitating a proinflammatory environment; however, its role during antigenic tolerance induction is unknown. Using a mouse model of asthma, we investigated the role of Opn during antigenic tolerance induction and its effects on associated regulatory cellular populations prior to disease initiation. Our experiments demonstrate that Opn drives protective antigenic tolerance by inducing accumulation of IFN-beta-producing plasmacytoid dendritic cells, as well as regulatory T cells, in mediastinal lymph nodes. We also show that, in the absence of TLR triggers, recombinant Opn, and particularly its SLAYGLR motif, directly induces IFN-beta expression in Ag-primed plasmacytoid dendritic cells, which renders them extra protective against induction of allergic airway disease upon transfer into recipient mice. Lastly, we show that blockade of type I IFNR prevents antigenic tolerance induction against experimental allergic asthma. Overall, we unveil a new role for Opn in setting up a tolerogenic milieu boosting antigenic tolerance induction, thus leading to prevention of allergic airway inflammation. Our results provide insight for the future design of immunotherapies against allergic asthma</style></abstract><notes><style face="normal" font="default">IS - 1550-6606 (Electronic)IS - 0022-1767 (Linking)LA - engPT - Journal ArticleCO - Greece -CO - Germany -CO - Belgium -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.4049/jimmunol.1701345</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29330321">PM:29330321</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol\20180112-Alisaffi.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol\20180112-Alisaffi.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180112, Alisaffi T</style></custom2><misc3><style face="normal" font="default">10.4049/jimmunol.1701345</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87385</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,W.</style></author><author><style face="normal" font="default"> Zeng,Q.</style></author><author><style face="normal" font="default"> Zhou,L.</style></author><author><style face="normal" font="default"> Luo,R.</style></author><author><style face="normal" font="default"> Dong,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China</style></auth-address><titles><title><style face="normal" font="default">Association of leptin with disease severity and inflammation indicators in Chinese obese children with allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">BACKGROUND: The prevalence of both obesity and allergic diseases in children has increased over the last several decades. However, the direct relationship between diverse allergic diseases and obesity has varied in different studies. Therefore, we aimed to examine the effect of obesity on the incidence and severity of allergic rhinitis (AR) and the possible key inflammation mediators during AR. METHODS: A total of 3,126 healthy students (without chronic diseases) were recruited from 14 randomly selected secondary schools in Guangzhou, China. Body mass index (BMI), waist circumference (WC), waist-to-height ratio (WHR) and body fat percentage (PBF) were measured and compared. The effect of obesity indicators and leptin level (exposures) on the incidence (primary outcome) and severity of AR (secondary outcomes) were analyzed. Inflammatory markers were detected and compared among groups. RESULTS: The symptom score (9.5+/-3.1 vs 8.2+/-3.5, P&lt;0.05) and medication score (3.6+/-1.6 vs 2.9+/-1.8, P&lt;0.05) were significantly higher in obese children with AR than in non-obese children with AR. After adjusted for potential confounders, multiple linear regression analysis showed that the serum leptin concentration was significantly correlated with the levels of T help (TH) 2 cytokines (coefficient, 0.48[95%CI, 0.05-0.91]), TH17 cytokines (coefficient, 0.39[95%CI, 0.11-0.89]), regulatory T cell cytokines (IL-10, coefficient, -0.43[95%CI, -0.02-0.65];TGF-beta, coefficient, -0.65[95%CI, -0.06-1.35]) in patients with AR. CONCLUSIONS: Our study shows that obesity exacerbates inflammation and contributes to disease severity in AR. Our study provides evidence that leptin was involved in enhanced TH inflammation as well as the accumulation and activation of inflammatory cells in obese children with AR. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12856</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29314270">PM:29314270</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-LiuW.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-LiuW.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Liu W</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12856</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87386</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Muller-Rompa,S.E.K.</style></author><author><style face="normal" font="default"> Markevych,I.</style></author><author><style face="normal" font="default"> Hose,A.J.</style></author><author><style face="normal" font="default"> Loss,G.</style></author><author><style face="normal" font="default"> Wouters,I.M.</style></author><author><style face="normal" font="default"> Genuneit,J.</style></author><author><style face="normal" font="default"> Braun-Fahrlander,C.</style></author><author><style face="normal" font="default"> Horak,E.</style></author><author><style face="normal" font="default"> Boznanski,A.</style></author><author><style face="normal" font="default"> Heederik,D.</style></author><author><style face="normal" font="default"> von Mutius,E.</style></author><author><style face="normal" font="default"> Heinrich,J.</style></author><author><style face="normal" font="default"> Ege,M.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dr von Hauner Children's Hospital, LMU Munich, Munich, Germany</style></auth-address><titles><title><style face="normal" font="default">An approach to the asthma-protective farm effect by geocoding: good farms and better farms</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">BACKGROUND: The highly consistent association of growing up on a farm with a reduced asthma risk has so far been attributed to direct farm exposure. In contrast, geographical determinants of the larger environment have never been assessed. In this study, the effects of proximity to farms and environmental variables in relation to the residential address on asthma and atopy were assessed. METHODS: Addresses of 2,265 children of the Bavarian arm of the GABRIELA-study were converted into geocodes. Proximity to the nearest cow farm was calculated, and environmental characteristics were derived from satellite data or terrestrial monitoring. Bacterial diversity in mattress dust samples was assessed in 501 children by sequencing of the 16S rRNA amplicons. Logistic regression models were used to calculate associations between outcomes and exposure variables. RESULTS: Asthma and atopy were inversely associated with presence of a farm within a radius of maximum 100m.The environmental variables greenness, tree cover, soil sealing, altitude, air pollution differed not only between farm and non-farm children, but also between farm children with and without another farm nearby. The latter distinction revealed strong associations with characteristics of traditional farms including a broader diversity of microbial exposure, which mainly contributed to the protective effect on asthma. In non-farm children, the protective effect of a farm nearby was completely explained by consumption of farm milk. CONCLUSIONS: Clustering of farms within a neighborhood of 100m is strongly associated with the protective effect on asthma and may represent a more traditional style of farming with broader microbial exposure. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - United States -CO - Netherlands -CO - Switzerland -CO - Austria -CO - Poland -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12861</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29314275">PM:29314275</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-MullerRompaSE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-MullerRompaSE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170104, Muller-Rompa SE</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12861</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87387</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Aranda,C.S.</style></author><author><style face="normal" font="default"> Cocco,R.R.</style></author><author><style face="normal" font="default"> Pierotti,F.F.</style></author><author><style face="normal" font="default"> Mallozi,M.</style></author><author><style face="normal" font="default"> Franco,J.M.</style></author><author><style face="normal" font="default"> Porto,A.C.</style></author><author><style face="normal" font="default"> Goudouris,E.</style></author><author><style face="normal" font="default"> Moraes,L.</style></author><author><style face="normal" font="default"> Rosario,N.A.</style></author><author><style face="normal" font="default"> Wandalsen,N.F.</style></author><author><style face="normal" font="default"> Pastorino,A.C.</style></author><author><style face="normal" font="default"> Sarinho,E.</style></author><author><style face="normal" font="default"> Sano,F.</style></author><author><style face="normal" font="default"> Chavarria,M.L.</style></author><author><style face="normal" font="default"> Borres,M.P.</style></author><author><style face="normal" font="default"> Sole,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Universidade Federal de Sao Paulo, Sao Paulo, SP, Brazil</style></auth-address><titles><title><style face="normal" font="default">Increased sensitization to several allergens over a 12-year period in Brazilian children</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">The prevalence of allergic sensitization and diseases, especially in the last decades, appears to have increased worldwide ((1,2)) . Change of habits and climate has been discussed as major contributing factors ((1,3)) . The first Brazilian Allergy Project (PROAL I) study was carried out in 2004 with the objective of documenting the sensitization rates to the major allergens in Brazilian allergic children ((4)) . This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - LetterCO - Brazil -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12860</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29314278">PM:29314278</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-ArandaCS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-ArandaCS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Aranda CS</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12860</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87388</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Petersen,T.H.</style></author><author><style face="normal" font="default"> Mortz,C.G.</style></author><author><style face="normal" font="default"> Bindslev-Jensen,C.</style></author><author><style face="normal" font="default"> Eller,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Odense Research Center for Anaphylaxis (ORCA), Dept. of Dermatology &amp; Allergy Center, Odense University Hospital, Odense, Denmark</style></auth-address><titles><title><style face="normal" font="default">Cow's milk allergic children - Can component resolved diagnostics predict duration and severity?</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">BACKGROUND: Cow's Milk Allergy (CMA) affects 2% of all children. This study investigates CRD to cow's milk proteins in children suspected for CMA, by correlating the level of CRD with outcome of the oral challenge. Furthermore, we evaluate the ability of serial CRD measurements to distinguish children with persistent CMA from children developing tolerance. METHODS: We included data from 78 children referred to the Allergy Centre during a 13 years period. Results from oral food challenges including threshold, severity and sensitization data (IgE antibodies to whole milk protein, IgE components towards milk and skin prick test (SPT)) were collected. The milk allergic children were re-evaluated with sensitization data and re-challenges regularly. RESULTS: Thirty-nine children had negative first challenges and 39 had positive first challenges. The positive group was re-challenged and separated into 3 groups depending on time to remission. At inclusion children with persistent CMA had significantly larger size of SPT and higher levels of s-IgE to milk and CRD compared to the other groups. SPT wheal-size was significantly larger in children with persistent CMA compared to children outgrowing CMA. Furthermore, a correlation between s-IgE level to cow's milk and Casein and the severity of the allergic reaction elicited by food challenges was found. CONCLUSION: Oral food challenge cannot be replaced by s-IgE to whole milk protein or milk components nor SPT in the diagnosis of CMA, however high levels of milk components and s-IgE to milk increase the risk of a long lasting or persisting CMA. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12854</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29314279">PM:29314279</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-PetersenTH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20180104-PetersenTH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Petersen TH</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12854</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87398</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kjaerbolling,I.</style></author><author><style face="normal" font="default"> Vesth,T.C.</style></author><author><style face="normal" font="default"> Frisvad,J.C.</style></author><author><style face="normal" font="default"> Nybo,J.L.</style></author><author><style face="normal" font="default"> Theobald,S.</style></author><author><style face="normal" font="default"> Kuo,A.</style></author><author><style face="normal" font="default"> Bowyer,P.</style></author><author><style face="normal" font="default"> Matsuda,Y.</style></author><author><style face="normal" font="default"> Mondo,S.</style></author><author><style face="normal" font="default"> Lyhne,E.K.</style></author><author><style face="normal" font="default"> Kogle,M.E.</style></author><author><style face="normal" font="default"> Clum,A.</style></author><author><style face="normal" font="default"> Lipzen,A.</style></author><author><style face="normal" font="default"> Salamov,A.</style></author><author><style face="normal" font="default"> Ngan,C.Y.</style></author><author><style face="normal" font="default"> Daum,C.</style></author><author><style face="normal" font="default"> Chiniquy,J.</style></author><author><style face="normal" font="default"> Barry,K.</style></author><author><style face="normal" font="default"> LaButti,K.</style></author><author><style face="normal" font="default"> Haridas,S.</style></author><author><style face="normal" font="default"> Simmons,B.A.</style></author><author><style face="normal" font="default"> Magnuson,J.K.</style></author><author><style face="normal" font="default"> Mortensen,U.H.</style></author><author><style face="normal" font="default"> Larsen,T.O.</style></author><author><style face="normal" font="default"> Grigoriev,I.V.</style></author><author><style face="normal" font="default"> Baker,S.E.</style></author><author><style face="normal" font="default"> Andersen,M.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biotechnology and Biomedicine, Technical University of Denmark, 2800 Lyngby, Denmark</style></auth-address><titles><title><style face="normal" font="default">Linking secondary metabolites to gene clusters through genome sequencing of six diverse Aspergillus species</style></title><secondary-title><style face="normal" font="default">Proc Natl Acad Sci U S A</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Proc Natl Acad Sci U S A</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> biosynthesis</style></keyword><keyword><style face="normal" font="default"> Phylogeny</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">The fungal genus of Aspergillus is highly interesting, containing everything from industrial cell factories, model organisms, and human pathogens. In particular, this group has a prolific production of bioactive secondary metabolites (SMs). In this work, four diverse Aspergillus species (A. campestris, A. novofumigatus, A. ochraceoroseus, and A. steynii) have been whole-genome PacBio sequenced to provide genetic references in three Aspergillus sections. A. taichungensis and A. candidus also were sequenced for SM elucidation. Thirteen Aspergillus genomes were analyzed with comparative genomics to determine phylogeny and genetic diversity, showing that each presented genome contains 15-27% genes not found in other sequenced Aspergilli. In particular, A. novofumigatus was compared with the pathogenic species A. fumigatus This suggests that A. novofumigatus can produce most of the same allergens, virulence, and pathogenicity factors as A. fumigatus, suggesting that A. novofumigatus could be as pathogenic as A. fumigatus Furthermore, SMs were linked to gene clusters based on biological and chemical knowledge and analysis, genome sequences, and predictive algorithms. We thus identify putative SM clusters for aflatoxin, chlorflavonin, and ochrindol in A. ochraceoroseus, A. campestris, and A. steynii, respectively, and novofumigatonin, ent-cycloechinulin, and epi-aszonalenins in A. novofumigatus Our study delivers six fungal genomes, showing the large diversity found in the Aspergillus genus; highlights the potential for discovery of beneficial or harmful SMs; and supports reports of A. novofumigatus pathogenicity. It also shows how biological, biochemical, and genomic information can be combined to identify genes involved in the biosynthesis of specific SMs</style></abstract><notes><style face="normal" font="default">IS - 1091-6490 (Electronic)IS - 0027-8424 (Linking)LA - engPT - Journal ArticleCO - Denmark -CO - United States -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1073/pnas.1715954115</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29317534">PM:29317534</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Proc Natl Acad Sci U S A\20180109-KjaerbollingI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Proc Natl Acad Sci U S A\20180109-KjaerbollingI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180109, Kjaerbolling I</style></custom2><misc3><style face="normal" font="default">10.1073/pnas.1715954115</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87400</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Daboussi,S.</style></author><author><style face="normal" font="default"> Mhamdi,S.</style></author><author><style face="normal" font="default"> Aichaouia,C.</style></author><author><style face="normal" font="default"> Moetamri,Z.</style></author><author><style face="normal" font="default"> Mejri,I.</style></author><author><style face="normal" font="default"> Khadraoui,M.</style></author><author><style face="normal" font="default"> Cheikh,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">Sublingual allergen immunotherapy in Tunisia: Safety and efficacy profile</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Angioedema</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword><keyword><style face="normal" font="default"> Symptoms score</style></keyword><keyword><style face="normal" font="default"> Tunisia</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">Allergen immunotherapy is currently the only treatment likely to impact the natural history of allergic disease. The sublingual route appears to exhibit better safety and has confirmed clinical efficacy. However, further research is required on aspects such as patient selection, use of optimal dosing, long-term effects, and management of adverse reactions. In addition, the widely heterogeneous nature of studies on sublingual allergen immunotherapy (SLIT) performed to date and variations in the application of the subcutaneous immunotherapy make it difficult for the prescribing clinician to draw accurate and useful conclusions. In this study, we aim to describe the treatment regimens for sublingual allergen immunotherapy practiced routinely in Tunisia. The secondary objectives include description of the respiratory allergies leading to treatment and evaluation of the efficacy and safety of treatment, patient satisfaction and compliance, and patient management practices. This was a longitudinal prospective study in 200-ápatients presenting allergic disease in whom sublingual immunotherapy was initiated in accordance with the ultra rush protocol. The average patient age was 18-áyears (range: 3 to 44-áyears). Specific immunotherapy was selected for severe persistent allergic rhinitis, either alone (25%) or associated with mild-to-moderate persistent asthma (75%). Sensitivity to dust mites was established in all our patients and confirmed by ACT (100%). The local adverse effects noted consisted of oral pruritus (12% of cases). No serious systemic effects such as anaphylactic shock, angioedema, or moderate or severe asthma attack, were observed in our study. Assessment of symptom intensity during SLIT showed a 77% decrease in symptoms score and a 55% decrease in medication score. No transition from rhinitis to asthma occurred and no new allergies emerged. Our study demonstrated that SLIT is effective and tolerable in Tunisian patients presenting allergic rhino-conjunctivitis and/or asthma. Further long-term controlled trials are required to reinforce the present results</style></abstract><notes><style face="normal" font="default">LA - FRECO - Tunisia -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.11.002</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.11.002</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\20180105-DaboussiS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\20180105-DaboussiS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180105, Daboussi S</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.11.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87404</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Timm,K.</style></author><author><style face="normal" font="default"> Mueller,R.S.</style></author><author><style face="normal" font="default"> Nett-Mettler,C.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">vetderm.ch, Ennetseeklinik fur Kleintiere AG, Rothusstrasse 2, 6331, Hunenberg, SwitzerlandZentrum fur klinische Tiermedizin, LMU Munich, Veterinaerstrasse 13, 80539, Munich, Germanyvetderm.ch, Ennetseeklinik fur Kleintiere AG, Rothusstrasse 2, 6331, Hunenberg, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Long-term effects of intralymphatic immunotherapy (ILIT) on canine atopic dermatitis</style></title><secondary-title><style face="normal" font="default">Vet Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Vet Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="12" Month="1" Year="2018">2018/1/12</year></dates><abstract><style face="normal" font="default">BACKGROUND: Subcutaneous allergen immunotherapy (SCIT) is an established and efficacious therapy for canine atopic dermatitis (AD). In humans, intralymphatic immunotherapy (ILIT) was reported to be associated with fewer and less severe adverse effects than subcutaneous allergen immunotherapy and to be efficacious for several years after three intralymphatic injections. OBJECTIVE: To evaluate safety and effects of ILIT in a case series of dogs with (AD). ANIMALS: Fifty one privately owned dogs with AD. METHODS: Dogs received injections of 0.2 mL alum-precipitated allergen extract into the popliteal lymph nodes at monthly intervals for 3-5 months. Lesion scores, pruritus and medication scores were determined before and at three and 12 months after beginning immunotherapy, and compared in a per protocol analysis (PP) and an intention-to-treat analysis (ITT). RESULTS: Twenty two dogs completed the study and 29 dogs did not fulfil study completion criteria due to lack of a final study visit (21 of 29) or due to insufficient improvement (14 of 29). All scores improved during the study with both analyses. For pruritus and Quality of Life scores this improvement was significant with both analyses; for Canine Atopic Dermatitis Extent and Severity Index (CADESI)-03 values and medication scores only with PP. The only rare adverse effects observed included mild swelling of the lymph node post-injection and increased pruritus. CONCLUSION AND CLINICAL RELEVANCE: ILIT is safe and feasible, and provides long-lasting relief in some atopic dogs with a limited number of injections</style></abstract><notes><style face="normal" font="default">IS - 1365-3164 (Electronic)IS - 0959-4493 (Linking)LA - engPT - Journal ArticleCO - Switzerland -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/vde.12517</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29327474">PM:29327474</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Vet Dermatol\20180112-TimmK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Vet Dermatol\20180112-TimmK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180112, Timm K</style></custom2><misc3><style face="normal" font="default">10.1111/vde.12517</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87405</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Carnett,M.J.H.</style></author><author><style face="normal" font="default"> Plant,J.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">SkinVet Clinic, Suite 120, 15800 SW Upper Boones Ferry Road, Lake Oswego, OR, 97035, USASkinVet Clinic, Suite 120, 15800 SW Upper Boones Ferry Road, Lake Oswego, OR, 97035, USA</style></auth-address><titles><title><style face="normal" font="default">Percutaneous prick test irritant threshold concentrations for eight allergens in healthy nonsedated dogs in the USA</style></title><secondary-title><style face="normal" font="default">Vet Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Vet Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword></keywords><dates><year Day="8" Month="1" Year="2018">2018/1/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: Percutaneous testing (PT) is preferred to intradermal testing in humans for the in vivo identification of allergen hypersensitivity, but the methodology has not been well described for use in dogs with atopic dermatitis. HYPOTHESIS/OBJECTIVES: To identify the irritant threshold concentrations (ITC) of eight aeroallergens using a commercial prick test device in normal dogs. ANIMALS: Twenty healthy, privately owned dogs. METHODS: Percutaneous testing was performed using the GREER((R)) Pick((R)) System (Stallergenes Greer; Lenoir, NC, USA). Five dilutions of glycerinated extracts of Bromis inermis, Sorghum halepense, Chenopodium album, Ambrosia psilostachya, Salix nigra and Acer negundo, as well as four dilutions of Dermatophagoides farinae and D. pteronyssinus were included. Glycerinated histamine (6 mg/ml) and glycerin/Coca's solution were used for the positive and negative controls, respectively. Orthogonal wheal diameters were measured for each test site every 5 min for 25 min. Reactions were considered significant when the average wheal diameter was equal to or greater than the mean of the positive and negative controls. RESULTS: Significant reactions were noted in five of 20 (25%) of dogs. The ITC (&lt;/=10% of dogs reacting) were 1:20 w/v for B. inermis and S. nigra, 1:400 w/v for D. farinae and 1:200 w/v for D. pteronyssinus. CONCLUSIONS AND CLINICAL IMPORTANCE: These results suggest that the pollen allergens evaluated in this study can be used for PT at their undiluted concentration (1:20 w/v) with a reasonable assurance of few false positive reactions in dogs. Dust mites require dilution for testing at the ITC</style></abstract><notes><style face="normal" font="default">IS - 1365-3164 (Electronic)IS - 0959-4493 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/vde.12514</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29315920">PM:29315920</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Vet Dermatol\20180108-CarnettMJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Vet Dermatol\20180108-CarnettMJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180108, Carnett MJ</style></custom2><misc3><style face="normal" font="default">10.1111/vde.12514</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87411</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ashley,J.</style></author><author><style face="normal" font="default"> Shukor,Y.</style></author><author><style face="normal" font="default"> D'Aurelio,R.</style></author><author><style face="normal" font="default"> Trinh,L.</style></author><author><style face="normal" font="default"> Rodgers,T.L.</style></author><author><style face="normal" font="default"> Temblay,J.</style></author><author><style face="normal" font="default"> Pleasants,M.</style></author><author><style face="normal" font="default"> Tothill,I.E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Synthesis of MIP Nanoparticles for alpha-Casein Detection using SPR as a Milk Allergen Sensor</style></title><secondary-title><style face="normal" font="default">ACS Sens</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">ACS Sens</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">Food recalls due to undeclared allergens or contamination are costly to the food manufacturing industry worldwide. As the industry strives for better manufacturing efficiencies over a diverse range of food products, there is a need for the development of new analytical techniques to improve monitoring the presence of unintended food allergens during the food manufacturing process. In particular, the monitoring of wash samples from cleaning in place systems (CIP), used in the cleaning of food processing equipment, would allow for the effective removal of allergen containing ingredients in between food batches. Casein proteins constitute the biggest group of proteins in milk and hence are the most commonly milk protein allergen in food ingredients. As such, these proteins could present an ideal analyte for cleaning validation. In this work, molecularly imprinted polymer-nanoparticles (nanoMIPs) with high affinity towards bovine alpha-casein were synthesized using solid-phase imprinting method. The nanoMIPs were then characterized and incorporated into label free surface plasmon resonance (SPR) based sensor. The nanoMIPs demonstrated good binding affinity and selectivity towards alpha-casein (KD ~10 x 10-9 M). This simple affinity sensor demonstrated the quantitative detection of alpha-casein achieving a detection limit of 127 +/- 97.6 ng ml-1 (0.127 ppm) which is far superior to existing commercially available ELISA kits. Recoveries from spiked CIP waste water samples were within the acceptable range (87-120%). The reported sensor could allow food manufacturers to adequately monitor and manage food allergen risk in food processing environments while insuring that the food produced is safe for the consumer</style></abstract><notes><style face="normal" font="default">IS - 2379-3694 (Electronic)IS - 2379-3694 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1021/acssensors.7b00850</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29333852">PM:29333852</url></web-urls><pdf-urls><url ppv-ref="no">i.tothill@cranfield.ac.uk</url></pdf-urls></urls><custom2><style face="normal" font="default">20180115, Ashley J</style></custom2><misc3><style face="normal" font="default">10.1021/acssensors.7b00850</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87413</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kulmala,P.</style></author><author><style face="normal" font="default"> Pelkonen,A.S.</style></author><author><style face="normal" font="default"> Kuitunen,M.</style></author><author><style face="normal" font="default"> Paassilta,M.</style></author><author><style face="normal" font="default"> Remes,S.</style></author><author><style face="normal" font="default"> Schultz,R.</style></author><author><style face="normal" font="default"> Dunder,T.</style></author><author><style face="normal" font="default"> Turunen,S.</style></author><author><style face="normal" font="default"> Makela,M.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">PEDEGO Research Unit and Medical Research Center (MRC) Oulu, University of Oulu, and Oulu University Hospital, Oulu, Finland</style></auth-address><titles><title><style face="normal" font="default">Wheat oral immunotherapy was moderately successful but was associated with very frequent adverse events in children aged 6-18 years</style></title><secondary-title><style face="normal" font="default">Acta Paediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Acta Paediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">AIM: This study investigated oral immunotherapy for children aged 6-18 years with wheat allergies. METHODS: Well-cooked wheat spaghetti was given to 100 children with wheat allergies every day for 17 weeks, increasing from 0.3mg to 2,000mg of wheat protein, followed by three-month and nine-month maintenance phases. Blood samples were taken before therapy and at follow-up visits. The study was carried out in 2009-2015 in four Finnish paediatric allergology units. RESULTS: The children (67% male) had a mean age of 11.6 years (range 6.1 to 18.6) and 57 were using wheat daily 16 months after the initiation of therapy. Allergic symptoms occurred in 94/100 children: mild in 34, moderate in 36 and severe in 24. Specific immunoglobulin E for omega-5-gliadin was significantly higher in patients who did not reach the target dose and were related to the intensity of reactions. CONCLUSION: The majority (57%) of children with wheat allergies could use wheat in their daily diet 16 months after the initiation of oral immunotherapy, but 94/100 had adverse reactions and 60 were moderate or severe. Specific immunoglobulin E to omega-5-gliadin may provide a biomarker for how much wheat can be tolerated and the intensity of the reactions to immunotherapy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1651-2227 (Electronic)IS - 0803-5253 (Linking)LA - engPT - Journal ArticleCO - Finland -</style></notes><work-type><style face="normal" font="default">10.1111/apa.14226</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29345001">PM:29345001</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Paediatr\20180118-KulmalaP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Paediatr\20180118-KulmalaP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Kulmala P</style></custom2><misc3><style face="normal" font="default">10.1111/apa.14226</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87414</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Frandsen,A.</style></author><author><style face="normal" font="default"> McClure,M.</style></author><author><style face="normal" font="default"> Chung,M.K.</style></author><author><style face="normal" font="default"> LaRiccia,P.J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Autonomic Response Testing Compared With Immunoglobulin E Allergy Panel Test Results: Preliminary Report</style></title><secondary-title><style face="normal" font="default">Altern Ther Health Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Altern Ther Health Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">Context * Chronically ill patients who have failed standard medical assessment and therapies are often assessed by integrative medical providers for atypical manifestations of allergies as the possible source or contributing factor(s) to their condition. Skin testing and immunoglobulin E (IgE) allergy panels increase the cost of care in these patients. Objective * The objective of this study was to determine the accuracy of autonomic response testing (ART) as compared with IgE allergy panel blood tests. Design * This study was a retrospective chart review of patients who had ART and blood drawn for an IgE allergy panel at the same office visit. Outcome Measures * Sensitivity, specificity, positive predictive value, negative predictive value, overall accuracy, phi coefficient, and Cohen's kappa were calculated. Results * A total of 14 charts were reviewed. All measures of accuracy were of either useful or excellent strength. The strength of association measures of the phi coefficient and Cohen's kappa were strong. Conclusion * This first and preliminary evaluation of the allergy assessment utility of ART is very promising and reveals the need for more vigorous follow-up studies</style></abstract><notes><style face="normal" font="default">IS - 1078-6791 (Print)IS - 1078-6791 (Linking)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29332023">PM:29332023</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180115, Frandsen A</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87416</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhou,L.</style></author><author><style face="normal" font="default"> Chen,L.</style></author><author><style face="normal" font="default"> Li,X.</style></author><author><style face="normal" font="default"> Li,T.</style></author><author><style face="normal" font="default"> Dong,Z.</style></author><author><style face="normal" font="default"> Wang,Y.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing 400014, PR China</style></auth-address><titles><title><style face="normal" font="default">Food allergy induces alteration in brain inflammatory status and cognitive impairments</style></title><secondary-title><style face="normal" font="default">Behav Brain Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Behav Brain Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="12" Month="1" Year="2018">2018/1/12</year></dates><abstract><style face="normal" font="default">Accumulating evidence supports an increase in emotional and behavioral problems in patients with food allergy, but the underlying mechanism remains poorly understood. Here we found that in addition to inducing an increase of allergic factors in serum, food allergy also increased levels of antigen-specific immunoglobulins and mast cell marker in the brain. In particular, food allergy increased the number of total microglia and the percentage of active microglia in the cerebral cortex and hippocampal CA1 areas, and induced the increase of TNF-alpha in the cerebral cortex. Importantly, these brain allergic responses were associated with behavioral impairments, including motor and learning deficits. Taken together, our study provides some evidence for profound effects of food allergy on brain functions, and thereby provides scientific basis for a better explanation of emotional and behavioral problems among patients with food allergy</style></abstract><notes><style face="normal" font="default">IS - 1872-7549 (Electronic)IS - 0166-4328 (Linking)LA - engPT - Journal ArticleCO - China -CO - Canada -</style></notes><work-type><style face="normal" font="default">10.1016/j.bbr.2018.01.011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29339006">PM:29339006</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Behav Brain Res\20180112-ZhouL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Behav Brain Res\20180112-ZhouL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180112, Zhou L</style></custom2><misc3><style face="normal" font="default">10.1016/j.bbr.2018.01.011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87417</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yamada,Y.</style></author><author><style face="normal" font="default"> Takabayashi,S.</style></author><author><style face="normal" font="default"> Kato,H.</style></author><author><style face="normal" font="default"> Ishiwata,K.</style></author><author><style face="normal" font="default"> Watanabe,N.</style></author><author><style face="normal" font="default"> Sasaki,E.</style></author><author><style face="normal" font="default"> Habu,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Molecular Life Science, Tokai University School of Medicine</style></auth-address><titles><title><style face="normal" font="default">The response of common marmoset immunity against cedar pollen extract</style></title><secondary-title><style face="normal" font="default">Biosci Trends</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biosci Trends</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">The in vivo model of pollinosis has been established using rodents, but the model cannot completely mimic human pollinosis. We used Callithrix jacchus, the common marmoset (CM), to establish a pollinosis animal model using intranasal weekly administration of cedar pollen extract with cholera toxin adjuvant. Some of the treated CMs exhibited the symptoms of snitching, excess nasal mucus and/or sneezing, but the period was very short, and the symptoms disappeared after several weeks. The CD4+CD25+ cell ratio in the peripheral blood increased in CMs quickly after the nasal administration of cedar pollen extract, but the timing was not parallel with the symptoms. IL-10 mRNA was enhanced in the peripheral blood mononuclear cells (PBMCs), suggesting CM-induced tolerance for cedar pollen administration. Similarly, Foxp3 mRNA was also detected in the PBMC. Additive sensitization of these CMs with Ascaris egg administration did not enhance chronic inflammation of type 1 allergy to induce the symptoms. These results suggest that the environmental immune cells develop transient allergic symptoms and subsequent immune-tolerance in the intranasally sensitized CMs</style></abstract><notes><style face="normal" font="default">IS - 1881-7823 (Electronic)IS - 1881-7815 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.5582/bst.2017.01219</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29332927">PM:29332927</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biosci Trends\20180115-YamadaY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biosci Trends\20180115-YamadaY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Yamada Y</style></custom2><misc3><style face="normal" font="default">10.5582/bst.2017.01219</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87418</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Weisenberg,S.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, New York University School of Medicine, New York City, New York, USA</style></auth-address><titles><title><style face="normal" font="default">Chronic strongyloidiasis with recurrent asthma exacerbations and steroid-associated 'hives'</style></title><secondary-title><style face="normal" font="default">BMJ Case Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMJ Case Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">A 74-year-old man experienced worsening asthma for several years. Oral steroids were required on multiple occasions for asthma treatment. During his steroid courses, he developed a hive-like rash, which would resolve after completion of each steroid course. He was from Romania, and had lived in the USA for many years. Laboratory testing had shown eosinophilia. He was eventually diagnosed with strongyloidiasis by serology. Treatment with ivermectin led to marked improvement but not resolution of his long-term asthma. His hive-like rash, which was likely larva currens, did not recur with a subsequent steroid course. Improved recognition of strongyloidiasis, particularly in steroid-treated patients, is needed</style></abstract><notes><style face="normal" font="default">IS - 1757-790X (Electronic)IS - 1757-790X (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1136/bcr-2017-221877</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29348277">PM:29348277</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMJ Case Rep\20180117-WeisenbergSA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMJ Case Rep\20180117-WeisenbergSA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Weisenberg SA</style></custom2><misc3><style face="normal" font="default">10.1136/bcr-2017-221877</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87419</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Thyssen,J.P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Allergy, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark</style></auth-address><titles><title><style face="normal" font="default">Could conjunctivitis in dupilumab treated atopic dermatitis patients be caused by colonization with demodex and increased IL-17 levels?</style></title><secondary-title><style face="normal" font="default">Br J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> complications</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">de Bruin-Weller et al., reported alarmingly high rates of unspecified and allergic conjunctivitis in trial patients with moderate-to-severe atopic dermatitis (AD) who underwent treatment with dupilumab; an antibody that inhibits signaling of IL-4 and IL-13.(1) Importantly, the exact pathogenic mechanism behind incident conjunctivitis in dupilumab-treated patients is unclear. While all, but one case, were considered to be of mild or moderate severity, and most resolved after treatment discontinuation, ocular complications may ultimately deprive AD patients from effective treatment with dupilumab. For these reasons, the medical community needs to rapidly identify the pathogenic mechanism. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2133 (Electronic)IS - 0007-0963 (Linking)LA - engPT - LetterCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1111/bjd.16330</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29333603">PM:29333603</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Dermatol\20180115-ThyssenJP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Dermatol\20180115-ThyssenJP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Thyssen JP</style></custom2><misc3><style face="normal" font="default">10.1111/bjd.16330</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87421</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Agarwal,R.</style></author><author><style face="normal" font="default"> Dhooria,S.</style></author><author><style face="normal" font="default"> Sehgal,I.S.</style></author><author><style face="normal" font="default"> Aggarwal,A.N.</style></author><author><style face="normal" font="default"> Garg,M.</style></author><author><style face="normal" font="default"> Saikia,B.</style></author><author><style face="normal" font="default"> Behera,D.</style></author><author><style face="normal" font="default"> Chakrabarti,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">A randomized trial of itraconazole versus prednisolone in acute-stage ABPA complicating asthma</style></title><secondary-title><style face="normal" font="default">Chest</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Chest</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Allergic bronchopulmonary aspergillosis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">BACKGROUND AND AIMS: Whether itraconazole monotherapy is effective in the acute-stage of allergic bronchopulmonary aspergillosis (ABPA) remains unknown. Herein, we compare the efficacy and safety of itraconazole and prednisolone monotherapy in ABPA. METHODS: We randomized treatment-naive subjects with ABPA complicating asthma (January 2012 to December 2013) to receive either oral itraconazole or prednisolone for four months. The study was not blinded. The primary outcomes were proportion of subjects showing composite response after six weeks, percentage decline in IgE after treatment, and numbers of subjects experiencing exacerbation. The secondary outcomes included the time to first exacerbation, change in lung function, and treatment-related adverse effects. RESULTS: One hundred and thirty-one subjects (prednisolone: n=63; itraconazole: n=68) were included in the study. The number of subjects demonstrating composite response was significantly higher in the prednisolone group compared to itraconazole (100% vs. 88%; p=0.007). The percentage decline in IgE after six weeks and three months; and, the numbers of subjects with exacerbations after one and two years of treatment were similar in the two groups. The time to first exacerbation (mean, 437 vs. 442 days) and the improvement in lung function after six weeks was also similar in the two groups. The occurrence of side-effects was significantly higher in the glucocorticoid arm (p&lt;0.001). CONCLUSIONS: Prednisolone was more effective in inducing response than itraconazole in acute-stage ABPA. However, itraconazole is also effective in a considerable number; and, with lesser side-effects compared to prednisolone, remains an attractive alternative in the initial treatment of ABPA. [clinicaltrials.gov: NCT01321827]</style></abstract><notes><style face="normal" font="default">IS - 1931-3543 (Electronic)IS - 0012-3692 (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.1016/j.chest.2018.01.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331473">PM:29331473</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Chest\20180110-AgarwalR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Chest\20180110-AgarwalR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Agarwal R</style></custom2><misc3><style face="normal" font="default">10.1016/j.chest.2018.01.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87422</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wu,W.</style></author><author><style face="normal" font="default"> Lin,L.</style></author><author><style face="normal" font="default"> Shi,B.</style></author><author><style face="normal" font="default"> Jing,J.</style></author><author><style face="normal" font="default"> Cai,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Maternal and Child Health , School of Public Health, Sun Yat-sen University , Guangzhou , Guangdong Province 510080 , People's Republic of China</style></auth-address><titles><title><style face="normal" font="default">The effects of Early Life Polyunsaturated Fatty Acids and Ruminant Trans Fatty Acids on Allergic Diseases: A systematic review and meta-analysis</style></title><secondary-title><style face="normal" font="default">Crit Rev Food Sci Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Crit Rev Food Sci Nutr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">Early life nutritional exposures could modify the gene expression and susceptibility of allergic diseases (AD). This systematic review aimed to evaluate whether early life (the first 1,000 days) natural exposure to polyunsaturated fatty acids (PUFA) and ruminant trans fatty acids (R-TFA) could affect the AD risk. We searched PubMed, EMBASE, PsycINFO, Scopus, the Cochrane Library, and ClinicalTrials.gov from inception through September 10, 2017 for observational studies. The quality of studies was examined by the Newcastle-Ottawa Scale, and the best evidence synthesis (BES) was applied. We included 26 observational studies, and 8 of them showed high quality. BES showed a moderate evidence for the protective effect of vaccenic acid (VA) on eczema, while insufficient or no evidence was found in other associations. Meta-analysis showed that higher n-6/n-3 ratio and linoleic acid were associated with higher risk of eczema (pooled odds ratio [OR] = 1.06, 95% confidence intervals [CI]: 1.00-1.13; 1.08, 95% CI: 1.02-1.15). However, VA was inversely associated with eczema pooled OR = 0.43, 95% CI: 0.26-0.72). Early life natural exposure to VA showed evident benefit on decreasing the risk of eczema, while PUFA and other R-TFA showed limited effects on AD. More robust studies especially for R-TFA are required</style></abstract><notes><style face="normal" font="default">IS - 1549-7852 (Electronic)IS - 1040-8398 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1080/10408398.2018.1429382</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29341787">PM:29341787</url></web-urls><pdf-urls><url ppv-ref="no">caili5@mail.sysu.edu.cn</url><url ppv-ref="no">jingjin@mail.sysu.edu.cn</url></pdf-urls></urls><custom2><style face="normal" font="default">20180117, Wu W</style></custom2><misc3><style face="normal" font="default">10.1080/10408398.2018.1429382</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87423</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Roger,A.</style></author><author><style face="normal" font="default"> Basagana,M.</style></author><author><style face="normal" font="default"> Teniente-Serra,A.</style></author><author><style face="normal" font="default"> Depreux,N.</style></author><author><style face="normal" font="default"> Jurgens,Y.</style></author><author><style face="normal" font="default"> Padro,C.</style></author><author><style face="normal" font="default"> Miquel,S.</style></author><author><style face="normal" font="default"> Elduque,C.</style></author><author><style face="normal" font="default"> Martinez-Caceres,E.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Section, University Hospital Germans Trias i Pujol, Badalona. Spain</style></auth-address><titles><title><style face="normal" font="default">Immunotheraphy In Allergic Diseases</style></title><secondary-title><style face="normal" font="default">Curr Pharm Des</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Pharm Des</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">Nowadays, specific immunotherapy is the only successful disease-modifying therapy for IgE-mediated allergic diseases. In this review we analyse different antigen-specific immunotherapies according to administration route, type of antigens and adjuvants, and we address the special case of food allergy</style></abstract><notes><style face="normal" font="default">IS - 1873-4286 (Electronic)IS - 1381-6128 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.2174/1381612824666180116094048</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29336248">PM:29336248</url></web-urls></urls><custom2><style face="normal" font="default">20180115, Roger A</style></custom2><misc3><style face="normal" font="default">10.2174/1381612824666180116094048</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87424</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Eckmann,J.D.</style></author><author><style face="normal" font="default"> Ravi,K.</style></author><author><style face="normal" font="default"> Katzka,D.A.</style></author><author><style face="normal" font="default"> Davis,D.R.</style></author><author><style face="normal" font="default"> See,J.A.</style></author><author><style face="normal" font="default"> Geno,D.R.</style></author><author><style face="normal" font="default"> Kryzer,L.A.</style></author><author><style face="normal" font="default"> Alexander,J.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA</style></auth-address><titles><title><style face="normal" font="default">Efficacy of Atopy Patch Testing in Directed Dietary Therapy of Eosinophilic Esophagitis: A Pilot Study</style></title><secondary-title><style face="normal" font="default">Dig Dis Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Dig Dis Sci</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Adult</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> Biopsy</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Eosinophilic esophagitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">BACKGROUND: Atopy patch testing (APT) has shown potential for predicting dietary food triggers in studies of children and adolescents with eosinophilic esophagitis (EoE). AIMS: To assess the efficacy of APT in adults with EoE. METHODS: We conducted a prospective open-label pilot study of patients >/= 18 years old with diagnosis of EoE at Mayo Clinic in Rochester, Minnesota, from November 2014 to January 2016. All patients underwent patch testing using intact food products, followed by a six food elimination diet and stepwise food reintroduction. Response to elimination diet was assessed with serial endoscopy with biopsies as well as clinical symptoms. APT results were directly compared to elimination diet results for assessment of efficacy. Correlation between clinical symptoms, endoscopic score, and histology was also qualitatively evaluated. RESULTS: Fifty percent of the patients had a positive APT, while only 16% had an APT result confirmed histologically during food reintroduction. Sensitivity of APT was calculated to be 5.9%, with specificity of 92.0%. Furthermore, we found significant qualitative inter-patient heterogeneity in the correlation between clinical symptoms, EREFS score, and histology. CONCLUSIONS: APT does not reliably predict food triggers identified by food elimination diet in adult patients with EoE. As a result, APT does not have a clear role in the evaluation of patients with EoE</style></abstract><notes><style face="normal" font="default">IS - 1573-2568 (Electronic)IS - 0163-2116 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s10620-018-4928-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29349695">PM:29349695</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Dig Dis Sci\20180118-EckmannJD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Dig Dis Sci\20180118-EckmannJD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Eckmann JD</style></custom2><misc3><style face="normal" font="default">10.1007/s10620-018-4928-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87426</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,G.X.</style></author><author><style face="normal" font="default"> Tu,Z.</style></author><author><style face="normal" font="default"> Yang,W.</style></author><author><style face="normal" font="default"> Wang,H.</style></author><author><style face="normal" font="default"> Zhang,L.</style></author><author><style face="normal" font="default"> Ma,D.</style></author><author><style face="normal" font="default"> Huang,T.</style></author><author><style face="normal" font="default"> Liu,J.</style></author><author><style face="normal" font="default"> Li,X.</style></author></authors></contributors><titles><title><style face="normal" font="default">Investigation into allergenicity reduction and glycation sites of glycated +¦-lactoglobulin with ultrasound pretreatment by high-resolution mass spectrometry</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">+¦-lactoglobulin</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> antigenic epitopes</style></keyword><keyword><style face="normal" font="default"> Conformation</style></keyword><keyword><style face="normal" font="default"> glycation</style></keyword><keyword><style face="normal" font="default"> specific glycation sites</style></keyword><keyword><style face="normal" font="default"> ultrasound pretreatment</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0308-8146</style></isbn><abstract><style face="normal" font="default">Ultrasound treatment could change the conformation of +¦-lactoglobulin (+¦-Lg) and improve the glycation reaction in aqueous solution under neutral condition. However, the effect of ultrasound pretreatment on glycation of +¦-Lg with pentose at dry-state remains ambiguous, and the relationship between glycation and allergenicity of +¦-Lg with ultrasound pretreatment is unclear. This study aimed to evaluate the effect of ultrasound pretreatment on glycation and allergenicity of +¦-Lg. Markedly decreased allergenicity of +¦-Lg was observed after glycation with ribose before and after ultrasound pretreatment with the minimum found at 400 W. Orbitrap LC-MS/MS showed that the glycation degree of some peptides in glycated +¦-Lg with and without ultrasound pretreatment were different although the content of free amino group and molecular mass were insignificantly different. Therefore, ultrasound pretreatment promoted the reduction in allergenicity by improving the glycation extent of some glycation sites although it hardly enhanced the whole glycation degree of +¦-Lg</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2018.01.086</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.foodchem.2018.01.086</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\20180112-LiuGX.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\20180112-LiuGX.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180112, Liu GX</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2018.01.086</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87430</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Turner,D.L.</style></author><author><style face="normal" font="default"> Goldklang,M.</style></author><author><style face="normal" font="default"> Cvetkovski,F.</style></author><author><style face="normal" font="default"> Paik,D.</style></author><author><style face="normal" font="default"> Trischler,J.</style></author><author><style face="normal" font="default"> Barahona,J.</style></author><author><style face="normal" font="default"> Cao,M.</style></author><author><style face="normal" font="default"> Dave,R.</style></author><author><style face="normal" font="default"> Tanna,N.</style></author><author><style face="normal" font="default"> D'Armiento,J.M.</style></author><author><style face="normal" font="default"> Farber,D.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY 10032</style></auth-address><titles><title><style face="normal" font="default">Biased Generation and In Situ Activation of Lung Tissue-Resident Memory CD4 T Cells in the Pathogenesis of Allergic Asthma</style></title><secondary-title><style face="normal" font="default">J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">Asthma is a chronic inflammatory disease mediated by allergen-specific CD4 T cells that promote lung inflammation through recruitment of cellular effectors into the lung. A subset of lung T cells can persist as tissue-resident memory T cells (TRMs) following infection and allergen induction, although the generation and role of TRM in asthma persistence and pathogenesis remain unclear. In this study, we used a mouse model of chronic exposure to intranasal house dust mite (HDM) extract to dissect how lung TRMs are generated and function in the persistence and pathogenesis of allergic airway disease. We demonstrate that both CD4(+) and CD8(+) T cells infiltrate into the lung tissue during acute HDM exposure; however, only CD4(+) TRMs, and not CD8(+) TRMs, persist long term following cessation of HDM administration. Lung CD4(+) TRMs are localized around airways and are rapidly reactivated upon allergen re-exposure accompanied by the rapid induction of airway hyperresponsiveness independent of circulating T cells. Lung CD4(+) TRM activation to HDM challenge is also accompanied by increased recruitment and activation of dendritic cells in the lungs. Our results indicate that lung CD4(+) TRMs can perpetuate allergen-specific sensitization and direct early inflammatory signals that promote rapid lung pathology, suggesting that targeting lung CD4(+) TRMs could have therapeutic benefit in alleviating recurrent asthma episodes</style></abstract><notes><style face="normal" font="default">IS - 1550-6606 (Electronic)IS - 0022-1767 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.4049/jimmunol.1700257</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29343554">PM:29343554</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol\20180117-TurnerDL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol\20180117-TurnerDL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Turner DL</style></custom2><misc3><style face="normal" font="default">10.4049/jimmunol.1700257</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87431</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Leo,G.</style></author><author><style face="normal" font="default"> Incorvaia,C.</style></author><author><style face="normal" font="default"> Cazzavillan,A.</style></author><author><style face="normal" font="default"> Consonni,D.</style></author><author><style face="normal" font="default"> Zuccotti,G.V.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Allergy and Respiratory Pathophysiology Unit,Department of Pediatrics,Vittore Buzzi Children's Hospital,University of Milan,Italy</style></auth-address><titles><title><style face="normal" font="default">Could seasonal allergy be a risk factor for acute rhinosinusitis in children?</style></title><secondary-title><style face="normal" font="default">J Laryngol Otol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Laryngol Otol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Symptoms score</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To evaluate the incidence of acute rhinosinusitis in children with grass pollen induced rhinitis during the period of grass pollinosis. METHODS: Children with nasal symptoms from grass pollen induced rhinitis but without rhinosinusitis symptoms were selected. Their parents were asked to complete a diary during pollen exposure to report nasal symptoms and drugs used daily. When rhinosinusitis was suspected, the confirmatory diagnosis of acute rhinosinusitis was made by fibro-endoscopy. Children without inhalant allergy served as controls. RESULTS: Seventeen out of 242 children (7.0 per cent) had a diagnosis of acute rhinosinusitis, confirmed by fibro-endoscopy, during grass pollination, compared to 3 out of 65 (4.6 per cent) in the control group (p = 0.49). Among allergic children, those with acute rhinosinusitis had symptoms for a greater number of days and/or a higher symptoms score than children without acute rhinosinusitis. CONCLUSION: Children with grass pollen induced rhinitis during exposure to pollen have an incidence of endoscopically confirmed acute rhinosinusitis comparable to non-allergic children. This suggests that grass pollen induced rhinitis is a negligible risk factor for acute rhinosinusitis</style></abstract><notes><style face="normal" font="default">IS - 1748-5460 (Electronic)IS - 0022-2151 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1017/S0022215118000038</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29343309">PM:29343309</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Laryngol Otol\20180118-LeoG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Laryngol Otol\20180118-LeoG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Leo G</style></custom2><misc3><style face="normal" font="default">10.1017/S0022215118000038</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87432</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bastan,I.</style></author><author><style face="normal" font="default"> Ge,X.N.</style></author><author><style face="normal" font="default"> Dileepan,M.</style></author><author><style face="normal" font="default"> Greenberg,Y.G.</style></author><author><style face="normal" font="default"> Guedes,A.G.</style></author><author><style face="normal" font="default"> Hwang,S.H.</style></author><author><style face="normal" font="default"> Hammock,B.D.</style></author><author><style face="normal" font="default"> Washabau,R.J.</style></author><author><style face="normal" font="default"> Rao,S.P.</style></author><author><style face="normal" font="default"> Sriramarao,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Veterinary Clinical Sciences, University of Minnesota, St. Paul, Minnesota</style></auth-address><titles><title><style face="normal" font="default">Inhibition of soluble epoxide hydrolase attenuates eosinophil recruitment and food allergen-induced gastrointestinal inflammation</style></title><secondary-title><style face="normal" font="default">J Leukoc Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Leukoc Biol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">Prevalence of food allergies in the United States is on the rise. Eosinophils are recruited to the intestinal mucosa in substantial numbers in food allergen-driven gastrointestinal (GI) inflammation. Soluble epoxide hydrolase (sEH) is known to play a pro-inflammatory role during inflammation by metabolizing anti-inflammatory epoxyeicosatrienoic acids (EETs) to pro-inflammatory diols. We investigated the role of sEH in a murine model of food allergy and evaluated the potential therapeutic effect of a highly selective sEH inhibitor (trans-4-{4-[3-(4-trifluoromethoxyphenyl)-ureido]-cyclohexyloxy}-benzoic acid [t-TUCB]). Oral exposure of mice on a soy-free diet to soy protein isolate (SPI) induced expression of intestinal sEH, increased circulating total and antigen-specific IgE levels, and caused significant weight loss. Administration of t-TUCB to SPI-challenged mice inhibited IgE levels and prevented SPI-induced weight loss. Additionally, SPI-induced GI inflammation characterized by increased recruitment of eosinophils and mast cells, elevated eotaxin 1 levels, mucus hypersecretion, and decreased epithelial junction protein expression. In t-TUCB-treated mice, eosinophilia, mast cell recruitment, and mucus secretion were significantly lower than in untreated mice and SPI-induced loss of junction protein expression was prevented to variable levels. sEH expression in eosinophils was induced by inflammatory mediators TNF-alpha and eotaxin-1. Treatment of eosinophils with t-TUCB significantly inhibited eosinophil migration, an effect that was mirrored by treatment with 11,12-EET, by inhibiting intracellular signaling events such as ERK (1/2) activation and eotaxin-1-induced calcium flux. These studies suggest that sEH induced by soy proteins promotes allergic responses and GI inflammation including eosinophilia and that inhibition of sEH can attenuate these responses</style></abstract><notes><style face="normal" font="default">IS - 1938-3673 (Electronic)IS - 0741-5400 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/JLB.3MA1017-423R</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29345370">PM:29345370</url></web-urls><pdf-urls><url ppv-ref="no">psrao@umn.edu</url></pdf-urls><related-urls><url ppv-ref="no">presto - sito non funzionante</url></related-urls></urls><custom2><style face="normal" font="default">20180117, Bastan I</style></custom2><misc3><style face="normal" font="default">10.1002/JLB.3MA1017-423R</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87433</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nikolic,J.</style></author><author><style face="normal" font="default"> Nesic,A.</style></author><author><style face="normal" font="default"> Kull,S.</style></author><author><style face="normal" font="default"> Schocker,F.</style></author><author><style face="normal" font="default"> Jappe,U.</style></author><author><style face="normal" font="default"> Gavrovic-Jankulovic,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biochemistry, Faculty of Chemistry, University of Belgrade, Belgrade, SerbiaDepartment of Biochemistry, Faculty of Chemistry, University of Belgrade, Belgrade, Serbia.</style></auth-address><titles><title><style face="normal" font="default">Employment of proteomic and immunological based methods for the identification of catalase as novel allergen from banana</style></title><secondary-title><style face="normal" font="default">J Proteomics</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Proteomics</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> Components</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="10" Month="1" Year="2018">2018/1/10</year></dates><abstract><style face="normal" font="default">Diagnostic reagents based on food allergen extracts often lack sufficient sensitivity. The introduction of well characterized food allergens in molecular allergy diagnosis has been recognized as valid approach to circumvent unstandardized allergen extracts. Banana fruit (Musa acuminata) is a well-established allergen source which besides six characterized allergens, contains unidentified IgE reactive proteins whose clinical relevance remains undefined. By employment of a combinatorial peptide ligand library (CPLL) methodology with 2-D PAGE, mass spectrometric and 2-D immunoblot analysis, a novel allergen from banana fruit was detected in banana as catalase. A recombinant homologue of natural catalase was produced, isolated and biochemically characterized. The recombinant protein showed IgE reactivity in 7 out of 13 tested patients with suspected allergy to banana in immunoblot. Novel banana fruit allergens should be added as components to allergen-microarrays for the diagnosis and the monitoring of banana allergy. SIGNIFICANCE: By employment of CPLL methodology with 2-D PAGE, mass spectrometric and 2-D immunoblot analysis catalase from banana fruit is identified as a novel allergen, with proposed designation as Mus a 7. IgE reactive recombinant Mus a 7 was produced and should be included in a component-resolved allergy diagnosis</style></abstract><notes><style face="normal" font="default">IS - 1876-7737 (Electronic)IS - 1874-3919 (Linking)LA - engPT - Journal ArticleCO - Serbia -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jprot.2018.01.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331514">PM:29331514</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Proteomics\20180111-NikolicJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Proteomics\20180111-NikolicJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180111, Nikolic J</style></custom2><misc3><style face="normal" font="default">10.1016/j.jprot.2018.01.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87435</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,W.</style></author><author><style face="normal" font="default"> Tu,Z.</style></author><author><style face="normal" font="default"> Wang,H.</style></author><author><style face="normal" font="default"> Zhang,L.</style></author><author><style face="normal" font="default"> Song,Q.</style></author></authors></contributors><auth-address><style face="normal" font="default">State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, Jiangxi, 330047, China</style></auth-address><titles><title><style face="normal" font="default">Glycation of ovalbumin after high-intensity ultrasound pretreatment: Effects on conformation, IgG/IgE binding ability and antioxidant activity</style></title><secondary-title><style face="normal" font="default">J Sci Food Agric</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Sci Food Agric</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Absorption</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Conformation</style></keyword><keyword><style face="normal" font="default"> glycation</style></keyword><keyword><style face="normal" font="default"> High intensity ultrasound</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> ultrasound pretreatment</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">BACKGROUND: Ovalbumin (OVA), a protein with excellent nutritional and processing properties, is the major allergen of hen egg white. Previous study showed that high-intensity ultrasound treatment increased the IgG and IgE binding abilities by unfolding the conformational structure of OVA. It may allow modifying the IgG and IgE binding of OVA by combining high-intensity ultrasound with other methods, such as glycation, a promising method for the improvement of protein properties. RESULTS: Glycation with mannose (M) after ultrasound pretreatment at 0-600 W significantly reduced the IgG and IgE binding abilities and dramatically enhanced the antioxidant activity of OVA-M conjugates, with the lowest values of IgG and IgE binding and highest values of antioxidant capacity observed at 600W. The polyacrylamide gel electrophoresis showed that the molecular weight of OVA-M conjugates with ultrasound pretreatment increased more than non-pretreatment sample, implying ultrasound pretreatment promoted glycation. The alpha-helix content and UV absorption of OVA were observably increased while beta-sheet content, intrinsic fluorescence and surface hydrophobicity were notably decreased, indicating the tertiary and secondary structure of OVA were markedly changed. CONCLUSION: High-intensity ultrasound pretreatment can be conducive to reducing the IgG and IgE binding abilities and enhancing the antioxidant activity of OVA-M conjugates. Therefore, glycation combined with high-intensity ultrasound pretreatment might be a promising method for producing hypo-allergenic and high-antioxidant OVA products</style></abstract><notes><style face="normal" font="default">IS - 1097-0010 (Electronic)IS - 0022-5142 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1002/jsfa.8890</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29344948">PM:29344948</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Sci Food Agric\20180118-YangW.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Sci Food Agric\20180118-YangW.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Yang W</style></custom2><misc3><style face="normal" font="default">10.1002/jsfa.8890</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87436</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Clausen,M.L.</style></author><author><style face="normal" font="default"> Agner,T.</style></author><author><style face="normal" font="default"> Lilje,B.</style></author><author><style face="normal" font="default"> Edslev,S.M.</style></author><author><style face="normal" font="default"> Johannesen,T.B.</style></author><author><style face="normal" font="default"> Andersen,P.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Bispebjerg University Hospital, Copenhagen, Denmark</style></auth-address><titles><title><style face="normal" font="default">Association of Disease Severity With Skin Microbiome and Filaggrin Gene Mutations in Adult Atopic Dermatitis</style></title><secondary-title><style face="normal" font="default">JAMA Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">JAMA Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> genetics</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">Importance: Skin microbiome correlates with disease severity for lesional and nonlesional skin, indicating a global influence of atopic dermatitis (AD). A relation between skin microbiome and filaggrin gene (FLG) mutations proposes a possible association between skin microbiome and host genetics. Objectives: To assess skin and nasal microbiome diversity and composition in patients with AD and compare with healthy controls, and to investigate the microbiome in relation to disease severity and FLG mutations in patients with AD. Design, Setting, and Participants: An observational case-control study of 45 adult healthy controls and 56 adult patients with AD was carried out from January 2015 to June 2015 in a tertiary referral center, Department of Dermatology, Bispebjerg Hospital, Denmark. Exposures: Bacterial swabs were taken from patients with AD (lesional skin, nonlesional skin, and anterior nares) and from healthy controls (nonlesional skin and anterior nares). Eczema severity was assessed and FLG mutations noted. Bacterial DNA was extracted from swabs, and V3-V4 16S rDNA regions amplified with PCR. Samples were analyzed at Statens Serum Institut September 2015 to September 2016. Bioinformatics analyses of the microbiome were analyzed using R statistical software (version 3.3.1, R Foundation Inc). Main Outcomes and Measures: Skin microbiomes were investigated using next-generation sequencing targeting 16S ribosomal RNA. Results: Microbiome alpha diversity was lower in patients with AD compared with healthy controls in nonlesional skin (effect size, 0.710; 95% CI, 0.27-1.15; P = .002), lesional skin (effect size, 0.728; 95% CI, 0.35-1.33; P = .001), and nose (effect size, 1.111; 95% CI, 0.48-0.94; P &lt; .001). Alpha diversity was inversely correlated with disease severity for lesional (effect size, 0.530; 95% CI, 0.23-1.64; P = .02) and nonlesional skin (effect size, 0.451; 95% CI, 0.04-2.44; P = .04) in patients with AD. Microbiome composition in AD nonlesional skin was linked to FLG mutations. Conclusions and Relevance: An altered microbiome composition in patients with AD in nonlesional skin, lesional skin, as well as nose, suggests a global influence of AD. Microbiome composition in AD nonlesional skin is associated with FLG mutations, proposing a possible association between the skin microbiome and host genetics</style></abstract><notes><style face="normal" font="default">IS - 2168-6084 (Electronic)IS - 2168-6068 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1001/jamadermatol.2017.5440</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29344612">PM:29344612</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\JAMA Dermatol\20180117-ClausenML.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\JAMA Dermatol\20180117-ClausenML.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Clausen ML</style></custom2><misc3><style face="normal" font="default">10.1001/jamadermatol.2017.5440</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87438</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Watkins,T.N.</style></author><author><style face="normal" font="default"> Liu,H.</style></author><author><style face="normal" font="default"> Chung,M.</style></author><author><style face="normal" font="default"> Hazen,T.H.</style></author><author><style face="normal" font="default"> Dunning Hotopp,J.C.</style></author><author><style face="normal" font="default"> Filler,S.G.</style></author><author><style face="normal" font="default"> Bruno,V.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">1Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA</style></auth-address><titles><title><style face="normal" font="default">Comparative transcriptomics of Aspergillus fumigatus strains upon exposure to human airway epithelial cells</style></title><secondary-title><style face="normal" font="default">Microb Genom</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Microb Genom</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">Aspergillus fumigatus is an opportunistic, ubiquitous, saprophytic mould that can cause severe allergic responses in atopic individuals as well as life-threatening infections in immunocompromised patients. A critical step in the establishment of infection is the invasion of airway epithelial cells by the inhaled fungi. Understanding how A. fumigatus senses and responds to airway cells is important to understand the pathogenesis of invasive pulmonary aspergillosis. Here, we analysed the transcriptomes of two commonly used clinical isolates, Af293 and CEA10, during infection of the A549 type II pneumocyte cell line in vitro. We focused our RNA-seq analysis on the core set of genes that are present in the genomes of the two strains. Our results suggest that: (a) A. fumigatus does not mount a conserved transcriptional response to airway epithelial cells in our in vitro model and (b) strain background and time spent in the tissue culture media have a greater impact on the transcriptome than the presence of host cells. Our analyses reveal both common and strain-specific transcriptional programmes that allow for the generation of hypotheses about gene function as it pertains to pathogenesis and the significant phenotypic heterogeneity that is observed among A. fumigatus isolates</style></abstract><notes><style face="normal" font="default">IS - 2057-5858 (Electronic)IS - 2057-5858 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1099/mgen.0.000154</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29345613">PM:29345613</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Microb Genom\20180118-WatkinsTN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Microb Genom\20180118-WatkinsTN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Watkins TN</style></custom2><misc3><style face="normal" font="default">10.1099/mgen.0.000154</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87439</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lei,W.</style></author><author><style face="normal" font="default"> Zeng,D.</style></author><author><style face="normal" font="default"> Liu,G.</style></author><author><style face="normal" font="default"> Zhu,Y.</style></author><author><style face="normal" font="default"> Wang,J.</style></author><author><style face="normal" font="default"> Wu,H.</style></author><author><style face="normal" font="default"> Jiang,J.</style></author><author><style face="normal" font="default"> Huang,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Crucial role of OX40/OX40L signaling in a murine model of asthma</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">The aim of the present study was to explore the roles of OX40/OX40 ligand (OX40L) signaling and OX40+ T cells in ovalbumin (OVA)induced mouse asthma model. Asthma was induced by OVA exposure and subsequent cotreatment with OX40L protein, neutralizing antiOX40L blocking antibody, OX40+ T cells or PBS. The protein expression levels of interleukin (IL)4, IL6, IL13, IL17, tumor necrosis factor (TNF)alpha and interferon (IFN)gamma in bronchoalveolar lavage fluid (BALF) were examined using murine cytokinespecific ELISA. Eosinophil accumulation as well as proliferation and apoptosis of T cells in BALF were detected by Cell Counting kit8 and flow cytometric assays. Expression of the apoptosisrelated protein cleaved caspase3 was examined in OX40+ T cells using western blot assay. Flow cytometric analysis revealed that OVAtreated mice that were cotreated with OX40L or OX40+ T cells exhibited higher eosinophil infiltration compared with control mice treated only with OVA, whereas neutralizing antiOX40L blocking antibody inhibited eosinophil infiltration. ELISA assays demonstrated that the expression of IL4, IL6, IL13, IL17, TNFalpha and IFNgamma in BALF in OX40Ltreated and OX40+ T celltreated mice was increased compared with expression levels in control mice. Treatment with OX40L protein effectively reduced apoptosis of T cells and the expression of cleaved caspase3 in T cells. OX40Ltreated and OX40+ T celltreated mice exhibited increased asthma through OX40/OX40L signaling, which probably promoted inflammatory factor expression, eosinophil infiltration and T cell proliferation</style></abstract><notes><style face="normal" font="default">IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2018.8453.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29344664">PM:29344664</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180118, Lei W</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2018.8453.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87440</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Manabe,T.</style></author><author><style face="normal" font="default"> Oku,N.</style></author><author><style face="normal" font="default"> Aihara,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Kanagawa Prefectural Ashigarakami Hospital, Matsuda, Kanagawa, Japan</style></auth-address><titles><title><style face="normal" font="default">Food-dependent exercise-induced anaphylaxis in Japanese elementary school children</style></title><secondary-title><style face="normal" font="default">Pediatr Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">BACKGROUND: In 2012, we clarified that the prevalence of food-dependent exercise-induced anaphylaxis (FDEIA) was 0.018% among junior-high students in Yokohama, Japan. Furthermore, although different from FDEIA, one student who had completed oral immunotherapy developed anaphylaxis during exercise after eating causative food. However, there have been few large-scale epidemiological studies of FDEIA in elementary school children, so we conducted the epidemiological study among elementary school children in Yokohama to clarify the frequency and characteristic of FDEIA. METHODS: We sent a questionnaire regarding the occurrence of FDEIA to all 348 public elementary school nurses in Yokohama. We also compared the results with those for junior-high school that we previously reported. We excluded children with past history of immediate food allergy from FDEIA and defined as desensitization status and exercise induced anaphylaxis (DEIA). RESULTS: Of 348 school nurses, 317 responded (91.1%). Overall, 8 of 170,146 children were diagnosed with FDEIA, which was significantly lower than the prevalence in junior-high school students (0.0047% vs 0.018%, p= 0.0009). The causative foods were wheat (4 cases), and soy, fruit, crustaceans, and squid (1 case each). Four children had DEIA and the causative foods were wheat and milk (2 cases each). Multiple episodes occurred in 5 children with FDEIA and 3 children with.DEIA. CONCLUSIONS: FDEIA was far less common in elementary school than in junior-high school, and wheat was the major causative food among afflicted children. The emergence of DEIA was notable. Decreasing episode recurrence remains an issue that needs to be resolved. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1442-200X (Electronic)IS - 1328-8067 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/ped.13520</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29341364">PM:29341364</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Int\20180117-ManabeT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Int\20180117-ManabeT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Manabe T</style></custom2><misc3><style face="normal" font="default">10.1111/ped.13520</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87441</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ishii,T.</style></author><author><style face="normal" font="default"> Niikura,Y.</style></author><author><style face="normal" font="default"> Kurata,K.</style></author><author><style face="normal" font="default"> Muroi,M.</style></author><author><style face="normal" font="default"> Tanamoto,K.I.</style></author><author><style face="normal" font="default"> Nagase,T.</style></author><author><style face="normal" font="default"> Sakaguchi,M.</style></author><author><style face="normal" font="default"> Yamashita,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pharmacotherapy, Research Institute of Pharmaceutical Sciences, Musashino University, Tokyo, Japan</style></auth-address><titles><title><style face="normal" font="default">Time-dependent distinct roles of Toll-like receptor 4 in a house-dust-mite-induced asthma mouse model</style></title><secondary-title><style face="normal" font="default">Scand J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Scand J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="16" Month="1" Year="2018">2018/1/16</year></dates><abstract><style face="normal" font="default">House dust mites (HDMs) are a common source of allergens that trigger both allergen-specific and innate immune responses in humans. Here we examined the effect of allergen concentration and the involvement of Toll-like receptor 4 (TLR4) in the process of sensitization to house dust mite allergens in an HDM-extract-induced asthma mouse model. Intranasal administration of HDM extract induced an immunoglobulin E response and eosinophilic inflammation in a dose-dependent manner from 2.5 to 30 mug/dose. In TLR4-knockout mice, the infiltration of eosinophils and neutrophils into the lung was decreased compared with that in wild-type mice in the early phase of inflammation (total of three doses). However, in the late phase of inflammation (total of seven doses), eosinophil infiltration was significantly greater in TLR4-knockout mice than in wild-type mice. This suggests that the roles of TLR4 signaling are different between the early phase and the later phase of HDM-allergen-induced inflammation. Thus, innate immune response through TLR4 regulated the response to HDM allergens, and the regulation was altered during the phase of inflammation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-3083 (Electronic)IS - 0300-9475 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/sji.12641</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29337391">PM:29337391</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Scand J Immunol\20180116-IshiiT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Scand J Immunol\20180116-IshiiT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180116, Ishii T</style></custom2><misc3><style face="normal" font="default">10.1111/sji.12641</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87445</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Batista,C.V.F.</style></author><author><style face="normal" font="default"> Martins,J.G.</style></author><author><style face="normal" font="default"> Restano-Cassulini,R.</style></author><author><style face="normal" font="default"> Coronas,F.I.V.</style></author><author><style face="normal" font="default"> Zamudio,F.Z.</style></author><author><style face="normal" font="default"> Procopio,R.</style></author><author><style face="normal" font="default"> Possani,L.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratorio Universitario de Proteomica, Instituto de Biotecnologia, Universidad Nacional Autonoma de Mexico, Avenida Universidad 2001, Apartado Postal 510-3, Cuernavaca, Morelos 62210, Mexico</style></auth-address><titles><title><style face="normal" font="default">Venom characterization of the Amazonian scorpion Tityus metuendus</style></title><secondary-title><style face="normal" font="default">Toxicon</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Toxicon</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Amino Acid Sequence</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Components</style></keyword><keyword><style face="normal" font="default"> Enzymes</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="11" Month="1" Year="2018">2018/1/11</year></dates><abstract><style face="normal" font="default">The soluble venom from the scorpion Tityus metuendus was characterized by various methods. In vivo experiments with mice showed that it is lethal. Extended electrophysiological recordings using seven sub-types of human voltage gated sodium channels (hNav1.1 to 1.7) showed that it contains both alpha- and beta-scorpion toxin types. Fingerprint analysis by mass spectrometry identified over 200 distinct molecular mass components. At least 60 sub-fractions were recovered from HPLC separation. Five purified peptides were sequenced by Edman degradation, and their complete primary structures were determined. Additionally, three other peptides have had their N-terminal amino acid sequences determined by Edman degradation and reported. Mass spectrometry analysis of tryptic digestion of the soluble venom permitted the identification of the amino acid sequence of 111 different peptides. Search for similarities of the sequences found indicated that they probably are: sodium and potassium channel toxins, metalloproteinases, hyaluronidases, endothelin and angiotensin-converting enzymes, bradykinin-potentiating peptide, hypothetical proteins, allergens, other enzymes, other proteins and peptides</style></abstract><notes><style face="normal" font="default">IS - 1879-3150 (Electronic)IS - 0041-0101 (Linking)LA - engPT - Journal ArticleCO - Mexico -CO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.toxicon.2018.01.006</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29337221">PM:29337221</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Toxicon\20180112-BatistaCV.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Toxicon\20180112-BatistaCV.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180112, Batista CV</style></custom2><misc3><style face="normal" font="default">10.1016/j.toxicon.2018.01.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87420</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">de Bruin-Weller,M.</style></author><author><style face="normal" font="default"> Graham,N.M.H.</style></author><author><style face="normal" font="default"> Pirozzi,G.</style></author><author><style face="normal" font="default"> Shumel,B.</style></author></authors></contributors><auth-address><style face="normal" font="default">University Medical Center Utrecht, Utrecht, Netherlands</style></auth-address><titles><title><style face="normal" font="default">Could conjunctivitis in dupilumab treated atopic dermatitis patients be caused by colonization with Demodex and increased IL-17 levels? Reply from authors</style></title><secondary-title><style face="normal" font="default">Br J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">In studies in atopic dermatitis (AD), dupilumab has been associated with higher rates of conjunctivitis compared with placebo. Consistent with previous studies, in LIBERTY AD CAFE (NCT02755649), all cases but one were mild or moderate, most (62-89%) were recovered/resolved or recovering/resolving by end of treatment, and no patients permanently discontinued study treatment because of conjunctivitis.(1) No patients reported atopic keratoconjunctivitis in this study. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2133 (Electronic)IS - 0007-0963 (Linking)LA - engPT - LetterCO - Netherlands -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/bjd.16348</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29336016">PM:29336016</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Dermatol\20180115-deBruinWellerM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Dermatol\20180115-deBruinWellerM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, de Bruin-Weller M</style></custom2><misc3><style face="normal" font="default">10.1111/bjd.16348</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87452</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Abrams,E.M.</style></author><author><style face="normal" font="default"> Chan,E.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Section of Allergy and Clinical Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.</style></auth-address><titles><title><style face="normal" font="default">Potential Pitfalls in Applying Screening Criteria in Infants at Risk of Peanut Allergy</style></title><secondary-title><style face="normal" font="default">J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6833 (Electronic)IS - 0022-3476 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1016/j.jpeds.2017.12.011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29352591">PM:29352591</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pediatr\20180117-AbramsEM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pediatr\20180117-AbramsEM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Abrams EM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jpeds.2017.12.011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87453</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Di Nardo,G.</style></author><author><style face="normal" font="default"> Cremon,C.</style></author><author><style face="normal" font="default"> Frediani,S.</style></author><author><style face="normal" font="default"> Lucarelli,S.</style></author><author><style face="normal" font="default"> Villa,M.P.</style></author><author><style face="normal" font="default"> Stanghellini,V.</style></author><author><style face="normal" font="default"> La Torre,G.</style></author><author><style face="normal" font="default"> Martemucci,L.</style></author><author><style face="normal" font="default"> Barbara,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Gastroenterology Unit, Santobono-Pausilipon Children's Hospital, Naples, Italy; Pediatric Gastroenterology Unit, International Hospital Salvator Mundi, Rome, Italy</style></auth-address><titles><title><style face="normal" font="default">Allergic Proctocolitis Is a Risk Factor for Functional Gastrointestinal Disorders in Children</style></title><secondary-title><style face="normal" font="default">J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> Multivariate Analysis</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To test the hypothesis that allergic proctocolitis, a cause of self-limiting rectal bleeding in infants, can predispose to the development of functional gastrointestinal disorders (FGIDs) later in childhood. STUDY DESIGN: We studied a cohort of 80 consecutive patients diagnosed with allergic proctocolitis. Their sibling or matched children presenting to the same hospital for minor trauma served as controls. Parents of the patients with allergic proctocolitis and controls participated in a telephone interview every 12 months until the child was at least 4 years old. At that time, they were asked to complete the parental Questionnaire on Pediatric Gastrointestinal Symptoms, Rome III version. RESULTS: Sixteen of the 160 subjects (10.0%) included in the study met the Rome III criteria for FGIDs. Among the 80 patients with allergic proctocolitis, 12 (15.0%) reported FGIDs, compared with 4 of 80 (5.0%) controls (P = .035). After adjustment for age and sex, the OR for FGIDs in allergic proctocolitis group was 4.39 (95% CI, 1.03-18.68). FGIDs were significantly associated with iron deficiency anemia, duration of hematochezia, and younger age at presentation. In a multivariate analysis, only the duration of hematochezia was significantly associated with the development of FGIDs (OR, 3.14; 95% CI,1.72-5.74). CONCLUSIONS: We have identified allergic proctocolitis as a new risk factor for the development of FGIDs in children. Our data suggest that not only infection, but also a transient early-life allergic inflammatory trigger may induce persistent digestive symptoms, supporting the existence of "postinflammatory" FGIDs</style></abstract><notes><style face="normal" font="default">IS - 1097-6833 (Electronic)IS - 0022-3476 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.jpeds.2017.10.073</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29352590">PM:29352590</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pediatr\20180115-DiNardoG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pediatr\20180115-DiNardoG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Di Nardo G</style></custom2><misc3><style face="normal" font="default">10.1016/j.jpeds.2017.10.073</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87451</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">van Wijck,Y.</style></author><author><style face="normal" font="default"> de Kleijn,S.</style></author><author><style face="normal" font="default"> John-Schuster,G.</style></author><author><style face="normal" font="default"> Mertens,T.C.J.</style></author><author><style face="normal" font="default"> Hiemstra,P.S.</style></author><author><style face="normal" font="default"> Muller,A.</style></author><author><style face="normal" font="default"> Smits,H.H.</style></author><author><style face="normal" font="default"> Taube,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pulmonology, Leiden University Medical Center, 2300 RC Leiden, the Netherlands</style></auth-address><titles><title><style face="normal" font="default">Therapeutic Application of an Extract of Helicobacter pylori Ameliorates the Development of Allergic Airway Disease</style></title><secondary-title><style face="normal" font="default">J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="19" Month="1" Year="2018">2018/1/19</year></dates><abstract><style face="normal" font="default">Epidemiological and experimental studies have shown that exposure to the gastric bacterium Helicobacter pylori, especially in early life, prevents the development of asthma. Recent mouse studies have shown that this protective effect does not require live bacteria and that treatment with an extract of H. pylori in neonates prevents the development of airway inflammation and goblet cell metaplasia. In the current study, the effect of administration of an extract of H. pylori was assessed in a therapeutic study design with application of the extract just prior to allergen challenge. C57BL/6 mice were sensitized and challenged with OVA or house dust mite. Treatment with H. pylori extract just prior to the challenge significantly reduced airway inflammation, as assessed in bronchoalveolar lavage fluid and lung tissue, and reduced airway remodeling, as assessed by goblet cell quantification. These effects were apparent in the OVA model and in the house dust mite model. Injection of H. pylori extract reduced the processing of allergen by dendritic cells in the lungs and mediastinal lymph node. Bone marrow-derived dendritic cells exposed to H. pylori extract were affected with regard to their ability to process Ag. These data show that application of H. pylori extract after sensitization effectively inhibits allergic airway disease</style></abstract><notes><style face="normal" font="default">IS - 1550-6606 (Electronic)IS - 0022-1767 (Linking)LA - engPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.4049/jimmunol.1700987</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29352004">PM:29352004</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol\20180119-vanWijckY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol\20180119-vanWijckY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180119, van Wijck Y</style></custom2><misc3><style face="normal" font="default">10.4049/jimmunol.1700987</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87450</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Takeda,K.</style></author><author><style face="normal" font="default"> Webb,T.L.</style></author><author><style face="normal" font="default"> Ning,F.</style></author><author><style face="normal" font="default"> Shiraishi,Y.</style></author><author><style face="normal" font="default"> Regan,D.P.</style></author><author><style face="normal" font="default"> Chow,L.</style></author><author><style face="normal" font="default"> Smith,M.J.</style></author><author><style face="normal" font="default"> Ashino,S.</style></author><author><style face="normal" font="default"> Guth,A.M.</style></author><author><style face="normal" font="default"> Hopkins,S.</style></author><author><style face="normal" font="default"> Gelfand,E.W.</style></author><author><style face="normal" font="default"> Dow,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Division of Cell Biology, National Jewish Health, Denver, CO 80206</style></auth-address><titles><title><style face="normal" font="default">Mesenchymal Stem Cells Recruit CCR2(+) Monocytes To Suppress Allergic Airway Inflammation</style></title><secondary-title><style face="normal" font="default">J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="19" Month="1" Year="2018">2018/1/19</year></dates><abstract><style face="normal" font="default">Mesenchymal stem cells (MSC) exert immune modulatory properties and previous studies demonstrated suppressive effects of MSC treatment in animal models of allergic airway inflammation. However, the underlying mechanisms have not been fully elucidated. We studied the role of MSC in immune activation and subsequent recruitment of monocytes in suppressing airway hyperresponsiveness and airway inflammation using a mouse model of allergic airway inflammation. MSC administration prior to or after allergen challenge inhibited the development of airway inflammation in allergen-sensitized mice. This was accompanied by an influx of CCR2-positive monocytes, which were localized around injected MSC in the lungs. Notably, IL-10-producing monocytes and/or macrophages were also increased in the lungs. Systemic administration of liposomal clodronate or a CCR2 antagonist significantly prevented the suppressive effects of MSC. Activation of MSC by IFN-gamma leading to the upregulation of CCL2 expression was essential for the suppressive effects, as administration of wild-type MSC into IFN-gamma-deficient recipients, or IFN-gamma receptor-deficient or CCL2-deficient MSC into wild-type mice failed to suppress airway inflammation. These results suggest that MSC activation by IFN-gamma, followed by increased expression of CCL2 and recruitment of monocytes to the lungs, is essential for suppression by MSC in allergen-induced airway hyperresponsiveness and airway inflammation</style></abstract><notes><style face="normal" font="default">IS - 1550-6606 (Electronic)IS - 0022-1767 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.4049/jimmunol.1700562</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29352000">PM:29352000</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol\20180119-TakedaK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol\20180119-TakedaK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180119, Takeda K</style></custom2><misc3><style face="normal" font="default">10.4049/jimmunol.1700562</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87449</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sutherland,T.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Faculty of Biology, Medicine and Health, Manchester Collaborative Centre for Inflammation Research, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9NT, U.K.</style></auth-address><titles><title><style face="normal" font="default">Chitinase-like proteins as regulators of innate immunity and tissue repair: helpful lessons for asthma?</style></title><secondary-title><style face="normal" font="default">Biochem Soc Trans</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biochem Soc Trans</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Enzymes</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword></keywords><dates><year Day="19" Month="1" Year="2018">2018/1/19</year></dates><abstract><style face="normal" font="default">Chitinases and chitinase-like proteins (CLPs) belong to the glycoside hydrolase family 18 of proteins. Chitinases are expressed in mammals and lower organisms, facilitate chitin degradation, and hence act as host-defence enzymes. Gene duplication and loss-of-function mutations of enzymatically active chitinases have resulted in the expression of a diverse range of CLPs across different species. CLPs are genes that are increasingly associated with inflammation and tissue remodelling not only in mammals but also across distant species. While the focus has remained on understanding the functions and expression patterns of CLPs during disease in humans, studies in mouse and lower organisms have revealed important and overlapping roles of the CLP family during physiology, host defence and pathology. This review will summarise recent insights into the regulatory functions of CLPs on innate immune pathways and discuss how these effects are not only important for host defence and tissue injury/repair after pathogen invasion, but also how they have extensive implications for pathological processes involved in diseases such as asthma</style></abstract><notes><style face="normal" font="default">IS - 1470-8752 (Electronic)IS - 0300-5127 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1042/BST20170108</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29351964">PM:29351964</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biochem Soc Trans\20180119-SutherlandTE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biochem Soc Trans\20180119-SutherlandTE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180119, Sutherland TE</style></custom2><misc3><style face="normal" font="default">10.1042/BST20170108</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87454</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sikoparija,B.</style></author><author><style face="normal" font="default"> Marko,O.</style></author><author><style face="normal" font="default"> Panic,M.</style></author><author><style face="normal" font="default"> Jakovetic,D.</style></author><author><style face="normal" font="default"> Radisic,P.</style></author></authors></contributors><titles><title><style face="normal" font="default">How to prepare a pollen calendar for forecasting daily pollen concentrations of Ambrosia, Betula and Poaceae?</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Prediction</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">Forecasting daily airborne pollen concentrations is of great importance for management of seasonal allergies. This paper explores the performance of the pollen calendar as the most basic observation-oriented model for predicting daily concentrations of airborne Ambrosia, Betula and Poaceae pollen. Pollen calendars were calculated as the mean or median value of pollen concentrations on the same date in previous years of the available historic dataset, as well as the mean or median value of pollen concentrations of the smoothed dataset, pre-processed using moving mean and moving median. The performance of the models was evaluated by comparing forecasted to measured pollen concentrations at both daily and 10-day-average resolutions. This research demonstrates that the interpolation of missing data and pre-processing of the calibration dataset yields lower prediction errors. The increase in the number of calibration years corresponds to an improvement in the performance of the calendars in predicting daily pollen concentrations. However, the most significant improvement was obtained using four calibration years. The calendar models correspond well to the shape of the pollen curve. It was also found that daily resolution instead of 10-day averages adds to their value by emphasising variability in pollen exposure, which is important for personal assessment of dose-response for pollen-sensitive individuals</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Serbia -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-018-9507-9</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-018-9507-9</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20180123-SikoparijaB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20180123-SikoparijaB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180123, Sikoparija B</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-018-9507-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87455</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sola,J.P.</style></author><author><style face="normal" font="default"> Pedreno,Y.</style></author><author><style face="normal" font="default"> Cerezo,A.</style></author><author><style face="normal" font="default"> Penalver-Mellado,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Probelte Pharma S.L.U., Spain</style></auth-address><titles><title><style face="normal" font="default">Development and characterization of an allergoid of cat dander for immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergy to cats is a frequent cause of sensitization to indoor allergens and currently there are few alternatives to specific immunotherapy with cat native extracts. The objective is to develop and characterize a new allergoid to increase the tools available for use in clinical practice. METHODS: The allergoid cat dander extract (ACD) was developed from a native cat dander extract (NCD) by modification with glutaraldehyde, and the optimal process control was determined by SDS-PAGE, DOT BLOT and determination of free amine groups. The ACD was characterized in protein profile by SDS-PAGE, size exclusion chromatography (SEC) and peptide footprint. The allergenic profile of ACD was determined by immunoblot, IgE CAP inhibition and IgG competition ELISA. The major allergen content in NCD was obtained by the ELISA sandwich protocol and was extrapolated to ACD. RESULTS: The control process determined the optimal development of the allergoid. The ACD obtained contains 182.28mug/mg of protein and 11.90mug/mg of Fel d 1. SDS-PAGE and SEC confirmed the presence of high molecular weight proteins in ACD, and the peptide footprint showed the presence of Fel d 1 and Fel d 7. The high degree of polymerization was evidenced with the determination of the reduction of lysine residues in the allergoid, resulting 91.96%. The ACD showed a significant loss of allergenicity respect to NCD, while the IgG-binding capacity was maintained. CONCLUSIONS: The ACD obtained presents a good safety profile, so would be a good alternative for treatment of cat allergy</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.12.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29342409">PM:29342409</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180113-SolaJP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180113-SolaJP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Sola JP</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.12.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87456</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Miceli Sopo,S.</style></author><author><style face="normal" font="default"> Fantacci,C.</style></author><author><style face="normal" font="default"> Bersani,G.</style></author><author><style face="normal" font="default"> Romano,A.</style></author><author><style face="normal" font="default"> Monaco,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Agostino Gemelli Hospital, Sacred Heart Catholic University, Rome, Italy.</style></auth-address><titles><title><style face="normal" font="default">Loss of tolerance for fishes previously tolerated in children with fish food protein induced enterocolitis syndrome</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Children</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="12" Month="1" Year="2018">2018/1/12</year></dates><abstract><style face="normal" font="default">We describe two case reports presenting some novel information on fish FPIES. Fish FPIES to one fish does not always start at the same time to other fish. Additionally, development of tolerance to the index fish do not necessarily imply tolerance to other reactive fish. This reflects on the best management of children with FPIES fish</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.029</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29338963">PM:29338963</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180112-MiceliSopoS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20180112-MiceliSopoS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180112, Miceli Sopo S</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.029</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87457</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Revez,J.A.</style></author><author><style face="normal" font="default"> Killian,K.J.</style></author><author><style face="normal" font="default"> O'Byrne,P.M.</style></author><author><style face="normal" font="default"> Boulet,L.P.</style></author><author><style face="normal" font="default"> Upham,J.W.</style></author><author><style face="normal" font="default"> Gauvreau,G.M.</style></author><author><style face="normal" font="default"> Ferreira,M.A.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia</style></auth-address><titles><title><style face="normal" font="default">Sputum cytology during late phase responses to inhalation challenge with different allergens</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> cytology</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword></keywords><dates><year Day="16" Month="1" Year="2018">2018/1/16</year></dates><abstract><style face="normal" font="default">BACKGROUND: In mouse models of allergic asthma, exposure to different allergens can trigger distinct inflammatory subtypes in the airways. We investigated if this observation extends to humans. METHODS: We compared the frequency of sputum inflammatory subtypes between mild allergic asthma subjects (n=129) exposed to different allergens in inhalation challenge tests. These tests were performed using a standardized protocol as part of clinical trials of experimental treatments for asthma, prior to drug randomization. Five allergen types were represented: the house dust mites Dermatophagoides pteronyssinus and Dermatophagoides farinae, ragweed, grass and cat. RESULTS: Of 118 individuals with a sputum sample collected before allergen challenge (baseline), 45 (38%) had paucigranulocytic, 51 (43%) eosinophilic, 11 (9%) neutrophilic and 11 (9%) mixed granulocytic sputum. Of note, most individuals with baseline paucigranulocytic sputum developed eosinophilic (48%) or mixed granulocytic (43%) sputum seven hours after allergen challenge, highlighting the dynamic nature of sputum inflammatory subtype in asthma. Overall, there was no difference in the frequency of sputum inflammatory subtypes following challenge with different allergen types. Similar results were observed at 24 hours after allergen challenge. CONCLUSIONS: Unlike reported in mice, in humans the sputum inflammatory subtype observed after an allergen-induced asthma exacerbation is unlikely to be influenced by the type of allergen used. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Australia -CO - Canada -</style></notes><work-type><style face="normal" font="default">10.1111/all.13415</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29337345">PM:29337345</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180116-RevezJA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180116-RevezJA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180116, Revez JA</style></custom2><misc3><style face="normal" font="default">10.1111/all.13415</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87458</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Einhorn,L.</style></author><author><style face="normal" font="default"> Hofstetter,G.</style></author><author><style face="normal" font="default"> Brandt,S.</style></author><author><style face="normal" font="default"> Hainisch,E.K.</style></author><author><style face="normal" font="default"> Fukuda,I.</style></author><author><style face="normal" font="default"> Kusano,K.</style></author><author><style face="normal" font="default"> Scheynius,A.</style></author><author><style face="normal" font="default"> Mittermann,I.</style></author><author><style face="normal" font="default"> Resch-Marat,Y.</style></author><author><style face="normal" font="default"> Vrtala,S.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author><author><style face="normal" font="default"> Marti,E.</style></author><author><style face="normal" font="default"> Rhyner,C.</style></author><author><style face="normal" font="default"> Crameri,R.</style></author><author><style face="normal" font="default"> Satoh,R.</style></author><author><style face="normal" font="default"> Teshima,R.</style></author><author><style face="normal" font="default"> Tanaka,A.</style></author><author><style face="normal" font="default"> Sato,H.</style></author><author><style face="normal" font="default"> Matsuda,H.</style></author><author><style face="normal" font="default"> Pali-Scholl,I.</style></author><author><style face="normal" font="default"> Jensen-Jarolim,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">The interuniversity Messerli Research Institute, University of Veterinary Medicine Vienna, Medical University Vienna and University Vienna, Vienna, AustriaAllergyCare, Allergy Diagnosis and Study Center, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Molecular allergen profiling in horses by microarray reveals Fag e 2 from buckwheat as a frequent sensitizer</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="19" Month="1" Year="2018">2018/1/19</year></dates><abstract><style face="normal" font="default">BACKGROUND: Companion animals are also affected by IgE-mediated allergies, but the eliciting molecules are largely unknown. We aimed at refining an allergen microarray to explore sensitization in horses and compare it to the human IgE reactivity profiles. METHODS: Custom-designed allergen microarray was produced on the basis of the IimmunoCAP ISAC technology containing 131 allergens. Sera from 51 horses derived from Europe or Japan were tested for specific IgE reactivity. The included horse patients were diagnosed for eczema due to insect bite hypersensitivity, chronic coughing, recurrent airway obstruction, urticaria, or were clinically asymptomatic. RESULTS: Horses showed individual IgE binding patterns irrespective of their health status, indicating sensitization. In contrast to European and Japanese human sensitization patterns, frequently recognized allergens were Aln g 1 from alder and Cyn d 1 from Bermuda grass, likely due to specific respiratory exposure around paddocks and near the ground. The most prevalent allergen for 72.5% of the tested horses (37/51) was the 2S-albumin Fag e 2 from buckwheat, which recently gained importance not only in human but also in horse diet. CONCLUSION: In line with the One Health concept, covering human health, animal health and environmental health, allergen microarrays provide novel information on the allergen sensitization patterns of the companion animals around us, which may form a basis for allergen-specific preventive and therapeutic concepts. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - Japan -CO - Sweden -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/all.13417</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29350763">PM:29350763</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20180119-EinhornL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20180119-EinhornL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180119, Einhorn L</style></custom2><misc3><style face="normal" font="default">10.1111/all.13417</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87460</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lin,R.</style></author><author><style face="normal" font="default"> Choi,Y.H.</style></author><author><style face="normal" font="default"> Zidar,D.A.</style></author><author><style face="normal" font="default"> Walker,J.K.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Duke University School of Medicine, 12277, Durham, North Carolina, United States</style></auth-address><titles><title><style face="normal" font="default">beta arrestin-2-dependent Signaling Promotes CCR4-mediated Chemotaxis of Murine T Helper Type 2 Cells</style></title><secondary-title><style face="normal" font="default">Am J Respir Cell Mol Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Respir Cell Mol Biol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="23" Month="1" Year="2018">2018/1/23</year></dates><abstract><style face="normal" font="default">Allergic asthma is a complex inflammatory disease that leads to significant healthcare costs and reduction in quality of life. Although many cell types are implicated in the pathogenesis of asthma, CD4+ T helper type 2 cells (Th2) are centrally involved. We previously reported that the asthma phenotype is virtually absent in ovalbumin-sensitized and -challenged mice that lack global expression of betaarrestin-2 and that CD4+ T cells from these mice displayed significantly reduced C-C motif chemokine 22 (CCL22)-mediated chemotaxis. Since CCL22-mediated activation of C-C chemokine receptor type 4 (CCR4) plays a role in Th2 cell regulation in asthmatic inflammation, we hypothesized that CCR4-mediated migration of CD4+ Th2 cells to the lung in asthma may utilize betaarrestin-dependent signaling. To test this hypothesis we assessed the effect of various signaling inhibitors on CCL22-induced chemotaxis using in vitro-polarized primary CD4+ Th2 cells from betaarrestin-2-KO and WT mice. Our results show, for the first time, that CCL22-induced, CCR4-mediated Th2 cell chemotaxis is dependent, in part, on a betaarrestin-2-dependent signaling pathway. Additionally, we show that this chemotactic signaling mechanism involves activation of P-p38 and Rho-associated protein kinase. These findings point to a pro-inflammatory role for betaarrestin-2-dependent signaling and support betaarrestin-2 as a novel therapeutic target in asthma</style></abstract><notes><style face="normal" font="default">IS - 1535-4989 (Electronic)IS - 1044-1549 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1165/rcmb.2017-0240OC</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29361236">PM:29361236</url></web-urls><pdf-urls><url ppv-ref="no">rui.lin.rao@gmail.com</url><url ppv-ref="no">walke082@mc.duke.edu</url></pdf-urls><related-urls><url ppv-ref="no">presto - 1 anno</url></related-urls></urls><custom2><style face="normal" font="default">20180123, Lin R</style></custom2><misc3><style face="normal" font="default">10.1165/rcmb.2017-0240OC</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87461</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Amison,R.T.</style></author><author><style face="normal" font="default"> Cleary,S.</style></author><author><style face="normal" font="default"> Riffo-Vasquez,Y.</style></author><author><style face="normal" font="default"> Bajwa,M.</style></author><author><style face="normal" font="default"> Page,C.P.</style></author><author><style face="normal" font="default"> Pitchford,S.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">King's College London, Institute of Pharmaceutical Science, London, United Kingdom of Great Britain and Northern Ireland</style></auth-address><titles><title><style face="normal" font="default">Platelets Play a Central Role in Sensitization to Allergen</style></title><secondary-title><style face="normal" font="default">Am J Respir Cell Mol Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Respir Cell Mol Biol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">BACKGROUND: Platelet activation occurs in patients with allergic inflammation, and platelets can be activated directly by allergen via an IgE-dependent process. Platelets activate antigen-presenting cells (APCs) such as CD11c+ dendritic cells (DCs) in vitro. Whilst CD11c+ DCs are requisite for allergen sensitization, the role of platelets in this process is unknown. OBJECTIVES: We investigated whether platelets were necessary for allergen sensitization. METHODS: Balb/c mice sensitised to ovalbumin (OVA), were exposed to subsequent aerosolized allergen (OVA challenge). We analysed lung CD11c+ cell activation, co-localization with platelets, and some other indices of inflammation. The role of platelets at the time of allergen sensitization was assessed through platelet depletion experiments restricted to the period of sensitization. RESULTS: Platelets co-localized with airway CD11c+ cells, and this association increased after allergen sensitization, and after subsequent allergen exposure. Temporary platelet depletion (>95%) at the time of allergen sensitization led to a suppression of IgE and IL-4 synthesis, and a decrease in the pulmonary recruitment of eosinophils, macrophages, and lymphocytes after subsequent allergen exposure. Furthermore, in mice previously depleted of platelets at the time of sensitization, the recovered platelet population were shown to have reduced expression of FcvarepsilonRI. Pulmonary CD11c+ cell recruitment was suppressed in these mice after allergen challenge, suggesting the migration of CD11c+ cells in vivo may be dependent on direct platelet recognition of allergen. CONCLUSION: Platelets are necessary for efficient host sensitization to allergen. This propagates the subsequent inflammatory response during secondary allergen exposure, and increases platelet association with airway CD11c+ cells</style></abstract><notes><style face="normal" font="default">IS - 1535-4989 (Electronic)IS - 1044-1549 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1165/rcmb.2017-0401OC</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29365287">PM:29365287</url></web-urls><pdf-urls><url ppv-ref="no">richard.amison@kcl.ac.uk</url><url ppv-ref="no">simon.pitchford@kcl.ac.uk</url></pdf-urls><related-urls><url ppv-ref="no">presto - 1 anno</url></related-urls></urls><custom2><style face="normal" font="default">20180124, Amison RT</style></custom2><misc3><style face="normal" font="default">10.1165/rcmb.2017-0401OC</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87462</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hsieh,M.C.</style></author><author><style face="normal" font="default"> Wu,Y.C.</style></author><author><style face="normal" font="default"> Huang,S.H.</style></author><author><style face="normal" font="default"> Kuo,Y.R.</style></author><author><style face="normal" font="default"> Lee,S.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">A Single-Center, Randomized, Double-Blind, Placebo-Controlled Clinical Trial of the Effectiveness of ANT1 Soybean Extract Cream on Skin Recovery After Nd: YAG Laser Treatment</style></title><secondary-title><style face="normal" font="default">Ann Plast Surg</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Plast Surg</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Aged</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> complications</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="25" Month="1" Year="2018">2018/1/25</year></dates><abstract><style face="normal" font="default">Nd:YAG laser has been used extensively for its versatility in treating many common aesthetic problems, but numerous adverse effects are often complained by recipients of Nd:YAG laser. This study introduces the ANT1 soybean extract cream, which was formulated to alleviate adverse effects after laser therapy. This study explores whether ANT1 enhances the repair mechanism of the postlaser skin, decreases laser-induced complication, and shortens recovery time. The study also aims to pinpoint the ANT1 concentration that is most effective in improving the skin condition after Nd-YAG laser therapy. MATERIALS AND METHODS: This study was a single-center, randomized, double-blind, placebo-controlled trial. Patients eligible for the study were Asian women, aged 25 to 40 years, who were free of dermatological diseases and allergic reaction. There were a total of 45 subjects. Each subject received a session of Nd-YAG laser therapy every 2 weeks, totaling 3 sessions. Facial skin assessment was achieved via VISIA complexion analysis. VISIA complexion analysis quantitatively assessed the skin condition and tracked the recovery progress of each subject at baseline, immediately after all 3 laser sessions, and a week after the final laser treatment. RESULTS: Skin condition was evaluated by VISIA complexion analysis. Skin condition was recorded in aspects of pigmented spots, wrinkles, texture, pores, and red area. After Nd-YAG laser therapy, postlaser inflammation was observed in all subjects. Throughout the laser sessions and the outpatient follow-up clinic, the adverse effects of laser therapy, such as redness, spots, wrinkles, pores, and textures, decreased with the use of ANT1 cream. There has been a marked effect in wrinkle reduction in the patients who received a higher concentration of ANT1 cream (P &lt;/= 0.05). Statistically significant improvement in spots and pores is also seen (P &lt;/= 0.05). CONCLUSIONS: Through this study, the results suggest that the application of ANT1 soybean extract cream ameliorates the complications and enhances the cosmetic effects of Nd-YAG laser therapy. A higher concentration of the ANT1 cream significantly reduces wrinkles and redness after laser. All in all, this study proves that the ANT1 soy extract cream may be a useful addition to postlaser care for an overall enhancement in skin condition and recovery</style></abstract><notes><style face="normal" font="default">IS - 1536-3708 (Electronic)IS - 0148-7043 (Linking)LA - engPT - Journal ArticleCO - Taiwan -</style></notes><work-type><style face="normal" font="default">10.1097/SAP.0000000000001287</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29369914">PM:29369914</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Plast Surg\20180125-HsiehMC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Plast Surg\20180125-HsiehMC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180125, Hsieh MC</style></custom2><misc3><style face="normal" font="default">10.1097/SAP.0000000000001287</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87465</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kono,M.</style></author><author><style face="normal" font="default"> Akiyama,M.</style></author><author><style face="normal" font="default"> Inoue,Y.</style></author><author><style face="normal" font="default"> Nomura,T.</style></author><author><style face="normal" font="default"> Hata,A.</style></author><author><style face="normal" font="default"> Okamoto,Y.</style></author><author><style face="normal" font="default"> Takeichi,T.</style></author><author><style face="normal" font="default"> Muro,Y.</style></author><author><style face="normal" font="default"> McLean,W.H.I.</style></author><author><style face="normal" font="default"> Shimizu,H.</style></author><author><style face="normal" font="default"> Sugiura,K.</style></author><author><style face="normal" font="default"> Suzuki,Y.</style></author><author><style face="normal" font="default"> Shimojo,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Nagoya University Graduate School of Medicine, Nagoya, Japan</style></auth-address><titles><title><style face="normal" font="default">Filaggrin gene mutations may influence the persistence of food allergies in Japanese primary school children</style></title><secondary-title><style face="normal" font="default">Br J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="25" Month="1" Year="2018">2018/1/25</year></dates><abstract><style face="normal" font="default">Mutations in FLG are the underlying cause of ichthyosis vulgaris and are an important predisposing factor for atopic dermatitis (AD).(1) In 2011, FLG mutations were reported to increase the risk of peanut allergy(2) , and they have been proven to increase the risk of other food sensitizations and allergies.(3,4) In this study, we comprehensively screened 411 children in Japan for 10 Japanese-population-specific FLG mutations and suggested that FLG mutations influence the persistence of food allergies (FAs). This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2133 (Electronic)IS - 0007-0963 (Linking)LA - engPT - LetterCO - Japan -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/bjd.16375</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29369340">PM:29369340</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Dermatol\20180125-KonoM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Dermatol\20180125-KonoM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180125, Kono M</style></custom2><misc3><style face="normal" font="default">10.1111/bjd.16375</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87466</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Curto-Barredo,L.</style></author><author><style face="normal" font="default"> Spertino,J.</style></author><author><style face="normal" font="default"> Figueras-Nart,I.</style></author><author><style face="normal" font="default"> Exposito-Serrano,V.</style></author><author><style face="normal" font="default"> Guilabert,A.</style></author><author><style face="normal" font="default"> Mele-Ninot,G.</style></author><author><style face="normal" font="default"> Cubiro,X.</style></author><author><style face="normal" font="default"> Bonfill-Orti,M.</style></author><author><style face="normal" font="default"> Garcias-Ladaria,J.</style></author><author><style face="normal" font="default"> Villar,M.</style></author><author><style face="normal" font="default"> Garcia-Navarro,X.</style></author><author><style face="normal" font="default"> Bielsa-Marsol,I.</style></author><author><style face="normal" font="default"> Vilavella,M.</style></author><author><style face="normal" font="default"> Aparicio,G.</style></author><author><style face="normal" font="default"> Baliu-Pique,C.</style></author><author><style face="normal" font="default"> Alvarez,A.</style></author><author><style face="normal" font="default"> Lamas-Domenech,N.</style></author><author><style face="normal" font="default"> Duran-Jorda,X.</style></author><author><style face="normal" font="default"> Serra-Baldrich,E.</style></author><author><style face="normal" font="default"> Gimenez-Arnau,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Hospital del Mar Medical Research Institute (IMIM), Universitat Autonoma Barcelona, (UAB) - Dermatology, Barcelona, Catalunya, Spain</style></auth-address><titles><title><style face="normal" font="default">Omalizumab updosing allows disease activity control in refractory patients with chronic spontaneous urticaria</style></title><secondary-title><style face="normal" font="default">Br J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Omalizumab</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">Omalizumab has been shown to be a very effective drug in chronic spontaneous urticaria (CSU) improving patients' quality of life.(1) Phase III clinical trials ASTERIA I/II and GLACIAL showed respectively 58.8-52.4% of patients achieving a twice daily average Urticaria Activity Score 7 (UAS7td)&lt;/=6 at week 12.(2) Outside of clinical trials, the response varies between 77-83%.(3) However, some patients do not achieve well-controlled activity of the disease with the licensed dose of omalizumab (300mg/4 weeks). This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2133 (Electronic)IS - 0007-0963 (Linking)LA - engPT - LetterCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1111/bjd.16379</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29368377">PM:29368377</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Dermatol\20180124-CurtoBarredoL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Dermatol\20180124-CurtoBarredoL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180124, Curto-Barredo L</style></custom2><misc3><style face="normal" font="default">10.1111/bjd.16379</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87467</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Willen,S.M.</style></author><author><style face="normal" font="default"> Rodeghier,M.</style></author><author><style face="normal" font="default"> Strunk,R.C.</style></author><author><style face="normal" font="default"> Bacharier,L.B.</style></author><author><style face="normal" font="default"> Rosen,C.L.</style></author><author><style face="normal" font="default"> Kirkham,F.J.</style></author><author><style face="normal" font="default"> DeBaun,M.R.</style></author><author><style face="normal" font="default"> Cohen,R.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Division of Hematology/Oncology, Vanderbilt-Meharry Center for Excellence in Sickle Cell Disease, Vanderbilt University Medical Center, Nashville, TN, USA</style></auth-address><titles><title><style face="normal" font="default">Aeroallergen sensitization predicts acute chest syndrome in children with sickle cell anaemia</style></title><secondary-title><style face="normal" font="default">Br J Haematol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Haematol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Aged</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">Asthma is associated with higher rates of acute chest syndrome (ACS) and vaso-occlusive pain episodes among children with sickle cell anaemia (SCA). Aeroallergen sensitization is a risk factor for asthma. We hypothesized that aeroallergen sensitization is associated with an increased incidence of hospitalizations for ACS and pain. Participants in a multicentre, longitudinal cohort study, aged 4-18 years with SCA, underwent skin prick testing to ten aeroallergens. ACS and pain episodes were collected from birth until the end of the follow-up period. The number of positive skin tests were tested for associations with prospective rates of ACS and pain. Multivariable models demonstrated additive effects of having positive skin tests on future rates of ACS (incidence rate ratio (IRR) for each positive test 1.23, 95% confidence interval [CI] 1.11-1.36, P &lt; 0.001). Aeroallergen sensitization was not associated with future pain (IRR 1.14, 95%CI 0.97-1.33, P = 0.11). Our study demonstrated that children with SCA and aeroallergen sensitization are at increased risk for future ACS. Future research is needed to determine whether identification of specific sensitizations and allergen avoidance and treatment reduce the risk of ACS for children with SCA</style></abstract><notes><style face="normal" font="default">IS - 1365-2141 (Electronic)IS - 0007-1048 (Linking)LA - engPT - Journal ArticleCO - United States -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/bjh.15076</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29363738">PM:29363738</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Haematol\20180124-WillenSM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Haematol\20180124-WillenSM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180124, Willen SM</style></custom2><misc3><style face="normal" font="default">10.1111/bjh.15076</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87468</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Soongrung,T.</style></author><author><style face="normal" font="default"> Mongkorntanyatipa,K.</style></author><author><style face="normal" font="default"> Peepim,T.</style></author><author><style face="normal" font="default"> Buaklin,A.</style></author><author><style face="normal" font="default"> Le Mignon,M.</style></author><author><style face="normal" font="default"> Malainual,N.</style></author><author><style face="normal" font="default"> Nony,E.</style></author><author><style face="normal" font="default"> Jacquet,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Chula Vaccine Research Center, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand</style></auth-address><titles><title><style face="normal" font="default">The Blomia tropicalis allergen Blo t 7 stimulates innate immune signaling pathways through TLR2</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Amino Acid Sequence</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="22" Month="1" Year="2018">2018/1/22</year></dates><abstract><style face="normal" font="default">BACKGROUND: Although the house dust mite species Blomia tropicalis is a leading cause of allergic diseases in tropical and subtropical regions, the identification and characterization of the allergenic proteins remains incomplete. OBJECTIVE: We aimed to characterize a recombinant form of Blo t 7 (rBlo t 7) in terms of IgE reactivity, lipid binding activity and ability to stimulate innate immunity. METHODS: The mature Blo t 7 cDNA was cloned by PCR methods for the expression of a secreted form of the allergen in P. pastoris. The IgE reactivity to purified rBlo t 7 as well as the potential cross-reactivity with Der p 7 were determined by ELISA. The lipid binding capacity of rBlo t 7 was assayed using fluorescent lipid probes. The stimulation of TLR2 signaling pathway by rBlo t 7 was examined in cell activation and reporter assays. RESULTS: The amplified mature Blo t 7 cDNA revealed the presence of a 60 base pair insertion compared with the reference sequence registered in the GENBANK database. Multiple protein sequence alignments of group 7 mite allergens confirmed that this longer deduced amino acid sequence was the authentic Blo t 7 polypeptide chain. Analysis of IgE reactivity can classify rBlo t 7 as an intermediate B. tropicalis allergen which displayed weak cross-reactivity with Der p 7. Purified rBlo t 7 was shown to bind selectively the naturally fluorescent lipid probe cis-parinaric (cPNA) with a dissociation constant of 2 muM. The group 7 Blomia allergen stimulated the TLR2-, NF-kB- and MAPK-dependent production of IL-8 and GM-CSF in respiratory epithelial cells. CONCLUSIONS &amp; CLINICAL RELEVANCE: Through its propensity to transport fatty acids/lipids and to stimulate TLR2 signaling pathways in airway epithelial cells, Blo t 7 can represent a key allergen for the initiation of the B. tropicalis-induced airway inflammation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Thailand -CO - France -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13098</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29356186">PM:29356186</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20180122-SoongrungT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20180122-SoongrungT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180122, Soongrung T</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13098</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87469</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,Y.S.</style></author><author><style face="normal" font="default"> Kim,M.N.</style></author><author><style face="normal" font="default"> Lee,K.E.</style></author><author><style face="normal" font="default"> Hong,J.Y.</style></author><author><style face="normal" font="default"> Oh,M.S.</style></author><author><style face="normal" font="default"> Kim,S.Y.</style></author><author><style face="normal" font="default"> Kim,K.W.</style></author><author><style face="normal" font="default"> Sohn,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Severance Hospital, Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea</style></auth-address><titles><title><style face="normal" font="default">Activated leukocyte cell adhesion molecule (ALCAM/CD166) regulates T cell responses in a murine model of food allergy</style></title><secondary-title><style face="normal" font="default">Clin Exp Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">Food allergy is a major public health problem. Studies have shown that long-term interactions between activated leukocyte cell adhesion molecule (ALCAM/CD166), on the surface of antigen presenting cells, and CD6, a co-stimulatory molecule, influence immune responses. However, there are currently no studies on the functions of ALCAM in food allergy. Therefore, we aimed to identify the functions of ALCAM in ovalbumin (OVA)-induced food allergy using ALCAM-deficient mice. Wild-type (WT) and ALCAM-deficient (ALCAM(-/-) ) mice were intraperitoneally sensitized with and orally fed OVA. The mice were sacrificed, and parameters related to food allergy and TH 2 immune responses were analyzed. ALCAM serum levels increased and mRNA expression decreased in OVA-challenged WT mice. Serum IgE levels, TH 2 cytokine mRNA, and histological injuries were higher in OVA-challenged WT mice than in control mice, and these were attenuated in ALCAM(-/-) mice. T cell proliferation of total cells, CD3(+) CD4(+) T cell, and activated T cells in immune tissues were diminished in OVA-challenged ALCAM(-/-) mice. Proliferation of co-cultured T cells and dendritic cells (DCs) was decreased by the anti-CD6 antibody. In addition, WT mice sensitized by adoptive transfer of OVA-pulsed ALCAM(-/-) BM-derived DCs showed reduced immune responses. Lastly, serum ALCAM levels were higher in children with food allergy than in control subjects. In this study, serum levels of ALCAM were elevated in food allergy-induced WT mice and children with food allergy. Moreover, immune responses and T cell activation were attenuated in OVA-challenged ALCAM(-/-) mice. These results indicate that ALCAM regulates food allergy by affecting T cell activation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2249 (Electronic)IS - 0009-9104 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1111/cei.13104</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29363753">PM:29363753</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Immunol\20180124-KimYS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Immunol\20180124-KimYS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180124, Kim YS</style></custom2><misc3><style face="normal" font="default">10.1111/cei.13104</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87471</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cook,Q.S.</style></author><author><style face="normal" font="default"> Burks,A.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy, Immunology, and Rheumatology, Department of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.</style></auth-address><titles><title><style face="normal" font="default">Peptide and Recombinant Allergen Vaccines for Food Allergy</style></title><secondary-title><style face="normal" font="default">Clin Rev Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Rev Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Components</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Systemic reaction</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">Food allergy is a significant public health problem, with no suitable treatments available for patients. Currently, patients are limited to avoidance and the use of readily available emergency medications. Immunotherapy is an appealing therapeutic strategy for inducing tolerance. Studies with whole native allergens have demonstrated the efficacy of immunotherapy for food allergy; however, the risk of IgE-mediated reactions with such treatment is significant. Advances in molecular biology techniques, including purification, sequencing, and cloning, have allowed researchers to identify specific allergen components and T cell binding epitopes. Support for the use of recombinant and peptide vaccines for food allergy comes from prior studies involving aeroallergens and hymenoptera venom. By manipulating allergen structure and IgE binding, allergenicity can be reduced, thereby reducing systemic reactions, making recombinant and peptide vaccines a safe and effective form of immunotherapy. Pre-clinical studies using in vitro and murine models demonstrated a more tolerant state following the use of these therapies. Studies with human subjects will be necessary to characterize the effects of recombinant and peptide food allergy vaccines and to demonstrate a safe treatment option for patients</style></abstract><notes><style face="normal" font="default">IS - 1559-0267 (Electronic)IS - 1080-0549 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s12016-018-8673-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29368278">PM:29368278</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Rev Allergy Immunol\20180124-CookQS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Rev Allergy Immunol\20180124-CookQS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180124, Cook QS</style></custom2><misc3><style face="normal" font="default">10.1007/s12016-018-8673-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87472</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Guajardo,J.R.</style></author><author><style face="normal" font="default"> Zegarra-Bustamante,M.A.</style></author><author><style face="normal" font="default"> Brooks,E.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pulmonary Medicine, Department of Pediatrics, UT Health San Antonio, 7703 Floyd Curl Drive, San Antonio, TX, 78229, USA</style></auth-address><titles><title><style face="normal" font="default">Does Aeroallergen Sensitization Cause or Contribute to Eosinophilic Esophagitis?</style></title><secondary-title><style face="normal" font="default">Clin Rev Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Rev Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Eosinophilic esophagitis</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Inhalant allergen</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="22" Month="1" Year="2018">2018/1/22</year></dates><abstract><style face="normal" font="default">Eosinophilic esophagitis is an atopic disease defined clinically by esophageal symptoms in combination with a dense esophageal eosinophilia. EoE is triggered and maintained by exposure to certain foods and it is known that dietary modification controls symptoms and achieves disease remission. Recently, aeroallergens have been implicated in the pathogenesis of EoE. To examine the role of aeroallergens in EoE, we reviewed the published literature. Sensitization and production of IgE antibodies to foods and aeroallergens in subjects with EoE has been demonstrated. However, the evidence suggests only a minor role for IgE-mediated immune reactions in EoE. There is some evidence to support an association of EoE diagnosis and flares with environmental allergen exposure, and animal studies support the notion that EoE may be induced by exposure to inhalant allergens. Some studies show that newly diagnosed cases of EoE follow a seasonal pollen distribution (summer and spring), but the weight of evidence does not support the seasonal occurrence of diagnosis or worsening of symptoms. Overall, we conclude that the current evidence does not support causality in inhalant allergen exposure and the genesis nor exacerbations of EoE in humans, although there is a possibility that inhalant allergen sensitization could play a modifying role in EoE in the context of cross-reacting food allergens</style></abstract><notes><style face="normal" font="default">IS - 1559-0267 (Electronic)IS - 1080-0549 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s12016-018-8671-6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29356936">PM:29356936</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Rev Allergy Immunol\20180122-GuajardoJR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Rev Allergy Immunol\20180122-GuajardoJR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180122, Guajardo JR</style></custom2><misc3><style face="normal" font="default">10.1007/s12016-018-8671-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87476</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Han,S.H.</style></author><author><style face="normal" font="default"> Cheon,H.I.</style></author><author><style face="normal" font="default"> Hur,M.S.</style></author><author><style face="normal" font="default"> Kim,M.J.</style></author><author><style face="normal" font="default"> Jung,W.H.</style></author><author><style face="normal" font="default"> Lee,Y.W.</style></author><author><style face="normal" font="default"> Choe,Y.B.</style></author><author><style face="normal" font="default"> Ahn,K.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Konkuk University School of Medicine, Seoul, Korea</style></auth-address><titles><title><style face="normal" font="default">Analysis of the skin mycobiome in adult patients with atopic dermatitis</style></title><secondary-title><style face="normal" font="default">Exp Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Exp Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="21" Month="1" Year="2018">2018/1/21</year></dates><abstract><style face="normal" font="default">With the recent availability of culture-independent sequencing methods, studies have been conducted to analyze skin microorganisms present in patients with atopic dermatitis (AD). However, the database on the skin fungal communities, "mycobiome," has been relatively restrictive compared with the bacterial world. We aimed to comparatively analyze the overall skin mycobiome between patients with AD and healthy individuals in the Korean population. We analyzed skin swab samples obtained from the antecubital fossae of 8 patients with AD and 8 healthy controls. Using sequencing method followed by direct DNA extraction and molecular PCR, taxonomic compositions of fungi at stepwise level ranks were analyzed. The phylogenic marker used was internal transcribed spacer 2 regions of DNA. We observed the tendency of higher intra- and inter-personal taxonomic diversity at genus and species levels in AD samples. Non-Malassezia fungal diversity was also noticeable in the patient group compared with healthy controls. Malassezia globosa and Malassezia restricta were prevalent in all samples across both study groups, and some Malassezia species, including Malassezia sloofiae and dermatis characterized AD. Our data might provide a new insight into the mycobiome of adult AD, which contributes to building a systemic mycobiome database in AD. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1600-0625 (Electronic)IS - 0906-6705 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1111/exd.13500</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29356103">PM:29356103</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Exp Dermatol\20180121-HanSH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Exp Dermatol\20180121-HanSH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180121, Han SH</style></custom2><misc3><style face="normal" font="default">10.1111/exd.13500</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87482</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Che,D.</style></author><author><style face="normal" font="default"> Cao,J.</style></author><author><style face="normal" font="default"> Liu,R.</style></author><author><style face="normal" font="default"> Wang,J.</style></author><author><style face="normal" font="default"> Hou,Y.</style></author><author><style face="normal" font="default"> Zhang,T.</style></author><author><style face="normal" font="default"> Wang,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">a School of Pharmacy , Xi'an Jiaotong University , Xi'an , China</style></auth-address><titles><title><style face="normal" font="default">Harpagoside-induced anaphylactic reaction in an IgE-independent manner both in vitro and in vivo</style></title><secondary-title><style face="normal" font="default">Immunopharmacol Immunotoxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunopharmacol Immunotoxicol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="22" Month="1" Year="2018">2018/1/22</year></dates><abstract><style face="normal" font="default">BACKGROUND: Harpagoside (HAR) is an active component of Scrophularia ningpoensis (SN), which has anti-inflammatory and anti-immune effects. SN is used widely in China to treat various diseases. Recently, SN has been used as a traditional Chinese medicine injection and used clinically. However, allergic responses to these injections are frequently reported. AIM: We examined whether the main component of SN, HAR, is associated with the allergic reaction to SN. METHODS: This study assessed the effects of HAR in mice and mast cell activation to characterize its anaphylactic effects and underlying mechanisms. Mice hindpaw swelling, serum allergy factor detection, enzyme-linked immunosorbent assays, and degranulation assays were performed to measure allergic mediators both in vivo and in vitro. RESULTS: The present study indicated that HAR induced paw swelling, interleukin-6, inositol triphosphate, tumor necrosis factor-alpha, and histamine increases in mice. Our in vitro data also showed that HAR induced beta-hexosaminidase, inositol triphosphate, and interleukin-6 release, leading to mast cell degranulation. In contrast, neither C48/80 nor HAR induced local anaphylaxis in STOCK Kit(W-sh)/HNihrJaeBsmJNju mice. CONCLUSIONS: HAR is a potential sensitization compound in SN, and these results provide information for the safe clinical use of SN</style></abstract><notes><style face="normal" font="default">IS - 1532-2513 (Electronic)IS - 0892-3973 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1080/08923973.2018.1424900</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29355053">PM:29355053</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunopharmacol Immunotoxicol\20180122-CheD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunopharmacol Immunotoxicol\20180122-CheD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180122, Che D</style></custom2><misc3><style face="normal" font="default">10.1080/08923973.2018.1424900</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87483</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Geeta,M.</style></author><author><style face="normal" font="default"> Riyaz,A.</style></author><author><style face="normal" font="default"> Krishnan,C.</style></author><author><style face="normal" font="default"> Scaria,V.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Govt. Medical College, Kozhikode, Kerala, India.</style></auth-address><titles><title><style face="normal" font="default">Rapid Transition of Facial Features from Early to Mid - Adolescence in Autosomal Dominant Hyper IgE Syndrome with a STAT3 Variation</style></title><secondary-title><style face="normal" font="default">Indian J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Indian J Pediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">IgE</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 0973-7693 (Electronic)IS - 0019-5456 (Linking)LA - engPT - LetterCO - India -</style></notes><work-type><style face="normal" font="default">10.1007/s12098-017-2603-y</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29368105">PM:29368105</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Indian J Pediatr\20180124-GeetaM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Indian J Pediatr\20180124-GeetaM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180124, Geeta M</style></custom2><misc3><style face="normal" font="default">10.1007/s12098-017-2603-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87484</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tharakan,A.</style></author><author><style face="normal" font="default"> Dobzanski,A.</style></author><author><style face="normal" font="default"> London,N.R.,Jr.</style></author><author><style face="normal" font="default"> Khalil,S.M.</style></author><author><style face="normal" font="default"> Surya,N.</style></author><author><style face="normal" font="default"> Lane,A.P.</style></author><author><style face="normal" font="default"> Ramanathan,M.,Jr.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD</style></auth-address><titles><title><style face="normal" font="default">Characterization of a novel, papain-inducible murine model of eosinophilic rhinosinusitis</style></title><secondary-title><style face="normal" font="default">Int Forum Allergy Rhinol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Forum Allergy Rhinol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">BACKGROUND: Eosinophilic chronic rhinosinusitis (ECRS) is a disease characterized by eosinophilic inflammatory infiltrate and a local type 2 cytokine milieu. Current animal models fail to recapitulate many of the innate and adaptive immunologic hallmarks of the disease, thus hindering the development of effective therapeutics. In the present study, mice were exposed intranasally to the cysteine protease papain, which shares functional similarities with parasitic proteases and aeroallergens, to generate a rapidly inducible murine model of eosinophilic rhinosinusitis. METHODS: C57BL/6 mice were intranasally instilled with 20 mug papain or heat-inactivated papain (HP) on days 0-2 and days 7-10, and then euthanized on day 11. Nasal lavage fluid (NALF) was analyzed to quantify eosinophils and inflammatory cytokine secretion. Sinonasal tissue was sectioned and stained for goblet cells or homogenized to analyze cytokine levels. Serum samples were assayed for immunoglobulin E (IgE) by enzyme-linked immunoassay. Sinonasal mucosal tissue was dissociated and analyzed by flow cytometry. RESULTS: Compared with HP treatment, papain induced significant eosinophilia in NALF, goblet cell hyperplasia, innate and adaptive immune cell infiltration, type 2 cytokine production, and IgE responses. Flow cytometric analysis of sinonasal tissues revealed significant inflammatory cell infiltration and interleukin-13-producing cell populations. CONCLUSION: In this study, we demonstrated that the cysteine protease papain induces allergic sinonasal eosinophilic rhinosinusitis and resembles T-helper 2 cell inflammation and innate immune characteristics of ECRS. This model permits further study into the molecular mechanisms underlying ECRS pathology and provides a model system for the evaluation of potential pharmacologic interventions</style></abstract><notes><style face="normal" font="default">IS - 2042-6984 (Electronic)IS - 2042-6976 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/alr.22072</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29341450">PM:29341450</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20180117-TharakanA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20180117-TharakanA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Tharakan A</style></custom2><misc3><style face="normal" font="default">10.1002/alr.22072</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87486</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Araujo Fonseca,C.H.</style></author><author><style face="normal" font="default"> Carvalho Marques,B.</style></author><author><style face="normal" font="default"> Bispo Reis,L.</style></author><author><style face="normal" font="default"> Cardoso Lima,D.A.</style></author><author><style face="normal" font="default"> Silva Mota,L.H.</style></author><author><style face="normal" font="default"> dos Santos Andrade,R.</style></author><author><style face="normal" font="default"> Andrade dos Santos,G.</style></author><author><style face="normal" font="default"> Moreno Amor,A.L.</style></author></authors></contributors><titles><title><style face="normal" font="default">ENTEROPARASITES, RESPIRATORY ALLERGY AND OTHER SIGNS AND SYMPTOMS IN CHILDS AND YOUTH POPULATION OF RECÔNCAVO OF BAHIA</style></title><secondary-title><style face="normal" font="default">J Adv Allergy Immunol Dis</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Adv Allergy Immunol Dis</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Aged</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Respiratory allergies may develop at any age, but the onset are more frequent in childhood and juvenile population due to genetic factors and to development of the immune system, which may presents as rhinitis and/or asthma. In Brazil, asthma is the second cause of hospital admission in children aged four to nine years old and the third in adolescents. Exposure to pathogens, particularly helminths, and their products are common in developing countries, and it appears to protect against the development of autoimmune and allergic diseases in experimental and human models. Based on these data, the present study investigated the presence of allergic conditions, infection by intestinal parasites and symptomatology on the juvenile population of the rural area of Santo Antônio de Jesus (Bahia - Brazil), from July to October, 2015. A questionnaire was applied to evaluate asthma and allergic symptoms and the parasitological feces exam was performed in 47 individuals. The study identified 81% of the positive samples for at least one parasite species; 45% polyparasitism; and the prevalence to Endolimax nana (48%) and hookworms (39%); eczema as the predominant allergic manifestation (34%) and headache, fatigue after physical activity, urticaria, itching in the head and nervousness as the most frequent signs and symptoms. The prevalence of enteroparasites, respiratory allergy and the symptoms associated with each of them are present in the studied population, and it may be related not only to the infection, but also to the presence of previous or overlapping diseases.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.25177/JAAID.2.1.5</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.25177/JAAID.2.1.5</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Adv Allergy Immunol Dis\20180120-AraujoFonsecaCH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Adv Allergy Immunol Dis\20180120-AraujoFonsecaCH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180120, Araujo Fonseca CH</style></custom2><misc3><style face="normal" font="default">10.25177/JAAID.2.1.5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87487</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Niu,S.</style></author><author><style face="normal" font="default"> Liu,Q.</style></author><author><style face="normal" font="default"> Xia,J.M.</style></author><author><style face="normal" font="default"> Xie,C.L.</style></author><author><style face="normal" font="default"> Luo,Z.H.</style></author><author><style face="normal" font="default"> Shao,Z.</style></author><author><style face="normal" font="default"> Liu,G.M.</style></author><author><style face="normal" font="default"> Yang,X.W.</style></author></authors></contributors><titles><title><style face="normal" font="default">Polyketides from the Deep-Sea-Derived Fungus Graphostroma sp. MCCC 3A00421 Showed Potent Anti-Food Allergic Activities</style></title><secondary-title><style face="normal" font="default">J Agric Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Agric Food Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Components</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword></keywords><dates><year Day="22" Month="1" Year="2018">2018/1/22</year></dates><abstract><style face="normal" font="default">To discover anti-food allergic components from deep-sea-derived microorganisms. A systematic chemical investigation was conducted on the Atlantic hydrothermal fungus Graphostroma sp. MCCC 3A00421. Consequently, nine new (1-9) and 19 known (1028) polyketides were isolated. The planar structures of the new compounds were elucidated mainly by detailed analysis of their NMR and HRESIMS data, while the absolute configurations were established using the modified Mosher's method in association with ECD spectra. Graphostrin A (1) is a novel chlorinated polyketide derivate bearing an oxazole moiety. All isolates were tested for anti-food allergic bioactivities in immunoglobulin E (IgE)-mediated rat basophilic leukemia (RBL)-2H3 cells. Reticulol (10) significantly decreased degranulation and histamine release with IC50 values of 13.5 and 13.7 muM, respectively, suggesting reticulol could be a potential anti-food allergic medicine</style></abstract><notes><style face="normal" font="default">IS - 1520-5118 (Electronic)IS - 0021-8561 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1021/acs.jafc.7b04383</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29355320">PM:29355320</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Agric Food Chem\20180122-NiuS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Agric Food Chem\20180122-NiuS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180122, Niu S</style></custom2><misc3><style face="normal" font="default">10.1021/acs.jafc.7b04383</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87488</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Niederberger,V.</style></author><author><style face="normal" font="default"> Neubauer,A.</style></author><author><style face="normal" font="default"> Gevaert,P.</style></author><author><style face="normal" font="default"> Zidarn,M.</style></author><author><style face="normal" font="default"> Worm,M.</style></author><author><style face="normal" font="default"> Aberer,W.</style></author><author><style face="normal" font="default"> Malling,H.J.</style></author><author><style face="normal" font="default"> Pfaar,O.</style></author><author><style face="normal" font="default"> Klimek,L.</style></author><author><style face="normal" font="default"> Pfutzner,W.</style></author><author><style face="normal" font="default"> Ring,J.</style></author><author><style face="normal" font="default"> Darsow,U.</style></author><author><style face="normal" font="default"> Novak,N.</style></author><author><style face="normal" font="default"> Gerth van Wijk,R.</style></author><author><style face="normal" font="default"> Eckl-Dorna,J.</style></author><author><style face="normal" font="default"> Focke-Tejkl,M.</style></author><author><style face="normal" font="default"> Weber,M.</style></author><author><style face="normal" font="default"> Muller,H.H.</style></author><author><style face="normal" font="default"> Klinger,J.</style></author><author><style face="normal" font="default"> Stolz,F.</style></author><author><style face="normal" font="default"> Breit,N.</style></author><author><style face="normal" font="default"> Henning,R.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otorhinolaryngology, Medical University of Vienna, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Safety and efficacy of immunotherapy with the recombinant B-cell epitope-based grass pollen vaccine BM32</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="11" Month="1" Year="2018">2018/1/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: BM32 is a grass pollen allergy vaccine based on recombinant fusion proteins consisting of nonallergenic peptides from the IgE-binding sites of the 4 major grass pollen allergens and the hepatitis B preS protein. OBJECTIVE: We sought to study the safety and clinical efficacy of immunotherapy (allergen immunotherapy) with BM32 in patients with grass pollen-induced rhinitis and controlled asthma. METHODS: A double-blind, placebo-controlled, multicenter allergen immunotherapy field study was conducted for 2 grass pollen seasons. After a baseline season, subjects (n = 181) were randomized and received 3 preseasonal injections of either placebo (n = 58) or a low dose (80 mug, n = 60) or high dose (160 mug, n = 63) of BM32 in year 1, respectively, followed by a booster injection in autumn. In the second year, all actively treated subjects received 3 preseasonal injections of the BM32 low dose, and placebo-treated subjects continued with placebo. Clinical efficacy was assessed by using combined symptom medication scores, visual analog scales, Rhinoconjunctivitis Quality of Life Questionnaires, and asthma symptom scores. Adverse events were graded according to the European Academy of Allergy and Clinical Immunology. Allergen-specific antibodies were determined by using ELISA, ImmunoCAP, and ImmunoCAP ISAC. RESULTS: Although statistical significance regarding the primary end point was not reached, BM32-treated subjects, when compared with placebo-treated subjects, showed an improvement regarding symptom medication, visual analog scale, Rhinoconjunctivitis Quality of Life Questionnaire, and asthma symptom scores in both treatment years. This was accompanied by an induction of allergen-specific IgG without induction of allergen-specific IgE and a reduction in the seasonally induced increase in allergen-specific IgE levels in year 2. In the first year, more grade 2 reactions were observed in the active (n = 6) versus placebo (n = 1) groups, whereas there was almost no difference in the second year. CONCLUSIONS: Injections of BM32 induced allergen-specific IgG, improved clinical symptoms of seasonal grass pollen allergy, and were well tolerated</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - Belgium -CO - Slovenia -CO - Germany -CO - Denmark -CO - Netherlands -CO - Russia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.052</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29361332">PM:29361332</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180117-NiederbergerV.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180117-NiederbergerV.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Niederberger V</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.052</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87489</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Retterer,M.K.C.</style></author><author><style face="normal" font="default"> Workman,L.J.</style></author><author><style face="normal" font="default"> Bacon,J.R.</style></author><author><style face="normal" font="default"> Platts-Mills,T.A.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Asthma and Allergic Disease Center, Carter Immunology Center, Department of Medicine, University of Virginia Health System, Charlottesville, Va</style></auth-address><titles><title><style face="normal" font="default">Specific IgE to gelatin as a cause of anaphylaxis to zoster vaccine</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - LetterCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.08.047</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29361333">PM:29361333</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180118-RettererMK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180118-RettererMK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Retterer MK</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.08.047</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87490</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Smith,T.D.</style></author><author><style face="normal" font="default"> Camacho,J.</style></author><author><style face="normal" font="default"> Wang,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Clinical Immunology, Icahn School of Medicine at Mount Sinai, New York, NY</style></auth-address><titles><title><style face="normal" font="default">Behavioral risks associated with food allergy management in an urban pediatric population</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword></keywords><dates><year Day="19" Month="1" Year="2018">2018/1/19</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.12.012</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29371074">PM:29371074</url></web-urls><pdf-urls><url ppv-ref="no">julie.wang@mssm.edu</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180119, Smith TD</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.12.012</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87491</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gomez,T.E.</style></author><author><style face="normal" font="default"> Garcia,R.C.</style></author><author><style face="normal" font="default"> Veleiro,P.B.</style></author><author><style face="normal" font="default"> Bartolome,B.</style></author><author><style face="normal" font="default"> Prado,B.M.</style></author><author><style face="normal" font="default"> Garcia,R.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Section, Hospital General Universitario, Ciudad Real, Spain.</style></auth-address><titles><title><style face="normal" font="default">Occupational allergic respiratory disease (rinoconjunctivitis and asthma) in a cheese factory worker</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="13" Month="1" Year="2018">2018/1/13</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.12.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29342450">PM:29342450</url></web-urls><pdf-urls><url ppv-ref="no">egomezt.cr@gmail.com</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180117, Goemz TE</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.12.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87492</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Stone,C.A.,Jr.</style></author><author><style face="normal" font="default"> Hemler,J.A.</style></author><author><style face="normal" font="default"> Commins,S.P.</style></author><author><style face="normal" font="default"> Schuyler,A.J.</style></author><author><style face="normal" font="default"> Phillips,E.J.</style></author><author><style face="normal" font="default"> Peebles,R.S.,Jr.</style></author><author><style face="normal" font="default"> Fahrenholz,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tenn.</style></auth-address><titles><title><style face="normal" font="default">Reply (Refers to: Specific IgE to gelatin as a cause of anaphylaxis to zoster vaccine)</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="19" Month="1" Year="2018">2018/1/19</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - LetterCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.08.048</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29370925">PM:29370925</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180119-StoneCAJr.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20180119-StoneCAJr.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180119, Stone CA Jr</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.08.048</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87493</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Guttman-Yassky,E.</style></author><author><style face="normal" font="default"> Brunner,P.M.</style></author><author><style face="normal" font="default"> Neumann,A.U.</style></author><author><style face="normal" font="default"> Khattri,S.</style></author><author><style face="normal" font="default"> Pavel,A.B.</style></author><author><style face="normal" font="default"> Malik,K.</style></author><author><style face="normal" font="default"> Singer,G.K.</style></author><author><style face="normal" font="default"> Baum,D.</style></author><author><style face="normal" font="default"> Gilleaudeau,P.</style></author><author><style face="normal" font="default"> Sullivan-Whalen,M.</style></author><author><style face="normal" font="default"> Rose,S.</style></author><author><style face="normal" font="default"> Jim,On S.</style></author><author><style face="normal" font="default"> Li,X.</style></author><author><style face="normal" font="default"> Fuentes-Duculan,J.</style></author><author><style face="normal" font="default"> Estrada,Y.</style></author><author><style face="normal" font="default"> Garcet,S.</style></author><author><style face="normal" font="default"> Traidl-Hoffmann,C.</style></author><author><style face="normal" font="default"> Krueger,J.G.</style></author><author><style face="normal" font="default"> Lebwohl,M.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY, USA</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of fezakinumab (an anti-IL-22 monoclonal antibody) in adults with moderate-to-severe atopic dermatitis inadequately controlled by conventional treatments - A randomized, double-blind, phase 2a trial</style></title><secondary-title><style face="normal" font="default">J Am Acad Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Acad Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">BACKGROUND: IL-22 promotes epidermal hyperplasia and inhibits skin barrier function. OBJECTIVE: Evaluate IL-22 blockade in adults with moderate-to-severe atopic dermatitis (AD). METHODS: Randomized, double-blind, placebo-controlled trial with intravenous fezakinumab monotherapy every 2wks for 10wks, with follow-up assessments until 20wks. SCORAD change from baseline at 12wks served as primary endpoint. RESULTS: At 12wks, mean SCORAD decline was 13.8+/-2.7 (fezakinumab) vs. 8.0+/-3.1 (placebo) for the entire population (p=0.134). In severe patients (baseline SCORAD>/=50), SCORAD decline was significantly stronger in drug vs. placebo at 12wks (21.6+/-3.8 vs. 9.6+/-4.2, p=0.029) and 20wks (27.4+/-3.9 vs. 11.5+/-5.1, p=0.010). At 12wks, improvements were significantly stronger in drug vs. placebo (12.4%+/-2.4 vs. 6.2%+/-2.7; p=0.009) for BSA in the entire population, and for IGA in severe patients (0.7+/-0.2 vs. 0.3+/-0.1; p=0.034). All scores showed progressive improvements after last dosing (10wks) until end of study (20wks). Common adverse events were upper respiratory tract infections. LIMITATIONS: Limited sample size, lack of EASI and numerical rating scale (NRS) pruritus assessments; significance primarily obtained in severe AD. CONCLUSION: Fezakinumab was well-tolerated, with sustained clinical improvements after last drug dosing</style></abstract><notes><style face="normal" font="default">IS - 1097-6787 (Electronic)IS - 0190-9622 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Germany -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaad.2018.01.016</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29353025">PM:29353025</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Acad Dermatol\20180115-GuttmanYasskyE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Acad Dermatol\20180115-GuttmanYasskyE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Guttman-Yassky E</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaad.2018.01.016</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87494</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Simpson,E.L.</style></author><author><style face="normal" font="default"> Flohr,C.</style></author><author><style face="normal" font="default"> Eichenfield,L.F.</style></author><author><style face="normal" font="default"> Bieber,T.</style></author><author><style face="normal" font="default"> Sofen,H.</style></author><author><style face="normal" font="default"> Taieb,A.</style></author><author><style face="normal" font="default"> Owen,R.</style></author><author><style face="normal" font="default"> Putnam,W.</style></author><author><style face="normal" font="default"> Castro,M.</style></author><author><style face="normal" font="default"> DeBusk,K.</style></author><author><style face="normal" font="default"> Lin,C.Y.</style></author><author><style face="normal" font="default"> Voulgari,A.</style></author><author><style face="normal" font="default"> Yen,K.</style></author><author><style face="normal" font="default"> Omachi,T.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, School of Medicine, Oregon Health &amp; Science University, Portland, OR, USA</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of lebrikizumab (an anti-IL-13 monoclonal antibody) in adults with moderate-to-severe atopic dermatitis inadequately controlled by topical corticosteroids: A randomized, placebo-controlled phase II trial (TREBLE)</style></title><secondary-title><style face="normal" font="default">J Am Acad Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Acad Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">BACKGROUND: Interleukin (IL)-13 plays a key role in type 2 inflammation and is an emerging pathogenic mediator in atopic dermatitis. OBJECTIVE: We investigated the efficacy and safety of lebrikizumab, an anti-IL-13 monoclonal antibody, as add-on to topical corticosteroid (TCS). METHODS: A randomized, placebo-controlled, double-blind, phase II study. Adults with moderate-to-severe AD were required to use twice-daily TCS, and randomized (1:1:1:1) to lebrikizumab 125 mg single dose (SD), 250 mg SD, 125 mg once every 4 weeks (Q4W), or placebo Q4W for 12 weeks, after 2-week TCS run-in. Primary endpoint was percentage of patients achieving Eczema Area and Severity Index (EASI)-50 at Week 12. RESULTS: 209 patients received study drug. At Week 12, significantly more patients achieved EASI-50 with lebrikizumab 125 mg Q4W (82.4%; p=0.026) versus placebo (62.3%); patients receiving lebrikizumab SD showed no statistically significant improvements in EASI-50 versus placebo. Adverse events were similar between groups (66.7% all lebrikizumab vs 66.0% placebo), mostly mild or moderate. LIMITATIONS: Protocol-mandated twice-daily TCS limits understanding of lebrikizumab efficacy as monotherapy. Short study duration did not allow long-term efficacy or safety evaluation. CONCLUSIONS: Lebrikizumab 125 mg Q4W led to significant improvement in patients with moderate-to-severe AD, when added to TCS, and was well tolerated</style></abstract><notes><style face="normal" font="default">IS - 1097-6787 (Electronic)IS - 0190-9622 (Linking)LA - engPT - Journal ArticleCO - United States -CO - United Kingdom -CO - Germany -CO - France -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaad.2018.01.017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29353026">PM:29353026</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Acad Dermatol\20180115-SimpsonEL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Acad Dermatol\20180115-SimpsonEL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Simpson EL</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaad.2018.01.017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87495</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rams,A.</style></author><author><style face="normal" font="default"> Zolcinski,M.</style></author><author><style face="normal" font="default"> Zastrzezynska,W.</style></author><author><style face="normal" font="default"> Polanski,S.</style></author><author><style face="normal" font="default"> Serafin,A.</style></author><author><style face="normal" font="default"> Wilanska,J.</style></author><author><style face="normal" font="default"> Musial,J.</style></author><author><style face="normal" font="default"> Bazan-Socha,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Internal Medicine , Jagiellonian University Medical College , Krakow , Poland</style></auth-address><titles><title><style face="normal" font="default">Autoimmune polyendocrine syndrome type 2 in patient with severe allergic asthma treated with omalizumab</style></title><secondary-title><style face="normal" font="default">J Asthma</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Asthma</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> complications</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">Asthma therapy with monoclonal antibodies is a promising and effective approach for those with a severe and refractory type of disease. Although such a targeted therapy is considered to be safe, unusual complications may occur. We present a case of a 45 year-old female patient with severe allergic asthma and chronic spontaneous urticaria, who developed autoimmune polyendocrine syndrome type 2 (APS-2) after 26 months of omalizumab administration. The patient was diagnosed with primary adrenal insufficiency (Addison's disease) and Hashimoto's thyroiditis accompanied by autoimmune atrophic gastritis. According to our knowledge this is the first description of APS-2 that developed in conjunction with omalizumab treatment, although we have no evidence that the observed phenomenon indicated a cause-effect relationship to omalizumab</style></abstract><notes><style face="normal" font="default">IS - 1532-4303 (Electronic)IS - 0277-0903 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1080/02770903.2017.1414239</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29300536">PM:29300536</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Asthma\20180115-RamsA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Asthma\20180115-RamsA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Rams A</style></custom2><misc3><style face="normal" font="default">10.1080/02770903.2017.1414239</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87496</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Saito,A.</style></author><author><style face="normal" font="default"> Okiyama,N.</style></author><author><style face="normal" font="default"> Iwamoto,K.</style></author><author><style face="normal" font="default"> Inoue,S.</style></author><author><style face="normal" font="default"> Koguchi-Yoshioka,H.</style></author><author><style face="normal" font="default"> Fujimoto,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan</style></auth-address><titles><title><style face="normal" font="default">Case with anaphylactic shock induced by heparin-lock flush injection</style></title><secondary-title><style face="normal" font="default">J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="1" Year="2018">2018/1/25</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1346-8138 (Electronic)IS - 0385-2407 (Linking)LA - engPT - LetterCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/1346-8138.14216</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29369395">PM:29369395</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Dermatol\20180125-SaitoA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Dermatol\20180125-SaitoA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180125, Saito A</style></custom2><misc3><style face="normal" font="default">10.1111/1346-8138.14216</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87498</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zurzolo,G.A.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author><author><style face="normal" font="default"> Peters,R.L.</style></author><author><style face="normal" font="default"> Tang,M.L.</style></author><author><style face="normal" font="default"> Dharmage,S.</style></author><author><style face="normal" font="default"> de Court</style></author><author><style face="normal" font="default"> Mathai,M.L.</style></author><author><style face="normal" font="default"> Campbell,D.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre for Chronic Disease, College of Health and Biomedicine, Victoria University, Melbourne, Victoria, Australia</style></auth-address><titles><title><style face="normal" font="default">Anaphylaxis to packaged foods in Australasia</style></title><secondary-title><style face="normal" font="default">J Paediatr Child Health</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Paediatr Child Health</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">AIMS: To examine reports of anaphylaxis in Australasia from consumption of packaged food products with or without precautionary allergen labelling (PAL), where the known allergen triggers were not a listed ingredient. METHODS: A questionnaire was sent to all members of the Australasian Society of Clinical Immunology and Allergy (n = 548). Participants were asked to complete a survey reporting whether they have had seen any patients over the last 3 months reporting anaphylaxis following ingestion of a packaged food where the suspected food allergen was not a listed ingredient. RESULTS: Of the n = 548 members approached, n = 198 responded (response rate 36.1%).There were 14 reports of anaphylaxis to packaged foods (where the suspected allergen was not a listed ingredient), which met the case definition from a total of 198 respondents over the 9-month period. Of those reactions, 50.0% (confidence interval 95% 21-78) were reported from foods that did not have a PAL statement, and 50.0% (confidence interval 95% 21-78) were due to peanuts. CONCLUSION: Anaphylaxis to undeclared allergens was not rare and did not appear to depend on whether the product was labelled with precautionary advice. There is currently no reliable labelling system that can inform food-allergic consumers of safer food choices. Improvements in the regulation of food labelling with PAL are required</style></abstract><notes><style face="normal" font="default">IS - 1440-1754 (Electronic)IS - 1034-4810 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1111/jpc.13823</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29363215">PM:29363215</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Paediatr Child Health\20180124-ZurzoloGA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Paediatr Child Health\20180124-ZurzoloGA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180124, Zurzolo GA</style></custom2><misc3><style face="normal" font="default">10.1111/jpc.13823</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87506</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bidat,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Food protein-induced enterocolitis syndrome (FPIES): Various presentations</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Food-protein-induced enterocolitis syndrome</style></keyword><keyword><style face="normal" font="default"> Milk</style></keyword><keyword><style face="normal" font="default"> Vomiting</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">Food-protein-induced enterocolitis syndrome (FPIES) is an increasingly common form of non-IgE-mediated food allergy. Different phenotypes are possible, acute or chronic, with sub-phenotypes. FPIES manifested only by diarrhea can also occur. The incriminated food is primarily cow's milk but unusual food allergies are occasionally observed. The distribution of incriminated foods varies according to the different continents</style></abstract><notes><style face="normal" font="default">LA - FRECO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.12.001</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.12.001</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\20180117-BidatE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\20180117-BidatE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Bidat E</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.12.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86735</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Koplin,J.J.</style></author><author><style face="normal" font="default"> Peters,R.L.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre of Food and Allergy Research, Murdoch Children's Research Institute, Royal Children's Hospital, Flemington Road, Parkville, Melbourne, Victoria 3052, Australia</style></auth-address><titles><title><style face="normal" font="default">Prevention of Food Allergies</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="11" start="1">1-11</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">This review summarizes the current state of play with regard to food allergy prevention. Food allergy prevention strategies focused on promoting timely introduction of allergenic foods (predominantly peanut) into the infant diet have recently been introduced in several countries. Additional prevention strategies currently under investigation include optimizing infant vitamin D levels, modulating the gut microbiota through use of probiotics, and preventing eczema to reduce the risk of food sensitization through a damaged skin barrier</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132666">PM:29132666</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-1-11.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-1-11.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Koplin JJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86829</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sohn,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Severance Hospital, Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.</style></auth-address><titles><title><style face="normal" font="default">Efficacy and Safety of Subcutaneous Allergen Immunotherapy for Allergic Rhinitis</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Immunol Res</style></abbr-1></periodical><pages end="3" start="1">1-3</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2092-7355 (Print)IS - 2092-7355 (Linking)LA - engPT - EditorialCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4168/aair.2018.10.1.1</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29178670">PM:29178670</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-1-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-1-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Sohn MH</style></custom2><misc3><style face="normal" font="default">10.4168/aair.2018.10.1.1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87214</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sanchez-Salguero,C.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Allergy Unit, Hospital Universitario Puerto Real, Cadiz, Spain</style></auth-address><titles><title><style face="normal" font="default">Food Protein-Induced Proctocolitis. The shadow of allergic disorders</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="2" start="1">1-2</pages><volume><style face="normal" font="default">46</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - EditorialCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.10.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29291769">PM:29291769</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2018-46-1-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2018-46-1-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Sanchez-Salguero CA</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.10.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87230</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,S.H.</style></author><author><style face="normal" font="default"> Lee,P.H.</style></author><author><style face="normal" font="default"> Kim,B.G.</style></author><author><style face="normal" font="default"> Seo,H.J.</style></author><author><style face="normal" font="default"> Baek,A.R.</style></author><author><style face="normal" font="default"> Park,J.S.</style></author><author><style face="normal" font="default"> Lee,J.H.</style></author><author><style face="normal" font="default"> Park,S.W.</style></author><author><style face="normal" font="default"> Kim,D.J.</style></author><author><style face="normal" font="default"> Park,C.S.</style></author><author><style face="normal" font="default"> Jang,A.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Respiratory and Allergy, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon, Gyeonggi-do, 14584, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Annexin A1 in plasma from patients with bronchial asthma: its association with lung function</style></title><secondary-title><style face="normal" font="default">BMC Pulm Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMC Pulm Med</style></abbr-1></periodical><pages end="" start="1">1-</pages><volume><style face="normal" font="default">18</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">BACKGROUND: Annexin-A1 (ANXA1) is a glucocorticoid-induced protein with multiple actions in the regulation of inflammatory cell activation. The anti-inflammatory protein ANXA1 and its N-formyl peptide receptor 2 (FPR2) have protective effects on organ fibrosis. However, the exact role of ANXA1 in asthma remains to be determined. The aim of this study was to identify the role of ANXA1 in bronchial asthma. METHODS: In mice sensitized and challenged with ovalbumin (OVA-OVA mice) and mice sensitized with saline and challenged with air (control mice), we investigated the potential links between ANXA1 levels and bronchial asthma using ELISA, immunoblotting, and immunohistochemical staining. Moreover, we also determined ANXA1 levels in blood from 50 asthmatic patients (stable and exacerbated states). RESULTS: ANXA1 protein levels in lung tissue and bronchoalveolar lavage fluid were significantly higher in OVA-OVA mice compared with control mice. FPR2 protein levels in lung tissue were significantly higher in OVA-OVA mice compared with control mice. Plasma ANXA1 levels were increased in asthmatic patients compared with healthy controls. Plasma ANXA1 levels were significantly lower in exacerbated patients compared with stable patients with bronchial asthma (p &lt; 0.05). The plasma ANXA1 levels in controlled asthmatic patients were correlated with forced expiratory volume in 1 s (FEV1) (r = - 0.191, p = 0.033) and FEV1/forced vital capacity (FVC) (r = -0.202, p = 0.024). CONCLUSION: These results suggest that ANXA1 may be a potential marker and therapeutic target for asthma</style></abstract><notes><style face="normal" font="default">IS - 1471-2466 (Electronic)IS - 1471-2466 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1186/s12890-017-0557-5.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29301525">PM:29301525</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMC Pulm Med\2018- 18-1.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMC Pulm Med\2018- 18-1.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Lee SH</style></custom2><misc3><style face="normal" font="default">10.1186/s12890-017-0557-5.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87238</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Castelli,S.</style></author><author><style face="normal" font="default"> Arasi,S.</style></author><author><style face="normal" font="default"> Pawankar,R.</style></author><author><style face="normal" font="default"> Matricardi,P.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Paediatric Pneumology &amp; Immunology, Charite - Universitatsmedizin Berlin, Berlin, Germany</style></auth-address><titles><title><style face="normal" font="default">Collection of nasal secretions and tears and their use in allergology</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="9" start="1">1-9</pages><volume><style face="normal" font="default">18</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Absorption</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: The identification of immunological markers in nasal secretions and tears is becoming essential in the study of allergic diseases. The collection procedure of nasal and ocular secretions directly influences the results, thus it is of paramount importance to validate and standardize the sampling process. RECENT FINDINGS: Current techniques for nasal secretions sampling are mainly based on three principles: collection of spontaneous secretions, nasal washings, and absorption. Collection of spontaneous secretions is appropriate in subjects with nasal hypersecretion, whereas in healthy individuals the collected volume is frequently insufficient. Nasal washings are associated with an unpredictable, high dilution and concentrations of markers often fall below detection limits of immunological assays. Absorption seem to provide the best compromise between sufficient sample amounts and detectability of inflammatory mediators and immunoglobulin E. Tear samples can be obtained by glass capillary tubes, filter paper strips and ophthalmic sponges. Volumes are however small or highly diluted through reflex tearing. SUMMARY: Secretions reflect the local inflammatory activity and provide valuable information about the immunological reaction to allergens at the target organ. There is increasing evidence of the potential clinical role of their analysis, for diagnosis, and monitoring of allergic rhino-conjunctivitis. Appropriate collection and processing is very important and requires special attention</style></abstract><notes><style face="normal" font="default">IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Japan -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000412</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29135513">PM:29135513</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2018-18-1-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2018-18-1-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Castelli S</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000412</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87285</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Manorak,W.</style></author><author><style face="normal" font="default"> Idahosa,C.</style></author><author><style face="normal" font="default"> Gupta,K.</style></author><author><style face="normal" font="default"> Roy,S.</style></author><author><style face="normal" font="default"> Panettieri,R.,Jr.</style></author><author><style face="normal" font="default"> Ali,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pathology, School of Dental Medicine, University of Pennsylvania, 240 South 40th Street, Philadelphia, PA, 19104-6030, USA</style></auth-address><titles><title><style face="normal" font="default">Upregulation of Mas-related G Protein coupled receptor X2 in asthmatic lung mast cells and its activation by the novel neuropeptide hemokinin-1</style></title><secondary-title><style face="normal" font="default">Respir Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Res</style></abbr-1></periodical><pages end="" start="1">1-</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="3" Month="1" Year="2018">2018/1/3</year></dates><abstract><style face="normal" font="default">Hemokinin-1 (HK-1) is a novel neuropeptide produced by human bronchial cells and macrophages and causes contraction of human bronchi ex vivo. It is also generated by antigen/IgE-activated murine mast cells (MCs) and contributes to experimental chronic allergic airway inflammation via the activation of the neurokinin receptor-1 (NK-1R) expressed on murine MCs. We found elevated MC numbers in the lungs of individuals who died from asthma (asthma) when compared to lungs of individuals who died from other causes (non-asthma). Mas-related G Protein coupled receptor X2 (MRGPRX2) is a novel G-protein coupled receptor (GPCR) that is expressed predominantly on human MCs. We detected low level of MRGPRX2 in non-asthma lung MCs but its expression was significantly upregulated in asthma lung MCs. HK-1 caused degranulation in a human MC line (LAD2) and RBL-2H3 cells stably expressing MRGPRX2 and this response was resistant to inhibition by an NK-1R antagonist. However, knockdown of MRGPRX2 in LAD2 cells resulted in substantial inhibition of HK-1-induced degranulation. These findings suggest that while HK-1 contributes to the development of experimental asthma in mice via NK-1R on murine MCs the effect of this neuropeptide on human bronchoconstriction likely reflects the activation of MRGPRX2 on lung MCs. Thus, development of selective MRGPRX2 antagonists could serve as novel target for the modulation of asthma</style></abstract><notes><style face="normal" font="default">IS - 1465-993X (Electronic)IS - 1465-9921 (Linking)LA - engPT - LetterCO - United States -</style></notes><work-type><style face="normal" font="default">10.1186/s12931-017-0698-3</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29295703">PM:29295703</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Res\2018-19-1.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Res\2018-19-1.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Manorak W</style></custom2><misc3><style face="normal" font="default">10.1186/s12931-017-0698-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87301</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cherrez Ojeda,I.</style></author><author><style face="normal" font="default"> Vanegas,E.</style></author><author><style face="normal" font="default"> Felix,M.</style></author><author><style face="normal" font="default"> Mata,V.</style></author><author><style face="normal" font="default"> Cherrez,S.</style></author><author><style face="normal" font="default"> Simancas-Racines,D.</style></author><author><style face="normal" font="default"> Greiding,L.</style></author><author><style face="normal" font="default"> Cano,J.</style></author><author><style face="normal" font="default"> Cherrez,A.</style></author><author><style face="normal" font="default"> Calderon,J.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Etiology of chronic urticaria: the Ecuadorian experience</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="1">1-</pages><volume><style face="normal" font="default">11</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">The purpose of this study was to identify chronic urticaria (CU) etiologies and treatment modalities in Ecuador. We propose that the sample distribution fits the expected one, and that there is an association between the etiology and its treatment</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Ecuador -CO - Argentina -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0181-0</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0181-0</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2018-11-1.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2018-11-1.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Cherrez Ojeda I</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0181-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87330</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Quirt,J.</style></author><author><style face="normal" font="default"> Gagnon,R.</style></author><author><style face="normal" font="default"> Ellis,A.K.</style></author><author><style face="normal" font="default"> Kim,H.L.</style></author></authors></contributors><titles><title><style face="normal" font="default">CSACI position statement: prescribing sublingual immunotherapy tablets for aeroallergens</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Clin Immunol</style></abbr-1></periodical><pages end="" start="1">1-</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1710-1492</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1186/s13223-017-0225-6</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s13223-017-0225-6</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-14-1.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-14-1.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180109, Quirt J</style></custom2><misc3><style face="normal" font="default">10.1186/s13223-017-0225-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87368</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Burks,A.W.</style></author><author><style face="normal" font="default"> Sampson,H.A.</style></author><author><style face="normal" font="default"> Plaut,M.</style></author><author><style face="normal" font="default"> Lack,G.</style></author><author><style face="normal" font="default"> Akdis,C.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, University of North Carolina, Chapel Hill, NC.</style></auth-address><titles><title><style face="normal" font="default">Treatment for food allergy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="9" start="1">1-9</pages><volume><style face="normal" font="default">141</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">The prevalence of IgE-mediated food allergy is an increasing public health concern effecting millions of persons worldwide. The current standard of treatment is strict avoidance of the offending food or foods, and to date, there are no regulatory approved treatments for food allergy. A significant amount of research has been directed at various forms of food immunotherapy, including oral, sublingual, and epicutaneous delivery routes. Although oral immunotherapy has shown the greatest promise for efficacy in terms of the amount of protein that can be ingested, it has also demonstrated less tolerability and a less favorable safety profile compared with sublingual immunotherapy and epicutaneous immunotherapy, which offers the least protection but has the best safety and tolerability profile. Studies have been conducted with adding adjuvants and anti-IgE to enhance either the efficacy or safety of food immunotherapy. Multiple concepts of food immunotherapy beyond these first-generation treatments are in either animal or early phase 1 studies</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -CO - United Kingdom -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29307409">PM:29307409</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\2018-141-1-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\2018-141-1-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Burks AW</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87375</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wilson,J.M.</style></author><author><style face="normal" font="default"> Platts-Mills,T.A.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Immunology, University of Virginia, Charlottesville, Va</style></auth-address><titles><title><style face="normal" font="default">Home Environmental Interventions for House Dust Mite</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="7" start="1">1-7</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">It has been 50 years since the dust mite was first appreciated to be a major source of allergen in house dust, and by extension a key trigger of allergic respiratory disease. Since that time a number of protein allergens have been identified and characterized, mainly from mite feces, and standardized mite extracts and IgE assays have been developed. Insights into the lifecycle of dust mites and aspects of mite allergen biology have shed light on the mechanisms that lead to respiratory disease and to the development of interventions that can minimize dust mite allergen exposure. It is now clear that dust mite allergy is a key contributor to asthma in many parts of the world, and that long-term avoidance can be effective for preventing sensitization and minimizing the development and severity of respiratory disease. Here, we discuss the evidence linking dust mites with respiratory disease, outline studies that support the efficacy of home environmental interventions, and highlight practical methods that have been shown to be effective as part of a multifaceted approach to dust mite avoidance</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29310755">PM:29310755</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180105, Wilson JM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87425</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rahmoun,N.</style></author><author><style face="normal" font="default"> El Mecherfi,K.E.</style></author><author><style face="normal" font="default"> Bouchetara,A.</style></author><author><style face="normal" font="default"> Lardjem,H.S.</style></author><author><style face="normal" font="default"> Dahmani,A.C.</style></author><author><style face="normal" font="default"> Adda,N.L.</style></author><author><style face="normal" font="default"> Boudjema,A.</style></author><author><style face="normal" font="default"> Zemani-Fodil,F.</style></author><author><style face="normal" font="default"> Saidi,D.</style></author><author><style face="normal" font="default"> Kheroua,O.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Laboratoire de Genetique Moleculaire et Cellulaire , Universite des Sciences et de la Technologie d'Oran-Mohamed Boudiaf -US</style></auth-address><titles><title><style face="normal" font="default">Association of REL Polymorphism with Cow's Milk Proteins Allergy in Pediatric Algerian Population. Association REL Polymorphism with Cow's Milk Proteins Allergy</style></title><secondary-title><style face="normal" font="default">Fetal Pediatr Pathol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Fetal Pediatr Pathol</style></abbr-1></periodical><pages end="10" start="1">1-10</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword></keywords><dates><year Day="16" Month="1" Year="2018">2018/1/16</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Cow's milk proteins allergy (CMPA) pathogenesis involves complex immunological mechanisms with the participation of several cells and molecules involved in food allergy. The association of polymorphisms in the interleukin 4, Forkhead box P3 and the avian reticuloendotheliosis genes was investigated in an infant population with CMPA of Western Algeria. MATERIALS AND METHODS: We obtained DNA and clinical data from milk allergic subjects during active phase and from a group of non-atopic control subjects. RESULTS: Our findings showed that the allele G of the cRel gene intronic polymorphism at +7883 positions was significantly higher among cow's milk proteins allergic patients compared to control subjects. CONCLUSION: The results of this study suggest a possible association of CMPA with cRel G+7883T polymorphism</style></abstract><notes><style face="normal" font="default">IS - 1551-3823 (Electronic)IS - 1551-3815 (Linking)LA - engPT - Journal ArticleCO - Algeria -</style></notes><work-type><style face="normal" font="default">10.1080/15513815.2017.1405468</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29336650">PM:29336650</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Fetal Pediatr Pathol\20180116-RahmounN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Fetal Pediatr Pathol\20180116-RahmounN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180116, Rahmoun N</style></custom2><misc3><style face="normal" font="default">10.1080/15513815.2017.1405468</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87240</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shin,Y.S.</style></author><author><style face="normal" font="default"> Jung,C.G.</style></author><author><style face="normal" font="default"> Park,H.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy and Clinical Immunology, Ajou University School of Medicine, SuwonDivision of Allergy and Clinical Immunology, Department of Internal Medicine, Keimyung University, Dongsan Medical Center, Daegu, South KoreaDepartment of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon</style></auth-address><titles><title><style face="normal" font="default">Prevalence and clinical characteristics of local allergic rhinitis to house dust mites</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="15" start="10">10-15</pages><volume><style face="normal" font="default">18</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: Local allergic rhinitis (LAR) is a recently classified subtype of rhinitis defined by a nasal allergic response in patients without systemic evidence of atopy. Recent studies have reported the prevalence, clinical course, culprit allergens, diagnostic methods and treatment outcomes of LAR. The purpose of this review is to summarize the most relevant and updated scientific evidence for LAR, especially focusing on its prevalence and clinical characteristics. RECENT FINDINGS: LAR is found in a significant proportion (3.7-61.9%) of patients previously diagnosed with nonallergic rhinitis, but the prevalence may differ among ethnic groups and countries. Common allergens of LAR are similar to those of allergic rhinitis, in which house dust mites are the most common cause, followed by grass pollen, tree pollen, weed pollen and animal dander confirmed by provocation tests. Although the nasal provocation test to a single allergen is considered the gold standard method, the detection of allergen-specific IgE and other inflammatory mediators from nasal secretions and the basophil activation test can assist in the diagnosis of LAR. Conjunctivitis and asthma are the most common comorbid conditions, and the occurrence rate of asthma increases over period. However, the conversion rate to allergic rhinitis was not significantly different between LAR and healthy controls. SUMMARY: LAR is a well-differentiated entity of rhinitis, which should be considered in patients with persistent and severe symptoms without any systemic evidence of atopy. Further research is needed to investigate the long-term outcome, and geographic and ethnic differences of LAR</style></abstract><notes><style face="normal" font="default">IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000413</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29135514">PM:29135514</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2018-18-10-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2018-18-10-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Shin YS</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000413</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87355</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hedge,V.L.</style></author><author><style face="normal" font="default"> Mahesh,P.A.</style></author><author><style face="normal" font="default"> Venkatesh,Y.P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Skin prick test analysis reveals cross-sensitization to tomato profilin and grass pollen in nasobronchialallergic patients with history of tomato food allergy</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="18" start="10">10-18</pages><volume><style face="normal" font="default">50</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">The association between grass pollen sensitization and food allergy to tomato is of great interest. We report here, the first such study in Indian population. We investigated 246 allergic rhinitis / asthma patients by diagnostic case history and skin prick test (SPT); grass pollen mix, tomato extract and purified tomato profilin were used for SPT. Tomato profilin was purified by affinity chromatography, and analyzed by HPLC (95% purity) and SDS-PAGE (14 kDa). We observed that 38% of the patients had sensitization to both grass pollen and tomato fruit, of which 92% were sensitized to tomato profilin. Among patients with a history of food allergy to tomato fruit, the association was more pronounced (66%). Tomato profilin appears to be an important cross-sensitizing panallergen in respiratory allergic patients in the Indian subcontinent.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - India -CO - United States -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.27</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.23822/EurAnnACI.1764-1489.27</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-10-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-10-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Hedge VL</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.27</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87366</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Guardone,L.</style></author><author><style face="normal" font="default"> Nucera,D.</style></author><author><style face="normal" font="default"> Lodola,L.B.</style></author><author><style face="normal" font="default"> Tinacci,L.</style></author><author><style face="normal" font="default"> Acutis,P.L.</style></author><author><style face="normal" font="default"> Guidi,A.</style></author><author><style face="normal" font="default"> Armani,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">FishLab, Department of Veterinary Sciences, University of Pisa, Viale delle Piagge 2, 56124, Pisa, Italy</style></auth-address><titles><title><style face="normal" font="default">Anisakis spp. larvae in different kinds of ready to eat products made of anchovies (Engraulis encrasicolus) sold in Italian supermarkets</style></title><secondary-title><style face="normal" font="default">Int J Food Microbiol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Int J Food Microbiol</style></full-title></periodical><pages end="18" start="10">10-18</pages><volume><style face="normal" font="default">268</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anchovy</style></keyword><keyword><style face="normal" font="default"> Anisakidosis</style></keyword><keyword><style face="normal" font="default"> Anisakis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">In this study the occurrence of visible anisakid larvae in semi-preserved anchovy products sold on the Italian market was investigated. Totally, 107 ready to eat products (33 salted-ripened, 49 in oil and 25 marinated) were sampled. Each sample was digested, then the digested material was observed under natural and UV light. Parasites were counted, collected and microscopically identified to genus level. A representative subset was molecularly identified using the cox2 gene. At least one visible Anisakis sp. larva was found in 54.2% of the total 107 products analysed and totally 1283 dead larvae were collected. Anisakis sp. larvae were found in all the 33 salted products and 1139 (88.8%) larvae were collected, with a range of 1-105 parasites per product. Larval density per gram was 0.13. Anisakis sp. larvae were found in 49.0% of the products in oil and 143 (11.1%) larvae were isolated, with a range of 0-28 and a density of 0.03. Only 1 larva was found in the 25 marinated products (4.0%, density 0.00). A highly significant difference between all the product categories in respect of number of larvae per product, frequency of products contaminated by at least one larva and larval density per gram was found. Within the subset of larvae molecularly analysed (n=122), 92 (75.4%) were identified as A. pegreffii and 30 (24.6%) as A. simplex. This study showed that semi-preserved anchovy products heavily contaminated with Anisakis spp. larvae reach the market. Beyond the negligible risk for anisakidosis, the presence of dead visible parasites may cause immediate rejection in consumers. In addition, the potential risk related to allergic reactions in sensitized individuals needs to be further assessed. In order to avoid commercialization of obviously contaminated products, fresh anchovies' batches intended for the production of such products should be accurately selected by the processing industry applying inspection methods</style></abstract><notes><style face="normal" font="default">IS - 1879-3460 (Electronic)IS - 0168-1605 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.ijfoodmicro.2017.12.030</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29306733">PM:29306733</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Food Microbiol\2018-268-10-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Food Microbiol\2018-268-10-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Guardone L</style></custom2><misc3><style face="normal" font="default">10.1016/j.ijfoodmicro.2017.12.030</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86744</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,X.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Division of Allergy and Immunology, Jaffe Food Allergy Institute, Center for Integrative Medicine for Immunology and Wellness, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.</style></auth-address><titles><title><style face="normal" font="default">Complementary and Alternative Medicine for Treatment of Food Allergy</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="124" start="103">103-124</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">The prevalence of food allergy is increasing. Food allergy can be life threatening and there is no approved treatment available. Allergen avoidance and rescue medication remain the sole management tools. Complementary and alternative medicine (CAM) use is common in the United States. However, research into safety and efficacy for food allergy is limited. Continued scientific research into food allergy herbal formula 2 (FAHF-2), refined methods of formulation, purified compounds, and other modalities are needed. Traditional Chinese medicine is the main component of CAM in the United States. Conventional doctors, CAM practitioners, and patients' families must collaborate to comanage these patients</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.012</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132667">PM:29132667</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-103-24.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-103-24.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Li XM</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.012</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86879</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fernandes,T.J.R.</style></author><author><style face="normal" font="default"> Costa,J.</style></author><author><style face="normal" font="default"> Oliveira,M.B.</style></author><author><style face="normal" font="default"> Mafra,I.</style></author></authors></contributors><titles><title><style face="normal" font="default">Exploiting 16S rRNA gene for the detection and quantification of fish as a potential allergenic food: A comparison of two real-time PCR approaches</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="1041" start="1034">1034-1041</pages><volume><style face="normal" font="default">245</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">EvaGreen dye</style></keyword><keyword><style face="normal" font="default"> Fish allergen</style></keyword><keyword><style face="normal" font="default"> Fish detection</style></keyword><keyword><style face="normal" font="default"> Mitochondrial DNA</style></keyword><keyword><style face="normal" font="default"> Quantitative real-time PCR</style></keyword><keyword><style face="normal" font="default"> TaqMan probe</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0308-8146</style></isbn><abstract><style face="normal" font="default">Fish is one of the most common allergenic foods that should be accurately labelled to protect the health of allergic consumers. In this work, two real-time PCR systems based on the EvaGreen dye and a TaqMan probe are proposed and compared. New primers were designed to target the 16S rRNA gene, as a universal maker for fish detection, with fully demonstrated specificity for a wide range of fish species. Both systems showed similar absolute sensitivities, down to 0.01</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç»pg of fish DNA, and adequate real-time PCR performance parameters. The probe system showed higher relative sensitivity and dynamic range (0.0001</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô50%) than the EvaGreen (0.05</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô50%). They were both precise, but trueness was compromised at the highest tested level with the EvaGreen assay. Therefore, both systems were successful, although the probe one exhibited the best performance. Its application to verify labelling compliance of foodstuffs suggested a high level of mislabelling and/or fraudulent practices</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Portugal -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2017.11.068</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29287319">PM:29287319</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\20171120-FernandesTJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\20171120-FernandesTJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Fernandes TJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2017.11.068</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87444</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lianto,P.</style></author><author><style face="normal" font="default"> Han,S.</style></author><author><style face="normal" font="default"> Li,X.</style></author><author><style face="normal" font="default"> Ogutu,F.O.</style></author><author><style face="normal" font="default"> Zhang,Y.</style></author><author><style face="normal" font="default"> Fan,Z.</style></author><author><style face="normal" font="default"> Che,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, 100083, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Quail egg homogenate alleviates food allergy induced eosinophilic esophagitis like disease through modulating PAR-2 transduction pathway in peanut sensitized mice</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="1049">1049-</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Eosinophilic esophagitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">The present pharmacotherapy for eosinophilic esophagitis (EoE) fundamentally depend on inhaled corticosteroids. Despite the fact that oral intake of topical steroids can be successful in restricting EoE-related inflammation, there are concerns with respect to the long term utilization of steroids, especially in kids. In the current research, we assess the effect of quail egg, which is reportedly a known serine protease inhibitor, on symptomatology and immune responses in a peanut-sensitized mouse model of food allergy induced EoE. Daily oral treatment with quail egg attenuated mice symptomatology and immune response. Treatment with quail egg inhibited antigen-prompted increments in mouse tryptase and eosinophil cationic protein (ECP) in serum and eosinophil in inflamed tissues like oesophagus, lung, and digestive system. Quail egg treatment resulted in decreased antibody specific IgE and IgG1 and a variety of inflammatory genes that were abnormally expressed in EoE. Other effects included increased IL-10, decreased PAR-2 activation and NF-kB p65 in inflamed tissues. Our results suggest that quail egg treatment may have therapeutic potential in attenuating the symptoms of food allergy induced EoE like disease through regulating PAR-2 downstream pathway by blocking the activation of the transcription factor NF-kB p65 activity</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-018-19309-x</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29348584">PM:29348584</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-1049.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-1049.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Lianto P</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-018-19309-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87443</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Khor,S.S.</style></author><author><style face="normal" font="default"> Morino,R.</style></author><author><style face="normal" font="default"> Nakazono,K.</style></author><author><style face="normal" font="default"> Kamitsuji,S.</style></author><author><style face="normal" font="default"> Akita,M.</style></author><author><style face="normal" font="default"> Kawajiri,M.</style></author><author><style face="normal" font="default"> Yamasaki,T.</style></author><author><style face="normal" font="default"> Kami,A.</style></author><author><style face="normal" font="default"> Hoshi,Y.</style></author><author><style face="normal" font="default"> Tada,A.</style></author><author><style face="normal" font="default"> Ishikawa,K.</style></author><author><style face="normal" font="default"> Hine,M.</style></author><author><style face="normal" font="default"> Kobayashi,M.</style></author><author><style face="normal" font="default"> Kurume,N.</style></author><author><style face="normal" font="default"> Kamatani,N.</style></author><author><style face="normal" font="default"> Tokunaga,K.</style></author><author><style face="normal" font="default"> Johnson,T.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan</style></auth-address><titles><title><style face="normal" font="default">Genome-wide association study of self-reported food reactions in Japanese identifies shrimp and peach specific loci in the HLA-DR/DQ gene region</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="1069">1069-</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergen immunotherapy</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> genetics</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Peach</style></keyword></keywords><dates><year Day="18" Month="1" Year="2018">2018/1/18</year></dates><abstract><style face="normal" font="default">Food allergy is an increasingly important health problem in the world. Several genome-wide association studies (GWAS) focused on European ancestry samples have identified food allergy-specific loci in the HLA class II region. We conducted GWAS of self-reported reactivity with common foods using the data from 11011 Japanese women and identified shrimp and peach allergy-specific loci in the HLA-DR/DQ gene region tagged by rs74995702 (P = 6.30 x 10(-17), OR = 1.91) and rs28359884 (P = 2.3 x 10(-12), OR = 1.80), respectively. After HLA imputation using a Japanese population-specific reference, the most strongly associated haplotype was HLA-DRB1*04:05-HLA-DQB1*04:01 for shrimp allergy (P = 3.92 x 10(-19), OR = 1.99) and HLA-DRB1*09:01-HLA-DQB1*03:03 for peach allergy (P = 1.15 x 10(-7), OR = 1.68). Additionally, both allergies' associated variants were eQTLs for several HLA genes, with HLA-DQA2 the single eQTL gene shared between the two traits. Our study suggests that allergy to certain foods may be related to genetic differences that tag both HLA alleles having particular epitope binding specificities as well as variants modulating expression of particular HLA genes. Investigating this further could increase our understanding of food allergy aetiology and potentially lead to better therapeutic strategies for allergen immunotherapies</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-18241-w</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29348432">PM:29348432</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-1069.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-1069.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-1069-data1.xlsxC:\A&amp;H HMW Papers\Sci Rep\2018-8-1069-data2.xlsxC:\A&amp;H HMW Papers\Sci Rep\2018-8-1069-worksheets.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-1069-data1.xlsxF:\A&amp;H HMW Papers\Sci Rep\2018-8-1069-data2.xlsxF:\A&amp;H HMW Papers\Sci Rep\2018-8-1069-worksheets.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20180118, Khor SS</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-18241-w</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87049</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cherrez Ojeda,I.</style></author><author><style face="normal" font="default"> Vanegas,E.</style></author><author><style face="normal" font="default"> Greiding,L.</style></author><author><style face="normal" font="default"> Cherrez,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Universidad Especialidades Espiritu Santo, School of Medicine, Samborondon, Ecuador</style></auth-address><titles><title><style face="normal" font="default">Urticarial vasculitis and autoimmune thyroid disease: Do we have enough data?</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="108" start="107">107-108</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - LetterCO - Ecuador -CO - Argentina -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.291</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273120">PM:29273120</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-107-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-107-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Cherrez Ojeda I</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.291</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87270</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bauters,T.</style></author><author><style face="normal" font="default"> Bordon,V.</style></author><author><style face="normal" font="default"> Willems,J.</style></author><author><style face="normal" font="default"> De Wilde,B.</style></author><author><style face="normal" font="default"> Laureys,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">1 Department of Pediatric Hemato-Oncology and Hematopoietic Stem Cell Transplantation, Ghent University Hospital, Ghent, Belgium</style></auth-address><titles><title><style face="normal" font="default">Severe anaphylactic reaction following anti-thymocyte globulin administration in a pediatric stem cell transplantation patient</style></title><secondary-title><style face="normal" font="default">J Oncol Pharm Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Oncol Pharm Pract</style></abbr-1></periodical><pages end="" start="1078155217699989">1078155217699989-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Guidelines</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">We present a case of a severe reaction after anti-thymocyte administration despite premedication and strict adherence to administration guidelines during the conditioning regimen. Due to the severity of the adverse drug reaction, we believe that this case should be reported</style></abstract><notes><style face="normal" font="default">IS - 1477-092X (Electronic)IS - 1078-1552 (Linking)LA - engPT - Journal ArticleCO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1177/1078155217699989</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29284348">PM:29284348</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Oncol Pharm Pract\20180101-BautersT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Oncol Pharm Pract\20180101-BautersT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180101, Bauters</style></custom2><misc3><style face="normal" font="default">10.1177/1078155217699989</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87047</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chatain,C.</style></author><author><style face="normal" font="default"> Boccon-Gibod,I.</style></author><author><style face="normal" font="default"> Bouillet,L.</style></author><author><style face="normal" font="default"> Leccia,M.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Allergology and Photobiology, Centre Hospitalier Universitaire de Grenoble, Grenoble, France.</style></auth-address><titles><title><style face="normal" font="default">Protracted severe food anaphylaxis: Should we incriminate expired epinephrine pen or clonal mast cell disorder?</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="109">109-</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - LetterCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.292</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273123">PM:29273123</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-109.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-109.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Chatain C</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.292</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86960</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Salzano,A.M.</style></author><author><style face="normal" font="default"> Sobolev,A.</style></author><author><style face="normal" font="default"> Carbone,V.</style></author><author><style face="normal" font="default"> Petriccione,M.</style></author><author><style face="normal" font="default"> Renzone,G.</style></author><author><style face="normal" font="default"> Capitani,D.</style></author><author><style face="normal" font="default"> Vitale,M.</style></author><author><style face="normal" font="default"> Minasi,P.</style></author><author><style face="normal" font="default"> Pasquariello,M.S.</style></author><author><style face="normal" font="default"> Novi,G.</style></author><author><style face="normal" font="default"> Zambrano,N.</style></author><author><style face="normal" font="default"> Scortichini,M.</style></author><author><style face="normal" font="default"> Mannina,L.</style></author><author><style face="normal" font="default"> Scaloni,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Proteomics &amp; Mass Spectrometry Laboratory, ISPAAM, National Research Council, 80147 Naples, Italy</style></auth-address><titles><title><style face="normal" font="default">A proteometabolomic study of Actinidia deliciosa fruit development</style></title><secondary-title><style face="normal" font="default">J Proteomics</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Proteomics</style></abbr-1></periodical><pages end="24" start="11">11-24</pages><volume><style face="normal" font="default">172</style></volume><reprint-status status="in-file"/><keywords/><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1876-7737 (Electronic)IS - 1874-3919 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.jprot.2017.11.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29133123">PM:29133123</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Proteomics\2018-172-11-24.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Proteomics\2018-172-11-24.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Proteomics\2018-172-11-24-mmc3.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Proteomics\2018-172-11-24-mmc3.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20171207, Salzano AM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jprot.2017.11.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87273</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Thrastardottir,A.R.</style></author><author><style face="normal" font="default"> Thordardottir,F.R.</style></author><author><style face="normal" font="default"> Torfadottir,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre for Public Health SciencesUniversity of IcelandUniversity Hospital</style></auth-address><titles><title><style face="normal" font="default">[Protocols Related to Food Allergies and Intolerances in Preschools in Reykjavik, Iceland]</style></title><secondary-title><style face="normal" font="default">Laeknabladid</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Laeknabladid</style></abbr-1></periodical><pages end="17" start="11">11-17</pages><volume><style face="normal" font="default">104</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">INTRODUCTION: The aim of the study was to explore prevalence of food allergies and intolerances among children in preschools in Reykjavik, Iceland. Also, to investigate how well preschools maintain a safe environment for children with food allergies. MATERIALS AND METHODS: In 2014, a questionnaire designed specifically for this study, was sent to 65 preschools. Forty-nine participated (75%) representing a total of 4225 children. Prevalence of food allergy and intolerance was determined based on medical certificates from physi-cians delivered to the preschools. Descriptive statistics were used to assess whether there were protocols related to food allergy, and if there was a difference between schools based on staff's education and number of children. RESULTS: The prevalence of documented food allergies/intolerances in children aged 2-6 years was 5%, 1% had severe allergy and 1% had multiple food allergies. Lactose intolerance was most frequent (2%), then milk allergy (2%) and egg allergy (1%). Only 41% preschools had a protocol that was activated if food with an allergen was accidentally given. Moreover, only 55% of preschools with children with severe -allergy reported all of their staff to have knowledge of symptoms related to anaphylaxis and only 64% were trained to respond to an anaphylactic shock. The education of preschool principals, kitchen employees and number of children in preschool were not related to having an active protocol at site. CONCLUSION: Prevalence of food allergy and intolerance was 5% in preschools in Reykjavik. Strategy for an active protocol related to food allergy was lacking in 59% of pre-schools</style></abstract><notes><style face="normal" font="default">IS - 0023-7213 (Print)IS - 0023-7213 (Linking)LA - icePT - English AbstractPT - Journal ArticleCO - Iceland -</style></notes><work-type><style face="normal" font="default">10.17992/lbl.2018.01.168</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29303109">PM:29303109</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Laeknabladid\2018-104-11-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Laeknabladid\2018-104-11-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Thrastardottir AR</style></custom2><misc3><style face="normal" font="default">10.17992/lbl.2018.01.168</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87502</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Eftekhar,N.</style></author><author><style face="normal" font="default"> Moghimi,A.</style></author><author><style face="normal" font="default"> Boskabady,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran</style></auth-address><titles><title><style face="normal" font="default">Prophylactic effect of rosmarinic acid on tracheal responsiveness, white blood cell count and oxidative stress markers in lung lavage of sensitized rats</style></title><secondary-title><style face="normal" font="default">Pharmacol Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pharmacol Rep</style></abbr-1></periodical><pages end="125" start="119">119-125</pages><volume><style face="normal" font="default">70</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">BACKGROUND: Rosmarinic acid (RA) as an active component of several medicinal plants, has shown anti-inflammatory and anti-oxidant effects. In this study, the effect of RA on tracheal responsiveness (TR), lung inflammatory cells, oxidant biomarkers in sensitized rats were evaluated. METHODS: TR to methacholine and ovalbumin (OVA) as well as total and differential white blood cell (WBC) count and levels of nitrogen dioxide, nitrate, malondialdehyde, thiol, superoxide dismutase, and catalase in bronchoalveolar lavage fluid were measured in control (groupC) rats, sensitized animals to OVA and given drinking water alone (group S), S groups receiving drinking water containing three concentrations of RA (0.125, 0.250 and 0.500mg/mL) and dexamethasone (1.25mug/mL), (n=6 in each group). RESULTS: Increased TR to methacholine and OVA, total WBC count, percentages of eosinophils, monocytes, neutrophils and levels of oxidant biomarkers but decreased other measured parameters were observed in group S compared to group C. Percentages of lymphocytes and antioxidant biomarkers were significantly increased but other measured parameters were significantly decreased in S group treated with dexamethasone and in rats treated with the two higher concentrations of RA compared to S group. The effect of RA medium concentration on percentage of eosinophils and RA high concentration on total WBC count and percentages of eosinophils and lymphocytes, were significantly higher than those of dexamethasone. CONCLUSION: These results showed the concentration-dependent effect of RA on tracheal responses, lung inflammatory cells and oxidant-antioxidant parameters which was comparable to that of dexamethasone at used concentrations in sensitized rats</style></abstract><notes><style face="normal" font="default">IS - 1734-1140 (Print)IS - 1734-1140 (Linking)LA - engPT - Journal ArticleCO - Iran -</style></notes><work-type><style face="normal" font="default">10.1016/j.pharep.2017.08.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29355815">PM:29355815</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pharmacol Rep\2018-70-119-25.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pharmacol Rep\2018-70-119-25.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170830, Eftekhar N</style></custom2><misc3><style face="normal" font="default">10.1016/j.pharep.2017.08.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87382</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zheng,B.</style></author><author><style face="normal" font="default"> Zhang,H.</style></author><author><style face="normal" font="default"> Wang,L.</style></author><author><style face="normal" font="default"> Guo,Y.</style></author><author><style face="normal" font="default"> Chen,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of Biochemistry and Molecular Biology, College of Life Science, Northwest A&amp;F University, Yangling, China</style></auth-address><titles><title><style face="normal" font="default">Characterization of 16-kDa major allergen with alpha-amylase inhibitor domain in tartary buckwheat seeds</style></title><secondary-title><style face="normal" font="default">Mol Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Immunol</style></abbr-1></periodical><pages end="130" start="121">121-130</pages><volume><style face="normal" font="default">94</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword></keywords><dates><year Day="3" Month="1" Year="2018">2018/1/3</year></dates><abstract><style face="normal" font="default">Tartary buckwheat (Fagopyrum tataricum, TB) is an important functional food containing proteins with balanced amino acid composition and more flavonoids than common buckwheat (Fagopyrum esculentum, CB). Buckwheat contains highly potent allergens that trigger an allergic reaction via an IgE mediated response. In this work, the full-length cDNA encoding Fag t 2 from tartary buckwheat seeds was cloned by screening the cDNA library of seed-filling period. The recombinant Fag t 2 (rFag t 2) expressed in Pichia pastoris SMD1168H was purified by purified by immobilized metal affinity chromatography. It demonstrated that Fag t 2 was a major allergen in tartary buckwheat with the activity of IgE binding and pepsin resistance, along with the thermal stability. The identification of natural Fag t 2 (n Fag t 2) confirmed that the Fag t 2 protein belongs to the 2S albumin family, only existing in embryo. Most interesting, we discovered that Fag t 2 had a alpha-amylase inhibitor domain near the end of C-terminal. The possible activity of alpha-amylase inhibitor of Fag t 2 will be detected in subsequent studies</style></abstract><notes><style face="normal" font="default">IS - 1872-9142 (Electronic)IS - 0161-5890 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.molimm.2017.12.024</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29306152">PM:29306152</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Immunol\2018-94-121-30.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Immunol\2018-94-121-30.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Zhang B</style></custom2><misc3><style face="normal" font="default">10.1016/j.molimm.2017.12.024</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86739</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wilson,J.M.</style></author><author><style face="normal" font="default"> McGowan,E.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Immunology, Department of Medicine, University of Virginia, PO Box 801355, Charlottesville, VA 22908, USA</style></auth-address><titles><title><style face="normal" font="default">Diagnosis and Management of Eosinophilic Esophagitis</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="139" start="125">125-139</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">Unlike traditional food allergies, immunoglobulin E (IgE) is not a key mediator of eosinophilic esophagitis (EoE). Nonetheless, foods antigens are important triggers of EoE, and allergists play an important role in management of this chronic disease. This review addresses insights into the diagnosis and management as it relates to our evolving understanding about the pathogenesis of EoE</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132668">PM:29132668</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-125-39.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-125-39.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Wilson JM</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86835</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rai,G.</style></author><author><style face="normal" font="default"> Ansari,M.A.</style></author><author><style face="normal" font="default"> Dar,S.A.</style></author><author><style face="normal" font="default"> Datt,S.</style></author><author><style face="normal" font="default"> Gupta,N.</style></author><author><style face="normal" font="default"> Sharma,S.</style></author><author><style face="normal" font="default"> Haque,S.</style></author><author><style face="normal" font="default"> Ramachandran,V.G.</style></author><author><style face="normal" font="default"> Mazumdar,A.</style></author><author><style face="normal" font="default"> Rudramurthy,S.</style></author><author><style face="normal" font="default"> Chakrabarti,A.</style></author><author><style face="normal" font="default"> Das,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Microbiology, University College of Medical Sciences (University of Delhi) &amp; Guru Teg Bahadur Hospital, Delhi, India</style></auth-address><titles><title><style face="normal" font="default">Serum Cytokine Profile in Patients with Chronic Rhinosinusitis with Nasal Polyposis Infected by Aspergillus flavus</style></title><secondary-title><style face="normal" font="default">Ann Lab Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Lab Med</style></abbr-1></periodical><pages end="131" start="125">125-131</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">methods</style></keyword></keywords><dates><year Day="0" Month="3" Year="2018">2018/3</year></dates><abstract><style face="normal" font="default">BACKGROUND: Fungi, especially Aspergillus flavus, can cause chronic rhinosinusitis with nasal polyposis and modulate host innate immune components. The objective of this study was to examine the serum levels of T helper (Th) cell subset Th1, Th2, and Th17 cytokines and total IgE in patients having chronic rhinosinusitis with nasal polyposis and Aspergillus flavus infection. METHODS: A case-control study including 40 patients with chronic rhinosinusitis with nasal polyposis and 20 healthy controls was conducted. Aspergillus flavus infection was confirmed by standard potassium hydroxide (KOH) testing, culture, and PCR. Serum samples of all patients and controls were analyzed for various cytokines (interleukins [IL]-1beta, IL-2, IL-4, IL-6, IL-17, IL-21, IL-27, TGF-beta) and total IgE by ELISA. Data from patients with Aspergillus flavus infection and healthy volunteers were compared using the independent t-test and non-parametric Mann-Whitney U test. RESULTS: Aspergillus flavus infection was found in 31 (77.5%) patients with chronic rhinosinusitis with nasal polyposis. IL-1beta, IL-17, IL-21, and TGF-beta serum levels were significantly higher in these patients than in controls; however, IL-2, IL-4, IL-6, and IL-27 levels were lower. Compared with nine (22.5%) patients without Aspergillus flavus infection, IL-17 level was higher while IL-2 level was lower in patients with Aspergillus flavus infection. Total IgE was significantly higher in patients with Aspergillus flavus infection than in controls. CONCLUSIONS: High levels of IL-17 and its regulatory cytokines in patients with chronic rhinosinusitis with nasal polyposis infected by Aspergillus flavus raise a concern about effective disease management and therapeutic recovery. Surgical removal of the nasal polyp being the chief management option, the choice of post-operative drugs may differ in eosinophilic vs. non-eosinophilic nasal polyposis. The prognosis is likely poor, warranting extended care</style></abstract><notes><style face="normal" font="default">IS - 2234-3814 (Electronic)IS - 2234-3806 (Linking)LA - engPT - Journal ArticleCO - India -CO - Saudi Arabia -</style></notes><work-type><style face="normal" font="default">10.3343/alm.2018.38.2.125</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29214756">PM:29214756</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Lab Med\2018-38-125-31.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Lab Med\2018-38-125-31.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Rai G</style></custom2><misc3><style face="normal" font="default">10.3343/alm.2018.38.2.125</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87120</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yu,K.</style></author><author><style face="normal" font="default"> Wang,Y.</style></author><author><style face="normal" font="default"> Wan,T.</style></author><author><style face="normal" font="default"> Zhai,Y.</style></author><author><style face="normal" font="default"> Cao,S.</style></author><author><style face="normal" font="default"> Ruan,W.</style></author><author><style face="normal" font="default"> Wu,C.</style></author><author><style face="normal" font="default"> Xu,Y.</style></author></authors></contributors><titles><title><style face="normal" font="default">Tacrolimus nanoparticles based on chitosan combined with nicotinamide: enhancing percutaneous delivery and treatment efficacy for atopic dermatitis and reducing dose</style></title><secondary-title><style face="normal" font="default">Int J Nanomedicine</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Int J Nanomedicine</style></full-title></periodical><pages end="142" start="129">129-142</pages><volume><style face="normal" font="default">13</style></volume><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Background: Topical application of tacrolimus (FK506) was effective in the treatment of atopic dermatitis (AD); however, adverse effects frequently occurred with the increase of FK506 dose during long-term treatment. Objective: The objective of this project was to develop a hybrid skin targeting system encapsulating FK506 based on nicotinamide (NIC) and chitosan nanoparticles (CS-NPs), ie, FK506-NIC-CS-NPs, which took advantages of both of NIC and CS-NPs to obtain the synergetic effects of percutaneous delivery and treatment efficacy enhancement along with dose reduction. Methods: The formulation of FK506-NIC-CS-NPs was optimized and characterized. In vitro and in vivo skin permeation studies were performed. AD-like skin lesions were constructed with BALB/c mice by 1-chloro-2, 4-dinitrobenzene (DNCB)-induced, and FK506-NIC-CS-NPs containing different dose of FK506 were topically administered to treat AD-like skin lesions in comparison with Protopic. Results: NIC was found to significantly increase the FK506 EE to 92.2% by CS-NPs. In comparison with commercial FK506 ointment (Protopic), in vitro and in vivo skin permeation studies demonstrated that NIC-CS-NPs system significantly enhanced FK506 permeation through and into the skin, and deposited more FK506 into the skin. The treatment efficacy on clinical symptoms, histological analysis, and molecular biology of the AD-mice demonstrated that NIC-CS-NPs with ~1/3 dose of FK506 of Protopic was superior to that of Protopic, and NIC-CS-NPs vehicle exhibited the adjuvant therapy and moderate anti-AD effects. Conclusion: The system of NIC-CS-NPs enhances the permeability of FK506, plays an adjuvant role in anti-AD, reduces the dose of FK506 in treating AD, and is therefore a promising nanoscale system of FK506 for the effective treatment of AD.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.2147/IJN.S150319</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29317821">PM:29317821</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Nanomedicine\2018-13-129-42.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Nanomedicine\2018-13-129-42.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171216, Yu K</style></custom2><misc3><style face="normal" font="default">10.2147/IJN.S150319</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86736</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dunlop,J.H.</style></author><author><style face="normal" font="default"> Keet,C.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pediatric Allergy and Immunology, Johns Hopkins University School of Medicine, The Johns Hopkins Hospital, CMSC 1102, 600 North Wolfe Street, Baltimore, MD 21287, USA</style></auth-address><titles><title><style face="normal" font="default">Epidemiology of Food Allergy</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="25" start="13">13-25</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> ASIA</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">Understanding the epidemiology of food allergy is complicated by the difficulty of identifying it on a large scale. The prevalence of food allergy is higher in younger age groups and decreases with age. Allergy to peanut and egg seems to be more common in Northern Europe, the United States, Canada and Australia compared with Southern Europe, Eastern Europe and Asia, whereas shellfish and fish allergies may be more common in Asia. The rate of transient unrecognized food allergy may be high and variable recognition of food allergy may explain some of the differences seen in food allergy prevalence</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132669">PM:29132669</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-13-25.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-13-25.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Dunlop JH</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87508</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Schiener,M.</style></author><author><style face="normal" font="default"> Hilger,C.</style></author><author><style face="normal" font="default"> Eberlein,B.</style></author><author><style face="normal" font="default"> Pascal,M.</style></author><author><style face="normal" font="default"> Kuehn,A.</style></author><author><style face="normal" font="default"> Revets,D.</style></author><author><style face="normal" font="default"> Planchon,S.</style></author><author><style face="normal" font="default"> Pietsch,G.</style></author><author><style face="normal" font="default"> Serrano,P.</style></author><author><style face="normal" font="default"> Moreno-Aguilar,C.</style></author><author><style face="normal" font="default"> de la Roca,F.</style></author><author><style face="normal" font="default"> Biedermann,T.</style></author><author><style face="normal" font="default"> Darsow,U.</style></author><author><style face="normal" font="default"> Schmidt-Weber,C.B.</style></author><author><style face="normal" font="default"> Ollert,M.</style></author><author><style face="normal" font="default"> Blank,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Center of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, Member of the German Center of Lung Research (DZL), Munich, Germany</style></auth-address><titles><title><style face="normal" font="default">The high molecular weight dipeptidyl peptidase IV Pol d 3 is a major allergen of Polistes dominula venom</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="1318">1318-</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Honeybee</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="22" Month="1" Year="2018">2018/1/22</year></dates><abstract><style face="normal" font="default">Hymenoptera venom allergy can cause severe anaphylaxis in untreated patients. Polistes dominula is an important elicitor of venom allergy in Southern Europe as well as in the United States. Due to its increased spreading to more moderate climate zones, Polistes venom allergy is likely to gain importance also in these areas. So far, only few allergens of Polistes dominula venom were identified as basis for component-resolved diagnostics. Therefore, this study aimed to broaden the available panel of important Polistes venom allergens. The 100 kDa allergen Pol d 3 was identified by mass spectrometry and found to be a dipeptidyl peptidase IV. Recombinantly produced Pol d 3 exhibited sIgE-reactivity with approximately 66% of Polistes venom-sensitized patients. Moreover, its clinical relevance was supported by the potent activation of basophils from allergic patients. Cross-reactivity with the dipeptidyl peptidases IV from honeybee and yellow jacket venom suggests the presence of exclusive as well as conserved IgE epitopes. The obtained data suggest a pivotal role of Pol d 3 as sensitizing component of Polistes venom, thus supporting its status as a major allergen of clinical relevance. Therefore, Pol d 3 might become a key element for proper diagnosis of Polistes venom allergy</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Luxembourg -CO - Spain -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-018-19666-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29358620">PM:29358620</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-1318.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-1318.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180122, Schiener M</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-018-19666-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87288</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Salmon,J.H.</style></author><author><style face="normal" font="default"> Perotin,J.M.</style></author><author><style face="normal" font="default"> Morel,J.</style></author><author><style face="normal" font="default"> Drame,M.</style></author><author><style face="normal" font="default"> Cantagrel,A.</style></author><author><style face="normal" font="default"> Ziegler,L.E.</style></author><author><style face="normal" font="default"> Ravaud,P.</style></author><author><style face="normal" font="default"> Sibilia,J.</style></author><author><style face="normal" font="default"> Pane,I.</style></author><author><style face="normal" font="default"> Mariette,X.</style></author><author><style face="normal" font="default"> Gottenberg,J.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Rheumatology Department, Maison Blanche Hospital, Reims University Hospitals, Reims</style></auth-address><titles><title><style face="normal" font="default">Serious infusion-related reaction after rituximab, abatacept and tocilizumab in rheumatoid arthritis: prospective registry data</style></title><secondary-title><style face="normal" font="default">Rheumatology (Oxford)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rheumatology (Oxford)</style></abbr-1></periodical><pages end="139" start="134">134-139</pages><volume><style face="normal" font="default">57</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Abatacept</style></keyword><keyword><style face="normal" font="default"> Adult</style></keyword><keyword><style face="normal" font="default"> adverse effects</style></keyword><keyword><style face="normal" font="default"> Aged</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Antibodies,Monoclonal,Humanized</style></keyword><keyword><style face="normal" font="default"> Antirheumatic Agents</style></keyword><keyword><style face="normal" font="default"> Arthritis,Rheumatoid</style></keyword><keyword><style face="normal" font="default"> Autoimmunity</style></keyword><keyword><style face="normal" font="default"> chemically induced</style></keyword><keyword><style face="normal" font="default"> Drug Eruptions</style></keyword><keyword><style face="normal" font="default"> drug therapy</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> etiology</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Hypertension</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Infusions,Intravenous</style></keyword><keyword><style face="normal" font="default"> Logistic Models</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Middle Aged</style></keyword><keyword><style face="normal" font="default"> Multivariate Analysis</style></keyword><keyword><style face="normal" font="default"> Peptides,Cyclic</style></keyword><keyword><style face="normal" font="default"> Pharyngitis</style></keyword><keyword><style face="normal" font="default"> Registries</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Rituximab</style></keyword><keyword><style face="normal" font="default"> Severity of Illness Index</style></keyword><keyword><style face="normal" font="default"> therapeutic use</style></keyword></keywords><dates><year Day="1" Month="1" Year="2018">2018/1/1</year></dates><abstract><style face="normal" font="default">Objective: The aim was to evaluate the incidence of serious infusion-related reactions (SIRRs) in RA treated by non-TNF-targeted biologics. Methods: We analysed data from three independent prospective registers, namely autoimmunity and rituximab, Orencia (abatacept) and RA (ORA) and Registry RoAcTEmra (tocilizumab), promoted by the French Society of Rheumatology and including patients with RA. SIRRs were defined by an occurrence during or within 24 h of an infusion and requiring discontinuation of treatment. Characteristics of patients with SIRRs were extracted from the electronic database. Results: Among the 4145 patients, SIRRs occurred in 100 patients: 56 patients with the rituximab cohort (2.8% or 0.7/100 patient-years), 15 with the abatacept cohort (1.5% or 0.6/100 patient-years) and 29 with tocilizumab (1.9% or 1/100 patient-years). No fatal SIRR occurred. A previous mild infusion reaction to non-TNF-targeted biologics was observed in a quarter of patients with SIRRs. After pooled multivariate analysis, positive anti-CCP was associated with a higher risk of SIRR (odds ratio = 2.5; 95% CI: 1.01, 6.17). Absence of concomitant treatment with a synthetic DMARD tended to be associated with a higher risk of SIRR (odds ratio = 1.67; 95% CI: 1.00, 2.86). Conclusion: In daily practice, SIRRs are slightly more frequent than in clinical trials and rarely life threatening. In common practice, serological status (anti-CCP positivity) and absence of concomitant treatment with a synthetic DMARD increase the risk of SIRR</style></abstract><notes><style face="normal" font="default">IS - 1462-0332 (Electronic)IS - 1462-0324 (Linking)LA - engPT - Journal ArticleRN - 0 (Antibodies, Monoclonal, Humanized)RN - 0 (Antirheumatic Agents)RN - 0 (Peptides, Cyclic)RN - 0 (cyclic citrullinated peptide)RN - 4F4X42SYQ6 (Rituximab)RN - 7D0YB67S97 (Abatacept)RN - I031V2H011 (tocilizumab)SB - AIMSB - IMCO - France -</style></notes><work-type><style face="normal" font="default">10.1093/rheumatology/kex403</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29069471">PM:29069471</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180101, Salmon JH</style></custom2><misc3><style face="normal" font="default">10.1093/rheumatology/kex403</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86740</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bingemann,T.A.</style></author><author><style face="normal" font="default"> Sood,P.</style></author><author><style face="normal" font="default"> Jarvinen,K.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy, Immunology and Rheumatology, Rochester Regional Health, 222 Alexander Street, Suite 3000, Rochester, NY 14607, USA</style></auth-address><titles><title><style face="normal" font="default">Food Protein-Induced Enterocolitis Syndrome</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="152" start="141">141-152</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated food allergy that usually presents in infancy. Cow's milk, soy, and grains are the most common food triggers. FPIES can present as a medical emergency with symptoms including delayed persistent emesis or diarrhea that can lead to severe dehydration and hemodynamic instability with abnormal laboratory markers. Diagnosis can often be made based on clinical history and noted improvement in symptoms once the suspected triggers have been removed from the diet, with oral food challenge as the gold standard for confirmation of diagnosis in unclear cases</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132670">PM:29132670</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-141-52.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-141-52.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Bingemann TA</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87507</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jones,A.C.</style></author><author><style face="normal" font="default"> Troy,N.M.</style></author><author><style face="normal" font="default"> White,E.</style></author><author><style face="normal" font="default"> Hollams,E.M.</style></author><author><style face="normal" font="default"> Gout,A.M.</style></author><author><style face="normal" font="default"> Ling,K.M.</style></author><author><style face="normal" font="default"> Kicic,A.</style></author><author><style face="normal" font="default"> Stick,S.M.</style></author><author><style face="normal" font="default"> Sly,P.D.</style></author><author><style face="normal" font="default"> Holt,P.G.</style></author><author><style face="normal" font="default"> Hall,G.L.</style></author><author><style face="normal" font="default"> Bosco,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Telethon Kids Institute, The University of Western Australia, Perth, Australia</style></auth-address><titles><title><style face="normal" font="default">Persistent activation of interlinked type 2 airway epithelial gene networks in sputum-derived cells from aeroallergen-sensitized symptomatic asthmatics</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="1511">1511-</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">Atopic asthma is a persistent disease characterized by intermittent wheeze and progressive loss of lung function. The disease is thought to be driven primarily by chronic aeroallergen-induced type 2-associated inflammation. However, the vast majority of atopics do not develop asthma despite ongoing aeroallergen exposure, suggesting additional mechanisms operate in conjunction with type 2 immunity to drive asthma pathogenesis. We employed RNA-Seq profiling of sputum-derived cells to identify gene networks operative at baseline in house dust mite-sensitized (HDM(S)) subjects with/without wheezing history that are characteristic of the ongoing asthmatic state. The expression of type 2 effectors (IL-5, IL-13) was equivalent in both cohorts of subjects. However, in HDM(S)-wheezers they were associated with upregulation of two coexpression modules comprising multiple type 2- and epithelial-associated genes. The first module was interlinked by the hubs EGFR, ERBB2, CDH1 and IL-13. The second module was associated with CDHR3 and mucociliary clearance genes. Our findings provide new insight into the molecular mechanisms operative at baseline in the airway mucosa in atopic asthmatics undergoing natural aeroallergen exposure, and suggest that susceptibility to asthma amongst these subjects involves complex interactions between type 2- and epithelial-associated gene networks, which are not operative in equivalently sensitized/exposed atopic non-asthmatics</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-018-19837-6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29367592">PM:29367592</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-1511.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-1511.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-1511.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-1511.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20180124, Jones AC</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-018-19837-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86741</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hammond,C.</style></author><author><style face="normal" font="default"> Lieberman,J.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, The University of Tennessee Health Science Center, 51 North Dunlap, Suite 400, Memphis, TN 38105, USA</style></auth-address><titles><title><style face="normal" font="default">Unproven Diagnostic Tests for Food Allergy</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="163" start="153">153-163</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">The gold standard for diagnosis of immunoglobulin E (IgE)-mediated food allergy remains the oral food challenge, with serum IgE testing and skin prick testing serving as acceptable alternatives. However, the increase in prevalence of food allergy (both physician diagnosed and patient suspected) has led patients to pursue a variety of other alternative diagnostic procedures for suspected food allergy, which are reviewed in this article. These procedures (IgG testing, electrodermal testing, cytotoxic testing, provocation/neutralization, and applied kinesiology) have largely been unproven and may lead to unnecessary elimination diets</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132671">PM:29132671</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-153-63.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-153-63.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Hammond C</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87017</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ahn,M.J.</style></author><author><style face="normal" font="default"> Yu,J.E.</style></author><author><style face="normal" font="default"> Jeong,J.</style></author><author><style face="normal" font="default"> Sim,D.W.</style></author><author><style face="normal" font="default"> Koh,Y.I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea</style></auth-address><titles><title><style face="normal" font="default">A Case of Schnitzler's Syndrome without Monoclonal Gammopathy-Associated Chronic Urticaria Treated with Anakinra</style></title><secondary-title><style face="normal" font="default">Yonsei Med J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Yonsei Med J</style></abbr-1></periodical><pages end="157" start="154">154-157</pages><volume><style face="normal" font="default">59</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Cyclosporine</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Chronic urticaria may often be associated with interleukin (IL)-1-mediated autoinflammatory disease, which should be suspected if systemic inflammation signs are present. Here, we report a case of Schnitzler's syndrome without monoclonal gammopathy treated successfully with the IL-1 receptor antagonist anakinra. A 69-year-old man suffered from a pruritic urticarial rash for 12 years. It became aggravated episodically and was accompanied by high fever, arthralgia, leukocytosis, and an elevated C-reactive protein and erythrocyte sedimentation rate. The episodes each lasted for over one week. Neutrophilic and eosinophilic inflammation was found on skin biopsy. However, serum and urine electrophoresis showed no evidence of monoclonal gammopathy. The cutaneous lesions were unresponsive to various kinds of anti-histamines, systemic glucocorticoids, colchicine, cyclosporine, dapsone, and methotrexate, which were administered over a span of 3 years immediately preceding successful treatment. A dramatic response, however, was observed after a daily administration of anakinra. This observation suggests that the correct diagnosis of this case is Schnitzler's syndrome without monoclonal gammopathy. For an adult patient with refractory chronic urticaria and systemic inflammation, Schnitzler's syndrome could be considered as a possible differential diagnosis. Although the typical form of Schnitzler's syndrome exhibits the presence of monoclonal gammopathy as a diagnostic criterion, monoclonal gammopathy may be absent in an atypical form. In such a situation, an IL-1 antagonist should be effective for the management of chronic urticaria</style></abstract><notes><style face="normal" font="default">IS - 1976-2437 (Electronic)IS - 0513-5796 (Linking)LA - engPT - Case ReportsCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.3349/ymj.2018.59.1.154</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29214791">PM:29214791</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Yonsei Med J\2018-59-154-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Yonsei Med J\2018-59-154-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Ahn MJ</style></custom2><misc3><style face="normal" font="default">10.3349/ymj.2018.59.1.154</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87239</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zheng,M.</style></author><author><style face="normal" font="default"> Wang,X.</style></author><author><style face="normal" font="default"> Zhang,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University</style></auth-address><titles><title><style face="normal" font="default">Association between allergic and nonallergic rhinitis and obstructive sleep apnea</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="25" start="16">16-25</pages><volume><style face="normal" font="default">18</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> airway</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: Allergic rhinitis and nonallergic rhinitis (NAR) are common disorders, which have been considered as potential risk factors for obstructive sleep apnea (OSA). This review summarizes the proposed underlying pathophysiological mechanisms to provide a better understanding of the relationship between these conditions. RECENT FINDINGS: In adults, allergic rhinitis and NAR may be considered as symptoms potentiating, rather than risk potentiating factors in the pathophysiology of OSA, whereas in children, these are considered to be independent predictors for sleep-disordered breathing (SDB) and failure of adeno-tonsillectomy, the recommended first-line therapy for children with OSA. Current advances suggest IL-6 may be important in regulating the sleep-wake cycle, and serum soluble IL-6 receptor (sIL-6R) levels may reflect the severity of OSA. Elevated Th17/Treg ratio correlates positively with apnea-hypopnea index of OSA patients, and Th17 and Treg imbalances caused by allergic rhinitis and OSA, respectively, may possibly promote each other, leading to further imbalance. Moreover, obesity is a strong risk factor for OSA, and leptin plays an important role in ventilatory function and upper airway obstruction. The variant trigeminocardiac reflex and nasotrigeminal reflex may also be involved in the association between rhinitis and OSA. SUMMARY: Allergic rhinitis/NAR and OSA are closely associated, and each condition can be detrimental to the other. Thus, clinicians should pay attention to the potential presence of allergic rhinitis/NAR in OSA patients and vice versa</style></abstract><notes><style face="normal" font="default">IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000414</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29135515">PM:29135515</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2018-18-16-25.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2018-18-16-25.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Zheng M</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000414</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87408</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Otsuka,H.</style></author><author><style face="normal" font="default"> Otsuka,K.</style></author><author><style face="normal" font="default"> Matsune,S.</style></author><author><style face="normal" font="default"> Okubo,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">From the Otsuka Ear, Nose, and Throat Clinic, Kanagawa, Japan</style></auth-address><titles><title><style face="normal" font="default">Assessing the onset of allergic rhinitis by nasal cytology and immunoglobulin E antibody levels in children</style></title><secondary-title><style face="normal" font="default">Am J Rhinol Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Rhinol Allergy</style></abbr-1></periodical><pages end="22" start="16">16-22</pages><volume><style face="normal" font="default">32</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="1" Year="2018">2018/1/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: It is difficult to identify the onset of allergic rhinitis in infants because making a conclusive diagnosis can be challenging. OBJECTIVE: We used a combination of cell differentials in nasal swabs and immunoglobulin E (sIgE) antibody values to food and inhalant allergens to make the diagnosis and identify relevant allergens for investigation of the onset of allergic rhinitis. METHODS: We studied 302 children, 2 to 120 months old, who visited our clinic for rhinorrhea. Nasal swabs were taken from all children, and neutrophils (N), eosinophils (Eo), and mast cells (Mc) were identified by nasal cytology and their numbers were estimated. Levels of sIgE antibodies to various food and inhalant allergens were determined in patients with nasal Eo and Mc. RESULTS: Percentages of participants with Eo-Mc and Eo-Mc-N at 2-14 (n = 84), 15-24 (n = 57), 25-60 (n = 73), and 61-120 months of age (n = 88) were 20, 23, 58, and 65%, respectively. There were no significant differences between the 2-14 and 15-24, and 25-60 and 61-120 months age groups, but there was a significant difference between the 15-24 and 25-60 months age groups (p = 0.00013). The percentages of participants with sIgE antibodies to food and inhalant allergens as solitary or main allergen were 12%/0% at 2-14 months old, 10.5%/7% at 15-24 months old, 1.3%/42.4% at 25-60 months old, and 0%/56.8% at 61-120 months old, respectively with a significant difference between 15-24 and 25-60 months old groups (p = 0.00025) for inhalant allergens. CONCLUSION: Allergic rhinitis associated with inhalant allergens in infants &lt;15 months of age is rare, but it is tempting to postulate that symptoms of rhinitis in these infants may be associated with sIgE antibodies to food allergens. Transition of sIgE responses from food to inhalant allergens occurred after 15 months of age, and sIgE antibodies to inhalant allergens were predominant after 25 months</style></abstract><notes><style face="normal" font="default">IS - 1945-8932 (Electronic)IS - 1945-8932 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.2500/ajra.2018.32.4503</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29336284">PM:29336284</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180101, Otsuka H</style></custom2><misc3><style face="normal" font="default">10.2500/ajra.2018.32.4503</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87505</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mahmutovic Persson,I.</style></author><author><style face="normal" font="default"> Menzel,M.</style></author><author><style face="normal" font="default"> Ramu,S.</style></author><author><style face="normal" font="default"> Cerps,S.</style></author><author><style face="normal" font="default"> Akbarshahi,H.</style></author><author><style face="normal" font="default"> Uller,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department Experimental Medical Science Unit of Respiratory Immunopharmacology, BMC D12, Lund University, 221 84, Lund, Sweden</style></auth-address><titles><title><style face="normal" font="default">IL-1beta mediates lung neutrophilia and IL-33 expression in a mouse model of viral-induced asthma exacerbation</style></title><secondary-title><style face="normal" font="default">Respir Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Res</style></abbr-1></periodical><pages end="" start="16">16-</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="24" Month="1" Year="2018">2018/1/24</year></dates><abstract><style face="normal" font="default">BACKGROUND: Viral-induced asthma exacerbations, which exhibit both Th1-type neutrophilia and Th2-type inflammation, associate with secretion of Interleukin (IL)-1beta. IL-1beta induces neutrophilic inflammation. It may also increase Th2-type cytokine expression. We hypothesised that IL-1beta is causally involved in both Th1 and Th2 features of asthma exacerbations. This hypothesis is tested in our mouse model of viral stimulus-induced asthma exacerbation. METHOD: Wild-type (WT) and IL-1beta deficient (IL-1beta(-/-)) mice received house dust mite (HDM) or saline intranasally during three weeks followed by intranasal dsRNA (PolyI:C molecule known for its rhinovirus infection mimic) for three consecutive days to provoke exacerbation. Bronchoalveolar lavage fluid was analysed for inflammatory cells and total protein. Lung tissues were stained for neutrophilic inflammation and IL-33. Tissue homogenates were analysed for mRNA expression of Muc5ac, CXCL1/KC, TNF-alpha, CCL5, IL-25, TSLP, IL-33, IL-1beta, CCL11 and CCL2 using RT-qPCR. RESULTS: Expression of IL-1beta, neutrophil chemoattractants, CXCL1 and CCL5, the Th2-upstream cytokine IL-33, and Muc5ac were induced at exacerbation in WT mice and were significantly inhibited in IL-1beta(-/-) mice at exacerbation. Effects of HDM alone were not reduced in IL-1beta-deficient mice. CONCLUSION: Without being involved in the baseline HDM-induced allergic asthma, IL-1beta signalling was required to induce neutrophil chemotactic factors, IL-33, and Muc5ac expression at viral stimulus-induced exacerbation. We suggest that IL-1beta has a role both in neutrophilic and Th2 inflammation at viral-induced asthma exacerbations</style></abstract><notes><style face="normal" font="default">IS - 1465-993X (Electronic)IS - 1465-9921 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1186/s12931-018-0725-z</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29361942">PM:29361942</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Res\2018-19-16.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Res\2018-19-16.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180124, Mahmutovic Persson I</style></custom2><misc3><style face="normal" font="default">10.1186/s12931-018-0725-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87478</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Helbig,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">a School of Medicine in Katowice, Medical University of Silesia , Department of Hematology and Bone Marrow Transplantation , Katowice , Poland</style></auth-address><titles><title><style face="normal" font="default">Imatinib for the treatment of hypereosinophilic syndromes</style></title><secondary-title><style face="normal" font="default">Expert Rev Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Expert Rev Clin Immunol</style></abbr-1></periodical><pages end="170" start="163">163-170</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">blood</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Hypereosinophilic syndromes (HES) encompass a group of disorders defined by sustained peripheral blood hypereosinophilia >1500/mm(3) and evidence of eosinophilia-associated organ impairment. Approximately 10% of HES patients may harbor a cryptic deletion on chromosome 4 leading to formation of the FIP1L1-PDGFRA (F/P) fusion gene; these patients are diagnosed as F/P-mutated myeloid/lymphoid neoplasms with eosinophilia (MLN-eo). Areas covered: This review discusses the results of IM treatment in HES depending on mutation status. The literature on IM therapy in HES by searching PubMed for the terms 'imatinib mesylate', 'hypereosinophilic syndromes' and 'FIP1L1-PDGFRA' has been reviewed. The author's publications as well as his own experience in the field of HES treatment remain a significant contribution to this work. Expert commentary: Imatinib mesylate, a first generation tyrosine kinase inhibitor, has revolutionized the therapeutic approach to patients with hypereosinophilic syndromes and detectable F/P fusion gene. The response to IM in F/P-mutated MLN-eo is universal with minimal side effects. IM at 100mg per day induces complete molecular remission and even lower doses can be efficient to maintain durable response. Some patients may remain in continued remission after IM discontinuation. Resistance to IM is associated with dismal prognosis. IM is less effective in F/P-unmutated HES with short-lived response</style></abstract><notes><style face="normal" font="default">IS - 1744-8409 (Electronic)IS - 1744-666X (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1080/1744666X.2018.1425142</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29303368">PM:29303368</url></web-urls><pdf-urls><url ppv-ref="no">ghelbig@o2.pl</url></pdf-urls></urls><custom2><style face="normal" font="default">20180120, Helbig G</style></custom2><misc3><style face="normal" font="default">10.1080/1744666X.2018.1425142</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87473</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ljubojevic,H.S.</style></author><author><style face="normal" font="default"> Gojceta,B.S.</style></author><author><style face="normal" font="default"> Hadzavdic,A.</style></author><author><style face="normal" font="default"> Marinovic,K.S.</style></author><author><style face="normal" font="default"> Jurakic,T.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Venereology, University Hospital Centre Zagreb, School of Medicine, University of Zagreb, 10000, Zagreb, Croatia</style></auth-address><titles><title><style face="normal" font="default">Erythema of the penis after use of a latex condom - latex allergy or something else?</style></title><secondary-title><style face="normal" font="default">Contact Dermatitis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Contact Dermatitis</style></abbr-1></periodical><pages end="169" start="168">168-169</pages><volume><style face="normal" font="default">78</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1600-0536 (Electronic)IS - 0105-1873 (Linking)LA - engPT - Journal ArticleCO - Croatia -</style></notes><work-type><style face="normal" font="default">10.1111/cod.12879</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29341187">PM:29341187</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Contact Dermatitis\2018-78-168-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Contact Dermatitis\2018-78-168-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180120, Ljubojevic HS</style></custom2><misc3><style face="normal" font="default">10.1111/cod.12879</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87277</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Renz,H.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author><author><style face="normal" font="default"> Sicherer,S.H.</style></author><author><style face="normal" font="default"> Sampson,H.A.</style></author><author><style face="normal" font="default"> Lack,G.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author><author><style face="normal" font="default"> Oettgen,H.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Laboratory Medicine, Philipps University Marburg, Baldinger Strasse, 35043 Marburg, Germany</style></auth-address><titles><title><style face="normal" font="default">Food allergy</style></title><secondary-title><style face="normal" font="default">Nat Rev Dis Primers</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nat Rev Dis Primers</style></abbr-1></periodical><pages end="" start="17098">17098-</pages><volume><style face="normal" font="default">4</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">Food allergies manifest in a variety of clinical conditions within the gastrointestinal tract, skin and lungs, with the most dramatic and sometimes fatal manifestation being anaphylactic shock. Major progress has been made in basic, translational and clinical research, leading to a better understanding of the underlying immunological mechanisms that lead to the breakdown of clinical and immunological tolerance against food antigens, which can result in either immunoglobulin E (IgE)-mediated reactions or non-IgE-mediated reactions. Lifestyle factors, dietary habits and maternal-neonatal interactions play a pivotal part in triggering the onset of food allergies, including qualitative and quantitative composition of the microbiota. These factors seem to have the greatest influence early in life, an observation that has led to the generation of hypotheses to explain the food allergy epidemic, including the dual-allergen exposure hypothesis. These hypotheses have fuelled research in preventive strategies that seek to establish desensitization to allergens and/or tolerance to allergens in affected individuals. Allergen-nonspecific therapeutic strategies have also been investigated in a number of clinical trials, which will eventually improve the treatment options for patients with food allergy</style></abstract><notes><style face="normal" font="default">IS - 2056-676X (Electronic)IS - 2056-676X (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Germany -CO - Australia -CO - United States -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1038/nrdp.2017.98</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29300005">PM:29300005</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nat Rev Dis Primers\2018-4-17098.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nat Rev Dis Primers\2018-4-17098.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Renz H</style></custom2><misc3><style face="normal" font="default">10.1038/nrdp.2017.98</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86825</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,J.H.</style></author><author><style face="normal" font="default"> Kim,S.C.</style></author><author><style face="normal" font="default"> Choi,H.</style></author><author><style face="normal" font="default"> Jung,C.G.</style></author><author><style face="normal" font="default"> Ban,G.Y.</style></author><author><style face="normal" font="default"> Shin,Y.S.</style></author><author><style face="normal" font="default"> Nahm,D.H.</style></author><author><style face="normal" font="default"> Park,H.S.</style></author><author><style face="normal" font="default"> Ye,Y.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea</style></auth-address><titles><title><style face="normal" font="default">A Retrospective Study of Clinical Response Predictors in Subcutaneous Allergen Immunotherapy With House Dust Mites for Allergic Rhinitis</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Immunol Res</style></abbr-1></periodical><pages end="24" start="18">18-24</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">PURPOSE: House dust mites (HDM) are major allergens that cause allergic rhinitis (AR). Allergen-specific subcutaneous immunotherapy (SCIT) has been shown to be clinically beneficial in many clinical trials. Such trials, however, are not reflective of all patient populations. The aim of this study was to describe the efficacy and safety of SCIT in routine clinical practice in Korean adults with AR sensitized to HDM. METHODS: We reviewed medical records of 304 patients with AR treated at an allergy clinic of a tertiary hospital using SCIT with aluminum hydroxide-adsorbed allergen extract targeting HDM alone or with pollens for at least 1 year from 2000 to 2012. Patients with asthma were excluded. Rates of remission, defined as no further requirement of maintenance medication, over time were determined by means of life tables and extension of survival analysis. Specific immunoglobulin E (IgE) levels to HDM were categorized into 6 classes. RESULTS: The mean time until achieving remission was 4.9+/-0.1 years, and the cumulative incidence of remission from AR was 76.6%. Severe AR (odds ratio [OR], 0.40; 95% confidence interval [CI], 0.23-0.69; P=0.001), specific IgE levels to HDM >/=17.5 kU/L (OR, 1.85; 95% CI, 1.01-3.37; P=0.045), and duration of immunotherapy >/=3 years (OR, 7.37; 95% CI, 3.50-15.51; P&lt;0.001) were identified as significant predictors of clinical remission during SCIT for patients with AR sensitized to HDM. Overall, 73 patients (24.0%) experienced adverse reactions to SCIT, and only 1 case of anaphylaxis (0.3%) developed. CONCLUSIONS: SCIT with HDM was found to be effective and safe for patients with AR. Specific IgE levels to HDM and a duration of SCIT >/=3 years may be predictors of clinical responses to SCIT in AR patients</style></abstract><notes><style face="normal" font="default">IS - 2092-7355 (Print)IS - 2092-7355 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4168/aair.2018.10.1.18</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29178674">PM:29178674</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-18-24.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-18-24.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Lee JH</style></custom2><misc3><style face="normal" font="default">10.4168/aair.2018.10.1.18</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87182</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Teng,F.</style></author><author><style face="normal" font="default"> Yu,L.</style></author><author><style face="normal" font="default"> Sun,J.</style></author><author><style face="normal" font="default"> Wang,N.</style></author><author><style face="normal" font="default"> Cui,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Basic Medicine, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu 224005, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Homology modeling and prediction of Bcell and Tcell epitopes of the house dust mite allergen Der f 20</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="1812" start="1807">1807-1812</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">1</style></number><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Prediction</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">House dust mite allergens can cause allergic diseases, including asthma, atopic dermatitis and rhinitis. Der f 20 is a novel allergen of Dermatophagoides farina (Der f), which is an arginine kinase. In the present study, the Bcell and Tcell epitopes of Der f 20 were predicted. The protein attribution, patterns, physicochemical properties and secondary structure of Der f 20 were also predicted. Der f 20 is a member of the ATP:guanido phosphotransferase family and contains a phosphagen kinase pattern. Using homology modeling, the present study constructed a reasonable tertiary structure of Der f 20. Using BcePred, ABCpred, BCPred and BPAP systems, Bcell epitopes at 2025, 4149, 111118, 131141, 170174 and 312321 were predicted. Using NetMHCIIpan3.0 and NetMHCII2.2, Tcell epitopes were predicted at 194202, 239247 and 274282. These results provide a theoretical basis for the design off Der f 20 epitopebased vaccines</style></abstract><notes><style face="normal" font="default">IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.8066</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29257224">PM:29257224</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Med Rep\2018-17-1807-12.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Med Rep\2018-17-1807-12.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Teng F</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.8066</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87475</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,Z.R.</style></author><author><style face="normal" font="default"> Wang,Q.</style></author><author><style face="normal" font="default"> Sui,Y.</style></author><author><style face="normal" font="default"> Zhang,Z.L.</style></author><author><style face="normal" font="default"> Jia,F.J.</style></author><author><style face="normal" font="default"> Fan,J.</style></author><author><style face="normal" font="default"> Zhang,Z.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Dezhou Pepole's Hospital, Dezhou, Shandong, China.</style></auth-address><titles><title><style face="normal" font="default">Dexamethasone alleviates allergic asthma immature rat through Toll like receptor 4</style></title><secondary-title><style face="normal" font="default">Eur Rev Med Pharmacol Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Rev Med Pharmacol Sci</style></abbr-1></periodical><pages end="189" start="184">184-189</pages><volume><style face="normal" font="default">22</style></volume><number><style face="normal" font="default">1</style></number><reprint-status date="01/27/2018" status="on-request"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">OBJECTIVE: The allergic asthma model induced by ovalbumin (OVA) was established in the immature rat. Dexamethasone (DXM) was adopted for intervention to analyze the treatment effect and to explore the relationship with toll-like receptor 4 (TLR4). MATERIALS AND METHODS: Immature SD rat was treated by OVA to construct allergic asthma model and intervened by DXM. The rats were randomly divided into model group, experimental group, and control group. The changes in lung tissue were observed by light microscope. The EOS infiltration and reactivity of airway wall were compared. The expressions of TLR2 and TLR4 protein and mRNA in the lung tissue were tested by Western blot and RT-PCR. RESULTS: The lung tissue in the model group was infiltrated by a lot of inflammatory cells, and mucous membrane edema was observed, compared with that in the control group. There were only a few inflammatory cells in the interstitial tissue and pulmonary alveoli in the experimental group compared with that in the model group. EOS count of airway wall and airway reactivity decreased in the experimental group. The levels of TLR2 and TLR4 were significantly elevated in the third week compared with the first week (p&lt;0.05). CONCLUSIONS: The treatment of DXM can alleviate the pathological changes of the lung tissue in SD immature rat with allergic asthma, reduce EOS infiltration in the airway wall, decrease airway reactivity, and elevate expressions of TLR2 and TLR4</style></abstract><notes><style face="normal" font="default">IS - 2284-0729 (Electronic)IS - 1128-3602 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.26355/eurrev_201801_14116</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29364486">PM:29364486</url></web-urls><pdf-urls><url ppv-ref="no">zhaoruiwangbn@163.com</url></pdf-urls><related-urls><url ppv-ref="no">presto - MedLine</url></related-urls></urls><custom2><style face="normal" font="default">20180122, Wang ZR</style></custom2><misc3><style face="normal" font="default">10.26355/eurrev_201801_14116</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87353</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jiang,X.Y.</style></author><author><style face="normal" font="default"> Zhang,L.</style></author><author><style face="normal" font="default"> Jiang,X.</style></author><author><style face="normal" font="default"> Abdulaziz,A.T.A.</style></author><author><style face="normal" font="default"> Wang,Y.H.</style></author><author><style face="normal" font="default"> Li,J.M.</style></author><author><style face="normal" font="default"> Zhou,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China</style></auth-address><titles><title><style face="normal" font="default">Allergy in patients with anti-N-methyl-d-aspartate receptor encephalitis</style></title><secondary-title><style face="normal" font="default">Epilepsy Behav</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Epilepsy Behav</style></abbr-1></periodical><pages end="192" start="188">188-192</pages><volume><style face="normal" font="default">79</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> autoimmune diseases</style></keyword><keyword><style face="normal" font="default"> complications</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">BACKGROUND AND OBJECTIVE: Allergy is a potential outcome of dysregulated immune system. Previous studies have shown the association of allergy and autoimmune diseases, however, there is few study to investigate the relationship between allergy and anti-N-methyl-d-aspartate receptor (anti-NMDAR) encephalitis. Thus, we investigate the rate of allergy in patients with anti-NMDAR encephalitis and analyze the risk factors. METHOD: The rate of allergy was investigated in patients with anti-NMDAR encephalitis and was compared with patients with virus encephalitis. The clinical cutaneous characters were described in details. All patients with anti-NMDAR encephalitis were divided into allergic and nonallergic group. Clinical factors were compared in the two groups, and logistic regression model was also used to analyze possible risk factors of allergy. RESULTS: Patients with anti-NMDAR encephalitis had a higher rate of allergy than those with viral encephalitis (22.1% vs 9.2%, odds ratio (OR)=3.23, confidence interval (CI)=1.40-7.42, P=0.006). In patients with anti-NMDAR encephalitis, allergic patients exhibited longer days in hospital (30days vs 22days, P=0.005) and higher occurrence of decreased consciousness (81.5% vs 58.9%, P=0.031), higher rate of complications (77.8% vs 57.9%, P=0.046) and abnormal electroencephalography (EEG) (100% vs 78.6%, P=0.021) than patients without allergy. Cerebrospinal fluid (CSF) antibody titers of allergic patients during the disease course were also higher than nonallergic patients (P=0.004). However, further logistic regression analysis did not reveal independent predictors of allergy. CONCLUSIONS: Patients with anti-NMDAR encephalitis show higher allergic rate than those with virus encephalitis. Patients with allergy show higher CSF antibody titers and greater illness severity. However, the final outcome of anti-NMDAR encephalitis was not influenced</style></abstract><notes><style face="normal" font="default">IS - 1525-5069 (Electronic)IS - 1525-5050 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.yebeh.2017.12.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29306850">PM:29306850</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Epilepsy Behav\2018-79-188-92.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Epilepsy Behav\2018-79-188-92.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Jiang XY</style></custom2><misc3><style face="normal" font="default">10.1016/j.yebeh.2017.12.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87407</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fiocchi,A.</style></author><author><style face="normal" font="default"> Schunemann,H.</style></author><author><style face="normal" font="default"> Ansotegui,I.</style></author><author><style face="normal" font="default"> Assa'ad,A.</style></author><author><style face="normal" font="default"> Bahna,S.</style></author><author><style face="normal" font="default"> Canani,R.B.</style></author><author><style face="normal" font="default"> Bozzola,M.</style></author><author><style face="normal" font="default"> Dahdah,L.</style></author><author><style face="normal" font="default"> Dupont,C.</style></author><author><style face="normal" font="default"> Ebisawa,M.</style></author><author><style face="normal" font="default"> Galli,E.</style></author><author><style face="normal" font="default"> Li,H.</style></author><author><style face="normal" font="default"> Kamenwa,R.</style></author><author><style face="normal" font="default"> Lack,G.</style></author><author><style face="normal" font="default"> Martelli,A.</style></author><author><style face="normal" font="default"> Pawankar,R.</style></author><author><style face="normal" font="default"> Said,M.</style></author><author><style face="normal" font="default"> Sanchez-Borges,M.</style></author><author><style face="normal" font="default"> Sampson,H.</style></author><author><style face="normal" font="default"> Shamir,R.</style></author><author><style face="normal" font="default"> Spergel,J.</style></author><author><style face="normal" font="default"> Terracciano,L.</style></author><author><style face="normal" font="default"> Vandenplas,Y.</style></author><author><style face="normal" font="default"> Venter,C.</style></author><author><style face="normal" font="default"> Waserman,S.</style></author><author><style face="normal" font="default"> Wong,G.</style></author><author><style face="normal" font="default"> Brozek,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy, Department of Pediatrics, Pediatric Hospital Bambino Gesu, Piazza Sant'Onofrio, Vatican City, Rome Italy.</style></auth-address><titles><title><style face="normal" font="default">The global impact of the DRACMA guidelines cow's milk allergy clinical practice</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="2">2-</pages><volume><style face="normal" font="default">11</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Background: The 2010 Diagnosis and Rationale for Action against Cow's Milk Allergy (DRACMA) guidelines are the only Grading of Recommendations Assessment, Development and Evaluation (GRADE) guidelines for cow's milk allergy (CMA). They indicate oral food challenge (OFC) as the reference test for diagnosis, and suggest the choice of specific alternative formula in different clinical conditions. Their recommendations are flexible, both in diagnosis and in treatment. Objectives &amp; methods: Using the Scopus citation records, we evaluated the influence of the DRACMA guidelines on milk allergy literature. We also reviewed their impact on successive food allergy and CMA guidelines at national and international level. We describe some economic consequences of their application. Results: DRACMA are the most cited CMA guidelines, and the second cited guidelines on food allergy. Many subsequent guidelines took stock of DRACMA's metanalyses adapting recommendations to the local context. Some of these chose not to consider OFC as an absolute requirement for the diagnosis of CMA. Studies on their implementation show that in this case, the treatment costs may increase and there is a risk of overdiagnosis. Interestingly, we observed a reduction in the cost of alternative formulas following the publication of the DRACMA guidelines. Conclusions: DRACMA reconciled international differences in the diagnosis and management of CMA. They promoted a cultural debate, improved clinician's knowledge of CMA, improved the quality of diagnosis and care, reduced inappropriate practices, fostered the efficient use of resources, empowered patients, and influenced some public policies. The accruing evidence on diagnosis and treatment of CMA necessitates their update in the near future</style></abstract><notes><style face="normal" font="default">IS - 1939-4551 (Print)IS - 1939-4551 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Italy -CO - Canada -CO - Spain -CO - United States -CO - Argentina -CO - France -CO - Japan -CO - China -CO - Kenya -CO - United Kingdom -CO - Australia -CO - Venezuela -CO - Israel -CO - Belgium -CO - Hong Kong -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0179-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29308116">PM:29308116</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2018-11-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2018-11-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Fiocchi A</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0179-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87470</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Albanesi,M.</style></author><author><style face="normal" font="default"> Nico,A.</style></author><author><style face="normal" font="default"> Sinisi,A.</style></author><author><style face="normal" font="default"> Giliberti,L.</style></author><author><style face="normal" font="default"> Rossi,M.P.</style></author><author><style face="normal" font="default"> Rossini,M.</style></author><author><style face="normal" font="default"> Kourtis,G.</style></author><author><style face="normal" font="default"> Rucco,A.S.</style></author><author><style face="normal" font="default"> Loconte,F.</style></author><author><style face="normal" font="default"> Muolo,L.</style></author><author><style face="normal" font="default"> Zurlo,M.</style></author><author><style face="normal" font="default"> Di Bona,D.</style></author><author><style face="normal" font="default"> Caiaffa,M.F.</style></author><author><style face="normal" font="default"> Macchia,L.</style></author></authors></contributors><titles><title><style face="normal" font="default">A 13-year real-life study on efficacy, safety and biological effects of Vespula venom immunotherapy</style></title><secondary-title><style face="normal" font="default">Clin Mol Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Mol Allergy</style></abbr-1></periodical><pages end="" start="2">2-</pages><volume><style face="normal" font="default">16</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1476-7961</style></isbn><abstract><style face="normal" font="default">Hymenoptera venom immunotherapy (VIT) is a clinically effective treatment. However, little is known about its long-term clinical efficacy and biological effects. Several mechanisms have been proposed to account for VIT efficacy, including reduction of specific IgE and induction of allergen-specific IgG4, but the overall picture remains elusive. We investigated Vespula VIT clinical efficacy up to 8-áyears after discontinuation and the kinetics of Vespula-specific IgE and IgG4. Out of 686 consecutive patients we retrospectively selected and analysed a series of 23 patients with Vespula allergy that underwent a 5-year IT course, followed by a prolonged follow-up</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1186/s12948-017-0079-y</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s12948-017-0079-y</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Mol Allergy\2018-16-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Mol Allergy\2018-16-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Albanesi M</style></custom2><misc3><style face="normal" font="default">10.1186/s12948-017-0079-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87367</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dhondalay,G.K.</style></author><author><style face="normal" font="default"> Rael,E.</style></author><author><style face="normal" font="default"> Acharya,S.</style></author><author><style face="normal" font="default"> Zhang,W.</style></author><author><style face="normal" font="default"> Sampath,V.</style></author><author><style face="normal" font="default"> Galli,S.J.</style></author><author><style face="normal" font="default"> Tibshirani,R.</style></author><author><style face="normal" font="default"> Boyd,S.D.</style></author><author><style face="normal" font="default"> Maecker,H.</style></author><author><style face="normal" font="default"> Nadeau,K.C.</style></author><author><style face="normal" font="default"> Andorf,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, Calif; Institute for Immunity, Transplantation, and Infection, Stanford University School of Medicine, Stanford, Calif</style></auth-address><titles><title><style face="normal" font="default">Food allergy and omics</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="29" start="20">20-29</pages><volume><style face="normal" font="default">141</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Food allergy (FA) prevalence has been increasing over the last few decades and is now a global health concern. Current diagnostic methods for FA result in a high number of false-positive results, and the standard of care is either allergen avoidance or use of epinephrine on accidental exposure, although currently with no other approved treatments. The increasing prevalence of FA, lack of robust biomarkers, and inadequate treatments warrants further research into the mechanism underlying food allergies. Recent technological advances have made it possible to move beyond traditional biological techniques to more sophisticated high-throughput approaches. These technologies have created the burgeoning field of omics sciences, which permit a more systematic investigation of biological problems. Omics sciences, such as genomics, epigenomics, transcriptomics, proteomics, metabolomics, microbiomics, and exposomics, have enabled the construction of regulatory networks and biological pathway models. Parallel advances in bioinformatics and computational techniques have enabled the integration, analysis, and interpretation of these exponentially growing data sets and opens the possibility of personalized or precision medicine for FA</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29307411">PM:29307411</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\2018-141-20-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\2018-141-20-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Dhondalay GK</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87351</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gupta,R.K.</style></author><author><style face="normal" font="default"> Gupta,K.</style></author><author><style face="normal" font="default"> Sharma,A.</style></author><author><style face="normal" font="default"> Das,M.</style></author><author><style face="normal" font="default"> Ansari,I.A.</style></author><author><style face="normal" font="default"> Dwivedi,P.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Food, Drug and Chemical Toxicology Group, Indian Institute of Toxicology Research , Lucknow -, India</style></auth-address><titles><title><style face="normal" font="default">Maillard reaction in food allergy: Pros and cons</style></title><secondary-title><style face="normal" font="default">Crit Rev Food Sci Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Crit Rev Food Sci Nutr</style></abbr-1></periodical><pages end="226" start="208">208-226</pages><volume><style face="normal" font="default">58</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Maillard Reaction</style></keyword><keyword><style face="normal" font="default"> Reducing sugar</style></keyword><keyword><style face="normal" font="default"> Reducing sugars</style></keyword></keywords><dates><year Day="22" Month="1" Year="2018">2018/1/22</year></dates><abstract><style face="normal" font="default">Food allergens have a notable potential to induce various health concerns in susceptible individuals. The majority of allergenic foods are usually subjected to thermal processing prior to their consumption. However, during thermal processing and long storage of foods, Maillard reaction (MR) often takes place. The MR is a non-enzymatic glycation reaction between the carbonyl group of reducing sugars and compounds having free amino groups. MR may sometimes be beneficial by damaging epitope of allergens and reducing allergenic potential, while exacerbation in allergic reactions may also occur due to changes in the motifs of epitopes or neoallergen generation. Apart from these modulations, non-enzymatic glycation can also modify the food protein(s) with various type of advance glycation end products (AGEs) such as N-(carboxymethyl-)lysine (CML), pentosidine, pyrraline, and methylglyoxal-H1 derived from MR. These Maillard products may act as immunogen by inducing the activation and proliferation of various immune cells. Literature is available to understand pathogenesis of glycation in the context of various diseases but there is hardly any review that can provide a thorough insight on the impact of glycation in food allergy. Therefore, present review explores the pathogenesis with special reference to food allergy caused by non-enzymatic glycation as well as AGEs</style></abstract><notes><style face="normal" font="default">IS - 1549-7852 (Electronic)IS - 1040-8398 (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.1080/10408398.2016.1152949</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="26980434">PM:26980434</url></web-urls></urls><custom2><style face="normal" font="default">20180102, Gupta RK</style></custom2><misc3><style face="normal" font="default">10.1080/10408398.2016.1152949</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86968</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dore,K.A.</style></author><author><style face="normal" font="default"> Kashiwakura,J.I.</style></author><author><style face="normal" font="default"> McDonnell,J.M.</style></author><author><style face="normal" font="default"> Gould,H.J.</style></author><author><style face="normal" font="default"> Kawakami,T.</style></author><author><style face="normal" font="default"> Sutton,B.J.</style></author><author><style face="normal" font="default"> Davies,A.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">King's College London, Randall Centre for Cell and Molecular Biophysics, New Hunt's House, London, SE1 1UL, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Crystal structures of murine and human Histamine-Releasing Factor (HRF/TCTP) and a model for HRF dimerisation in mast cell activation</style></title><secondary-title><style face="normal" font="default">Mol Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Immunol</style></abbr-1></periodical><pages end="222" start="216">216-222</pages><volume><style face="normal" font="default">93</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">IgE</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">In allergic disease, mast cell activation is conventionally triggered by allergen-mediated cross-linking of receptor-bound IgE on the cell surface. In addition to its diverse range of intracellular roles in apoptosis, cell proliferation and cancer, Histamine-Releasing Factor (HRF) also activates mast cells and basophils. A subset of IgE antibodies bind HRF through their Fab regions, and two IgE binding sites on HRF have been mapped. HRF can form dimers, and a disulphide-linked dimer is critical for activity. The current model for the activity of HRF in mast cell activation involves cross-linking of receptor-bound IgE by dimeric HRF, mediated by HRF/Fab interactions. HRF crystal and solution structures have provided little insight into either the formation of disulphide-linked HRF dimers or the ability of HRF to activate mast cells. We report the first crystal structure of murine HRF (mHRF) to 4.0A resolution, revealing a conserved fold. We also solved the structure of human HRF (hHRF) in two new crystal forms, one at the highest resolution (1.4A) yet reported. The high resolution hHRF structure reveals a disulphide-linked dimer, in which the two molecules are closely associated, and provides a model for the role of both human and murine HRF in mast cell activation</style></abstract><notes><style face="normal" font="default">IS - 1872-9142 (Electronic)IS - 0161-5890 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.molimm.2017.11.022</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29216544">PM:29216544</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Immunol\2018-93-216-22.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Immunol\2018-93-216-22.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Dore KA</style></custom2><misc3><style face="normal" font="default">10.1016/j.molimm.2017.11.022</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87359</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lu,M.</style></author><author><style face="normal" font="default"> Jin,Y.</style></author><author><style face="normal" font="default"> Ballmer-Weber,B.</style></author><author><style face="normal" font="default"> Goodman,R.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Food Science and Technology, University of Nebraska Lincoln, Lincoln, NE, USA.</style></auth-address><titles><title><style face="normal" font="default">A comparative study of human IgE binding to proteins of a genetically modified (GM) soybean and six non-GM soybeans grown in multiple locations</style></title><secondary-title><style face="normal" font="default">Food Chem Toxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem Toxicol</style></abbr-1></periodical><pages end="223" start="216">216-223</pages><volume><style face="normal" font="default">112</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">Prior to commercialization, genetically modified (GM) crops are evaluated to determine the allergenicity of the newly expressed protein. Some regulators require an evaluation of endogenous allergens in commonly allergenic crops including soybean to determine if genetic transformation increased endogenous allergen concentrations, even asking for IgE testing using sera from individual sensitized subjects. Little is known about the variability of the expression of endogenous allergens among non-GM varieties or under different environmental conditions. We tested IgE binding to endogenous allergenic proteins in an experimental non-commercial GM line, a non-GM near-isoline control, and five non-GM commercial soybean lines replicated at three geographically separated locations. One-dimensional (1D) and two-dimensional (2D) immunoblotting and ELISA were performed using serum or plasma from eleven soybean allergic patients. The results of immunoblots and ELISA showed no significant differences in IgE binding between the GM line and its non-GM near-isoline control. However, some distinct differences in IgE binding patterns were observed among the non-GM commercial soybean lines and between different locations, highlighting the inherent variability in endogenous allergenic proteins. Understanding the potential variability in the levels of endogenous allergens is necessary to establish a standard of acceptance for GM soybeans compared to non-GM soybean events and lines</style></abstract><notes><style face="normal" font="default">IS - 1873-6351 (Electronic)IS - 0278-6915 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1016/j.fct.2018.01.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29307601">PM:29307601</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem Toxicol\2018-112-216-23.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem Toxicol\2018-112-216-23.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Lu M</style></custom2><misc3><style face="normal" font="default">10.1016/j.fct.2018.01.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87172</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Leickly,F.E.</style></author><author><style face="normal" font="default"> Kloepfer,K.M.</style></author><author><style face="normal" font="default"> Slaven,J.E.</style></author><author><style face="normal" font="default"> Vitalpur,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Section of Pediatric Pulmonology, Allergy, and Sleep Medicine, Department of Pediatrics, Indiana University School of Medicine and Riley Hospital for Children, Indiana University Health, Carmel, IN.</style></auth-address><titles><title><style face="normal" font="default">Peanut Allergy: An Epidemiologic Analysis of a Large Database</style></title><secondary-title><style face="normal" font="default">J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pediatr</style></abbr-1></periodical><pages end="228" start="223">223-228</pages><volume><style face="normal" font="default">192</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To confirm new observations on peanut allergy and answer current concerns that families and healthcare providers have about peanut allergy. STUDY DESIGN: Children who presented with a story of peanut allergy or peanut sensitization were asked to participate in a registry, which allowed an analysis focused on questions that a food allergy support group had about children with peanut allergy or sensitization. RESULTS: A total of 1070 children were entered into the registry over 5 years. Two-thirds had a reaction to peanut. Children with peanut allergy were predominantly male (63%), white (78%), and with private health insurance (80%). Most reactions involved the skin (55%) and anaphylaxis occurred in 35%. The median age of a reaction was 1 year old. Atopic dermatitis was noted in 60% and asthma in 41%. Additional food allergy was noted in 58%. When second exposures occurred 28% had a more severe reaction. Skin test size did not differentiate the type of a reaction and children with anaphylaxis had slightly higher specific IgE levels. Severe reactions with inadvertent exposure in children who were peanut sensitized was rare (&lt;1%). CONCLUSIONS: The strategies for peanut allergy prevention and treatment have evolved. The data obtained in this large registry can answer many questions that families and healthcare providers have during this transition</style></abstract><notes><style face="normal" font="default">IS - 1097-6833 (Electronic)IS - 0022-3476 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jpeds.2017.09.026</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29246346">PM:29246346</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pediatr\2018-192-223-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pediatr\2018-192-223-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Leickly FE</style></custom2><misc3><style face="normal" font="default">10.1016/j.jpeds.2017.09.026</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86637</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Purschke,B.</style></author><author><style face="normal" font="default"> Mendez Sanchez,Y.D.</style></author><author><style face="normal" font="default"> Jager,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Centrifugal fractionation of mealworm larvae (Tenebrio molitor, L.) for protein recovery and concentration</style></title><secondary-title><style face="normal" font="default">LWT - Food Sci Technol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">LWT - Food Sci Technol</style></full-title></periodical><pages end="228" start="224">224-228</pages><volume><style face="normal" font="default">89</style></volume><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Edible insects</style></keyword><keyword><style face="normal" font="default"> Protein isolation</style></keyword><keyword><style face="normal" font="default"> Experimental design</style></keyword><keyword><style face="normal" font="default"> Centrifugation force</style></keyword><keyword><style face="normal" font="default"> Centrifugation time</style></keyword><keyword><style face="normal" font="default"> Solubilization pH</style></keyword></keywords><dates><year Day="0" Month="3" Year="2018">2018/3</year></dates><isbn><style face="normal" font="default">0023-6438</style></isbn><abstract><style face="normal" font="default">The utilization of edible insect protein as a novel source and potential substitute for conventional proteins used in food/feed formulations has recently drawn attention in industrial countries. The development of efficient processes for the recovery of insect protein is of crucial importance and will help to gain industrial applicability. However, systematic studies about important unit operations of insect protein recovery procedures are scarce. The present study evaluates a centrifugal fractionation concept by investigating the impact of solubilization pH (7.0</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô10.5), centrifugation speed/force (4000-8850 min</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">êÆ1; 1860</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô9170-ág) and centrifugation time (10</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô30-ámin) on the protein recovery of mealworm larvae (Tenebrio molitor L.). Therefore, a 23 full factorial screening design was applied. The statistical evaluation identified the centrifugation force and solubilization pH as key parameters determining the protein content and recovery in the supernatant fraction. Within the experimental campaign, protein content was enhanced from initially 39-ág/100-ág dry base (db) in the larvae to 56</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô65 g/100-ág-ádb in the extracts while the recovery ranged from 31 to 58%. The results of this study elucidated the main factors determining the efficiency of the centrifugal separation step for mealworm protein concentration and recovery and provide a database for the design of industrial separation processes</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Austria -CO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.lwt.2017.10.057</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.lwt.2017.10.057</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\LWT - Food Sci Technol\2018-89-224-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\LWT - Food Sci Technol\2018-89-224-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Purschke B</style></custom2><misc3><style face="normal" font="default">10.1016/j.lwt.2017.10.057</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87409</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hong,S.D.</style></author><author><style face="normal" font="default"> Ryu,G.</style></author><author><style face="normal" font="default"> Seo,M.Y.</style></author><author><style face="normal" font="default"> Jeong,J.I.</style></author><author><style face="normal" font="default"> Kim,H.Y.</style></author><author><style face="normal" font="default"> Chung,S.K.</style></author><author><style face="normal" font="default"> Dhong,H.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">From the Department of Otorhinolaryngology-Head and Neck Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea</style></auth-address><titles><title><style face="normal" font="default">Optimal cutoff values of allergen-specific immunoglobulin E to house dust mites and animal dander based on skin-prick test results: Analysis in 16,209 patients with allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Am J Rhinol Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Rhinol Allergy</style></abbr-1></periodical><pages end="26" start="23">23-26</pages><volume><style face="normal" font="default">32</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="1" Year="2018">2018/1/25</year></dates><abstract><style face="normal" font="default">BACKGROUND: The most common tests for allergen sensitization in patients with allergic rhinitis are the skin-prick test (SPT) and an in vitro test to detect serum specific immunoglobulin E (sIgE). However, in vitro allergen test results were interpreted dichotomically as positive or negative at a threshold of 0.35 kU/L of sIgE, regardless of the patient characteristics or antigen types. OBJECTIVE: The purpose of this study was to determine the cutoff value for sIgE in house-dust mites and animal dander, and to analyze differences in cutoff value according to age and gender. METHODS: A total of 16,209 patients with more than one allergic rhinitis symptom who underwent both SPT and serum sIgE testing were retrospectively evaluated between March 2008 and May 2012. There were 9374 male (57.8%) and 6835 female (42.2%) patients. The mean age was 31.8 years (range, 2-89 years). The criterion standard for allergen sensitization was defined as a wheal of >3 mm or an allergen-to-histamine ratio of >/=1 in SPT results. The Youden index was used to calculate the cutoff value of sIgE. RESULTS: Cutoff values of sIgE for Dermatophagoides pteronyssinus, Dermatophagoides farinae, cat, and dog were 0.69, 1.16, 0.13, and 0.45 kU/L, respectively. The cutoff value of sIgE changed according to age for D. pteronyssinus and D. farinae but not for cat and dog allergens. When categorizing according to age group, the cutoff values of sIgE for D. pteronyssinus and D. farinae had a tendency to decrease with age. There was no significant difference in cutoff value according to gender. CONCLUSION: The cutoff value for sIgE differed for each antigen and changed with age. Physicians should select the proper cutoff value for sIgE for appropriate criteria according to antigen and patient age rather than using a uniform cutoff value</style></abstract><notes><style face="normal" font="default">IS - 1945-8932 (Electronic)IS - 1945-8932 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.2500/ajra.2018.32.4483</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29336285">PM:29336285</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180101, Hong SD</style></custom2><misc3><style face="normal" font="default">10.2500/ajra.2018.32.4483</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86951</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nguyen,T.H.</style></author><author><style face="normal" font="default"> Maltby,S.</style></author><author><style face="normal" font="default"> Tay,H.L.</style></author><author><style face="normal" font="default"> Eyers,F.</style></author><author><style face="normal" font="default"> Foster,P.S.</style></author><author><style face="normal" font="default"> Yang,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Priority Research Centre for Healthy Lungs, School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, The University of Newcastle, Callaghan, New South Wales 2308, Australia</style></auth-address><titles><title><style face="normal" font="default">Identification of IFN-gamma and IL-27 as Critical Regulators of Respiratory Syncytial Virus-Induced Exacerbation of Allergic Airways Disease in a Mouse Model</style></title><secondary-title><style face="normal" font="default">J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol</style></abbr-1></periodical><pages end="247" start="237">237-247</pages><volume><style face="normal" font="default">200</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Respiratory syncytial virus (RSV) infection induces asthma exacerbations, which leads to worsening of clinical symptoms and may result in a sustained decline in lung function. Exacerbations are the main cause of morbidity and mortality associated with asthma, and significantly contribute to asthma-associated healthcare costs. Although glucocorticoids are used to manage exacerbations, some patients respond to them poorly. The underlying mechanisms associated with steroid-resistant exacerbations remain largely unknown. We have previously established a mouse model of RSV-induced exacerbation of allergic airways disease, which mimics hallmark clinical features of asthma. In this study, we have identified key roles for macrophage IFN-gamma and IL-27 in the regulation of RSV-induced exacerbation of allergic airways disease. Production of IFN-gamma and IL-27 was steroid-resistant, and neutralization of IFN-gamma or IL-27 significantly suppressed RSV-induced steroid-resistant airway hyperresponsiveness and airway inflammation. We have previously implicated activation of pulmonary macrophage by TNF-alpha and/or MCP-1 in the mechanisms of RSV-induced exacerbation. Stimulation of pulmonary macrophages with TNF-alpha and/or MCP-1 induced expression of both IFN-gamma and IL-27. Our findings highlight critical roles for IFN-gamma and IL-27, downstream of TNF-alpha and MCP-1, in the mechanism of RSV-induced exacerbation. Thus, targeting the pathways that these factors activate may be a potential therapeutic approach for virus-induced asthma exacerbations</style></abstract><notes><style face="normal" font="default">IS - 1550-6606 (Electronic)IS - 0022-1767 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.4049/jimmunol.1601950</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29167232">PM:29167232</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol\20171122-NguyenTH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol\20171122-NguyenTH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171122, Nguyen TH</style></custom2><misc3><style face="normal" font="default">10.4049/jimmunol.1601950</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87464</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Olivry,T.</style></author><author><style face="normal" font="default"> Mueller,R.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC, 27607, USA. t</style></auth-address><titles><title><style face="normal" font="default">Critically appraised topic on adverse food reactions of companion animals (5): discrepancies between ingredients and labeling in commercial pet foods</style></title><secondary-title><style face="normal" font="default">BMC Vet Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMC Vet Res</style></abbr-1></periodical><pages end="" start="24">24-</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="22" Month="1" Year="2018">2018/1/22</year></dates><abstract><style face="normal" font="default">BACKGROUND: Elimination dietary trials for the diagnosis of adverse food reactions (food allergies) in dogs and cats are often conducted with commercial pet foods while relying on their label to select those not containing previously-eaten ingredients. There are concerns that industrial pet foods might contain unlisted food sources that could negate the usefulness of performing food trials. Furthermore, unidentified ingredients might cause clinical reactions in patients hypersensitive to such items. RESULTS: We searched two article databases on July 7, 2017 and January 12, 2018 for relevant articles, and we screened abstracts from the leading international veterinary dermatology congresses for suitable material. Additional citations were found in the selected papers. In all, we extracted data from 17 articles and one abstract. The studies varied both in the number of pet foods tested (median: 15; range: 1 to 210) and that of ingredients specifically evaluated (median: 4; range: 1 to 11). Studies most often employed either PCR to detect DNA or ELISA to identify proteins from one or more vegetal or animal species; two studies used mass spectrometry to increase the number of detectable proteins. The various methods found ingredients that were not on the label in 0 to 83% (median: 45%) of tested diets; this percentage varied between 33 and 83% in pet foods with "novel/limited" ingredients proposed for elimination diets. Similarly, ingredients were found to be missing from the label in 0 to 38% (median: 1%) of tested foods. Finally, six studies evaluated, among others, several hydrolysate-containing pet foods: mislabeling with unlabeled or missing ingredients was found only in one diet. CONCLUSIONS: The mislabeling of pet foods appears rather common, even in those with "novel" or "limited" ingredients proposed for elimination diets. Unexpected added ingredients are more frequently detected than those missing from the label. There is insufficient information to determine if the presence of a contaminating component will lead to a clinical reaction in a patient allergic to it, as challenges with the mislabeled foods were not performed in dogs or cats allergic to such ingredients. The testing of hydrolysate-containing pet foods found only one instance of possible mislabeling</style></abstract><notes><style face="normal" font="default">IS - 1746-6148 (Electronic)IS - 1746-6148 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1186/s12917-018-1346-y</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29357847">PM:29357847</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMC Vet Res\2018-14-24.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMC Vet Res\2018-14-24.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180122, Olivry T</style></custom2><misc3><style face="normal" font="default">10.1186/s12917-018-1346-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86824</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,P.H.</style></author><author><style face="normal" font="default"> Kim,B.G.</style></author><author><style face="normal" font="default"> Lee,S.H.</style></author><author><style face="normal" font="default"> Lee,J.H.</style></author><author><style face="normal" font="default"> Park,S.W.</style></author><author><style face="normal" font="default"> Kim,D.J.</style></author><author><style face="normal" font="default"> Park,C.S.</style></author><author><style face="normal" font="default"> Leikauf,G.D.</style></author><author><style face="normal" font="default"> Jang,A.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea</style></auth-address><titles><title><style face="normal" font="default">Alteration in Claudin-4 Contributes to Airway Inflammation and Responsiveness in Asthma</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Immunol Res</style></abbr-1></periodical><pages end="33" start="25">25-33</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">PURPOSE: Claudin-4 has been reported to function as a paracellular sodium barrier and is one of the 3 major claudins expressed in lung alveolar epithelial cells. However, the possible role of claudin-4 in bronchial asthma has not yet been fully studied. In this study, we aimed to elucidate the role of claudin-4 in the pathogenesis of bronchial asthma. METHODS: We determined claudin-4 levels in blood from asthmatic patients. Moreover, using mice sensitized and challenged with OVA, as well as sensitized and challenged with saline, we investigated whether claudin-4 is involved in the pathogenesis of bronchial asthma. Der p1 induced the inflammatory cytokines in NHBE cells. RESULTS: We found that claudin-4 in blood from asthmatic patients was increased compared with that from healthy control subjects. Plasma claudin-4 levels were significantly higher in exacerbated patients than in control patients with bronchial asthma. The plasma claudin-4 level was correlated with eosinophils, total IgE, FEV1% pred, and FEV1/FVC. Moreover, lung tissues from the OVA-OVA mice showed significant increases in transcripts and proteins of claudin-4 as well as in TJ breaks and the densities of claudin-4 staining. When claudin-4 was knocked down by transfecting its siRNA, inflammatory cytokine expressions, which were induced by Der p1 treatment, were significantly increased. CONCLUSIONS: These findings thus raise the possibility that regulation of lung epithelial barrier proteins may constitute a therapeutic approach for asthma</style></abstract><notes><style face="normal" font="default">IS - 2092-7355 (Print)IS - 2092-7355 (Linking)LA - engPT - Journal ArticleCO - South Korea -CO - United States -</style></notes><work-type><style face="normal" font="default">10.4168/aair.2018.10.1.25</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29178675">PM:29178675</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-25-33.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-25-33.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Lee PH</style></custom2><misc3><style face="normal" font="default">10.4168/aair.2018.10.1.25</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86946</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,B.K.</style></author><author><style face="normal" font="default"> Park,S.J.</style></author><author><style face="normal" font="default"> Nam,S.Y.</style></author><author><style face="normal" font="default"> Kang,S.</style></author><author><style face="normal" font="default"> Hwang,J.</style></author><author><style face="normal" font="default"> Lee,S.J.</style></author><author><style face="normal" font="default"> Im,D.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Molecular Inflammation Research Center for Aging Intervention (MRCA) and College of Pharmacy, Pusan National University, Busan 46241, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Anti-allergic effects of sesquiterpene lactones from Saussurea costus (Falc.) Lipsch. determined using in vivo and in vitro experiments</style></title><secondary-title><style face="normal" font="default">J Ethnopharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Ethnopharmacol</style></abbr-1></periodical><pages end="261" start="256">256-261</pages><volume><style face="normal" font="default">213</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">ETHNOPHARMACOLOGICAL RELEVANCE: Saussurea costus (Falc.) Lipsch. root has been used in Asian traditional medicine for the treatment of asthma, rheumatism, and other conditions. S. costus extracts were shown to alleviate house dust mite-induced atopic-like dermatitis in Nc/Nga mice; besides, sesquiterpene lactones were isolated from S. costus extracts. AIMS OF THE STUDY: We aimed to investigate the effects of sesquiterpene lactones (alantolactone, costunolide, and dehydrocostuslactone) in allergic asthma using female Balb/c mice and rat RBL-2H3 mast cells. MATERIALS AND METHODS: Antigen-induced degranulation was assessed by measuring beta-hexosaminidase activity in vitro. In addition, a murine ovalbumin-induced allergic asthma model was used to test the in vivo efficacy of sesquiterpene lactones. RESULTS: Sesquiterpene lactones inhibited antigen-induced degranulation, wherein dehydrocostuslactone > costunolide > alantolactone in potency. Administration of sesquiterpene lactones decreased the number of immune cells, particularly eosinophils, and reduced the expression and secretion of Th2 cytokines (IL-4 and IL-13) in the bronchoalveolar lavage fluid and lung tissues of mice with ovalbumin-induced allergic asthma. Histological studies showed that sesquiterpene lactones reduced inflammation and mucin production in the lungs. Similar to the in vitro study, dehydrocostuslactone showed the highest potency, followed by costunolide and alantolactone. CONCLUSION: These findings provide evidence that sesquiterpene lactones might be potential anti-allergic therapeutics</style></abstract><notes><style face="normal" font="default">IS - 1872-7573 (Electronic)IS - 0378-8741 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1016/j.jep.2017.11.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29158156">PM:29158156</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Ethnopharmacol\2018-213-256-61.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Ethnopharmacol\2018-213-256-61.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Lee BK</style></custom2><misc3><style face="normal" font="default">10.1016/j.jep.2017.11.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87173</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Salo,P.M.</style></author><author><style face="normal" font="default"> Zeldin,D.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">National Institute of Health Research Triangle Park, North CarolinaNational Institute of Health Research Triangle Park, North Carolina</style></auth-address><titles><title><style face="normal" font="default">Mite-impermeable bedding casings and severe asthma exacerbations</style></title><secondary-title><style face="normal" font="default">J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pediatr</style></abbr-1></periodical><pages end="269" start="266">266-269</pages><volume><style face="normal" font="default">192</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6833 (Electronic)IS - 0022-3476 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jpeds.2017.10.058</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29246350">PM:29246350</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pediatr\2018-192-266-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pediatr\2018-192-266-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Salo PM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jpeds.2017.10.058</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86737</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wambre,E.</style></author><author><style face="normal" font="default"> Jeong,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Benaroya Research Institute at Virginia Mason, 1201 Ninth Avenue, Seattle, WA 98101, USA.</style></auth-address><titles><title><style face="normal" font="default">Oral Tolerance Development and Maintenance</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="37" start="27">27-37</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">The gastrointestinal tract has an abundant mucosal immune system to develop and maintain oral tolerance. The oral route of administration takes advantage of the unique set of immune cells and pathways involved in the induction of oral tolerance. Food allergy results from a loss of oral tolerance toward ingested antigens. Oral immunotherapy is thought to initiate desensitization through interaction of an allergen with mucosal dendritic cells that initiate downstream immune system modulation through regulatory T cells and effector T cells</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132672">PM:29132672</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-27-37.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-27-37.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Wambre E</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87410</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Muluk,N.B.</style></author><author><style face="normal" font="default"> Cingi,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">From the Department of Otorhinolaryngology, Medical Faculty, Kirikkale University, Kirikkale, Turkey</style></auth-address><titles><title><style face="normal" font="default">Oral allergy syndrome</style></title><secondary-title><style face="normal" font="default">Am J Rhinol Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Rhinol Allergy</style></abbr-1></periodical><pages end="30" start="27">27-30</pages><volume><style face="normal" font="default">32</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="1" Year="2018">2018/1/1</year></dates><abstract><style face="normal" font="default">OBJECTIVES: To review oral allergy syndrome (OAS). METHODS: We searched several medical literature data bases with the following key words: "oral allergy syndrome," "OAS," "pollen-food allergy syndrome," "PFAS," "allergy," "diagnosis," "treatment." RESULTS: Oral allergy syndrome (OAS), also called "pollen-food allergy syndrome," is a type of food allergy brought about by flavors, nuts, raw fruit, and vegetables. The most well-known symptoms are mouth and throat itching, which starts rapidly after a food is placed in the mouth, and that, as a rule, continues for just a couple of minutes after the food has been swallowed. The frequency of OAS with pollen allergy has been reported as 5-8%; 1-2% of patients with OAS with pollen allergy show extreme responses, e.g., anaphylaxis. Birch tree pollen, ragweed pollen, and grass pollen hypersensitivity cause the symptoms. The diagnosis of OAS is confirmed by a positive history and positive skin-prick test result triggered by the food's fresh extract. Oral challenge result is normally positive with the raw food and negative with the similar cooked food. CONCLUSION: Patients with grass allergy may have a response to peaches, oranges, celery, tomatoes, and melons. Patients with ragweed allergy may show OAS symptoms with melon, cucumber, banana, and zucchini. Physicians should be aware of OAS and know the appropriate treatment</style></abstract><notes><style face="normal" font="default">IS - 1945-8932 (Electronic)IS - 1945-8932 (Linking)LA - engPT - Journal ArticleCO - Turkey -</style></notes><work-type><style face="normal" font="default">10.2500/ajra.2018.32.4489</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29336286">PM:29336286</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180101, Muluk NB</style></custom2><misc3><style face="normal" font="default">10.2500/ajra.2018.32.4489</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87354</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pahus,L.</style></author><author><style face="normal" font="default"> Gouitaa,M.</style></author><author><style face="normal" font="default"> Sofalvi,T.</style></author><author><style face="normal" font="default"> Alagha,K.</style></author><author><style face="normal" font="default"> Gras,D.</style></author><author><style face="normal" font="default"> Chanez,P.</style></author><author><style face="normal" font="default"> Charpin,D.</style></author></authors></contributors><titles><title><style face="normal" font="default">Cypress pollen allergy is responsible for two distinct phenotypes of allergic rhinitis different from other pollinosis</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="35" start="28">28-35</pages><volume><style face="normal" font="default">50</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Cypress pollen</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Different phenotypes of allergic rhinitis have been identified based on the seasonality of the allergen involved. Within pollinosis, importance has to be paid to the responsible pollen species. Guidelines for clinical management are mostly based on studies performed in patients with grass pollen allergy. Only few data is available on tree pollen allergy and more specifically on cypress pollen allergy. We focused on the clinical and biological features of cypress pollen allergy to determine whether it is associated with a specific phenotype of allergic rhinitis or not. Our results suggest that cypress pollen can be responsible for two distinct phenotypes of rhinitis, both different from other pollinosis. In the most common phenotype, cypress pollen was not responsible for bronchial hyperresponsiveness or systemic inflammation. Close attention has to be paid to the allergen involved in allergic rhinitis. Different phenotypes leading to different pharmacological strategies may apply.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - France -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.34</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.23822/EurAnnACI.1764-1489.34</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-28-35.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-28-35.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Pahus L</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.34</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87096</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ahmed,I.</style></author><author><style face="normal" font="default"> Lv,L.</style></author><author><style face="normal" font="default"> Lin,H.</style></author><author><style face="normal" font="default"> Li,Z.</style></author><author><style face="normal" font="default"> Ma,J.</style></author><author><style face="normal" font="default"> Guanzhi,C.</style></author><author><style face="normal" font="default"> Sun,L.</style></author><author><style face="normal" font="default"> Xu,L.</style></author></authors></contributors><titles><title><style face="normal" font="default">Effect of tyrosinase-aided crosslinking on the IgE binding potential and conformational structure of shrimp (Metapenaeus ensis) tropomyosin</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="295" start="287">287-295</pages><volume><style face="normal" font="default">248</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> Caffeic acid</style></keyword><keyword><style face="normal" font="default"> Cross-linking</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> Protein structure</style></keyword><keyword><style face="normal" font="default"> Shrimp Tropomyosin</style></keyword><keyword><style face="normal" font="default"> Tropomyosin</style></keyword><keyword><style face="normal" font="default"> Tyrosinase</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0308-8146</style></isbn><abstract><style face="normal" font="default">The present study was performed to determine crosslinking and oxidative reactions catalyzed by tyrosinase (Tyr), caffeic acid (CA) and their combination with respect to IgE binding potential and conformational structure of shrimp tropomyosin (TM). Cross-links and IgE binding potentials were analyzed by SDS-PAGE, western blot and indirect ELISA. While structural changes were characterized using surface hydrophobicity, ultraviolet (UV), fluorescence and circular dichroism (CD) spectroscopies. Maximum reduction in the IgG (37.19%) and IgE binding potentials (49.41%) were observed when treated with 2000 nkat/g Tyr + CA, as indicated by ELISA analyses. These findings correlated well with the denaturation of protein, as evident by slight blue shift and alterations in the ellipticities observed via structural analyses. The results demonstrated that addition of CA mediator with Tyr pronouncedly enhanced crosslinking, and altered the conformational structure, thereby mitigated allergenicity of TM, thus showing promise in developing novel food structures with reduced allergenic potential</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2017.12.071</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29329856">PM:29329856</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\20171211-AhmedI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\20171211-AhmedI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171211, Ahmed I</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2017.12.071</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87245</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Inman,S.E.</style></author><author><style face="normal" font="default"> Groves,K.</style></author><author><style face="normal" font="default"> McCullough,B.</style></author><author><style face="normal" font="default"> Quaglia,M.</style></author><author><style face="normal" font="default"> Hopley,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">LGC, Queens Road, Teddington, Middlesex TW11 0LY, United Kingdom.</style></auth-address><titles><title><style face="normal" font="default">Development of a LC-MS method for the discrimination between trace level Prunus contaminants of spices</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="296" start="289">289-296</pages><volume><style face="normal" font="default">245</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword></keywords><dates><year Day="15" Month="4" Year="2018">2018/4/15</year></dates><abstract><style face="normal" font="default">The need for an analytical procedure for the identification of allergens present at trace levels in foods was highlighted by conflicting results in a case of contamination of the spice cumin. The application of a bottom-up proteomics experiment was investigated to identify marker peptides for potential contaminant nuts which could then be monitored with high specificity and sensitivity by selective reaction monitoring experiments. The method developed allowed for the distinction between two closely related Prunus species, almond and mahaleb, in two different spices, cumin and paprika. The paprika sample was found to be contaminated with almond and the cumin sample, contaminated at a much lower level, was found to be contaminated with mahaleb. The method could be applied to any protein-dense food matrix allergen so long as suitable control and reference samples can be acquired</style></abstract><notes><style face="normal" font="default">IS - 0308-8146 (Print)IS - 0308-8146 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2017.10.101</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29287373">PM:29287373</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\2018-245-289-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\2018-245-289-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171021, Inman SE</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2017.10.101</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87184</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,H.</style></author><author><style face="normal" font="default"> Yang,N.</style></author><author><style face="normal" font="default"> Wang,T.</style></author><author><style face="normal" font="default"> Dai,B.</style></author><author><style face="normal" font="default"> Shang,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Vitamin D reduces inflammatory response in asthmatic mice through HMGB1/TLR4/NFkappaB signaling pathway</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="2920" start="2915">2915-2920</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">2</style></number><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> drug therapy</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">The present study aimed to investigate the effects of vitamin D (VD) on inflammatory responses in asthmatic mice and the underlying mechanism, providing a theoretical basis for clinical application of targeted drug therapy, and the development of novel drugs against asthma. Mouse models of asthma were established. Hematoxylineosin staining was performed to observe the pathological changes of the lung tissue. Pulmonary function tests were conducted to determine airway resistance in asthmatic mice. ELISA was performed to measure the serum levels of inflammatory factors. Western blot analysis and reverse transcriptionquantitative polymerase chain reaction were performed to determine the changes in apoptosisinducing factors, and high mobility group box 1 protein (HMGB1)/Tolllike receptor4 (TLR4)/nuclear factor (NF)kappaB signaling pathwayrelated proteins. VD reduced infiltrated inflammatory factors, attenuated the airway resistance of asthmatic mice, decreased serum levels of interleukin (IL)1beta, IL6, tumor necrosis factor (TNF)alpha, increased serum levels of IL10, decreased apoptotic factor Bcl2associated X and caspase3 expression, downregulated HMGB1 and TLR4, NFkappaB and phosphorylatedNFkappaB p65 expression. When TLR4 expression was inhibited, the antiinflammatory effects of VD were attenuated, and HMGB1, TLR4, NFkappaB and pNFkappaB p65 expression was increased. VD was able reduce the inflammatory response of asthmatic mice and apoptosis in lung tissue through the HMGB1/TLR4/NFkappaB signaling pathway</style></abstract><notes><style face="normal" font="default">IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.8216</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29257249">PM:29257249</url></web-urls><pdf-urls><url ppv-ref="no">shangyunx@sina.com</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171205, Zhang H</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.8216</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87255</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tchidjou,H.K.</style></author><author><style face="normal" font="default"> Vescio,M.F.</style></author><author><style face="normal" font="default"> Serafinelli,J.</style></author><author><style face="normal" font="default"> Giampaolo,R.</style></author><author><style face="normal" font="default"> Jenkner,A.</style></author><author><style face="normal" font="default"> Tadonkeng,M.C.</style></author><author><style face="normal" font="default"> Avellis,L.</style></author><author><style face="normal" font="default"> Fiocchi,A.</style></author><author><style face="normal" font="default"> Pezzotti,P.</style></author><author><style face="normal" font="default"> Rezza,G.</style></author><author><style face="normal" font="default"> Rossi,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Immunology and Infectious Diseases, University-Hospital Pediatric Department (DPUO), Bambino Gesu Children Hospital, Piazza Sant'Onofrio 4, 00165, Rome, Italy.</style></auth-address><titles><title><style face="normal" font="default">Susceptibility to allergy in adoptive children: a cross-sectional study at "Bambino Gesu Children's Hospital"</style></title><secondary-title><style face="normal" font="default">Ital J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ital J Pediatr</style></abbr-1></periodical><pages end="" start="3">3-</pages><volume><style face="normal" font="default">44</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">BACKGROUND: Prevalence of allergy has steeply increased during the past few decades, particularly in high-income countries. The development of atopy could present different characteristics in internationally adopted children with regard to incidence, specific patterns of allergies and timing of occurrence. We aimed to investigate the occurrence of allergic diseases among adopted children in Italy. METHODS: We collected demographic information, preadoption immunization data, infectious diseases screening results, immunological status, and performed hematological and biochemical tests according to a standardized protocol in 108 adopted children. RESULTS: At initial visit (mean age was 5.7 +/- 3.2 years), 48 children displayed elevated total serum IgE levels with a prevalence of 56.5% (95%CI: 0.45; 0.67). The prevalences of children screened positive for one or more food allergens and inhalants were 30.1% (95%CI: 19.9%; 42.0%) and 34.3% (95%CI: 23.3%; 46.6%) respectively, only 9 children exhibited abnormal absolute eosinophil counts, 23 (21.3%) had a parasitic infection and 60 (55.6%) had received at least one dose of vaccine. CONCLUSIONS: Children without medical records or with a past medical history suggestive of atopy should perform a thorough allergy evaluation at the time of adoption. Our study offers also a glimpse at the vaccination status and immune-allergic profiles of recent migrant children in Italy</style></abstract><notes><style face="normal" font="default">IS - 1824-7288 (Electronic)IS - 1720-8424 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1186/s13052-017-0440-2</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29301554">PM:29301554</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ital J Pediatr\2018-44-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ital J Pediatr\2018-44-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Tchidjou HK</style></custom2><misc3><style face="normal" font="default">10.1186/s13052-017-0440-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87501</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cvetkovski,B.</style></author><author><style face="normal" font="default"> Kritikos,V.</style></author><author><style face="normal" font="default"> Yan,K.</style></author><author><style face="normal" font="default"> Bosnic-Anticevich,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Sydney, Sydney, Australia.</style></auth-address><titles><title><style face="normal" font="default">Tell me about your hay fever: a qualitative investigation of allergic rhinitis management from the perspective of the patient</style></title><secondary-title><style face="normal" font="default">NPJ Prim Care Respir Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">NPJ Prim Care Respir Med</style></abbr-1></periodical><pages end="" start="3">3-</pages><volume><style face="normal" font="default">28</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Economic burden</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="23" Month="1" Year="2018">2018/1/23</year></dates><abstract><style face="normal" font="default">Allergic rhinitis (AR) is sub-optimally managed in the community and is responsible for a significant health and economic burden. Uncontrolled AR increases the risk of poorly controlled asthma and presents an increased susceptibility to thunderstorm asthma. With the availability of treatments over-the-counter, bypassing the health care professional (HCP), the role of the patient is paramount. Research on the role of the patient in AR management in the current environment is limited. This study aims to explore the patient perspective of AR management and understand why it is sub-optimally managed in the community. Patient perspectives of AR management were explored utilizing a qualitative, phenomenological approach. Adults with AR were included in the study and interviewed. Transcripts were analyzed for recurrent themes and emergent concepts. Forty-seven participants with AR were interviewed about their experiences. Patient reports of delayed diagnosis, treatment fatigue and confidence in the ability to manage their AR themselves, heavily influenced their management preferences. Patients also described barriers associated with AR management including financial expense as well as being mistaken for having an infectious disease. Patients described examples of the impact on their quality of life caused by their AR, yet they strongly believed they could manage it themselves. This belief that AR is a condition that should be entirely self-managed, contributes to its burden. It amplifies patients' separation from HCPs and having access to guidelines aimed at optimizing their AR control</style></abstract><notes><style face="normal" font="default">IS - 2055-1010 (Electronic)IS - 2055-1010 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1038/s41533-018-0071-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29362452">PM:29362452</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\NPJ Prim Care Respir Med\2018-23-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\NPJ Prim Care Respir Med\2018-23-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180123, Cvetkovski B</style></custom2><misc3><style face="normal" font="default">10.1038/s41533-018-0071-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87183</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Song,Y.</style></author><author><style face="normal" font="default"> Yan,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology, The Third Central Hospital of Tianjin, Tianjin 300170, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Exploring of the molecular mechanism of rhinitis via bioinformatics methods</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="3020" start="3014">3014-3020</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> biosynthesis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">The aim of this study was to analyze gene expression profiles for exploring the function and regulatory network of differentially expressed genes (DEGs) in pathogenesis of rhinitis by a bioinformatics method. The gene expression profile of GSE43523 was downloaded from the Gene Expression Omnibus database. The dataset contained 7 seasonal allergic rhinitis samples and 5 nonallergic normal samples. DEGs between rhinitis samples and normal samples were identified via the limma package of R. The webGestal database was used to identify enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of the DEGs. The differentially coexpressed pairs of the DEGs were identified via the DCGL package in R, and the differential coexpression network was constructed based on these pairs. A proteinprotein interaction (PPI) network of the DEGs was constructed based on the Search Tool for the Retrieval of Interacting Genes database. A total of 263 DEGs were identified in rhinitis samples compared with normal samples, including 125 downregulated ones and 138 upregulated ones. The DEGs were enriched in 7 KEGG pathways. 308 differential coexpression gene pairs were obtained. A differential coexpression network was constructed, containing 212 nodes. In total, 148 PPI pairs of the DEGs were identified, and a PPI network was constructed based on these pairs. Bioinformatics methods could help us identify significant genes and pathways related to the pathogenesis of rhinitis. Steroid biosynthesis pathway and metabolic pathways might play important roles in the development of allergic rhinitis (AR). Genes such as CDC42 effector protein 5, solute carrier family 39 member A11 and PR/SET domain 10 might be also associated with the pathogenesis of AR, which provided references for the molecular mechanisms of AR</style></abstract><notes><style face="normal" font="default">IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.8213</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29257233">PM:29257233</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Med Rep\2018-17-3014-20.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Med Rep\2018-17-3014-20.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Song Y</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.8213</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87434</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rochelle,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Departement de medecine familiale et de medecine d'urgence, Universite Laval, Quebec G0R 1Z0, Canada</style></auth-address><titles><title><style face="normal" font="default">Using randomised, double-blind, N-of-1 trials of food challenge to diagnose food allergy and assess the effectiveness of food allergen avoidance</style></title><secondary-title><style face="normal" font="default">J R Soc Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J R Soc Med</style></abbr-1></periodical><pages end="32" start="31">31-32</pages><volume><style face="normal" font="default">111</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1758-1095 (Electronic)IS - 0141-0768 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1177/0141076817748549</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29338598">PM:29338598</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J R Soc Med\2018-111-31-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J R Soc Med\2018-111-31-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180110, Rochelle P</style></custom2><misc3><style face="normal" font="default">10.1177/0141076817748549</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87372</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nickels,A.S.</style></author><author><style face="normal" font="default"> Wu,A.C.</style></author><author><style face="normal" font="default"> Stukus,D.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Asthma and Allergic Disease, Park Nicollet Health Services, St. Louis Park, Minn.</style></auth-address><titles><title><style face="normal" font="default">Social Media and the Allergist: Evidence Supports Increasing Our Engagement</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="314" start="313">313-314</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.09.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29310761">PM:29310761</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180105, Nickels AS</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.09.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86583</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nardiello,D.</style></author><author><style face="normal" font="default"> Natale,A.</style></author><author><style face="normal" font="default"> Palermo,C.</style></author><author><style face="normal" font="default"> Quinto,M.</style></author><author><style face="normal" font="default"> Centonze,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dipartimento di Scienze Agrarie, Degli Alimenti e dell'Ambiente, Universita Degli Studi di Foggia, Via Napoli, 25, 71122 Foggia, Italy.</style></auth-address><titles><title><style face="normal" font="default">Milk authenticity by ion-trap proteomics following multi-enzyme digestion</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="323" start="317">317-323</pages><volume><style face="normal" font="default">244</style></volume><reprint-status status="in-file"/><keywords/><dates><year Day="1" Month="4" Year="2018">2018/4/1</year></dates><abstract><style face="normal" font="default">The practice of adding adulterating substances in milk in order to raise profits is unfortunately worldwide. In addition, higher priced milk, coming from minor dairy species, is often illegally integrated with the lower priced cow milk. The presence of species-specific proteins, different from those declared in label, may be a serious problem for people with allergies. The development of proper analytical methods is therefore essential to protect consumer benefits and product authenticity. In this study, a proteomic approach for the detection of adulteration processes of specific milks in mixtures is proposed. Few microliters of milk samples have been digested with trypsin and chymotrypsin and analyzed by nanoLC-ESI-IT-MS/MS. A post-database processing was performed to obtain confident peptide sequence assignments, allowing the detection of milk adulteration at a level lower than 1%. Species-specific peptides from bovine beta-lactoglobulin and alphaS1 casein were identified as suitable peptide markers of milk authenticity</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 0308-8146 (Print)IS - 0308-8146 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2017.10.052</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29120788">PM:29120788</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\2018-244-317-23.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\2018-244-317-23.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Nardiello D</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2017.10.052</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87376</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Abramson,S.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Shannon Clinic/Shannon Medical Center, San Angelo, Texas.</style></auth-address><titles><title><style face="normal" font="default">Reducing Environmental Allergic Triggers: Policy Issues</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="35" start="32">32-35</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Occupational Exposure</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">The implementation of policies to reduce environmental allergic triggers can be an important adjunct to optimal patient care for allergic rhinitis and allergic asthma. Policies at the local level in schools and other public as well as private buildings can make an impact on disease morbidity. Occupational exposures for allergens have not yet been met with the same rigorous policy standards applied for exposures to toxicants by Occupational Safety and Health Administration. Further benefit may be obtained through policies by local, county, state, and national governments, and possibly through international cooperative agreements. The reduction of allergenic exposures can and should be affected by policies with strong scientific, evidence-based derivation. However, a judicious application of the precautionary principle may be needed in circumstances where the health effect of inaction could lead to more serious threats to vulnerable populations with allergic disease. This commentary covers the scientific basis, current implementation, knowledge gaps, and pro/con views on policy issues in reducing environmental allergic triggers</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.027</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29310764">PM:29310764</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180105, Abramson SL</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.027</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86774</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Grant,T.</style></author><author><style face="normal" font="default"> Matsui,E.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Breathing New Life Into Mite-Impermeable Bedcovers</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="322" start="321">321-322</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">1</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords/><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.018</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.10.018</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171120, Grant T</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87227</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lew,D.B.</style></author><author><style face="normal" font="default"> LeMesseurier,K.S.</style></author><author><style face="normal" font="default"> Palipane,M.</style></author><author><style face="normal" font="default"> Lin,Y.</style></author><author><style face="normal" font="default"> Samarasinghe,A.E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Saccharomyces cerevisiae-Derived Mannan Does Not Alter Immune Responses to Aspergillus Allergens</style></title><secondary-title><style face="normal" font="default">Biomed Res Int</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Biomed Res Int</style></full-title></periodical><pages end="" start="3298378">3298378-</pages><volume><style face="normal" font="default">2018</style></volume><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Severe asthma with fungal sensitization predominates in the population suffering from allergic asthma, to which there is no cure. While corticosteroids are the mainstay in current treatment, other means of controlling inflammation may be beneficial. Herein, we hypothesized that mannan from Saccharomyces cerevisiae would dampen the characteristics of fungal allergic asthma by altering the pulmonary immune responses. Using wild-type and transgenic mice expressing the human mannose receptor on smooth muscle cells, we explored the outcome of mannan administration during allergen exposure on the pathogenesis of fungal asthma through measurement of cardinal features of disease such as inflammation, goblet cell number, and airway hyperresponsiveness. Mannan treatment did not alter most hallmarks of allergic airways disease in wild-type mice. Transgenic mice treated with mannan during allergen exposure had an equivalent response to non-mannan-treated allergic mice except for a prominent granulocytic influx into airways and cytokine availability. Our studies suggest no role for mannan as an inflammatory regulator during fungal allergy.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1155/2018/3298378</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1155/2018/3298378</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biomed Res Int\2018-2018-3298378.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biomed Res Int\2018-2018-3298378.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Lew DB</style></custom2><misc3><style face="normal" font="default">10.1155/2018/3298378</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87219</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Assayag,M.</style></author><author><style face="normal" font="default"> Moshel,S.</style></author><author><style face="normal" font="default"> Kohan,M.</style></author><author><style face="normal" font="default"> Berkman,N.</style></author></authors></contributors><titles><title><style face="normal" font="default">The effect of omalizumab treatment on the low affinity immunoglobulin E receptor (CD23/fc epsilon RII) in patients with severe allergic asthma</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Proc</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Proc</style></abbr-1></periodical><pages end="42" start="36">36-42</pages><volume><style face="normal" font="default">39</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="1" Month="1" Year="2018">2018/1/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: Omalizumab is an anti-immunoglobulin E (IgE) monoclonal antibody used in the treatment of severe asthma. Its therapeutic efficacy is primarily attributed to reduction of serum-free IgE and in the expression of high-affinity IgE receptor, fc epsilon RI. However, its effect on the low-affinity IgE receptor fc epsilon RII/CD23 in vivo has not been evaluated. AIM: To determine whether CD23 plays a role in the inflammatory process in severe uncontrolled asthma and whether anti-IgE therapy modulates fc epsilon RII/CD23 expression in these patients. METHODS: We evaluated the expression of IgE receptors fc epsilon RI, fc epsilon RII/CD23, and soluble CD23 (sCD23), and the activation state of peripheral blood monocytes (tumor necrosis factor alpha, interleukin (IL) 1-beta, transforming growth factor (TGF) beta expression) in the patients with severe asthma before and after 24 weeks of omalizumab treatment and in the healthy controls. Cytokine expression of monocytes in response to different stimulation (IL-4, IL-4 plus IgE, IL-4 plus IgE plus anti-IgE, and IL-4 plus IgE plus anti-IgE plus anti-CD23 for 72 hours) was determined by enzyme-linked immunosorbent assay. RESULTS: Treatment with omalizumab (for 24 weeks) improved disease control and pulmonary function (forced expiratory volume in the first second of expiration, 64.5 versus 74%; p = 0.021). Mean +/- SE expression of fc epsilon RI on monocytes was higher in the patients with asthma versus the controls (45.7 +/- 12.2% versus 18.6 +/- 5.8%; p = 0.04) and was reduced after omalizumab treatment (45.7 +/- 12.2% versus 15.6 +/- 4.4%; p = 0.027). Mean +/- SE TGF-beta levels in supernatants from monocytes were reduced in the patients treated with omalizumab (211 +/- 6 pg/mL versus 184 +/- 9 pg/mL; p = 0.036). CONCLUSION: Modulation of the low affinity IgE receptor CD23 in severe asthma is complex, and sCD23 may inversely reflect disease activity. Treatment with omalizumab was associated with reduced monocyte activation</style></abstract><notes><style face="normal" font="default">IS - 1539-6304 (Electronic)IS - 1088-5412 (Linking)LA - engPT - Journal ArticleCO - Israel -</style></notes><work-type><style face="normal" font="default">10.2500/aap.2018.39.4106</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29279058">PM:29279058</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Proc\2018-39-36-42.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Proc\2018-39-36-42.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Assayag M</style></custom2><misc3><style face="normal" font="default">10.2500/aap.2018.39.4106</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87369</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hauptman,M.</style></author><author><style face="normal" font="default"> Peden,D.</style></author><author><style face="normal" font="default"> Phipatanakul,W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of General Pediatrics, Boston Children's Hospital, Boston, Mass; Department of Pediatrics, Harvard Medical School, Boston, Mass</style></auth-address><titles><title><style face="normal" font="default">Environmental Control: The First Tenet of Allergy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="37" start="36">36-37</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.022</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29310767">PM:29310767</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180105, Hauptman M</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.022</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87500</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jo,S.</style></author><author><style face="normal" font="default"> Kim,T.J.</style></author><author><style face="normal" font="default"> Lee,H.</style></author><author><style face="normal" font="default"> Min,Y.W.</style></author><author><style face="normal" font="default"> Min,B.H.</style></author><author><style face="normal" font="default"> Lee,J.H.</style></author><author><style face="normal" font="default"> Son,H.J.</style></author><author><style face="normal" font="default"> Rhee,P.L.</style></author><author><style face="normal" font="default"> Baek,S.Y.</style></author><author><style face="normal" font="default"> Kim,S.W.</style></author><author><style face="normal" font="default"> Kim,J.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea</style></auth-address><titles><title><style face="normal" font="default">Associations between Atopic Dermatitis and Risk of Gastric Cancer: A Nationwide Population-based Study</style></title><secondary-title><style face="normal" font="default">Korean J Gastroenterol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Korean J Gastroenterol</style></abbr-1></periodical><pages end="44" start="38">38-44</pages><volume><style face="normal" font="default">71</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="25" Month="1" Year="2018">2018/1/25</year></dates><abstract><style face="normal" font="default">Background/Aims: Epidemiologic and clinical data indicate that allergies may be associated with reduced risks for several cancers; however, to date, only a few studies have examined the associations between allergies and gastric cancer. This study aimed to examine the associations between allergies and gastric cancer using a large population-based dataset. Methods: This cross-sectional study obtained data from the Korea National Health and Nutrition Examination Survey between 2010 and 2014, involving a total of 24,089 participants. The associations between allergies and gastric cancer were analyzed using univariable and multivariable logistic regression analyses with complex sampling, while adjusting for confounding factors that included age, sex, body mass index, smoking status, alcohol intake, and level of education. Results: Multivariable logistic regression analyses that were adjusted for the potential confounders determined that a history of allergic diseases tended to be associated with reduced risk of gastric cancer; however, this relationship was not statistically significant (any allergy: odds ratio [OR], 0.62; 95% confidence interval [CI], 0.34-1.12; atopic dermatitis: OR, 0.34; 95% CI, 0.50-1.72; allergic rhinitis: OR, 0.71; 95% CI, 0.34-1.46; asthma: OR, 0.44; 95% CI, 0.15-1.29). Multivariable analysis showed that a history of atopic dermatitis was associated with reduced risk of gastric cancer in men (OR, 0.16; 95% CI, 0.03-0.75). Conclusions: This findings of this study suggest that individuals with allergies tend to have a reduced risk of gastric cancer, without a statistically significant association. Furthermore, atopic dermatitis was associated with reduced risk of gastric cancer, particularly in men</style></abstract><notes><style face="normal" font="default">IS - 2233-6869 (Electronic)IS - 1598-9992 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4166/kjg.2018.71.1.38</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29361812">PM:29361812</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Korean J Gastroenterol\2018-71-38-44.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Korean J Gastroenterol\2018-71-38-44.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180125, Jo S</style></custom2><misc3><style face="normal" font="default">10.4166/kjg.2018.71.1.38</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86734</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gupta,M.</style></author><author><style face="normal" font="default"> Cox,A.</style></author><author><style face="normal" font="default"> Nowak-Wegrzyn,A.</style></author><author><style face="normal" font="default"> Wang,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy &amp; Immunology, Department of Internal Medicine, University of Michigan, 24 Frank Lloyd Wright Drive, Suite H-2100, Ann Arbor, MI 48106, USA</style></auth-address><titles><title><style face="normal" font="default">Diagnosis of Food Allergy</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="52" start="39">39-52</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Diagnosis of food allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">Food allergy diagnosis remains challenging. Most standard methods are unable to differentiate sensitization from clinical allergy. Recognizing food allergy is of utmost importance to prevent life-threatening reactions. On the other hand, faulty interpretation of tests leads to overdiagnosis and unnecessary food avoidances. Highly predictive models have been established for major food allergens based on skin prick testing and food-specific immunoglobulin E but are lacking for most other foods. Although many newer diagnostic techniques are improving the accuracy of food allergy diagnostics, an oral food challenge remains the only definitive method of confirming a food allergy</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132673">PM:29132673</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-39-52.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-39-52.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Gupta M</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87485</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,L.</style></author><author><style face="normal" font="default"> Zhou,Y.</style></author><author><style face="normal" font="default"> Cui,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">1 Shandong Institute of Parasitic Diseases, Shandong Academy of Medical Sciences, Jining, China</style></auth-address><titles><title><style face="normal" font="default">lncRNA profiling in NCI-H292 cells after stimulation with Dermatophagoides farinae extracts</style></title><secondary-title><style face="normal" font="default">Int J Immunopathol Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Immunopathol Pharmacol</style></abbr-1></periodical><pages end="" start="394632017750997">394632017750997-</pages><volume><style face="normal" font="default">32</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> etiology</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Airway epithelium cells are the first line of defense against airborne allergens. When cultured, epithelial cells can be exposed to various allergens, providing an ideal model to investigate allergic disorders. This study sought to characterize the profile of long noncoding (lnc) RNAs, which can regulate gene expression and exert functions in diverse cellular processes, in airway epithelial cells exposed to house dust mite allergens. NCI-H292 cells were exposed to house dust mite extract for 24 h. RNA expression was profiled in exposed and unexposed cells. There were 270 lncRNAs that were differentially expressed (fold change >/= 2, P &lt; 0.05) in NCI-H292 cells after stimulation with Dermatophagoides farinae (house dust mite) extracts. Furthermore, 119 lncRNAs and 22 messenger RNAs were co-expressed. Gene Ontology analysis showed that these under-regulated and up-regulated lncRNAs were associated with biological process, cellular component, and molecular function. After bioinformatic analysis of significantly regulated signaling pathways, we found these lncRNAs may target 16 gene pathways, including glycolysis, axon guidance, ErbB signaling, and mitogen-activated protein kinases (MAPK) signaling. The identification of differentially regulated lncRNAs in NCI-H292 cells after stimulation with Dermatophagoides farinae extracts, as well as their target gene pathways, can provide insight to the etiology and pathogenesis of allergy</style></abstract><notes><style face="normal" font="default">IS - 2058-7384 (Electronic)IS - 0394-6320 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1177/0394632017750997</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29357711">PM:29357711</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Immunopathol Pharmacol\2018-32-394632017750997.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Immunopathol Pharmacol\2018-32-394632017750997.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180118, Wang L</style></custom2><misc3><style face="normal" font="default">10.1177/0394632017750997</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87358</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">O'Sullivan,A.J.</style></author><author><style face="normal" font="default"> Pigat,S.</style></author><author><style face="normal" font="default"> O'Mahony,C.</style></author><author><style face="normal" font="default"> Gibney,M.J.</style></author><author><style face="normal" font="default"> McKevitt,A.I.</style></author></authors></contributors><auth-address><style face="normal" font="default">a UCD Institute of Food and Health, School of Agriculture and Food Science , University College Dublin , Dublin , Republic of Ireland</style></auth-address><titles><title><style face="normal" font="default">Predictive modelling of the exposure to steviol glycosides in Irish patients aged 1-3 years with phenylketonuria and cow's milk protein allergy</style></title><secondary-title><style face="normal" font="default">Food Addit Contam Part A Chem Anal Control Expo Risk Assess</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Addit Contam Part A Chem Anal Control Expo Risk Assess</style></abbr-1></periodical><pages end="48" start="40">40-48</pages><volume><style face="normal" font="default">35</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Children with Phenylketonuria (PKU) and severe cow's milk protein allergy (CMPA) consume prescribed, specially formulated, foods for special medical purposes (FSMPs) as well as restricted amounts of normal foods. These patients are exposed to artificial sweeteners from the consumption of a combination of free and prescribed foods. Young patients with PKU and CMPA have a higher risk of exceeding acceptable daily intakes (ADI) for additives than age-matched healthy children. A predictive modelling approach has been adapted successfully to assess the additive exposure of young patients with PKU and CMPA to artificial sweeteners. Steviol glycosides (E960) are at various stages of regulatory approval for the various food categories in the EU but are not as yet permitted for use in products intended for young children. The aim of this study was to predict potential steviol glycoside exposure in young children with PKU and CMPA considering the potential for future provisions for the use of this sweetener. The recent introduction of steviol glycosides means that no exposure data are available for children with CMPA and PKU. Food consumption data were derived from the food consumption survey data of healthy young children in Ireland from the National Preschool and Nutrition Survey (NPNS, 2010-11). Specially formulated amino acid-based FSMPs are used to replace whole or milk protein foods and were included in the exposure model to replace restricted foods. The recommendations to ensure adequate protein intake in these patients were used to determine FSMP intake. Exposure assessment results indicated that the maximum permitted level (MPL) for FSMPs would warrant careful consideration to avoid exposures above the ADI. These data can be used to inform recommendations for the medical nutrition industry</style></abstract><notes><style face="normal" font="default">IS - 1944-0057 (Electronic)IS - 1944-0057 (Linking)LA - engPT - Journal ArticleCO - Ireland -</style></notes><work-type><style face="normal" font="default">10.1080/19440049.2017.1401737</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29111886">PM:29111886</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Addit Contam Part A Chem Anal Control Expo Risk Assess\2018-35-40-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Addit Contam Part A Chem Anal Control Expo Risk Assess\2018-35-40-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180105, O'Sullivan AJ</style></custom2><misc3><style face="normal" font="default">10.1080/19440049.2017.1401737</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87357</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sousa,M.J.</style></author><author><style face="normal" font="default"> Reis Ferreira,A.L.</style></author><author><style face="normal" font="default"> Moreira da Silva,J.P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Bodybuilding protein supplements and cow's milk allergy in adult</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="44" start="42">42-44</pages><volume><style face="normal" font="default">50</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">We report a case of a previously healthy 24-year-old man with a 3-month history of gastrointestinal symptoms during exercise and also few minutes after the ingestion of cow's milk (CM) without exercise. He reported the ingestion of a blend of hydrolyzed whey and casein proteins for bodybuilding for the last 2 years. The in vivo tests showed positivity to CM, á-lactalbumin, â-lactoglobulin and casein extracts, and also to the protein supplement. The serum specific IgE was positive for CM, â-lactoglobulin and á-lactalbumin. The in vivo and in vitro tests results suggested an IgE-mediated CMA. Adult-onset CMA has been rarely reported, and to our knowledge this is the first case possibly related to bodybuilding supplements. The authors theorize that the presentation of large amounts of proteins in the gastrointestinal tract may favor sensitization.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Portugal -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.28</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.23822/EurAnnACI.1764-1489.28</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-42-4.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-42-4.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Sousa MJ</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.28</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87474</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Maher,A.M.</style></author><author><style face="normal" font="default"> Ward,C.E.</style></author><author><style face="normal" font="default"> Pratt,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Shiitake Dermatitis After Consumption of Homemade Soup</style></title><secondary-title><style face="normal" font="default">Dermatitis</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Dermatitis</style></full-title></periodical><pages end="44" start="43">43-44</pages><volume><style face="normal" font="default">29</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">1710-3568</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1097/DER.0000000000000334</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1097/DER.0000000000000334</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Dermatitis\2018-29-43-4.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Dermatitis\2018-29-43-4.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180121, Maher AM</style></custom2><misc3><style face="normal" font="default">10.1097/DER.0000000000000334</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87356</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Uasuf,C.G.</style></author><author><style face="normal" font="default"> Torina,A.</style></author><author><style face="normal" font="default"> Ferrantelli,V.</style></author><author><style face="normal" font="default"> Brusca,I.</style></author></authors></contributors><titles><title><style face="normal" font="default">An unusual case of positive sIgE to Galactose-alpha-1,3-galactose from South Italy</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="47" start="45">45-47</pages><volume><style face="normal" font="default">50</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">We report the case of a 38-year-old man who was bitten several times during his life by a tick. He didn't report any previous history of anaphylaxis after the ingestion of red meat. The serum specific IgE showed positivity to alpha-Gal. The proximity of the bits didn't increase the titer of IgE antibodies to alpha-gal. We could hypothesize that the frequency of the exposure to the tick Corresponding author bites and the amount of tick bites during his lifetime induced a sort of tolerance in this patient.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Italy -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.25</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.23822/EurAnnACI.1764-1489.25</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-45-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2018-50-45-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Uasuf CG</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.25</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86722</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dharma,C.</style></author><author><style face="normal" font="default"> Lefebvre,D.L.</style></author><author><style face="normal" font="default"> Tran,M.M.</style></author><author><style face="normal" font="default"> Lou,W.Y.W.</style></author><author><style face="normal" font="default"> Subbarao,P.</style></author><author><style face="normal" font="default"> Becker,A.B.</style></author><author><style face="normal" font="default"> Mandhane,P.J.</style></author><author><style face="normal" font="default"> Turvey,S.E.</style></author><author><style face="normal" font="default"> Sears,M.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, McMaster University, Hamilton, Canada</style></auth-address><titles><title><style face="normal" font="default">Patterns of allergic sensitization and atopic dermatitis from 1 to 3 years: effects on allergic diseases</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="59" start="48">48-59</pages><volume><style face="normal" font="default">48</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: While allergic sensitization and atopic dermatitis (AD) are known to increase the risk for allergic diseases, the impact of different temporal and clinical patterns of sensitization and AD is less well defined. OBJECTIVE: We investigated patterns of sensitization and AD from early infancy to age 3, and the differential risk for developing allergic diseases within each pattern in a general cohort. METHODS: Children (n=2629) from the Canadian Healthy Infant Longitudinal Development (CHILD) Study underwent skin prick tests and were assessed clinically for AD at ages 1 and 3 years. We applied an unsupervised latent class analysis (LCA) to the following 5 factors at these ages: AD, food sensitization, inhalant sensitization, poly-sensitization to foods, and poly-sensitization to inhalants. The risks for developing asthma, allergic rhinitis and food allergy at 3 years were evaluated for each identified group. RESULTS: Five distinct classes were revealed by LCA: healthy (81.8%), atopic dermatitis (7.6%), inhalant sensitization (3.5%), transient sensitization (4.1%), and persistent sensitization (3.2%). Using healthy children as the baseline, children in the "atopic dermatitis" group had the next lowest risk for all allergic outcomes at 3 years; those in the "inhalant sensitization" group had the highest risk for allergic rhinitis; children in the "transient sensitization" group were at an increased risk for food allergy; while children in the "persistent sensitization" group had the highest risk for all allergic diseases. CONCLUSION AND CLINICAL RELEVANCE: There is substantial heterogeneity among allergen-sensitized children. Researchers and clinicians need to be aware of the non-specificity associated with labelling children simply as "atopic" and "non-atopic" without considering the timing of their atopic history, type of sensitization, and AD status. Children with AD who were poly-sensitized to foods at an early age appear to be at greatest risk of developing other allergic diseases. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171116IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13063</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29143385">PM:29143385</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171116-DharmaC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171116-DharmaC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171116, Dharma C</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13063</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86961</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cortes,A.</style></author><author><style face="normal" font="default"> Castillo,A.</style></author><author><style face="normal" font="default"> Sciaraffia,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Food allergy: Children's symptom levels are associated with mothers' psycho-socio-economic variables</style></title><secondary-title><style face="normal" font="default">J Psychosom Res</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Psychosom Res</style></full-title></periodical><pages end="54" start="48">48-54</pages><volume><style face="normal" font="default">104</style></volume><number><style face="normal" font="default">Supplement C</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Childcare</style></keyword><keyword><style face="normal" font="default"> Economic burden</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0022-3999</style></isbn><abstract><style face="normal" font="default">Allergies affect children's health as well as their quality of life, stress levels, and family budget. The available literature suggests that family, social and psychological factors are affected by allergic pathologies such as rhinitis, asthma and atopic dermatitis. However, few studies have focused on quantifying such association in child food allergy. This study aims to enhance the understanding of the associations between caregiver variables and children's Food Allergy (FA). The study involved 206 participants: 103 mothers plus 103 children with IgE mediated FA. The analyses excluded two outliers comprising 101 subjects. For statistical analyses, each dyad </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çômother/child- was considered to be one subject unity. A between-subjects one-way ANOVA determined the association of children's cutaneous, gastric and respiratory symptoms with anxiety, depression, perceived social support and socioeconomic factors in the mothers. There are significant associations between children's allergic symptoms (gastric and cutaneous) and mothers' psychological state (anxiety and depression); family budget; social interactions (with friends, family and partner); understanding of health care required by their child; and sleep disorders. Respiratory symptoms did not show any significant associations with the dependent variables. FA is a process in which children's symptoms are significantly associated with socioeconomic and psychological variables of the mothers. The presence or absence of some specific symptoms is directly associated with specific impacts on the mothers. An understanding of such dynamics supports the consideration of a comprehensive and multidisciplinary therapeutic approach to offer more ecological healthcare for </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£families living with FA.</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Chile -</style></notes><work-type><style face="normal" font="default">10.1016/j.jpsychores.2017.11.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29275785">PM:29275785</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Psychosom Res\2018-104SC-48-54.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Psychosom Res\2018-104SC-48-54.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171209, Cortes A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jpsychores.2017.11.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87401</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sookrung,N.</style></author><author><style face="normal" font="default"> Reamtong,O.</style></author><author><style face="normal" font="default"> Poolphol,R.</style></author><author><style face="normal" font="default"> Indrawattana,N.</style></author><author><style face="normal" font="default"> Seesuay,W.</style></author><author><style face="normal" font="default"> Saelim,N.</style></author><author><style face="normal" font="default"> Tantilipikorn,P.</style></author><author><style face="normal" font="default"> Bunnag,C.</style></author><author><style face="normal" font="default"> Chaicumpa,W.</style></author><author><style face="normal" font="default"> Tungtrongchitr,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Research and Development, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand</style></auth-address><titles><title><style face="normal" font="default">Glutathione S-transferase (GST) of American Cockroach, Periplaneta americana: Classes, Isoforms, and Allergenicity</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="484">484-</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Cockroaches</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword></keywords><dates><year Day="11" Month="1" Year="2018">2018/1/11</year></dates><abstract><style face="normal" font="default">Insect glutathione S-transferases (GSTs) play important roles in insecticide/drug resistance and stress response. Medically, GSTs of house dust mites (Dermatophagoides pteronyssinus and Blomia tropicalis) and German cockroach (Blattella germanica) are human allergens. In this study, classes, isoforms and B-cell and allergenic epitopes of GST of American cockroach, Periplaneta americana, the predominant species in the tropics and subtropics were investigated for the first time. Enzymatically active native and recombinant P. americana-GSTs bound to IgE in sera of all P. americana allergic patients that were tested. By gel-based proteomics and multiple sequence alignments, the native GST comprises three isoforms of delta and sigma classes. All isoforms interacted with serum IgE of the cockroach allergic subjects. Molecularly, the protein contains six B-cell epitopes; two epitopes located at beta1-alpha1 and beta4-alpha3 regions bound to patients' serum IgE, indicating that they are allergenic. P. americana are ubiquitous and their GST can sensitize humans to allergic diseases; thus, the protein should be included in the allergen array for component resolved diagnosis (CRD) of allergic patients, either by skin prick test or specific IgE determination. The GST is suitable also as a target of environmental allergen detection and quantification for intervention of cockroach sensitization and allergic morbidity</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Thailand -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-18759-z</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29323160">PM:29323160</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-484.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-484.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20181211, Sookrung N</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-18759-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87044</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Meadows,J.A.</style></author><author><style face="normal" font="default"> Imbeau,S.</style></author><author><style face="normal" font="default"> Finerfrock,B.</style></author><author><style face="normal" font="default"> Burke,R.</style></author><author><style face="normal" font="default"> Sublett,J.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Alabama Allergy &amp; Asthma, Montgomery, Alabama.</style></auth-address><titles><title><style face="normal" font="default">USP's revisions to sterile compounding standards and FDA guidance; impacts on mixing of allergen extracts</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="7" start="5">5-7</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engCO - United States -PT - Journal Article</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.11.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273129">PM:29273129</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-5-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-5-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Meadows JA</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.11.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87459</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tenn,M.W.</style></author><author><style face="normal" font="default"> Steacy,L.M.</style></author><author><style face="normal" font="default"> Ng,C.C.</style></author><author><style face="normal" font="default"> Ellis,A.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">1Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON Canada</style></auth-address><titles><title><style face="normal" font="default">Onset of action for loratadine tablets for the symptomatic control of seasonal allergic rhinitis in adults challenged with ragweed pollen in the Environmental Exposure Unit: a post hoc analysis of total symptom score</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Clin Immunol</style></abbr-1></periodical><pages end="" start="5">5-</pages><volume><style face="normal" font="default">14</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Background: Loratadine is a second-generation, non-sedating antihistamine used for the relief of allergic rhinitis symptoms. Previous studies reported that when loratadine was encapsulated, the onset of action for symptom relief was 180 min. However, unmodified loratadine tablets were not evaluated at that time. Using data from a previously published Environmental Exposure Unit (EEU) study comparing azelastine nasal spray with loratadine tablets, cetirizine tablets, and placebo, this post hoc analysis determines the onset of action of loratadine tablets (i.e. unmodified) by analyzing the total symptom score for the relief of nasal and ocular seasonal allergic rhinitis (SAR) symptoms. Methods: A Phase IV, randomized, single-center, double-blind, placebo-controlled, double-dummy, four-way crossover study was conducted in the EEU. Seventy participants were randomized sequentially into one of the four treatments during ragweed pollen exposure. Nasal and ocular symptom scores were self-reported by the participants and recorded. The original study analysis was carried out by evaluating the nasal symptom scores only. For this post hoc analysis, both nasal and ocular data from the loratadine and placebo treatment arms were analyzed. The primary endpoint for this analysis was the onset of action of loratadine as measured by the change in total symptom score (TSS) from baseline in comparison to placebo. The onset of ocular symptom relief using the total ocular symptom score (TOSS) was also reported. Results: Loratadine tablets demonstrated a significant and durable improvement in both TSS (P = .005) and TOSS (P = .013) at 75 min post-treatment administration compared to placebo. The mean proportion of participants reporting none or mild for all component symptoms of TSS and TOSS at 75 min and thereafter was significantly higher in the loratadine (TSS, P = .0005; TOSS, P &lt;/= .0001) vs. placebo treatment arm. Conclusions: The onset of action of loratadine tablets was 75 min for the relief of nasal and ocular symptoms in adults with SAR. These results suggest a faster onset of action for loratadine tablets (75 min) compared to previously reported studies which were conducted with modified (i.e. gelatin-encapsulated) loratadine tablets (180 min).Trial registration Clinicaltrials.gov identifier NCT00561717</style></abstract><notes><style face="normal" font="default">IS - 1710-1484 (Print)IS - 1710-1484 (Linking)LA - engPT - Journal ArticleCO - Canada -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1186/s13223-017-0227-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29371864">PM:29371864</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2018-14-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2018-14-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180116, Tenn MW</style></custom2><misc3><style face="normal" font="default">10.1186/s13223-017-0227-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86830</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,W.</style></author><author><style face="normal" font="default"> Shibamoto,T.</style></author><author><style face="normal" font="default"> Kuda,Y.</style></author><author><style face="normal" font="default"> Zhang,T.</style></author><author><style face="normal" font="default"> Tanida,M.</style></author><author><style face="normal" font="default"> Kurata,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Physiology II, Kanazawa Medical University, Uchinada, Japan</style></auth-address><titles><title><style face="normal" font="default">beta(2)-Adrenoceptor Blockade Deteriorates Systemic Anaphylaxis by Enhancing Hyperpermeability in Anesthetized Mice</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Immunol Res</style></abbr-1></periodical><pages end="61" start="52">52-61</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">PURPOSE: Patients treated with propranolol, a nonselective beta-adrenoceptor antagonist, develop severe anaphylaxis, but the mechanism remains unknown. We determined effects of beta(1)- and beta(2)-adrenoceptor antagonists on the anaphylaxis-induced increase in vascular permeability in mice. METHODS: In anesthetized ovalbumin-sensitized C57BL mice, mean arterial blood pressure (MBP) was measured, and Evans blue dye extravasation and hematocrit (Hct) were assessed at 20 minutes after antigen injection. The following pretreatment groups (n=7/group) were studied: (1) sensitized control (non-pretreatment), (2) propranolol, (3) the selective beta(2)-adrenoceptor antagonist ICI 118,551, (4) the selective beta(1)-adrenoceptor antagonist atenolol, (5) adrenalectomy, (6) the selective beta(2)-adrenoceptor agonist terbutaline, and (7) non-sensitized groups. RESULTS: The antigen injection decreased MBP, and increased Hct and vascular permeability in the kidney, lung, mesentery, and intestine, but not in the liver or spleen. Pretreatment with ICI 118,551, propranolol and adrenalectomy, but not atenolol, reduced the survival rate and augmented the increases in Hct and vascular permeability in the kidney, intestine, and lung as compared with the sensitized control group. Pretreatment with terbutaline abolished the antigen-induced alterations. Plasma epinephrine levels were increased significantly in the sensitize control mice. CONCLUSIONS: Blockade of beta(2)-adrenoceptor can deteriorate systemic anaphylaxis by augmenting hyperpermeability-induced increase in plasma extravasation by inhibiting beneficial effects of epinephrine released from the adrenal glands in anesthetized mice</style></abstract><notes><style face="normal" font="default">IS - 2092-7355 (Print)IS - 2092-7355 (Linking)LA - engPT - Journal ArticleCO - China -CO - Japan -</style></notes><work-type><style face="normal" font="default">10.4168/aair.2018.10.1.52</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29178678">PM:29178678</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-52-61.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-52-61.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Yang W</style></custom2><misc3><style face="normal" font="default">10.4168/aair.2018.10.1.52</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86733</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Davis,C.M.</style></author><author><style face="normal" font="default"> Kelso,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Section of Immunology, Allergy and Rheumatology, Baylor College of Medicine, Texas Children's Hospital, 1102 Bates Avenue, MC 330.01, Houston, TX 77030, USA.</style></auth-address><titles><title><style face="normal" font="default">Food Allergy Management</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="64" start="53">53-64</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">The management of food allergies requires the cooperation of the food allergic person, physician, family, and social contacts. For children, school management of food allergies is a key component of the overall approach. Recognition of the signs and symptoms of allergic reactions and preparation to administer the appropriate treatment of mild and severe symptoms in the event of accidental exposure is necessary. Avoidance of food allergens is facilitated by label reading and dietary guidance is extremely important to minimize nutritional deficiencies. Medications and vaccines with food-derived excipients generally do not need to be avoided because, in most cases, they contain little food protein</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132674">PM:29132674</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-53-64.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-53-64.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Davis CM</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87050</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bozek,A.</style></author><author><style face="normal" font="default"> Kolodziejczyk,K.</style></author><author><style face="normal" font="default"> Jarzab,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical Department of Internal Disease, Dermatology and Allergology in Zabrze, Medical University of Silesia, Katowice, Poland.</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of birch pollen immunotherapy for local allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="58" start="53">53-58</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: Local allergic rhinitis (LAR) is a relatively new disease. OBJECTIVE: To ascertain the effects of allergen-specific immunotherapy in LAR. METHODS: A randomized, double-blind, placebo-controlled trial of birch subcutaneous allergen immunotherapy (AIT) for LAR was performed in 28 patients. The therapy was performed for 24 months in 15 patients with AIT and 13 patients given placebo. The primary end point was decrease in symptom medication score (SMS). In addition, we monitored serum-specific immunoglobulin E (IgE), serum-specific immunoglobulin G4, nasal-specific IgE to Bet v 1, and safety and quality-of-life parameters. RESULTS: After 24 months of treatment, there was a significant decrease in the median area under the curve for SMS of the active group vs the placebo group: 2.14 (range, 1.22-4.51) vs 6.21 (range, 5.12-7.89), at the P &lt; .05 level. During AIT, the active group showed a significant decrease in SMS of up to 65% vs baseline. A significant increase in immunoglobulin G4 and decrease in nasal-specific IgE were observed in the active group during AIT compared with the placebo group. AIT was well-tolerated and without systemic reactions. CONCLUSION: This study demonstrates that AIT for birch pollen in patients with LAR was clinically effective and exhibited good tolerance. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03157505</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273130">PM:29273130</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-53-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-53-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Bozek A</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87095</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Incorvaia,C.</style></author><author><style face="normal" font="default"> Mauro,M.</style></author><author><style face="normal" font="default"> Gritti,B.L.</style></author><author><style face="normal" font="default"> Makri,E.</style></author><author><style face="normal" font="default"> Ridolo,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Cardiac/Pulmonary Rehabilitation , ASST Pini/CTO , Milan , Italy</style></auth-address><titles><title><style face="normal" font="default">Venom immunotherapy in patients with allergic reactions to insect stings</style></title><secondary-title><style face="normal" font="default">Expert Rev Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Expert Rev Clin Immunol</style></abbr-1></periodical><pages end="59" start="53">53-59</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Mastocytosis</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Allergy to Hymenoptera (Apis mellifera, Vespula species, Polistes species, Vespa crabro) venom can be safely and effectively treated by venom immunotherapy (VIT), which in the 40 years since its introduction has been able to prevent reactions to stings, and to treatment as well, though systemic reactions, occasionally severe, are possible. Areas covered: We reviewed the recent literature on VIT by searching in PubMed for the terms 'venom immunotherapy' and 'Hymenoptera venom immunotherapy' to highlight the current status of VIT and the likely development in the coming years. Expert commentary: VIT, provided the correct choice of the venom and adequate venom preparations and maintenance doses are used, is a treatment of great value in preventing systemic reactions to Hymenoptera stings. A 5-year duration ensures a prolonged tolerance to stings following VIT discontinuation, unless patients suffer from mastocytosis. In fact, due to reports of fatal reactions after stopping VIT, patients with mastocytosis, or with very severe reactions to stings, need an indefinite duration of treatment</style></abstract><notes><style face="normal" font="default">IS - 1744-8409 (Electronic)IS - 1744-666X (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1080/1744666X.2018.1413350</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202591">PM:29202591</url></web-urls></urls><custom2><style face="normal" font="default">20171213, Incorvaia C</style></custom2><misc3><style face="normal" font="default">10.1080/1744666X.2018.1413350</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87332</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hubert,J.</style></author><author><style face="normal" font="default"> Stejskal,V.</style></author><author><style face="normal" font="default"> Athanassiou,C.G.</style></author><author><style face="normal" font="default"> Throne,J.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Crop Research Institute, 161 06 Prague 6, Czechia</style></auth-address><titles><title><style face="normal" font="default">Health Hazards Associated with Arthropod Infestation of Stored Products</style></title><secondary-title><style face="normal" font="default">Annu Rev Entomol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Annu Rev Entomol</style></abbr-1></periodical><pages end="573" start="553">553-573</pages><volume><style face="normal" font="default">63</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Mites</style></keyword></keywords><dates><year Day="7" Month="1" Year="2018">2018/1/7</year></dates><abstract><style face="normal" font="default">Insects and mites are common inhabitants and accidental invaders of food, including durable commodities, and their presence can have both direct and indirect effects on human health. The most common direct effect is contamination of food with arthropod fragments and related contaminants, which may be allergenic or even carcinogenic. The most important indirect effect is that their presence can change the storage microenvironment, making durable products suitable for the rapid development of fungi and other microorganisms. Some of these fungi can produce toxins (e.g., aflatoxins) that endanger human health. Insects may actively or passively contribute to the spread of microorganisms, increasing product contamination, and they may host bacteria that have developed antibiotic resistance, contributing to their spread in food. Several species also may host, attract, or transmit tapeworms, predators, or parasitoids that may affect health. This review synthesizes research on these topics and suggests directions for future research</style></abstract><notes><style face="normal" font="default">IS - 1545-4487 (Electronic)IS - 0066-4170 (Linking)LA - engPT - Journal ArticleCO - Czechia -CO - Greece -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1146/annurev-ento-020117-043218</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29324037">PM:29324037</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180107, Hubert J</style></custom2><misc3><style face="normal" font="default">10.1146/annurev-ento-020117-043218</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87274</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Klimek,L.</style></author><author><style face="normal" font="default"> Groger,M.</style></author><author><style face="normal" font="default"> Becker,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Milbenallergie im HNO-Bereich: Bedeutung, Diagnostik und Therapieoptionen</style></title><secondary-title><style face="normal" font="default">Laryngorhinootologie</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Laryngorhinootologie</style></abbr-1></periodical><pages end="69" start="56">56-69</pages><volume><style face="normal" font="default">97</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> drug therapy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Allergic rhinitis (AR) affects ca. 20% of the population. Approximately one third of patients affected by AR are suffering from perennial rhinitis due to mite allergy. Perennial rhinitis is the form of the disease that is most frequently associated with other allergy-related comorbidities such as asthma and atopic dermatitis, sleep disorders, chronic sinusitis, eustachian tube dysfunction and others.The often non-specific symptoms and the insidious course may lead to misinterpretations in diagnosing the disease.Therapeutic options include allergen avoidance with regard to environmental measures, encasings and personal actions. Drug therapy in mite-AR consists mainly in the administration of mast cell stabilizers, H1-antihistamines, glucocorticosteroids (GCS), leukotriene receptor antagonists and decongestants. It is particularly important to ensure a good antiinflammatory activity. Thus, a combination of H1-antihistamine and topical nasal GCS seems to be a rational approach. The only causal treatment form besides allergen avoidance is allergen-specific immunotherapy 1</style></abstract><notes><style face="normal" font="default">IS - 1438-8685 (Electronic)IS - 0935-8943 (Linking)LA - gerPT - English AbstractPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1055/s-0043-121086</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29301162">PM:29301162</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Laryngorhinootologie\2018-97-56-69.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Laryngorhinootologie\2018-97-56-69.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Klimek L</style></custom2><misc3><style face="normal" font="default">10.1055/s-0043-121086</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87448</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Feng,B.W.</style></author><author><style face="normal" font="default"> Fu,S.M.</style></author><author><style face="normal" font="default"> Zhang,Q.S.</style></author><author><style face="normal" font="default"> Long,X.L.</style></author><author><style face="normal" font="default"> Xie,X.L.</style></author><author><style face="normal" font="default"> Ren,W.</style></author><author><style face="normal" font="default"> Liang,Z.T.</style></author><author><style face="normal" font="default"> Yang,Z.L.</style></author><author><style face="normal" font="default"> Chen,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Third Clinical Medical School of Southern Medical University, Zhongshan, Guangdong 528400, China.</style></auth-address><titles><title><style face="normal" font="default">[Influence of cow's milk protein allergy on the diagnosis of functional gastrointestinal diseases based on the Rome IV standard in infants and young children]</style></title><secondary-title><style face="normal" font="default">Zhongguo Dang Dai Er Ke Za Zhi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Zhongguo Dang Dai Er Ke Za Zhi</style></abbr-1></periodical><pages end="59" start="56">56-59</pages><volume><style face="normal" font="default">20</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To study the influence of cow's milk protein allergy (CMPA) on the diagnosis of functional gastrointestinal diseases (FGID) based on the Rome IV standard in infants and young children. METHODS: A total of 84 children aged 1 month to 3 years who were diagnosed with CMPA were enrolled as the case group, and 84 infants and young children who underwent physical examination and had no CMPA were enrolled as the control group. The pediatricians specializing in gastroenterology asked parents using a questionnaire for the diagnosis of FGID based on the Rome IV standard to assess clinical symptoms and to diagnose FGID. RESULTS: The case group had a significantly higher incidence rate of a family history of allergies than the control group (P&lt;0.05). In the case group, 38 (45%) met the Rome IV standard for the diagnosis of FGID, while in the control group, 13 (15%) met this standard (P&lt;0.05). According to the Rome IV standard for FGID, the case group had significantly higher diagnostic rates of reflex, functional diarrhea, difficult defecation, and functional constipation than the control group (P&lt;0.05). The children who were diagnosed with FIGD in the control group were given conventional treatment, and those in the case group were asked to avoid the intake of cow's milk protein in addition to the conventional treatment. After 3 months of treatment, the case group had a significantly higher response rate to the treatment than the control group (P&lt;0.05). CONCLUSIONS: In infants and young children, CMPA has great influence on the diagnosis of FGID based on the Rome IV standard. The possibility of CMPA should be considered during the diagnosis of FGID</style></abstract><notes><style face="normal" font="default">IS - 1008-8830 (Print)IS - 1008-8830 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29335084">PM:29335084</url></web-urls></urls><custom2><style face="normal" font="default">20180115, Feng BW</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87048</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tadrous,M.</style></author><author><style face="normal" font="default"> Khuu,W.</style></author><author><style face="normal" font="default"> Lebovic,G.</style></author><author><style face="normal" font="default"> Stanbrook,M.B.</style></author><author><style face="normal" font="default"> Martins,D.</style></author><author><style face="normal" font="default"> Paterson,J.M.</style></author><author><style face="normal" font="default"> Mamdani,M.M.</style></author><author><style face="normal" font="default"> Juurlink,D.N.</style></author><author><style face="normal" font="default"> Gomes,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Applied Health Research Centre, Li Ka Shing Knowledge Institute, St Michael's Hospital, Toronto, Ontario, Canada; Institute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada. Electronic address: tadrousm@smh.caInstitute for Clinical Evaluative Sciences, Toronto, Ontario, CanadaApplied Health Research Centre, Li Ka Shing Knowledge Institute, St Michael's Hospital, Toronto, Ontario, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario, CanadaInstitute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario, CanadaInstitute for Clinical Evaluative Sciences, Toronto, Ontario, CanadaInstitute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario, CanadaInstitute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario, Canada; Li Ka Shing Centre for Health care Analytics Research and Training, St. Michael's Hospital, Toronto, Ontario, CanadaInstitute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario, Canada; Sunnybrook Research Institute, Toronto, Ontario, CanadaApplied Health Research Centre, Li Ka Shing Knowledge Institute, St Michael's Hospital, Toronto, Ontario, Canada; Institute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario, Canada</style></auth-address><titles><title><style face="normal" font="default">Real-world health care utilization and effectiveness of omalizumab for the treatment of severe asthma</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="65" start="59">59-65</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Omalizumab is indicated for the treatment of moderate to severe asthma. There is limited observational evidence on the costs and effectiveness of omalizumab. OBJECTIVE: To examine the costs and effectiveness of omalizumab for treatment of severe asthma relative to nonusers. METHODS: We conducted a within-person repeated-measures matched cohort study in Ontario, Canada from April 1, 2012 to March 31, 2014. Continuous users of omalizumab were matched with up to 4 nonusers according to age, sex, recent specialist visits, oral corticosteroid use, asthma severity, and Charlson comorbidity score. The primary outcome was direct health care costs. Secondary outcomes were asthma-related hospitalizations or emergency department visits and oral corticosteroid use. The association between omalizumab use and each outcome was assessed using mixed-effects models adjusting for confounders. RESULTS: Ninety-five omalizumab users and 352 nonusers were matched. Among users, there was a significant increase in health care costs of $1,796 per person owing to the cost of the medication at treatment initiation (P &lt; .0001). Costs did not change significantly among nonusers ($85 increase in average monthly costs per person; P = .59). We found no significant changes in the rates of asthma-related hospitalizations or emergency department visits among omalizumab users (P = .44) or nonusers (P = .99) between pre- and postintervention periods. CONCLUSION: The use of omalizumab was associated with increased costs but no evidence of lower rates of clinically important outcomes. These results suggest omalizumab had limited effectiveness in our study population. Future studies should further explore subsets of patients most likely to benefit from omalizumab therapy</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.016.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28986124">PM:28986124</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-59-65.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-59-65.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Tadrous M</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.016.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87217</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Topcu,Z.I.K.</style></author><author><style face="normal" font="default"> Kaklikkaya,N.</style></author><author><style face="normal" font="default"> Baki,A.</style></author><author><style face="normal" font="default"> Orhan,F.</style></author></authors></contributors><titles><title><style face="normal" font="default">Characteristics of beef allergy in schoolchildren in Turkey</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Proc</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Proc</style></abbr-1></periodical><pages end="65" start="59">59-65</pages><volume><style face="normal" font="default">39</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="1" Month="1" Year="2018">2018/1/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: The prevalence of immunoglobulin E (IgE) mediated beef allergy in childhood is unknown. We investigated the prevalence and characteristics of IgE-mediated beef allergy in urban schoolchildren. METHODS: This cross-sectional study recruited 6000 randomly selected urban schoolchildren ages 6-17 years from the city center of Giresun in the eastern Black Sea region of Turkey during 2013. Children with suspected IgE-mediated beef allergy, determined by a self-administered questionnaire, after providing written consent, were skin-prick tested with commercial beef and cow's milk solutions and prick-prick tested with raw, boiled, and fried beef. Levels of serum-specific IgE to beef specific IgE and serum-specific IgE to cow's milk were determined by using fluorescent enzyme immunoassay. All children with suspected beef allergy were invited for a double-blind, placebo controlled food challenge (DBPCFC) to determine the prevalence of IgE-mediated beef allergy. RESULTS: The response rate to the questionnaire was 82.2%. The estimated prevalence of parental-reported IgE-mediated beef allergy was 2.6%. The prevalence of IgE-mediated beef allergy confirmed by DBPCFC was 0.30% (95% confidence interval, 0.18-0.5%). Positive challenge responses were observed in 70.6% (p = 0.027), 76.9% (p = 0.027), and 73.3% (p = 0.028) of the children with a positive family history of beef allergy, positive skin test results, and positive beef specific IgE values, respectively. A beef specific IgE value of >5 kUA/L alone or a combination of a positive family history of beef allergy, positive skin test results, and beef specific IgE values of >3 kUA/L yielded a positive response to DBPCFC. CONCLUSION: The presence of a family history of beef allergy, beef specific IgE value, and skin test result positivity are independently associated with positive DBPCFC results, and combined evaluation of these three parameters increased the positive predictive power of the tests</style></abstract><notes><style face="normal" font="default">IS - 1539-6304 (Electronic)IS - 1088-5412 (Linking)LA - engPT - Journal ArticleCO - Turkey -</style></notes><work-type><style face="normal" font="default">10.2500/aap.2018.39.4098</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29279061">PM:29279061</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Proc\2018-39-59-65.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Proc\2018-39-59-65.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Topcu ZI</style></custom2><misc3><style face="normal" font="default">10.2500/aap.2018.39.4098</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87244</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sanchiz,A.</style></author><author><style face="normal" font="default"> Cuadrado,C.</style></author><author><style face="normal" font="default"> Dieguez,M.C.</style></author><author><style face="normal" font="default"> Ballesteros,I.</style></author><author><style face="normal" font="default"> Rodriguez,J.</style></author><author><style face="normal" font="default"> Crespo,J.F.</style></author><author><style face="normal" font="default"> Cuevas,N.L.</style></author><author><style face="normal" font="default"> Rueda,J.</style></author><author><style face="normal" font="default"> Linacero,R.</style></author><author><style face="normal" font="default"> Cabanillas,B.</style></author><author><style face="normal" font="default"> Novak,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Food Technology, National Institute of Agricultural, Food Research, and Technology (INIA), Ctra. La Coruna Km. 7.5, 28040 Madrid, Spain</style></auth-address><titles><title><style face="normal" font="default">Thermal processing effects on the IgE-reactivity of cashew and pistachio</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="602" start="595">595-602</pages><volume><style face="normal" font="default">245</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> Food Technology</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword></keywords><dates><year Day="15" Month="4" Year="2018">2018/4/15</year></dates><abstract><style face="normal" font="default">Thermal processing can modify the structure and function of food proteins and may alter their allergenicity. This work aimed to elucidate the influence of moist thermal treatments on the IgE-reactivity of cashew and pistachio. IgE-western blot and IgE-ELISA were complemented by Skin Prick Testing (SPT) and mediator release assay to determine the IgE cross-linking capability of treated and untreated samples. Moist thermal processing diminished the IgE-binding properties of both nuts, especially after heat/pressure treatment. The wheal size in SPT was importantly reduced after application of thermally-treated samples. For cashew, heat/pressure treated-samples still retain some capacity to cross-link IgE and degranulate basophils, however, this capacity was diminished when compared with untreated cashew. For pistachio, the degranulation of basophils after challenge with the harshest heat/pressure treatment was highly decreased. Boiling produced more variable results, however this treatment applied to both nuts for 60min, led to an important decrease of basophil degranulation</style></abstract><notes><style face="normal" font="default">IS - 0308-8146 (Print)IS - 0308-8146 (Linking)LA - engPT - Journal ArticleCO - Spain -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2017.10.132</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29287414">PM:29287414</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\2018-245-595-602.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\2018-245-595-602.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171112, Sanchiz A</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2017.10.132</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87383</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Coscia,A.</style></author><author><style face="normal" font="default"> Bertino,E.</style></author><author><style face="normal" font="default"> Tonetto,P.</style></author><author><style face="normal" font="default"> Peila,C.</style></author><author><style face="normal" font="default"> Cresi,F.</style></author><author><style face="normal" font="default"> Arslanoglu,S.</style></author><author><style face="normal" font="default"> Moro,G.E.</style></author><author><style face="normal" font="default"> Spada,E.</style></author><author><style face="normal" font="default"> Milani,S.</style></author><author><style face="normal" font="default"> Giribaldi,M.</style></author><author><style face="normal" font="default"> Antoniazzi,S.</style></author><author><style face="normal" font="default"> Conti,A.</style></author><author><style face="normal" font="default"> Cavallarin,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Neonatal Unit of Turin University, City of Health and Science of Turin, Via Ventimiglia 3, 10126, Turin, Italy</style></auth-address><titles><title><style face="normal" font="default">Nutritional adequacy of a novel human milk fortifier from donkey milk in feeding preterm infants: study protocol of a randomized controlled clinical trial</style></title><secondary-title><style face="normal" font="default">Nutr J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nutr J</style></abbr-1></periodical><pages end="" start="6">6-</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="9" Month="1" Year="2018">2018/1/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: Fortification of human milk is a standard practice for feeding very low birth weight infants. However, preterm infants often still experience suboptimal growth and feeding intolerance. New fortification strategies and different commercially available fortifiers have been developed. Commercially available fortifiers are constituted by a blend of ingredients from different sources, including plant oils and bovine milk proteins, thus presenting remarkable differences in the quality of macronutrients with respect to human milk. Based on the consideration that donkey milk has been suggested as a valid alternative for children allergic to cow's milk proteins, due to its biochemical similarity to human milk, we hypothesized that donkey milk could be a suitable ingredient for developing an innovative human milk fortifier. The aim of the study is to evaluate feeding tolerance, growth and clinical short and long-term outcomes in a population of preterm infants fed with a novel multi-component fortifier and a protein concentrate derived from donkey milk, in comparison to an analogous population fed with traditional fortifier and protein supplement containing bovine milk proteins. METHODS: The study has been designed as a randomized, controlled, single-blind clinical trial. Infants born &lt;1500 g and &lt;32 weeks of gestational age were randomized to receive for 21 days either a combination of control bovine milk-based multicomponent fortifier and protein supplement, or a combination of a novel multicomponent fortifier and protein supplement derived from donkey milk. The fortification protocol followed is the same for the two groups, and the two diets were designed to be isoproteic and isocaloric. Weight, length and head circumference are measured; feeding tolerance is assessed by a standardized protocol. The occurrence of sepsis, necrotizing enterocolitis and adverse effects are monitored. DISCUSSION: This is the first clinical study investigating the use of a human milk fortifier derived from donkey milk for the nutrition of preterm infants. If donkey milk derived products will be shown to improve the feeding tolerance or either of the clinical, metabolic, neurological or auxological outcomes of preterm infants, it would be an absolute innovation in the field of feeding practices for preterm infants. TRIAL REGISTRATION: ISR</style></abstract><notes><style face="normal" font="default">IS - 1475-2891 (Electronic)IS - 1475-2891 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1186/s12937-017-0308-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29316931">PM:29316931</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nutr J\2018-17-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nutr J\2018-17-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180109, Coscia A</style></custom2><misc3><style face="normal" font="default">10.1186/s12937-017-0308-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86828</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jarupalee,T.</style></author><author><style face="normal" font="default"> Chatchatee,P.</style></author><author><style face="normal" font="default"> Komolpis,K.</style></author><author><style face="normal" font="default"> Suratannon,N.</style></author><author><style face="normal" font="default"> Roytrakul,S.</style></author><author><style face="normal" font="default"> Yingchutrakul,Y.</style></author><author><style face="normal" font="default"> Yimchuen,W.</style></author><author><style face="normal" font="default"> Butta,P.</style></author><author><style face="normal" font="default"> Jacquet,A.</style></author><author><style face="normal" font="default"> Palaga,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Graduate Program in Biotechnology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand</style></auth-address><titles><title><style face="normal" font="default">Detecting Allergens From Black Tiger Shrimp Penaeus monodon That Can Bind and Cross-link IgE by ELISA, Western Blot, and a Humanized Rat Basophilic Leukemia Reporter Cell Line RS-ATL8</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Immunol Res</style></abbr-1></periodical><pages end="76" start="62">62-76</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: Black tiger shrimp Penaeus monodon is one of the common causes of shellfish allergy that is increasing worldwide. One of the important problems in the management of shellfish allergy is the lack of accurate diagnostic assay because the biological and immunological properties of allergens in black tiger shrimp have not been well characterized. This study aims to detect proteins with the ability to bind and cross-link immunoglobulin E (IgE) from black tiger shrimp by enzyme-linked immunosorbent assay (ELISA), Western blot, and a humanized rat basophilic leukemia reporter cell line RS-ATL8. METHODS: Sera from shrimp allergic subjects were subjected to ELISA and Western blots using raw or cooked shrimp extract as antigens. Pooled sera were used to sensitize the RS-ATL8 reporter cell line and cells were activated by shrimp extract. Eluted protein extracts separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) were tested on the RS-ATL8 cell line and subjected to mass spectrometry to identify potential candidate allergens. RESULTS: Allergic sera reacted stronger to raw shrimp extract than cooked shrimp extract (P=0.009). Western blot demonstrated that major IgE reactivity protein bands were at 32-39 kDa and 91-230 kDa in both raw and cooked shrimp extracts. The eluted protein bands at the molecular weight of 38 and 115 kDa from raw shrimp extract induced IgE cross-linking as assayed by the RS-ATL8 cell line. These protein bands were subjected to mass spectrometry for analysis. Ubiquitin-activating enzyme and crustacyanin were identified as potential candidate novel shrimp allergens. CONCLUSIONS: The RS-ATL8 reporter cell line can be used to identify potential new shrimp allergens that can functionally cross-link IgE and induce mast cell degranulation</style></abstract><notes><style face="normal" font="default">IS - 2092-7355 (Print)IS - 2092-7355 (Linking)LA - engPT - Journal ArticleCO - Thailand -</style></notes><work-type><style face="normal" font="default">10.4168/aair.2018.10.1.62</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29178679">PM:29178679</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-62-76.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-62-76.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Jarupalee T</style></custom2><misc3><style face="normal" font="default">10.4168/aair.2018.10.1.62</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86738</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Robinson,M.L.</style></author><author><style face="normal" font="default"> Lanser,B.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, National Jewish Health, 1400 Jackson Street, K830, Denver, CO 80206, USA</style></auth-address><titles><title><style face="normal" font="default">The Role of Baked Egg and Milk in the Diets of Allergic Children</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="76" start="65">65-76</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">Baked egg and baked milk are tolerated by most children who are allergic to hen's egg and cow's milk. Incorporating baked goods into the diets of allergic children may help them outgrow their primary allergy more quickly, with changes observed akin to immunotherapy. Benefits may also include increased quality of life and improved nutritional status. The search for a reliable biomarker to predict tolerance to baked goods is ongoing. Most children with a milk or egg allergy who are not previously tolerating egg or milk in baked goods should be offered an observed oral food challenge</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132675">PM:29132675</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-65-76.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-65-76.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Robinson ML</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86721</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jogi,N.O.</style></author><author><style face="normal" font="default"> Svanes,C.</style></author><author><style face="normal" font="default"> Siiak,S.P.</style></author><author><style face="normal" font="default"> Logan,E.</style></author><author><style face="normal" font="default"> Holloway,J.W.</style></author><author><style face="normal" font="default"> Igland,J.</style></author><author><style face="normal" font="default"> Johannessen,A.</style></author><author><style face="normal" font="default"> Levin,M.</style></author><author><style face="normal" font="default"> Real,F.G.</style></author><author><style face="normal" font="default"> Schlunssen,V.</style></author><author><style face="normal" font="default"> Horsnell,W.G.C.</style></author><author><style face="normal" font="default"> Bertelsen,R.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Tartu, Tartu, Estonia</style></auth-address><titles><title><style face="normal" font="default">Zoonotic helminth exposure and risk of allergic diseases: a study of two generations in Norway</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="77" start="66">66-77</pages><volume><style face="normal" font="default">48</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Animal and human studies indicate that definitive host helminth infections may confer protection from allergies. However, zoonotic helminths, such as Toxocara species (spp.), have been associated with increased allergies. OBJECTIVE: We describe the prevalence of Toxocara spp. and Ascaris spp. seropositivity, and associations with allergic diseases and sensitisation, in two generations in Bergen, Norway. METHODS: Serum levels of total IgG4, anti-Toxocara spp. IgG4 and Ascaris spp. IgG4 were established by ELISA in two cohorts; parents born 1945-1972 (n=171) and their offspring born 1969-2003 (n=264). Allergic outcomes and covariates were recorded through interviews and clinical examinations including serum IgEs and skin prick tests. RESULTS: Anti-Ascaris spp. IgG4 was detected in 29.2% of parents and 10.3% of offspring, and anti-Toxocara spp. IgG4 in 17.5% and 8.0% of parents and offspring, respectively. Among offspring anti-Toxocara spp. IgG4 was associated with pet keeping before age 15 (OR=6.15; 95% CI=1.37-27.5) and increasing BMI (1.16[1.06-1.25] per kg/m2 ). Toxocara spp. seropositivity was associated with wheeze (2.97[1.45- 7.76]), hay fever (4.03[1.63-9.95]), eczema (2.89[1.08-7.76]) and cat sensitization (5.65[1.92-16.6]) among offspring, but was not associated with allergic outcomes among parents. Adjustment for childhood or current pet keeping did not alter associations with allergies. Parental Toxocara spp. seropositivity was associated with increased offspring allergies following a sex-specific pattern. CONCLUSIONS &amp; CLINICAL RELEVANCE: Zoonotic helminth exposure in Norway was less frequent in offspring than parents; however, Toxocara spp. seropositivity was associated with increased risk of allergic manifestations in the offspring generation, but not among parents. Changes in response to helminth exposure may provide insights into the increase in allergy incidence in affluent countries. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Estonia -CO - Norway -CO - South Africa -CO - United KIngdom -CO - Norway -CO - Denmark -CO - France -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13055</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29117468">PM:29117468</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171108-JogiNO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171108-JogiNO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Jogi NO</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13055</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87218</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jerzynska,J.</style></author><author><style face="normal" font="default"> Stelmach,W.</style></author><author><style face="normal" font="default"> Majak,P.</style></author><author><style face="normal" font="default"> Stelmach,R.</style></author><author><style face="normal" font="default"> Janas,A.</style></author><author><style face="normal" font="default"> Stelmach,I.</style></author></authors></contributors><titles><title><style face="normal" font="default">Comparison of the effect of 5-grass pollen sublingual immunotherapy tablets and drops in children with rhinoconjunctivitis</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Proc</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Proc</style></abbr-1></periodical><pages end="73" start="66">66-73</pages><volume><style face="normal" font="default">39</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="1" Month="1" Year="2018">2018/1/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: One of the most important aspects of sublingual immunotherapy (SLIT) is the regimen of administration. AIM: To find any differences in symptom-medication scores between the two groups of SLIT tablets and drops, given pre-coseasonally (starting 8 weeks before the pollen season) in children with rhinoconjunctivitis allergy to grass pollen. The secondary outcome were the differences in lung function and induction of T-regulatory forkhead box P3 (FOXP3) positive cells. METHODS: This was a retrospective, secondary analysis of pooled data obtained from our two prospective randomized placebo controlled trials that involved children who underwent SLIT. Forty-one children, ages 6-18 years, with allergic rhinitis (AR), sensitive to grass pollen, participated in the study. RESULTS: Treatment with both tablets and drops significantly reduced all symptoms (nasal, asthma, and ocular) within the groups; there was no significant difference between both groups. When compared with the tablet therapy, there was a trend for drops therapy to be more effective in the reduction of combined symptom-medication score, but the difference was not statistically significant (p = 0.1036); there was no significant difference in asthma and nasal scores. We showed a significant decrease in the fractional exhaled nitric oxide level comparable in both immunotherapy groups. There were no differences between the groups in the induction of CD4+ CD25+ FOXP3+-positive cells in peripheral blood. CONCLUSIONS: Both protocols showed similar decreases in symptom-medication scores; however, when compared with tablet therapy, there was a trend for drops therapy to be more effective in the reduction of combined symptom-medication score</style></abstract><notes><style face="normal" font="default">IS - 1539-6304 (Electronic)IS - 1088-5412 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.2500/aap.2018.39.4099</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29279062">PM:29279062</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Proc\2018-39-66-73.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Proc\2018-39-66-73.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Jerzynska J</style></custom2><misc3><style face="normal" font="default">10.2500/aap.2018.39.4099</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87276</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jabs,F.</style></author><author><style face="normal" font="default"> Plum,M.</style></author><author><style face="normal" font="default"> Laursen,N.S.</style></author><author><style face="normal" font="default"> Jensen,R.K.</style></author><author><style face="normal" font="default"> Molgaard,B.</style></author><author><style face="normal" font="default"> Miehe,M.</style></author><author><style face="normal" font="default"> Mandolesi,M.</style></author><author><style face="normal" font="default"> Rauber,M.M.</style></author><author><style face="normal" font="default"> Pfutzner,W.</style></author><author><style face="normal" font="default"> Jakob,T.</style></author><author><style face="normal" font="default"> Mobs,C.</style></author><author><style face="normal" font="default"> Andersen,G.R.</style></author><author><style face="normal" font="default"> Spillner,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunological Engineering, Department of Engineering, Aarhus University, 8000, Aarhus, Denmark</style></auth-address><titles><title><style face="normal" font="default">Trapping IgE in a closed conformation by mimicking CD23 binding prevents and disrupts FcepsilonRI interaction</style></title><secondary-title><style face="normal" font="default">Nat Commun</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nat Commun</style></abbr-1></periodical><pages end="" start="7">7-</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Conformation</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="2" Month="1" Year="2018">2018/1/2</year></dates><abstract><style face="normal" font="default">Anti-IgE therapeutics interfere with the ability of IgE to bind to its receptors on effector cells. Here we report the crystal structure of an anti-IgE single-domain antibody in complex with an IgE Fc fragment, revealing how the antibody inhibits interactions between IgE and the two receptors FcepsilonRI and CD23. The epitope overlaps only slightly with the FcepsilonRI-binding site but significantly with the CD23-binding site. Solution scattering studies of the IgE Fc reveal that antibody binding induces a half-bent conformation in between the well-known bent and extended IgE Fc conformations. The antibody acts as functional homolog of CD23 and induces a closed conformation of IgE Fc incompatible with FcepsilonRI binding. Notably the antibody displaces IgE from both CD23 and FcepsilonRI, and abrogates allergen-mediated basophil activation and facilitated allergen binding. The inhibitory mechanism might facilitate strategies for the future development of anti-IgE therapeutics for treatment of allergic diseases</style></abstract><notes><style face="normal" font="default">IS - 2041-1723 (Electronic)IS - 2041-1723 (Linking)LA - engPT - Journal ArticleCO - Denmark -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1038/s41467-017-02312-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29295972">PM:29295972</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nat Commun\2018-9-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nat Commun\2018-9-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Jabs F</style></custom2><misc3><style face="normal" font="default">10.1038/s41467-017-02312-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87045</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Greenhawt,M.</style></author><author><style face="normal" font="default"> DunnGalvin,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Clinical Immunology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan; Department of Pediatrics, Child Health Evaluation and Research Unit, University of Michigan Medical School, Ann Arbor, Michigan; Department of Pediatrics, Section of Allergy and Immunology, Children's Hospital Colorado, University of Colorado School of Medicine, Aurora, Colorado. Electronic address: Matthew.Greenhawt@childrenscolorado.orgDepartment of Pediatrics &amp; Child Health, University College Cork, Cork, Ireland</style></auth-address><titles><title><style face="normal" font="default">Preliminary psychometric analyses and clinical performance of a caregiver self-efficacy scale for food allergy self-management</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="79" start="73">73-79</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: Food allergy health-related quality of life has been defined, but self-efficacy is poorly described. OBJECTIVE: To examine the preliminary reliability, validity, and clinical performance of a novel food allergy self-efficacy index. METHODS: An 8-item Food Allergy Self-Efficacy Questionnaire (FASEQ) was adapted for food allergy-related themes and coadministered with the Food Allergy Quality of Life Parental Burden (FAQL-PB) index to caregivers self-reporting a food allergic child (group A) and those with children followed up at a food allergy referral center clinic (group B). FASEQ split-half reliability, 2-week recall, factor analysis, and construct and discriminative validity were assessed. Multiple linear regression was used to explore predictive associations between the FAQL-PB and the FASEQ. RESULTS: Among 2,308 caregivers, the mean FASEQ score was 2.69 (95% CI, 2.66-2.73) and was lower (better) among group A (mean FASEQ score, 2.52; 95% CI, 2.49-2.56) vs group B (mean FASEQ score, 3.75; 95% CI, 3.66-3.84; P &lt; .001). The FASEQ Cronbach alpha was 0.87, and the 2-week intraclass correlation coefficient (ICC) was 0.75. Total and 6 of 8 individual FASEQ domain scores were significantly lower among caregivers with children having anaphylaxis or epinephrine use vs none and peanut or tree nut allergy vs milk or egg allergy, demonstrating good discriminative validity. Total FASEQ score was associated with FAQL-PB score (ICC, 0.13; 95% CI, 0.06-0.19; P &lt; .001), with 6 of 8 FASEQ individual domains significantly associated (ICC range, -0.17 to 0.3; P &lt; .01 for all). Factor analysis revealed 2 domains (medical care and social functioning) with construct validity. CONCLUSION: We present preliminary evidence the FASEQ is a valid tool to assess caregiver food allergy self-efficacy. Self-efficacy is a distinct but related concept that captures aspects of self-management that are an important companion to health-related quality of life</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Ireland -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.060</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273132">PM:29273132</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-73-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-73-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Greenhawt M</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.060</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86742</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Parrish,C.P.</style></author><author><style face="normal" font="default"> Kim,E.H.</style></author><author><style face="normal" font="default"> Bird,J.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Food Allergy Center at Children's Medical Center, 1935 Medical District Drive, Dallas, TX 75235, USA</style></auth-address><titles><title><style face="normal" font="default">Interventional Therapies for the Treatment of Food Allergy</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="88" start="77">77-88</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">Treatment of IgE-mediated food allergies is limited to allergen avoidance and emergency treatment on accidental ingestion, which is not uncommon. In recent years, interest in interventional therapies to treat food allergy has increased significantly. Although oral, sublingual, and epicutaneous immunotherapy have shown promise in studies, none is approved as therapy for food allergy to date and questions remain regarding efficacy, safety, dosing, and duration of therapy</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.006</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132676">PM:29132676</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-77-88.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-77-88.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Parrish CP</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86826</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kaminuma,O.</style></author><author><style face="normal" font="default"> Nishimura,T.</style></author><author><style face="normal" font="default"> Kitamura,N.</style></author><author><style face="normal" font="default"> Saeki,M.</style></author><author><style face="normal" font="default"> Hiroi,T.</style></author><author><style face="normal" font="default"> Mori,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Center for Life Science Research, University of Yamanashi, Yamanashi, Japan</style></auth-address><titles><title><style face="normal" font="default">T-Helper Type 2 Cells Direct Antigen-Induced Eosinophilic Skin Inflammation in Mice</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Immunol Res</style></abbr-1></periodical><pages end="82" start="77">77-82</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Eosinophilic inflammation in combination with immunoglobulin E (IgE) production is a characteristic feature of atopic dermatitis. Although activated T-helper type (Th) 2 cells play critical roles in the local accumulation and activation of eosinophils, whether they induce eosinophilic skin inflammation, independent of the IgE-mediated pathway has been unclear. To address the functional role of T cells in allergic skin diseases, we herein transferred Th1/Th2-differentiated or naive DO11.10 T cells into unprimed BALB/c mice. Ovalbumin-specific Th2 cells, as well as eosinophils, accumulated in the skin upon antigen challenge, despite the absence of antigen-specific IgE. Neither antigen-specific Th1 nor naive T cells induced eosinophil accumulation, although Th1 cells by themselves migrated into the skin. Interleukin (IL)-4, IL-5, and eotaxin were specifically produced in the skin of antigen-challenged, Th2 cell-transferred mice, whereas interferon (IFN)-gamma and regulated on activation, normal T cell expressed and secreted (RANTES) were preferentially produced in Th1 cells-transferred mice. Production of monocyte chemoattractant protein (MCP)-1 and MCP-3 was enhanced by both Th1 and Th2 cells. The accumulation of eosinophils and Th2 cells in the skin was suppressed by both dexamethasone and FK506, indicating an essential role of Th2 cells in eosinophil recruitment. We conclude that Th2 cells can induce eosinophilic infiltration into the skin in the absence of antigen-specific IgE</style></abstract><notes><style face="normal" font="default">IS - 2092-7355 (Print)IS - 2092-7355 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.4168/aair.2018.10.1.77</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29178680">PM:29178680</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-77-82.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-77-82.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Kaminuma O</style></custom2><misc3><style face="normal" font="default">10.4168/aair.2018.10.1.77</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87043</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shtessel,M.</style></author><author><style face="normal" font="default"> Tversky,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, Division of Allergy and Clinical Immunology, Johns Hopkins University, Baltimore, Maryland</style></auth-address><titles><title><style face="normal" font="default">Reliability of allergy skin testing</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="83" start="80">80-83</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: Percutaneous allergen skin testing remains an established benchmark for diagnosing atopic disease. The reliability of skin testing depends greatly on the performance of allergen extracts used, methods used, and the presence of antihistamine medications. OBJECTIVE: To determine the differential effect of cetirizine on 2 different concentrations of histamine control solution and 5 common allergens used for percutaneous skin testing. METHODS: Twelve individuals underwent skin testing with histamine (1 and 6 mg/mL), control diluent, and 5 common aeroallergens. Wheal and flare measurements were measured in a masked fashion by a single operator. Cetirizine was administered for 4 consecutive days to determine the effect on both histamine and allergen wheal and flare responses. RESULTS: A total of 384 skin tests were performed on 12 volunteers. Cetirizine began to suppress wheal and flare responses at 1 hour (P &lt; .05), with maximum suppression at day 5 (P &lt; .05). Wheal and flare responses returned to greater than 90% baseline within 4 days of not taking cetirizine. Suppression was more apparent with 1 vs 6 mg/mL of histamine (62% vs 33%). Four of the 12 individuals taking cetirizine had a positive skin test result using 6 mg/mL of histamine control when the 1-mg/mL histamine test result was negative. Importantly, twice as many individuals had false-negative allergen responses using 6 mg/mL of histamine vs the 1 mg/mL as a positive control, although this finding did not reach statistical significance. CONCLUSION: The use of a 6-mg/mL histamine control for some percutaneous skin test devices may result in more false-negative allergen responses because of the inability to detect the presence of antihistamines</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">    10.1016/j.anai.2017.10.015</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273134">PM:29273134</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-80-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-80-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Shtessel M</style></custom2><misc3><style face="normal" font="default">    10.1016/j.anai.2017.10.015</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87446</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">An,T.J.</style></author><author><style face="normal" font="default"> Rhee,C.K.</style></author><author><style face="normal" font="default"> Kim,J.H.</style></author><author><style face="normal" font="default"> Lee,Y.R.</style></author><author><style face="normal" font="default"> Chon,J.Y.</style></author><author><style face="normal" font="default"> Park,C.K.</style></author><author><style face="normal" font="default"> Yoon,H.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pulmonary, Allergy and Critical Care Medicine, Department of Internal Medicine, Yeouido St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea</style></auth-address><titles><title><style face="normal" font="default">Effects of Macrolide and Corticosteroid in Neutrophilic Asthma Mouse Model</style></title><secondary-title><style face="normal" font="default">Tuberc Respir Dis (Seoul)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Tuberc Respir Dis (Seoul)</style></abbr-1></periodical><pages end="87" start="80">80-87</pages><volume><style face="normal" font="default">81</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: Asthma is a disease of chronic airway inflammation with heterogeneous features. Neutrophilic asthma is corticosteroid-insensitive asthma related to absence or suppression of TH2 process and increased TH1 and/or TH17 process. Macrolides are immunomodulatory drug that reduce airway inflammation, but their role in asthma is not fully known. The purpose of this study was to evaluate the role of macrolides in neutrophilic asthma and compare their effects with those of corticosteroids. METHODS: C57BL/6 female mice were sensitized with ovalbumin (OVA) and lipopolysaccharides (LPS). Clarithromycin (CAM) and/or dexamethasone (DXM) were administered at days 14, 15, 21, 22, and 23. At day 24, the mice were sacrificed. RESULTS: Airway resistance in the OVA+LPS exposed mice was elevated but was more attenuated after treatment with CAM+DXM compared with the monotherapy group (p&lt;0.05 and p&lt;0.01). In bronchoalveolar lavage fluid study, total cells and neutrophil counts in OVA+LPS mice were elevated but decreased after CAM+DXM treatment. In hematoxylin and eosin stain, the CAM+DXM-treated group showed less inflammation additively than the monotherapy group. There was less total protein, interleukin 17 (IL-17), interferon gamma, and tumor necrosis factor alpha in the CAM+DXM group than in the monotherapy group (p&lt;0.001, p&lt;0.05, and p&lt;0.001). More histone deacetylase 2 (HDAC2) activity was recovered in the DXM and CAM+DXM challenged groups than in the control group (p&lt;0.05). CONCLUSION: Decreased IL-17 and recovered relative HDAC2 activity correlated with airway resistance and inflammation in a neutrophilic asthma mouse model. This result suggests macrolides as a potential corticosteroid-sparing agent in neutrophilic asthma</style></abstract><notes><style face="normal" font="default">IS - 1738-3536 (Print)IS - 1738-3536 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4046/trd.2017.0108</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29332324">PM:29332324</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Tuberc Respir Dis (Seoul)\2018-81-80-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Tuberc Respir Dis (Seoul)\2018-81-80-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180112, An TJ</style></custom2><misc3><style face="normal" font="default">10.4046/trd.2017.0108</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87272</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jeong,S.Y.</style></author><author><style face="normal" font="default"> Lee,J.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">College of Pharmacy, Chung-Ang University, Seoul 06974, KoreaCollege of Pharmacy, Chung-Ang University, Seoul 06974, Korea</style></auth-address><titles><title><style face="normal" font="default">Inhibitory effects of 2,6-di-tert-butyl-4-hydroxymethylphenol on asthmatic responses to ovalbumin challenge in conscious guinea pigs</style></title><secondary-title><style face="normal" font="default">Korean J Physiol Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Korean J Physiol Pharmacol</style></abbr-1></periodical><pages end="89" start="81">81-89</pages><volume><style face="normal" font="default">22</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">This study evaluated the anti-asthmatic activities of 2,6-di-tert-butyl-4-hydroxymethylphenol (DBHP) that is a potent phenolic antioxidant in edible vegetable oil. The effects of DBHP on bronchial asthma were evaluated by determining the specific airway resistance (sRaw) and tidal volume (TV) during the immediate asthmatic response (IAR) and the late-phase asthmatic response (LAR) in guinea pigs with aerosolized ovalbumin-induced asthma. Recruitment of leukocytes and the levels of biochemical inflammatory mediators were determined in the bronchoalveolar lavage fluids (BALFs), and histopathological surveys performed in lung tissues. DBHP significantly inhibited the increased sRaw and improved the decreased TV on IAR and LAR, and also inhibited recruitment of eosinophils and neutrophils into the lung, and release of biochemical inflammatory mediators such as histamine and phospholipase A2 from these infiltrated leukocytes, and improved pathological changes. However, anti-asthmatic activities of DBHP at oral doses of 12.5 to 50 mg/kg was less than those of dexamethasone (5 mg/kg, p.o.) and cromoglycate (10 mg/kg, p.o.), but more potent or similar to that of salbutamol (5 mg/kg, p.o.). These results in the present study suggest that anti-asthmatic effects of DBHP in the guinea pigs model of OVA-induced asthmatic responses principally are mediated by inhibiting the recruitments of the leukocytes and the release of biochemical inflammatory mediators from these infiltrated leukocytes</style></abstract><notes><style face="normal" font="default">IS - 1226-4512 (Print)IS - 1226-4512 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4196/kjpp.2018.22.1.81</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29302215">PM:29302215</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Korean J Physiol Pharmacol\2018-22-81-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Korean J Physiol Pharmacol\2018-22-81-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Jeong SY</style></custom2><misc3><style face="normal" font="default">10.4196/kjpp.2018.22.1.81</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87415</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">no authors</style></author></authors></contributors><titles><title><style face="normal" font="default">[Food allergy in children: recommendations for diagnosis and treatment]</style></title><secondary-title><style face="normal" font="default">Arch Argent Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arch Argent Pediatr</style></abbr-1></periodical><pages end="" start="82">82-</pages><volume><style face="normal" font="default">116</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword></keywords><dates><year Day="1" Month="2" Year="2018">2018/2/1</year></dates><abstract><style face="normal" font="default">Food allergy arises from a specific immune response induced by food exposure. It is the first cause of anaphylaxis in childhood. Its prevalence increased exponentially in western countries. The proteins most frequently involved in infants are cow's milk and hen's egg; and in adults, seafood. Peanuts have the same frequency in both groups. The clinical manifestations and methodology of study are directly related to the pathophysiology of the disease. Clinical history, skin prick test, patch test, and food oral challenge are essential to arrive at a correct diagnosis, that will avoid unnecessary exclusions or exposures that carry life risk. The treatment is based on the correct avoidance of responsible food (considering hidden allergens), besides patient and their care giver's education, to maintain a good quality of life</style></abstract><notes><style face="normal" font="default">IS - 1668-3501 (Electronic)IS - 0325-0075 (Linking)LA - spaPT - English AbstractPT - Journal ArticleCO - Argentina -</style></notes><work-type><style face="normal" font="default">10.5546/aap.2018.S1</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29333846">PM:29333846</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Arch Argent Pediatr\2018-116-82.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Arch Argent Pediatr\2018-116-82.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180101, no authors</style></custom2><misc3><style face="normal" font="default">10.5546/aap.2018.S1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86827</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,Y.S.</style></author><author><style face="normal" font="default"> Park,S.H.</style></author><author><style face="normal" font="default"> Han,K.</style></author><author><style face="normal" font="default"> Lee,J.H.</style></author><author><style face="normal" font="default"> Kim,N.I.</style></author><author><style face="normal" font="default"> Roh,J.Y.</style></author><author><style face="normal" font="default"> Seo,S.J.</style></author><author><style face="normal" font="default"> Song,H.J.</style></author><author><style face="normal" font="default"> Lee,M.G.</style></author><author><style face="normal" font="default"> Choi,J.H.</style></author><author><style face="normal" font="default"> Park,Y.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, The Catholic University of Korea College of Medicine, Seoul, Korea</style></auth-address><titles><title><style face="normal" font="default">Clinical Course of Chronic Spontaneous Urticaria in the Korean Adult Population</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Immunol Res</style></abbr-1></periodical><pages end="87" start="83">83-87</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Knowledge of the clinical course of chronic spontaneous urticaria (CSU) remains unclear. The purpose of our study was to investigate the clinical course of CSU in the Korean adult population. Each patient in the CSU group who was defined by disease codes between 2003 and 2007 was tracked whether he or she went into remission or not until 2013. Kaplan-Meier survival analysis was carried out to analyze remission, and log-rank tests were performed for between-group comparisons. Demographic differences between subjects who went into remission 1 year after the initial diagnosis and those who did not were analyzed using chi(2) tests. A total of 13,969 subjects were included in the CSU group. The 1-, 2-, 3-, 4-, and 5-year remission rates of CSU were 21.5%, 33.0%, 38.9%, 42.6%, and 44.6%, respectively. The proportion of subjects in the 65+ age group (P=0.050) and with male gender (P=0.002) was significantly higher among subjects who did not go into remission 1 year after the initial diagnosis. Our study indicates that CSU could have a more persistent course than previously reported</style></abstract><notes><style face="normal" font="default">IS - 2092-7355 (Print)IS - 2092-7355 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4168/aair.2018.10.1.83</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29178681">PM:29178681</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-83-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Immunol Res\2018-10-83-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Kim YS</style></custom2><misc3><style face="normal" font="default">10.4168/aair.2018.10.1.83</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87041</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kannan,S.</style></author><author><style face="normal" font="default"> Perzanowski,M.S.</style></author><author><style face="normal" font="default"> Ganguri,H.B.</style></author><author><style face="normal" font="default"> Acevedo-Garcia,D.</style></author><author><style face="normal" font="default"> Acosta,L.M.</style></author><author><style face="normal" font="default"> Spatcher,M.</style></author><author><style face="normal" font="default"> Divjan,A.</style></author><author><style face="normal" font="default"> Chew,G.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Nutrition, School of Public Health and Health Sciences, University of Massachusetts, Amherst, Massachusetts</style></auth-address><titles><title><style face="normal" font="default">Complex relationships between vitamin D and allergic sensitization among Puerto Rican 2-year-old children</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="89" start="84">84-89</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: In the United States, Puerto Ricans have a higher prevalence of asthma than other Latino ethnicities. Low vitamin D levels for children living in northern climates could be a factor. OBJECTIVE: To assess serum 25-hydroxyvitamin D [25(OH)D] distributions (a marker of vitamin D) and associations among vitamin D, allergic sensitization, early wheeze, and home/demographic factors. METHODS: Puerto Rican infants born in New York City, with a maternal history of atopy, were enrolled in a birth cohort. Blood was collected at age 2 years (n = 154; 82 males and 72 females). Serum 25(OH)D and immunoglobulin E (IgE) (indoor allergen-specific and total) were determined using immunoassays. Home/demographic characteristics and respiratory symptoms were assessed by questionnaire. RESULTS: The median concentration of 25(OH)D was 22.6 ng/mL; 32% were at risk of deficiency or inadequacy (&lt;12 or 12-19 ng/mL). Serum 25(OH)D levels were lower in the heating (a surrogate for less sun exposure in colder months) compared with nonheating (26.1 vs 22.7 ng/mL, P = .02) season, but were not associated with allergen-specific IgE levels or with level of acculturation (measured by maternal birthplace). However, low 25(OH)D levels (below median) were associated with high total IgE >100 IU/mL (P = .01). Also, 25(OH)D concentrations differed between children who attended daycare and those who did not (21.8 vs 24.5 ng/mL; t test, P = .02). Serum 25(OH)D was not associated with wheeze or asthma by 2 years of age (P = .43). CONCLUSION: Vitamin D deficiency, possibly linked with allergic pathways, may partially explain the trajectory for disproportionate asthma burden among Puerto Ricans, especially those born and raised in colder climates</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.027</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273135">PM:29273135</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-84-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-84-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Kannan S</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.027</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86969</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Perez-Riverol,A.</style></author><author><style face="normal" font="default"> Fernandes,L.G.R.</style></author><author><style face="normal" font="default"> Musacchio Lasa,A.</style></author><author><style face="normal" font="default"> Dos Santos-Pinto,J.R.A.</style></author><author><style face="normal" font="default"> Moitinho,A.D.</style></author><author><style face="normal" font="default"> Izuka Moraes,G.H.</style></author><author><style face="normal" font="default"> Jabs,F.</style></author><author><style face="normal" font="default"> Miehe,M.</style></author><author><style face="normal" font="default"> Seismman,H.</style></author><author><style face="normal" font="default"> Palma,M.S.</style></author><author><style face="normal" font="default"> de Lima,Z.R.</style></author><author><style face="normal" font="default"> Spillner,E.</style></author><author><style face="normal" font="default"> Brochetto-Braga,M.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratorio de Biologia Molecular de Artropodes-LBMA-IBRC-UNESP (Univ Estadual Paulista), Av. 24-A, n_1515, CEP 13506-900, Bela Vista, Rio Claro, SP, Brazil.</style></auth-address><titles><title><style face="normal" font="default">Phospholipase A1-based cross-reactivity among venoms of clinically relevant Hymenoptera from Neotropical and temperate regions</style></title><secondary-title><style face="normal" font="default">Mol Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Immunol</style></abbr-1></periodical><pages end="93" start="87">87-93</pages><volume><style face="normal" font="default">93</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Honeybee</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Molecular cross-reactivity caused by allergen homology or cross-reactive carbohydrate determinants (CCDs) is a major challenge for diagnosis and immunotherapy of insect venom allergy. Venom phospholipases A1 (PLA1s) are classical, mostly non-glycosylated wasp and ant allergens that provide diagnostic benefit for differentiation of genuine sensitizations from cross-reactivity. As CCD-free molecules, venom PLA1s are not causative for CCD-based cross-reactivity. Little is known however about the protein-based cross-reactivity of PLA1 within vespid species. Here, we address PLA1-based cross-reactivity among ten clinically relevant Hymenoptera venoms from Neotropical and temperate regions including Polybia paulista (paulistinha) venom and Vespula vulgaris (yellow jacket) venom. In order to evaluate cross-reactivity, sera of mice sensitized with recombinant PLA1 (rPoly p 1) from P. paulista wasp venom were used. Pronounced IgE and IgG based cross-reactivity was detected for wasp venoms regardless the geographical region of origin. The cross-reactivity correlated well with the identity of the primary sequence and 3-D models of PLA1 proteins. In contrast, these mice sera showed no reaction with honeybee (HBV) and fire ant venom. Furthermore, sera from patients monosensitized to HBV and fire ants did not recognize the rPoly p 1 in immunoblotting. Our findings reveal the presence of conserved epitopes in the PLA1s from several clinically relevant wasps as major cause of PLA1-based in vitro cross-reactivity. These findings emphasize the limitations but also the potential of PLA1-based HVA diagnostics</style></abstract><notes><style face="normal" font="default">IS - 1872-9142 (Electronic)IS - 0161-5890 (Linking)LA - engPT - Journal ArticleCO - Brazil -CO - Cuba -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1016/j.molimm.2017.11.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29156294">PM:29156294</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Immunol\2018-93-87-93.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Immunol\2018-93-87-93.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Perez-Riverol A</style></custom2><misc3><style face="normal" font="default">10.1016/j.molimm.2017.11.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87442</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nieuwenhuizen,E.N.</style></author><author><style face="normal" font="default"> Kirstein,F.</style></author><author><style face="normal" font="default"> Hoving,J.C.</style></author><author><style face="normal" font="default"> Brombacher,F.</style></author></authors></contributors><auth-address><style face="normal" font="default">International Centre for Genetic Engineering and Biotechnology (ICGEB), Cape Town component, University of Cape Town, Cape Town, South Africa.</style></auth-address><titles><title><style face="normal" font="default">House dust mite induced allergic airway disease is attenuated in CD11c(cre)IL-4Ralpha(-/l) degrees (x) mice</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="885">885-</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">The precise mechanisms leading to development of T helper type (Th)2-driven allergic responses are unknown. We aimed to determine how IL-4 receptor alpha (IL-4Ralpha) signaling on CD11c(+) cells influences allergen-induced Th2 responses in mice. CD11c(cre)IL-4Ralpha(-/l) degrees (x) mice, deficient in IL-4Ralpha on dendritic cells and alveolar macrophages, were compared to IL-4Ralpha(-/l) degrees (x) littermate controls in models of allergic airway disease induced by OVA/alum, OVA alone or house dust mite. Cytokine responses, eosinophil and neutrophil infiltration into the lungs, airway hyperreactivity and mucus hypersecretion were evaluated after allergen challenge. In the OVA/alum model, CD11c(cre)IL-4Ralpha(-/lox) mice had similar airway hyperreactivity, eosinophil infiltration, Th2-type cytokine production and mucus hypersecretion to littermate controls. When alum was omitted during sensitization, CD11c(cre)IL-4Ralpha(-/lox) mice had similar airway hyperreactivity and mucus secretion but reduced Th2-type cytokine production and eosinophils, suggesting alum overrides the requirement for IL-4Ralpha signaling on CD11c(+) cells in enhancing Th2-type responses. In the house dust mite model, CD11c(cre)IL-4Ralpha(-/lox) mice showed similar mucus secretion, but reduced Th2 responses, eosinophils, neutrophils and airway hyperreactivity, unlike previously tested LysM(cre)IL-4Ralpha(-/lox) mice, which lack IL-4Ralpha on alveolar macrophages but not on dendritic cells. Therefore, our results indicate that IL-4Ralpha signaling on dendritic cells promotes allergen-induced Th2 responses and eosinophil infiltration into the lung</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - South Africa -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-19060-9</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29343807">PM:29343807</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2018-8-885.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2018-8-885.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Nieuwenhuizen EN</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-19060-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86743</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Loh,W.</style></author><author><style face="normal" font="default"> Tang,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy and Immune Disorders, Murdoch Children's Research Institute, Flemington Road, Parkville, Melbourne, Victoria 3052, Australia</style></auth-address><titles><title><style face="normal" font="default">Adjuvant Therapies in Food Immunotherapy</style></title><secondary-title><style face="normal" font="default">Immunol Allergy Clin North Am</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Allergy Clin North Am</style></abbr-1></periodical><pages end="101" start="89">89-101</pages><volume><style face="normal" font="default">38</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">Finding an effective curative treatment for food allergy is a research priority. Although oral immunotherapy (OIT) is effective at inducing desensitization, the temporary nature of this effect and high rates of adverse reactions have highlighted a need for novel strategies to improve tolerance induction and safety. One such strategy is the use of an adjuvant together with food immunotherapy to either suppress allergic reactions and/or modulate the underlying allergic immune response. In particular, the use of bacterial adjuvants seems to be a promising means of enhancing OIT-induced sustained unresponsiveness and warrants further investigation</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1557-8607 (Electronic)IS - 0889-8561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Australia -CO - Singapore -</style></notes><work-type><style face="normal" font="default">10.1016/j.iac.2017.09.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132677">PM:29132677</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-89-101.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Allergy Clin North Am\2018-38-89-101.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Loh W</style></custom2><misc3><style face="normal" font="default">10.1016/j.iac.2017.09.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87078</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Carrera,M.</style></author><author><style face="normal" font="default"> Canas,B.</style></author><author><style face="normal" font="default"> Gallardo,J.M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Advanced proteomics and systems biology applied to study food allergy</style></title><secondary-title><style face="normal" font="default">Curr Opin Food Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Food Sci</style></abbr-1></periodical><pages end="16" start="9">9-16</pages><volume><style face="normal" font="default">22</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="8" Year="2018">2018/8</year></dates><isbn><style face="normal" font="default">2214-7993</style></isbn><abstract><style face="normal" font="default">Food allergy is considered to be the fourth most important public health problem by the World Health Organization (WHO). As a consequence, accurate, sensitive and fast detection methods for food allergy control and investigation are highly recommendable. In this work, we present a short overview of the applications of the Advanced Proteomics and Systems Biology approaches for the study and control of food allergy. For this purpose, two consecutive proteomics strategies (Discovery and Targeted Proteomics) applied for the study and control of food allergy are reviewed in detail. In addition, from an integrative point of view, the emergence proteomics-based systems biology approaches applied for the study of the mechanisms of food allergy are described. Future directions and new perspectives are also provided</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.cofs.2017.12.001</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.cofs.2017.12.001</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Food Sci\2018-22-9-16.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Food Sci\2018-22-9-16.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171211, Carrera M</style></custom2><misc3><style face="normal" font="default">10.1016/j.cofs.2017.12.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87377</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ahluwalia,S.K.</style></author><author><style face="normal" font="default"> Matsui,E.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Uniformed Services University of the Heath Sciences, Bethesda, Md; Allergy, Immunology, and Immunizations Service, Walter Reed National Military Medical Center, Bethesda, Md</style></auth-address><titles><title><style face="normal" font="default">Indoor Environmental Interventions for Furry Pet Allergens, Pest Allergens, and Mold: Looking to the Future</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="19" start="9">9-19</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Pediatric</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Over the last 2 to 3 decades, significant advances have been made in understanding the role that indoor allergen exposures play with regard to respiratory health. Multiple studies have confirmed that sensitization and exposure to indoor allergens can be a risk factor for asthma morbidity. Environmental interventions targeting key indoor allergens have been evaluated with the aims of examining their causal effects on asthma-related outcomes and identifying clinically efficacious interventions to incorporate into treatment recommendations. Historically, it appeared that the most successful intervention, as performed in the Inner-City Asthma Study, was individually tailored, targeting multiple allergens in a predominantly low-income, minority, and urban pediatric population. Recent studies suggest that single-allergen interventions may be efficacious when targeting the most clinically relevant allergen for a population. In this article, we review recent literature on home environmental interventions and their effects on specific indoor allergen levels and asthma-related outcomes</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29310769">PM:29310769</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20180105, Ahluwalia SK</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87042</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bjelac,J.A.</style></author><author><style face="normal" font="default"> Blanch,M.B.</style></author><author><style face="normal" font="default"> Fernandez,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatric Allergy and Clinical Immunology, Cleveland Clinic, Cleveland, Ohio.</style></auth-address><titles><title><style face="normal" font="default">Allergic disease in patients with common variable immunodeficiency at a tertiary care referral center</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="92" start="90">90-92</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.075</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273136">PM:29273136</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-90-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-90-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Bjelac JA</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.075</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87275</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Crowley,M.P.</style></author><author><style face="normal" font="default"> McDonald,V.</style></author><author><style face="normal" font="default"> Scully,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Guy's and St. Thomas' Hospital, London, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Ofatumumab for TTP in a Patient with Anaphylaxis Associated with Rituximab</style></title><secondary-title><style face="normal" font="default">N Engl J Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">N Engl J Med</style></abbr-1></periodical><pages end="93" start="92">92-93</pages><volume><style face="normal" font="default">378</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Rituximab</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1533-4406 (Electronic)IS - 0028-4793 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1056/NEJMc1714146</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29298144">PM:29298144</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\N Engl J Med\2018-378-92-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\N Engl J Med\2018-378-92-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Crowley MP</style></custom2><misc3><style face="normal" font="default">10.1056/NEJMc1714146</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87338</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,Y.</style></author><author><style face="normal" font="default"> Dong,P.</style></author><author><style face="normal" font="default"> Zhao,J.</style></author><author><style face="normal" font="default"> Zhou,W.</style></author><author><style face="normal" font="default"> Zhou,Y.</style></author><author><style face="normal" font="default"> Xu,Y.</style></author><author><style face="normal" font="default"> Mei,C.</style></author><author><style face="normal" font="default"> Guo,F.</style></author><author><style face="normal" font="default"> Zheng,Y.</style></author><author><style face="normal" font="default"> Yang,J.Q.</style></author></authors></contributors><auth-address><style face="normal" font="default">Key Laboratory of National Health and Family Planning Commission on Parasitic Disease Control and Prevention, Jiangsu Provincial Key Laboratory on Parasite and Vector Control, Jiangsu Institute of Parasitic Diseases and Public Health Research Center of Jiangnan University, Wuxi, Jiangsu, China</style></auth-address><titles><title><style face="normal" font="default">PKC lambda/iota regulates Th17 differentiation and house dust mite-induced allergic airway inflammation</style></title><secondary-title><style face="normal" font="default">Biochim Biophys Acta</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biochim Biophys Acta</style></abbr-1></periodical><pages end="941" start="934">934-941</pages><volume><style face="normal" font="default">1864</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword></keywords><dates><year Day="3" Month="1" Year="2018">2018/1/3</year></dates><abstract><style face="normal" font="default">Asthma is a chronic airway inflammation in which Th2 and Th17 cells play critical roles in its pathogenesis. We have reported that atypical protein kinase (PKC) lambda/iota is a new regulator for Th2 differentiation and function. However, the role of PKClambda/iota for Th17 cells remains elusive. In this study, we explored the effect of PKClambda/iota on Th17 cells in the context of ex vivo cell culture systems and an in vivo murine model of allergic airway inflammation with the use of activated T cell-specific conditional PKClambda/iota-deficient mice. Our findings indicate that PKClambda/iota regulates Th17 cells. The secretion of Th17 effector cytokines, including IL-17, IL-21 and IL-22, were inhibited from PKClambda/iota-deficient T cells under non-skewing or Th17-skewing culture conditions. Moreover, the impaired Th17 differentiation and function by the PKClambda/iota-deficiency was associated with the downregulation of Stat3 and Rorgammat, key Th17 transcription factors. We developed a model of Th17 and neutrophil-involved allergic airway inflammation by intratracheal inoculation of house dust mites. PKClambda/iota-deficiency significantly inhibited airway inflammations. The infiltrating cells in the lungs and bronchoalveolar lavage fluids were significantly reduced in conditional PKClambda/iota-deficient mice. Th17 effector cytokines were reduced in the bronchoalveolar lavage fluids and lungs at protein and mRNA levels. Thus, PKClambda/iota emerges as a critical regulator of Th17 differentiation and allergic airway hyperresponsiveness</style></abstract><notes><style face="normal" font="default">IS - 0006-3002 (Print)IS - 0006-3002 (Linking)LA - engPT - Journal ArticleCO - China -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.bbadis.2018.01.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29305916">PM:29305916</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biochim Biophys Acta\2018-1864-934-41.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biochim Biophys Acta\2018-1864-934-41.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Yang Y</style></custom2><misc3><style face="normal" font="default">10.1016/j.bbadis.2018.01.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87046</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gordon,J.</style></author><author><style face="normal" font="default"> Reboulet,R.</style></author><author><style face="normal" font="default"> Gandhi,P.</style></author><author><style face="normal" font="default"> Matsui,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Inspirotec, Inc, Chicago, Illinois.</style></auth-address><titles><title><style face="normal" font="default">Validation of a novel sampling technology for airborne allergens in low-income urban homes</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="97" start="96">96-97</pages><volume><style face="normal" font="default">120</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273138">PM:29273138</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-96-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2018-120-96-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Gordon J</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87174</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sitton,C.</style></author><author><style face="normal" font="default"> Temples,H.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Practice Guidelines for Peanut Allergies</style></title><secondary-title><style face="normal" font="default">J Pediatr Health Care</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pediatr Health Care</style></abbr-1></periodical><pages end="102" start="98">98-102</pages><volume><style face="normal" font="default">32</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">This article reviews the latest recommendations and clinical practice guidelines for peanut allergies among the pediatric population. Recommendations in this paper were compiled using information collected from a variety of publications of accredited professional organizations. Peanut allergies are the body's response to what it sees to be an unwanted substance in the body. This article focuses on the causes, signs and symptoms, prevention, diagnosis, and management of peanut allergies</style></abstract><notes><style face="normal" font="default">IS - 1532-656X (Electronic)IS - 0891-5245 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.pedhc.2017.09.013</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29229067">PM:29229067</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pediatr Health Care\2018-32-98-102.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pediatr Health Care\2018-32-98-102.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Sitton C</style></custom2><misc3><style face="normal" font="default">10.1016/j.pedhc.2017.09.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87477</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Caraballo,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Institute for Immunological Research , University of Cartagena , Cartagena , Colombia</style></auth-address><titles><title><style face="normal" font="default">The tropics, helminth infections and hygiene hypotheses</style></title><secondary-title><style face="normal" font="default">Expert Rev Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Expert Rev Clin Immunol</style></abbr-1></periodical><pages end="102" start="99">99-102</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword></keywords><dates><year Day="0" Month="2" Year="2018">2018/2</year></dates><abstract><style face="normal" font="default">The Tropics is very appropriate to test the hypotheses raised to explain the increasing trends of allergy and other inflammatory diseases worldwide. The absence of parasite infection as a possible cause of the increase of allergic diseases was proposed by J. Gerrard a long time ago; however, the idea that helminth infections, which induce a strong Th2 could reduce allergy symptoms seems counterintuitive; but the fact is that they have a dual effect: they increase the Th2 responses but also exert immunosuppression and both effects influence the symptoms of allergy. Basic experimentation has provided valuable information about the mechanisms of allergic inflammation and more recently, about its control by helminth induced immunomodulation, discovering helminth molecules with anti-inflammatory properties that are meant to replace the live helminth therapeutic approaches. The immunosuppressive power of helminths makes them excellent candidates to be considered in the hygiene hypotheses. Future comprehensive studies evaluating simultaneously the role of microbial infections, helminth infections, microbiota, pollution and biodiversity will help to elucidate the causes of the increasing trends of allergic disorders. Doing this in the tropics, where all these variables are still present could be difficult but no doubt that will be more informative</style></abstract><notes><style face="normal" font="default">IS - 1744-8409 (Electronic)IS - 1744-666X (Linking)LA - engPT - Journal ArticleCO - Colombia -</style></notes><work-type><style face="normal" font="default">10.1080/1744666X.2018.1424543</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29300114">PM:29300114</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Expert Rev Clin Immunol\2018-14-99-102.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Expert Rev Clin Immunol\2018-14-99-102.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180120, Caraballo L</style></custom2><misc3><style face="normal" font="default">10.1080/1744666X.2018.1424543</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86878</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,Z.</style></author><author><style face="normal" font="default"> Zhang,X.</style></author><author><style face="normal" font="default"> Chen,W.</style></author><author><style face="normal" font="default"> Zhou,P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Conformation stability, in vitro digestibility and allergenicity of tropomyosin from shrimp (Exopalaemon modestus) as affected by high intensity ultrasound</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="1009" start="997">997-1009</pages><volume><style face="normal" font="default">245</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> Conformation</style></keyword><keyword><style face="normal" font="default"> Digestibility</style></keyword><keyword><style face="normal" font="default"> High intensity ultrasound</style></keyword><keyword><style face="normal" font="default"> Tropomyosin</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><isbn><style face="normal" font="default">0308-8146</style></isbn><abstract><style face="normal" font="default">The effects of high intensity ultrasound (HIU) modification (power: 100</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô800</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç»W, 15</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç»min) on the conformation stability, in vitro digestibility and allergenicity of tropomyosin (TM) from Exopalaemon modestus were investigated. HIU treatment oxidized the Cys, Met and Lys in TM and degraded TM to generate protein fragments by HIU-induced free radicals. The +¦-helix content decreased, while +¦-sheet, +¦-turn and random coil increased. The immunoblotting and ELISA data suggested HIU treatment reduced the allergenicity and contributed to higher digestibility of TM. TM had resistance to gastric digestion, while intestinal digestion totally hydrolyzed TM, and the sequential HIU-gastric-intestinal digestion most efficiently hydrolyzed TM and reduced the allergenicity of digestion products. Stronger HIU could loosen TM structure, strengthen the gastrointestinal digestibility of TM and reduce the allergenicity of TM and digestion products to low level</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2017.11.072</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29287471">PM:29287471</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\20171121-ZhangZ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\20171121-ZhangZ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Zhang Z</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2017.11.072</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87283</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,D.C.P.</style></author><author><style face="normal" font="default"> Tay,N.Q.</style></author><author><style face="normal" font="default"> Thian,M.</style></author><author><style face="normal" font="default"> Prabhu,N.</style></author><author><style face="normal" font="default"> Furuhashi,K.</style></author><author><style face="normal" font="default"> Kemeny,D.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunology Programme, Department of Microbiology and Immunology, Centre for Life Sciences, National University of Singapore, Singapore</style></auth-address><titles><title><style face="normal" font="default">Prior exposure to inhaled allergen enhances anti-viral immunity and T cell priming by dendritic cells</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0190063">e0190063-</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Influenza and asthma are two of the major public health concerns in the world today. During the 2009 influenza pandemic asthma was found to be the commonest comorbid illness of patients admitted to hospital. Unexpectedly, it was also observed that asthmatic patients admitted to hospital with influenza infection were less likely to die or require admission to intensive care compared with non-asthmatics. Using an in vivo model of asthma and influenza infection we demonstrate that prior exposure to Blomia tropicalis extract (BTE) leads to an altered immune response to influenza infection, comprised of less severe weight loss and faster recovery following infection. This protection was associated with significant increases in T cell numbers in the lungs of BTE sensitised and infected mice, as well as increased IFN-gamma production from these cells. In addition, elevated numbers of CD11b+ dendritic cells (DCs) were found in the lung draining lymph nodes following infection of BTE sensitised mice compared to infected PBS treated mice. These CD11b+ DCs appeared to be better at priming CD8 specific T cells both in vivo and ex vivo, a function not normally attributed to CD11b+ DCs. We propose that this alteration in cross-presentation and more efficient T cell priming seen in BTE sensitised mice, led to the earlier increase in T cells in the lungs and subsequently faster clearance of the virus and reduced influenza induced pathology. We believe this data provides a novel mechanism that explains why asthmatic patients may present with less severe disease when infected with influenza</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Singapore -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0190063</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29293541">PM:29293541</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2018-13-e0190063.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2018-13-e0190063.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Lee DC</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0190063</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87282</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ma,Y.</style></author><author><style face="normal" font="default"> Dawicki,W.</style></author><author><style face="normal" font="default"> Zhang,X.</style></author><author><style face="normal" font="default"> Gordon,J.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Respirology, Critical Care and Sleep Medicine, Department of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada</style></auth-address><titles><title><style face="normal" font="default">Contributions of direct versus indirect mechanisms for regulatory dendritic cell suppression of asthmatic allergen-specific IgG1 antibody responses</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0190414">e0190414-</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">IL-10-differentiated dendritic cells (DC10) can reverse the asthma phenotype in mice, but how they suppress the asthmatic B cell response is unclear. Herein we assessed the mechanism(s) by which DC10 and DC10-induced Treg affect IgG1 production in asthma. We observed a rapid decline in lung-resident OVA-specific IgG1-secreting B cells on cessation of airway allergen challenge, and intraperitoneal DC10 therapy did not amplify that (p>0.05). It did however increase the loss of IgG1-B cells from the bone marrow (by 45+/-7.2%; p&lt;/=0.01) and spleen (by 65+/-17.8%; p&lt;/=0.05) over 2 wk. Delivery of OVA-loaded DC10 directly into the airways of asthmatic mice decreased the lung IgG1 B cell response assessed 2 dy later by 33+/-9.7% (p&lt;/=0.01), while their co-culture with asthmatic lung cell suspensions reduced the numbers of IgG1-secreting cells by 56.5+/-9.7% (p&lt;/=0.01). This effect was dependent on the DC10 carrying intact allergen on their cell surface; DC10 that had phagocytosed and fully processed their allergen were unable to suppress B cell responses, although they did suppress asthmatic Th2 cell responses. We had shown that therapeutic delivery of DC10-induced Treg can effectively suppress asthmatic T and B cell (IgE and IgG1) responses; herein CD4+ cells or Treg from the lungs of DC10-treated OVA-asthmatic mice suppressed in vitro B cell IgG1 production by 52.2+/-8.7% (p&lt;/=0.001) or 44.6+/-12.2% (p&lt;/=0.05), respectively, but delivery of DC10-induced Treg directly into the airways of asthmatic mice had no discernible impact over 2 dy on the numbers of lung IgG1-secreting cells (p>/=0.05). In summary, DC10 treatment down-regulates OVA-specific B cell responses of asthmatic mice. While DC10 that carry intact allergen on their cell surface can dampen this response, DC10-induced Treg are critical for full realization of this outcome. This suggests that infectious tolerance is an essential element in regulatory DC control of the B cell response in allergic asthma</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0190414</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29293622">PM:29293622</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2018-13-e0190414.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2018-13-e0190414.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180102, Ma Y</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0190414</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87504</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Benede,S.</style></author><author><style face="normal" font="default"> Berin,M.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Jaffe Food Allergy Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America</style></auth-address><titles><title><style face="normal" font="default">Mast cell heterogeneity underlies different manifestations of food allergy in mice</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0190453">e0190453-</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">Food can trigger a diverse array of symptoms in food allergic individuals from isolated local symptoms affecting skin or gut to multi-system severe reactions (systemic anaphylaxis). Although we know that gastrointestinal and systemic manifestations of food allergy are mediated by tissue mast cells (MCs), it is not clear why allergen exposure by the oral route can result in such distinct clinical manifestations. Our aim was to assess the contribution of mast cell subsets to different manifestations of food allergy. We used two common models of IgE-mediated food allergy, one resulting in systemic anaphylaxis and the other resulting in acute gastrointestinal symptoms, to study the immune basis of allergic reactions. We used responders and non-responders in each model system, as well as naive controls to identify the association of mast cell activation with clinical reactivity rather than sensitization. Systemic anaphylaxis was uniquely associated with activation of connective tissue mast cells (identified by release of mouse mast cell protease (MMCP) -7 into the serum) and release of histamine, while activation of mucosal mast cells (identified by release of MMCP-1 in the serum) did not correlate with symptoms. Gastrointestinal manifestations of food allergy were associated with an increase of MMCP-1-expressing mast cells in the intestine, and evidence of both mucosal and connective tissue mast cell activation. The data presented in this paper demonstrates that mast cell heterogeneity is an important contributor to manifestations of food allergy, and identifies the connective tissue mast cell subset as key in the development of severe systemic anaphylaxis</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticlePT - Research Support, N.I.H., ExtramuralCO - United States -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0190453</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29370173">PM:29370173</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2018-13-e0190453.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2018-13-e0190453.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S1_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S2_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S3_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S4_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S5_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S6_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S7_Table.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S1_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S2_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S3_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S4_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S5_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S6_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S7_Table.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20180125, Benede S</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0190453</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87389</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Eyring,K.R.</style></author><author><style face="normal" font="default"> Pedersen,B.S.</style></author><author><style face="normal" font="default"> Maclean,K.N.</style></author><author><style face="normal" font="default"> Stabler,S.P.</style></author><author><style face="normal" font="default"> Yang,I.V.</style></author><author><style face="normal" font="default"> Schwartz,D.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, School of Medicine, University of Colorado, Aurora, CO, United States of America</style></auth-address><titles><title><style face="normal" font="default">Methylene-tetrahydrofolate reductase contributes to allergic airway disease</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0190916">e0190916-</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">RATIONALE: Environmental exposures strongly influence the development and progression of asthma. We have previously demonstrated that mice exposed to a diet enriched with methyl donors during vulnerable periods of fetal development can enhance the heritable risk of allergic airway disease through epigenetic changes. There is conflicting evidence on the role of folate (one of the primary methyl donors) in modifying allergic airway disease. OBJECTIVES: We hypothesized that blocking folate metabolism through the loss of methylene-tetrahydrofolate reductase (Mthfr) activity would reduce the allergic airway disease phenotype through epigenetic mechanisms. METHODS: Allergic airway disease was induced in C57BL/6 and C57BL/6Mthfr-/- mice through house dust mite (HDM) exposure. Airway inflammation and airway hyperresponsiveness (AHR) were measured between the two groups. Gene expression and methylation profiles were generated for whole lung tissue. Disease and molecular outcomes were evaluated in C57BL/6 and C57BL/6Mthfr-/- mice supplemented with betaine. MEASUREMENTS AND MAIN RESULTS: Loss of Mthfr alters single carbon metabolite levels in the lung and serum including elevated homocysteine and cystathionine and reduced methionine. HDM-treated C57BL/6Mthfr-/- mice demonstrated significantly less airway hyperreactivity (AHR) compared to HDM-treated C57BL/6 mice. Furthermore, HDM-treated C57BL/6Mthfr-/- mice compared to HDM-treated C57BL/6 mice have reduced whole lung lavage (WLL) cellularity, eosinophilia, and Il-4/Il-5 cytokine concentrations. Betaine supplementation reversed parts of the HDM-induced allergic airway disease that are modified by Mthfr loss. 737 genes are differentially expressed and 146 regions are differentially methylated in lung tissue from HDM-treated C57BL/6Mthfr-/- mice and HDM-treated C57BL/6 mice. Additionally, analysis of methylation/expression relationships identified 503 significant correlations. CONCLUSION: Collectively, these findings indicate that the loss of folate as a methyl donor is a modifier of allergic airway disease, and that epigenetic and expression changes correlate with this modification. Further investigation into the mechanisms that drive this observation is warranted</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0190916</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29329322">PM:29329322</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2018-13-e0190916.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2018-13-e0190916.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S1_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S2_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S3_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S4_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S5_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S6_Table.xlsxC:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S7_Table.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S1_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S2_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S3_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S4_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S5_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S6_Table.xlsxF:\A&amp;H HMW Papers\PLoS ONE\2018-13-e0190916S7_Table.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20180112, Eyring KR</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0190916</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87390</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shin,J.H.</style></author><author><style face="normal" font="default"> Roh,D.</style></author><author><style face="normal" font="default"> Lee,D.H.</style></author><author><style face="normal" font="default"> Kim,S.W.</style></author><author><style face="normal" font="default"> Kim,S.W.</style></author><author><style face="normal" font="default"> Cho,J.H.</style></author><author><style face="normal" font="default"> Kim,B.G.</style></author><author><style face="normal" font="default"> Kim,B.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology-Head and Neck Surgery, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Allergic rhinitis and rhinosinusitis synergistically compromise the mental health and health-related quality of life of Korean adults: A nationwide population-based survey</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0191115">e0191115-</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword></keywords><dates><year Day="0" Month="0" Year="2018">2018</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergic rhinitis (AR) and rhinosinusitis (RS) negatively impact psychological well-being and health-related quality of life (HRQoL). However, few population-based studies have investigated the effects of these conditions on mental health and HRQoL. PURPOSE: To explore independent associations of AR and/or RS with mental health and HRQoL using data from the 2013-2015 Korea National Health and Nutrition Examination Survey (KNHANES). METHODS: The KNHANES is a nationwide cross-sectional survey of the non-institutionalized population of Korea. A total of 15,441 adults completed the clinical examination and the health questionnaire. We divided all participants into four groups: AR-/RS-, AR-/RS+, AR+/RS-, and AR+/RS+. Logistic regression analyses were performed after adjustment for sociodemographic characteristics, general health behaviors, and other comorbidities. RESULTS: The AR+/RS+ group contained the highest proportion of subjects with perceived stress and depressed mood. Subjects with AR+/RS+ also had more frequent problems in terms of pain/discomfort and anxiety/depression. After adjusting for all confounders, the odds ratios (ORs) were 2.96 (p = 0.009) for depressed mood and 3.17 (p = 0.013) for suicidal ideation in the AR+/RS+ group compared with in the AR-/RS- group. The AR+/RS- group reported more perceived stress (OR, 1.56, p = 0.003) and depression (OR, 1.72, p = 0.024) compared with the AR-/RS- group. In terms of the ORs for HRQoL, the AR+/RS+ group reported more problems in terms of self-care (OR, 3.73, p = 0.038) and more pain/discomfort (OR 2.19, p = 0.006) compared with the AR-/RS- group. CONCLUSIONS: In the Korean population, AR and RS exerted a synergistic negative impact on mental health and HRQoL, especially suicidal ideation. Most patients seek help from clinicians for impaired HRQoL. Therefore, clinicians should consider the underlying mental health and HRQoL of patients with AR and/or RS, as these may be impaired by their conditions</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0191115</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29324857">PM:29324857</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2018-13-e0191115.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2018-13-e0191115.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180111, Shin JH</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0191115</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87503</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tamura,K.</style></author><author><style face="normal" font="default"> Matsumoto,K.</style></author><author><style face="normal" font="default"> Fukuyama,S.</style></author><author><style face="normal" font="default"> Kan,O.</style></author><author><style face="normal" font="default"> Ishii,Y.</style></author><author><style face="normal" font="default"> Tonai,K.</style></author><author><style face="normal" font="default"> Tatsuta,M.</style></author><author><style face="normal" font="default"> Enokizu,A.</style></author><author><style face="normal" font="default"> Inoue,H.</style></author><author><style face="normal" font="default"> Nakanishi,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan</style></auth-address><titles><title><style face="normal" font="default">Frequency-dependent airway hyperresponsiveness in a mouse model of emphysema and allergic inflammation</style></title><secondary-title><style face="normal" font="default">Physiol Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Physiol Rep</style></abbr-1></periodical><pages end="" start="e13568">e13568-</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> etiology</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="1" Year="2018">2018/1</year></dates><abstract><style face="normal" font="default">Asthma and chronic obstructive pulmonary disease (COPD), chronic airway inflammatory diseases characterized by airflow limitation, have different etiologies and pathophysiologies. Asthma-COPD Overlap (ACO) has recently been used for patients with mixed asthma and COPD. The pathophysiological mechanisms of ACO have not been clearly understood due to the lack of an appropriate murine model. To investigate its pathophysiology, we examined a murine model by allergen challenge in surfactant protein-D (SP-D)-deficient mice that spontaneously developed pulmonary emphysema. SP-D-deficient mice were sensitized and challenged by ovalbumin (OVA). Lungs and bronchoalveolar lavage fluid (BALF) were collected for analysis, and static lung compliance and airway hyperresponsiveness (AHR) were measured 48 h after the last OVA challenge. In SP-D-deficient, naive, or OVA-challenged mice, the mean linear intercept and static lung compliance were increased compared with wild-type (WT) mice. There was no significant difference in goblet cell hyperplasia and the gene expression of Mucin 5AC (MUC5AC) between SP-D-deficient and WT OVA-challenged mice. In SP-D-deficient OVA-challenged mice, airway hyperresponsiveness was significantly enhanced despite the lower eosinophil count and the concentration of interleukin (IL)-5 and IL-13 in BALF compared with WT OVA-challenged mice at 120 ventilations per minute. When mice were ventilated at a lower ventilation frequency of 100 ventilations per minute, elevated airway hyperresponsiveness in SP-D-deficient OVA-challenged mice was diminished. This model of emphysematous change with allergic airway inflammation raises the possibility that frequency-dependent airway hyperresponsiveness may be involved in the pathophysiology of ACO</style></abstract><notes><style face="normal" font="default">IS - 2051-817X (Electronic)IS - 2051-817X (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.14814/phy2.13568</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29368450">PM:29368450</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Physiol Rep\2018-6-e13568.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Physiol Rep\2018-6-e13568.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180123, Tamura K</style></custom2><misc3><style face="normal" font="default">10.14814/phy2.13568</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87252</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Qiao,M.</style></author><author><style face="normal" font="default"> Tu,M.</style></author><author><style face="normal" font="default"> Wang,Z.</style></author><author><style face="normal" font="default"> Mao,F.</style></author><author><style face="normal" font="default"> Chen,H.</style></author><author><style face="normal" font="default"> Qin,L.</style></author><author><style face="normal" font="default"> Du,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Food Science and Technology, Dalian Polytechnic University, National Engineering Research Center of Seafood, Dalian 116034, China.</style></auth-address><titles><title><style face="normal" font="default">Identification and Antithrombotic Activity of Peptides from Blue Mussel (Mytilus edulis) Protein</style></title><secondary-title><style face="normal" font="default">Int J Mol Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Mol Sci</style></abbr-1></periodical><pages end="" start="E138">E138-</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Binding Sites</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">The blue mussel (Mytilus edulis) reportedly contains many bioactive components of nutritional value. Water-, salt- and acid-soluble M. edulis protein fractions were obtained and the proteins were trypsinized. The resultant peptides were analyzed by ultra-performance liquid chromatography quadrupole time of flight tandem mass spectrometry (UPLC-Q-TOF-MS/MS). 387 unique peptides were identified that matched 81 precursor proteins. Molecular mass distributions of the proteins and peptides were analyzed by sodium dodecyl sulfate-polyacryl amide gel electrophoresis (SDS-PAGE). The differences between the three protein samples were studied by Venn diagram of peptide and protein compositions. Toxicity, allergic and antithrombotic activity of peptides was predicted using database website and molecular docking respectively. The antithrombotic activity of enzymatic hydrolysate from water-, salt- and acid-soluble M. edulis protein were 40.17%, 85.74%, 82.00% at 5 mg/mL, respectively. Active mechanism of antithrombotic peptide (ELEDSLDSER) was also research about amino acid binding sites and interaction, simultaneously</style></abstract><notes><style face="normal" font="default">IS - 1422-0067 (Electronic)IS - 1422-0067 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3390/ijms19010138</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29300301">PM:29300301</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Mol Sci\2018-19-E138.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Mol Sci\2018-19-E138.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Qiao M</style></custom2><misc3><style face="normal" font="default">10.3390/ijms19010138</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87253</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Maiz,L.</style></author><author><style face="normal" font="default"> Nieto,R.</style></author><author><style face="normal" font="default"> Canton,R.</style></author><author><style face="normal" font="default"> Gomez de la Pedrosa,G.</style></author><author><style face="normal" font="default"> Martinez-Garcia,M.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Servicio de Neumologia, Unidad de Bronquiectasias y Fibrosis Quistica, Hospital Universitario Ramon y Cajal, 28034 Madrid, Spain.</style></auth-address><titles><title><style face="normal" font="default">Fungi in Bronchiectasis: A Concise Review</style></title><secondary-title><style face="normal" font="default">Int J Mol Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Mol Sci</style></abbr-1></periodical><pages end="" start="E142">E142-</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="4" Month="1" Year="2018">2018/1/4</year></dates><abstract><style face="normal" font="default">Although the spectrum of fungal pathology has been studied extensively in immunosuppressed patients, little is known about the epidemiology, risk factors, and management of fungal infections in chronic pulmonary diseases like bronchiectasis. In bronchiectasis patients, deteriorated mucociliary clearance-generally due to prior colonization by bacterial pathogens-and thick mucosity propitiate, the persistence of fungal spores in the respiratory tract. The most prevalent fungi in these patients are Candida albicans and Aspergillus fumigatus; these are almost always isolated with bacterial pathogens like Haemophillus influenzae and Pseudomonas aeruginosa, making very difficult to define their clinical significance. Analysis of the mycobiome enables us to detect a greater diversity of microorganisms than with conventional cultures. The results have shown a reduced fungal diversity in most chronic respiratory diseases, and that this finding correlates with poorer lung function. Increased knowledge of both the mycobiome and the complex interactions between the fungal, viral, and bacterial microbiota, including mycobacteria, will further our understanding of the mycobiome's relationship with the pathogeny of bronchiectasis and the development of innovative therapies to combat it</style></abstract><notes><style face="normal" font="default">IS - 1422-0067 (Electronic)IS - 1422-0067 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.3390/ijms19010142</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29300314">PM:29300314</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Mol Sci\2018-19-E142.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Mol Sci\2018-19-E142.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180104, Naiz L</style></custom2><misc3><style face="normal" font="default">10.3390/ijms19010142</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87437</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Marcolino,M.S.</style></author><author><style face="normal" font="default"> Oliveira,J.A.Q.</style></author><author><style face="normal" font="default"> D'Agostino,M.</style></author><author><style face="normal" font="default"> Ribeiro,A.L.</style></author><author><style face="normal" font="default"> Alkmim,M.B.M.</style></author><author><style face="normal" font="default"> Novillo-Ortiz,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Medical School and Telehealth Center, University Hospital, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil</style></auth-address><titles><title><style face="normal" font="default">The Impact of mHealth Interventions: Systematic Review of Systematic Reviews</style></title><secondary-title><style face="normal" font="default">JMIR Mhealth Uhealth</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">JMIR Mhealth Uhealth</style></abbr-1></periodical><pages end="" start="e23">e23-</pages><volume><style face="normal" font="default">6</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="17" Month="1" Year="2018">2018/1/17</year></dates><abstract><style face="normal" font="default">BACKGROUND: Mobile phone usage has been rapidly increasing worldwide. mHealth could efficiently deliver high-quality health care, but the evidence supporting its current effectiveness is still mixed. OBJECTIVE: We performed a systematic review of systematic reviews to assess the impact or effectiveness of mobile health (mHealth) interventions in different health conditions and in the processes of health care service delivery. METHODS: We used a common search strategy of five major scientific databases, restricting the search by publication date, language, and parameters in methodology and content. Methodological quality was evaluated using the Measurement Tool to Assess Systematic Reviews (AMSTAR) checklist. RESULTS: The searches resulted in a total of 10,689 articles. Of these, 23 systematic reviews (371 studies; more than 79,665 patients) were included. Seventeen reviews included studies performed in low- and middle-income countries. The studies used diverse mHealth interventions, most frequently text messaging (short message service, SMS) applied to different purposes (reminder, alert, education, motivation, prevention). Ten reviews were rated as low quality (AMSTAR score 0-4), seven were rated as moderate quality (AMSTAR score 5-8), and six were categorized as high quality (AMSTAR score 9-11). A beneficial impact of mHealth was observed in chronic disease management, showing improvement in symptoms and peak flow variability in asthma patients, reducing hospitalizations and improving forced expiratory volume in 1 second; improving chronic pulmonary diseases symptoms; improving heart failure symptoms, reducing deaths and hospitalization; improving glycemic control in diabetes patients; improving blood pressure in hypertensive patients; and reducing weight in overweight and obese patients. Studies also showed a positive impact of SMS reminders in improving attendance rates, with a similar impact to phone call reminders at reduced cost, and improved adherence to tuberculosis and human immunodeficiency virus therapy in some scenarios, with evidence of decrease of viral load. CONCLUSIONS: Although mHealth is growing in popularity, the evidence for efficacy is still limited. In general, the methodological quality of the studies included in the systematic reviews is low. For some fields, its impact is not evident, the results are mixed, or no long-term studies exist. Exceptions include the moderate quality evidence of improvement in asthma patients, attendance rates, and increased smoking abstinence rates. Most studies were performed in high-income countries, implying that mHealth is still at an early stage of development in low-income countries</style></abstract><notes><style face="normal" font="default">IS - 2291-5222 (Print)IS - 2291-5222 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Brazil -CO - United States -</style></notes><work-type><style face="normal" font="default">10.2196/mhealth.8873</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29343463">PM:29343463</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\JMIR Mhealth Uhealth\2018-6-e23.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\JMIR Mhealth Uhealth\2018-6-e23.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180117, Marcolino MS</style></custom2><misc3><style face="normal" font="default">10.2196/mhealth.8873</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87428</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,L.</style></author><author><style face="normal" font="default"> Zhang,X.</style></author><author><style face="normal" font="default"> Zhang,J.</style></author><author><style face="normal" font="default"> Fan,W.</style></author><author><style face="normal" font="default"> Lu,M.</style></author><author><style face="normal" font="default"> Hu,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">State Key Laboratory of Tree Genetics and Breeding, Key Laboratory of Tree Breeding and Cultivation of the State Forestry Administration, Research Institute of Forestry, Chinese Academy of Forestry, Beijing 100091, China.</style></auth-address><titles><title><style face="normal" font="default">Proteomic Analysis and Identification of Possible Allergenic Proteins in Mature Pollen of Populus tomentosa</style></title><secondary-title><style face="normal" font="default">Int J Mol Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Mol Sci</style></abbr-1></periodical><pages end="" start="E250">E250-</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Components</style></keyword><keyword><style face="normal" font="default"> genetics</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="16" Month="1" Year="2018">2018/1/16</year></dates><abstract><style face="normal" font="default">Pollen grains from Populus tomentosa, a widely cultivated tree in northern area of China, are considered to be an important aeroallergen causing severe allergic diseases. To gain insight into their allergenic components, mature Populus tomentosa pollen proteins were analyzed by two-dimensional gel electrophoresis (2-DE) and matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF/TOF MS). A total of 412 spots from mature pollen were resolved on pH 4-7 immobilized pH gradient (IPG) strips and 159 distinct proteins were identified from 242 spots analyzed. The identified proteins were categorized based on their functional role in the pollen, which included proteins involved in energy regulation, protein fate, protein synthesis and processing, metabolism, defense/stress responses, development and other functional categories. Moreover, among the identified proteins, 27 proteins were identified as putative allergens using the Structural Database of Allergenic Proteins (SDAP) tool and Allergen Online. The expression patterns of these putative allergen genes indicate that several of these genes are highly expressed in pollen. The identified putative allergens have the potential to improve specific diagnosis and can be used to develop vaccines for immunotherapy against poplar pollen allergy</style></abstract><notes><style face="normal" font="default">IS - 1422-0067 (Electronic)IS - 1422-0067 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3390/ijms19010250</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29337913">PM:29337913</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Mol Sci\2018-19-E250.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Mol Sci\2018-19-E250.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20181216, Wang L</style></custom2><misc3><style face="normal" font="default">10.3390/ijms19010250</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87447</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Siebers,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, Wellington School of Medicine and Health Sciences, University of Otago, 23 Mein Street, Newtown, Wellington 6242, New Zealand.</style></auth-address><titles><title><style face="normal" font="default">Allergies in Animals and Humans</style></title><secondary-title><style face="normal" font="default">Vet Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Vet Sci</style></abbr-1></periodical><pages end="" start="E5">E5-</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> New Zealand</style></keyword></keywords><dates><year Day="15" Month="1" Year="2018">2018/1/15</year></dates><abstract><style face="normal" font="default">Allergy to inhalant and food allergens affects many patients worldwide [...]</style></abstract><notes><style face="normal" font="default">IS - 2306-7381 (Electronic)IS - 2306-7381 (Linking)LA - engPT - EditorialCO - New Zealand -</style></notes><work-type><style face="normal" font="default">10.3390/vetsci5010005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29342930">PM:29342930</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Vet Sci\2018-5-E5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Vet Sci\2018-5-E5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180115, Siebers R</style></custom2><misc3><style face="normal" font="default">10.3390/vetsci5010005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87499</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Beute,J.</style></author><author><style face="normal" font="default"> Lukkes,M.</style></author><author><style face="normal" font="default"> Koekoek,E.P.</style></author><author><style face="normal" font="default"> Nastiti,H.</style></author><author><style face="normal" font="default"> Ganesh,K.</style></author><author><style face="normal" font="default"> de Bruijn,M.J.</style></author><author><style face="normal" font="default"> Hockman,S.</style></author><author><style face="normal" font="default"> van,Nimwegen M.</style></author><author><style face="normal" font="default"> Braunstahl,G.J.</style></author><author><style face="normal" font="default"> Boon,L.</style></author><author><style face="normal" font="default"> Lambrecht,B.N.</style></author><author><style face="normal" font="default"> Manganiello,V.C.</style></author><author><style face="normal" font="default"> Hendriks,R.W.</style></author><author><style face="normal" font="default"> KleinJan,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pulmonary Medicine, Erasmus MC, 's-Gravendijkwal, Rotterdam, Netherlands</style></auth-address><titles><title><style face="normal" font="default">A pathophysiological role of PDE3 in allergic airway inflammation</style></title><secondary-title><style face="normal" font="default">JCI Insight</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">JCI Insight</style></abbr-1></periodical><pages end="" start="e94888">e94888-</pages><volume><style face="normal" font="default">3</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword></keywords><dates><year Day="25" Month="1" Year="2018">2018/1/25</year></dates><abstract><style face="normal" font="default">Phosphodiesterase 3 (PDE3) and PDE4 regulate levels of cyclic AMP, which are critical in various cell types involved in allergic airway inflammation. Although PDE4 inhibition attenuates allergic airway inflammation, reported side effects preclude its application as an antiasthma drug in humans. Case reports showed that enoximone, which is a smooth muscle relaxant that inhibits PDE3, is beneficial and lifesaving in status asthmaticus and is well tolerated. However, clinical observations also showed antiinflammatory effects of PDE3 inhibition. In this study, we investigated the role of PDE3 in a house dust mite-driven (HDM-driven) allergic airway inflammation (AAI) model that is characterized by T helper 2 cell activation, eosinophilia, and reduced mucosal barrier function. Compared with wild-type (WT) littermates, mice with a targeted deletion of the PDE3A or PDE3B gene showed significantly reduced HDM-driven AAI. Therapeutic intervention in WT mice showed that all hallmarks of HDM-driven AAI were abrogated by the PDE3 inhibitors enoximone and milrinone. Importantly, we found that enoximone also reduced the upregulation of the CD11b integrin on mouse and human eosinophils in vitro, which is crucial for their recruitment during allergic inflammation. This study provides evidence for a hitherto unknown antiinflammatory role of PDE3 inhibition in allergic airway inflammation and offers a potentially novel treatment approach</style></abstract><notes><style face="normal" font="default">IS - 2379-3708 (Electronic)IS - 2379-3708 (Linking)LA - engPT - Journal ArticleCO - Netherlands -CO - United States -CO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1172/jci.insight.94888</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29367458">PM:29367458</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\JCI Insight\2018-3-e94888.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\JCI Insight\2018-3-e94888.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180125, Beute J</style></custom2><misc3><style face="normal" font="default">10.1172/jci.insight.94888</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86501</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Larenas-Linnemann,D.E.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Investigational Unit, Hospital Medica Sur, Mexico City, Mexico. Electronic address: Marlar1@prodigy.net.mx</style></auth-address><titles><title><style face="normal" font="default">Worldwide allergen immunotherapy guidelines: Evidence and experience-based</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Mexico -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108768">PM:29108768</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-LarenasLinnemannDE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-LarenasLinnemannDE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Larenas-Linnemann DE</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86502</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ferrer,M.</style></author><author><style face="normal" font="default"> Madamba,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergology and Clinical Immunology, Clinica Universidad de Navarra, Pamplona, Spain. Electronic address: mferrerp@unav.eduDepartment of Allergology and Clinical Immunology, Clinica Universidad de Navarra, Pamplona, Spain</style></auth-address><titles><title><style face="normal" font="default">Biologics in chronic urticaria</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108771">PM:29108771</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-FerrerM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-FerrerM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Ferrer M</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86503</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rodriguez Del Rio,P.</style></author><author><style face="normal" font="default"> Cistero-Bahima,A.</style></author><author><style face="normal" font="default"> van Ree,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Servicio de Alergia del Hospital Nino Jesus de Madrid, Spain. Electronic address: prrio@yahoo.esServicio de Alergia del Institut Universitari Dexeus de Barcelona, SpainAcademisch Medisch Centrum Universiteit van Amsterdam, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">Debates in allergy, regarding the symposium on: "Position Statements and Therapeutic Guidelines"</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Spain -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.006</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108772">PM:29108772</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-RodriguezDelRioP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-RodriguezDelRioP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Rodriguez Del Rio P</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86504</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Timon,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Biological Products, Advanced Therapies and Biotechnology Division, Agencia Espanola de Medicamentos y Productos Sanitarios, Campezo 1, 28022 Madrid, Spain. Electronic address: mtimon@aemps.es</style></auth-address><titles><title><style face="normal" font="default">Proposals for harmonization of allergens regulation in the European Union</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">Allergen medicinal products in the European Union are regulated differently across the different Member States. Thus, whereas in some countries strict quality, safety and efficacy requirements are in place, in others, most allergens are on the market as Named Patient Products, without any regulatory oversight. This situation results on European allergic patients being exposed to totally different standards depending on where they live. Initiatives to correct this situation are needed</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108764">PM:29108764</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-TimonM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-TimonM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Timon M</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86505</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Quirce,S.</style></author><author><style face="normal" font="default"> Phillips-Angles,E.</style></author><author><style face="normal" font="default"> Dominguez-Ortega,J.</style></author><author><style face="normal" font="default"> Barranco,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy, Hospital La Paz Institute for Health Research (IdiPAZ), Madrid, Spain; CIBER de Enfermedades Respiratorias, CIBERES, Spain.</style></auth-address><titles><title><style face="normal" font="default">Biologics in the treatment of severe asthma</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">Severe asthma is defined as asthma which requires treatment with high dose inhaled corticosteroids and with a second controller drug to prevent it from becoming uncontrolled or which remains uncontrolled despite this therapy. Patients with uncontrolled severe asthma require additional treatment options as add-on therapy, including biologics. Biologic therapies in asthma are designed to block key immune regulators, such as IgE, or certain pro-inflammatory cytokines, e.g. interleukin (IL)-5, IL-4, IL-13 or IL-17. Patients with severe asthma and eosinophilic phenotype may benefit from biologic therapies aimed at reducing blood and tissue eosinophils, such as mepolizumab, reslizumab and benralizumab. Patients with Th2-high phenotype may also benefit from therapy with anti-IL-4/anti-IL-13 monoclonal antibodies (dupilumab). The main limitations of asthma treatment with biologic agents are the crossover and overlap of the different pathways in the pathogenesis of asthma which may cause lack of complete success of these therapies, in addition of high costs, which make pharmacoeconomic studies necessary to identify the ideal target patient population to receive these biologic drugs</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.012</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108767">PM:29108767</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-QuirceS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-QuirceS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Quirce S</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.012</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86506</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ibanez,E.E.</style></author><author><style face="normal" font="default"> Bartra,T.J.</style></author><author><style face="normal" font="default"> Hernandez Fernandez de Rojas,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy, Hospital Universitari i Politenic La Fe, Valencia, Spain. Electronic address: ibanez_eth@gva.esDepartment of Allergy, Hospital Clinic de Barcelona, Barcelona, SpainDepartment of Allergy, Hospital Universitari i Politenic La Fe, Valencia, Spain</style></auth-address><titles><title><style face="normal" font="default">Non-allergenic immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.014</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108769">PM:29108769</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-IbanezEE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-IbanezEE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Ibanez EE</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.014</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86507</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Barber,D.</style></author><author><style face="normal" font="default"> Escribese,M.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">IMMA, Institute of Applied Molecular Medicine, Faculty of Medicine, Universidad San Pablo CEU, Campus Monteprincipe, Boadilla del Monte, 28668 Madrid, Spain. Electronic address: domingo.barberhernandez@ceu.esIMMA, Institute of Applied Molecular Medicine, Faculty of Medicine, Universidad San Pablo CEU, Campus Monteprincipe, Boadilla del Monte, 28668 Madrid, Spain; Basic Medical Sciences Department, Faculty of Medicine, Universidad San Pablo CEU, Campus Monteprincipe, Boadilla del Monte, 28668 Madrid, Spain</style></auth-address><titles><title><style face="normal" font="default">Predictive biomarkers in allergen specific immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108770">PM:29108770</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-BarberD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-BarberD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Barber D</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86508</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Scheurer,S.</style></author><author><style face="normal" font="default"> Toda,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Molecular Allergology, Paul-Ehrlich-Institut, Langen, Germany. Electronic address: schst@pei.deMolecular Allergology, Paul-Ehrlich-Institut, Langen, Germany</style></auth-address><titles><title><style face="normal" font="default">Epicutaneous immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108765">PM:29108765</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-ScheurerS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-ScheurerS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Scheurer S</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86509</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Escribese,M.M.</style></author><author><style face="normal" font="default"> Barber,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Basic Medical Sciences Department, Faculty of Medicine, CEU San Pablo University, Campus Monteprincipe, Boadilla del Monte, 28668 Madrid, Spain</style></auth-address><titles><title><style face="normal" font="default">New insight into cancer immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">A key point for maintenance of the immune system homeostasis is the balance between the capacity to recognize and fight exogenous molecules and the capacity to avoid auto reactivity. The disruption of this balance induces the progression of several immune diseases such as autoimmune diseases, allergies, infections or cancer. A promising therapeutic approach to treat these diseases is immunotherapy. In cancer, both active and passive immunotherapies have been tested with promising results, such as the blocking of immunological checkpoints like CTLA-4 and PD-1. These treatments, in the market since a few years ago, aim to redirect the patient's immunological response by inhibiting the induction of regulatory T cells, both in the priming and effector phases. This strategy sheds light on the immunological mechanisms that control the regulatory response mediated by T cells and opens new lines of research into other immunological diseases such as allergy, in which the induction of a regulatory response is necessary to avoid allergic progression and which is the main objective of allergen-specific immunotherapies available today</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.013</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108766">PM:29108766</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-EscribeseMM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171107-EscribeseMM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Escribese MM</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86510</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Arita,T.</style></author><author><style face="normal" font="default"> Nomiyama,T.</style></author><author><style face="normal" font="default"> Asai,J.</style></author><author><style face="normal" font="default"> Katoh,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan</style></auth-address><titles><title><style face="normal" font="default">Successful treatment of refractory alopecia universalis by persuading a patient not to sleep with her dog</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - LetterCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.06.011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29092781">PM:29092781</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171102-AritaT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171102-AritaT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Arita T</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.06.011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86511</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hide,M.</style></author><author><style face="normal" font="default"> Igarashi,A.</style></author><author><style face="normal" font="default"> Yagami,A.</style></author><author><style face="normal" font="default"> Chinuki,Y.</style></author><author><style face="normal" font="default"> Inomata,N.</style></author><author><style face="normal" font="default"> Fukunaga,A.</style></author><author><style face="normal" font="default"> Kaiser,G.</style></author><author><style face="normal" font="default"> Wang,J.</style></author><author><style face="normal" font="default"> Matsushima,S.</style></author><author><style face="normal" font="default"> Greenberg,S.</style></author><author><style face="normal" font="default"> Khalil,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of omalizumab for the treatment of refractory chronic spontaneous urticaria in Japanese patients: Subgroup analysis of the phase 3 POLARIS study</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="11" Year="2017">2017/11/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: Omalizumab, a humanized anti-IgE monoclonal antibody, proved efficacious and well tolerated in patients with chronic spontaneous urticaria (CSU) refractory to H1 antihistamines (H1AH) in the POLARIS study (NCT02329223), a randomized, double-blind, placebo-controlled trial in East Asian patients. However, data in Japanese patients, who have specific baseline characteristics (e.g., low angioedema incidence, different background medications) that may impact clinical outcomes, are lacking. This pre-specified analysis presents additional patient-level data over time, pharmacokinetic and pharmacodynamics data for omalizumab and IgE, and efficacy and safety data for omalizumab in Japanese patients. METHODS: Japanese patients (N = 105) were randomized 1:1:1 to omalizumab 300 mg, 150 mg, or placebo by subcutaneous injection every 4 weeks. Efficacy and safety were assessed primarily based on changes from baseline to Week 12 in weekly itch-severity scores (ISS7) and weekly urticaria activity scores (UAS7), and incidence of adverse events (AEs), respectively. Patient-level UAS7 data over time were also reviewed. RESULTS: At Week 12, least squares mean (LSM) changes from baseline in ISS7 were greater with omalizumab vs. placebo (-9.54 and -7.29 for omalizumab 300 mg and 150 mg, respectively, vs. placebo [-5.17]). Corresponding LSM changes from baseline in UAS7 were -21.61 and -15.59 (vs. placebo [-10.88]). Most responders in the omalizumab 300 mg group displayed improvement of disease activity within 2-4 weeks and had well-controlled symptoms during the treatment period. Overall AE incidence was similar across treatment arms. CONCLUSIONS: This subgroup analysis demonstrated that omalizumab is a well-tolerated, beneficial option for treatment of CSU in H1AH-refractory Japanese patients</style></abstract><notes><style face="normal" font="default">DA - 20171105IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - Journal ArticleCO - Japan -CO - Switzerland -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.10.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29102514">PM:29102514</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171105-HideM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171105-HideM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171105, Hide M</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.10.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86512</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kanazawa,J.</style></author><author><style face="normal" font="default"> Masuko,H.</style></author><author><style face="normal" font="default"> Yamada,H.</style></author><author><style face="normal" font="default"> Yatagai,Y.</style></author><author><style face="normal" font="default"> Sakamoto,T.</style></author><author><style face="normal" font="default"> Kitazawa,H.</style></author><author><style face="normal" font="default"> Iijima,H.</style></author><author><style face="normal" font="default"> Naito,T.</style></author><author><style face="normal" font="default"> Hirota,T.</style></author><author><style face="normal" font="default"> Tamari,M.</style></author><author><style face="normal" font="default"> Hizawa,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pulmonary Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan</style></auth-address><titles><title><style face="normal" font="default">How important is allergic sensitization as a cause of atopic asthma?</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - LetterCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.10.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29103905">PM:29103905</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171106-KanazawaJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171106-KanazawaJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Kanazawa J</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.10.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86513</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rolla,G.</style></author><author><style face="normal" font="default"> Heffler,E.</style></author><author><style face="normal" font="default"> Boita,M.</style></author><author><style face="normal" font="default"> Doyen,V.</style></author><author><style face="normal" font="default"> Mairesse,M.</style></author><author><style face="normal" font="default"> Cvackova,M.</style></author><author><style face="normal" font="default"> Debarbieux,S.</style></author><author><style face="normal" font="default"> Kleine-Tebbe,J.</style></author><author><style face="normal" font="default"> Ollert,M.</style></author><author><style face="normal" font="default"> Raulf,M.</style></author><author><style face="normal" font="default"> Bircher,A.J.</style></author><author><style face="normal" font="default"> Hilger,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy and Clinical Immunology - Dept. Medical Sciences, University of Torino, Italy</style></auth-address><titles><title><style face="normal" font="default">Pigeon tick bite: a neglected cause of idiopathic nocturnal anaphylaxis</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">Anaphylaxis is a serious systemic allergic reaction with rapid onset and potentially life-threatening. We report in detail a case of severe nocturnal anaphylaxis due to pigeon tick bite showing the diagnostic value of the extract and the recombinant allergen in the diagnostic procedures (basophil activation test, IgE-immunoblot and experimental ImmunoCAP). Apart from the presented case we describe that, during the last 10 years, we have collected 28 cases of allergy to Argas reflexus from several European countries. We suspect that this allergy is underdiagnosed because of the lack of diagnostic reagents. Because of the growing number of pigeons in Middle and Southern Europe cities, some cases of idiopathic anaphylaxis could potentially be caused by Argas reflexus in those countries. The identification of pigeon ticks as a trigger of anaphylaxis would greatly improve medical care and advice for these patients as the parasite can be exterminated by eradication measures in order to avoid further incidents. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171030IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Italy -CO - Belgium -CO - Czechia -CO - France -CO - Germany -CO - Denmark -CO - Luxembourg -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/all.13344</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29083476">PM:29083476</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171030-RollaG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171030-RollaG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171030, Rolla G</style></custom2><misc3><style face="normal" font="default">10.1111/all.13344</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86514</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ertas,R.</style></author><author><style face="normal" font="default"> Ozyurt,K.</style></author><author><style face="normal" font="default"> Atasoy,M.</style></author><author><style face="normal" font="default"> Hawro,T.</style></author><author><style face="normal" font="default"> Maurer,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Kayseri Education and Research Hospital Dermatology Clinic, Turkey</style></auth-address><titles><title><style face="normal" font="default">The clinical response to omalizumab in CSU patients is linked to and predicted by IgE levels and their change</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">BACKGROUND: Omalizumab is an effective and well-tolerated treatment for chronic spontaneous urticaria (CSU). Markers and predictors of response are largely unknown, but needed to optimize omalizumab treatment. Omalizumab targets IgE, and IgE levels may be linked to the effects of treatment. We evaluated if response rates to treatment with omalizumab in patients with CSU are linked to their baseline IgE levels, their IgE levels after omalizumab treatment, and the ratio of on treatment IgE and baseline IgE levels. METHODS: CSU patients (n=113) were treated with omalizumab 300 mg/4 weeks for 12 weeks, when their treatment responses, i.e. no, partial, or complete response, were assessed by use of the urticaria activity score, physician and patient visual analog scale, and treatment effectiveness score. Total IgE levels were measured before treatment (bIgE) with omalizumab and 4 weeks thereafter (w4IgE). RESULTS: Non-responders to omalizumab had significantly lower bIgE levels (17.9IU/ml, 17.0-55.0IU/ml) than partial responders (82.0IU/ml, 46.2-126.5IU/ml, p=0.008) and complete responders (73.7IU/ml, 19.45-153.8IU/ml, p=0.032). Non-responders also had lower w4IgE levels and lower ratios of w4IgE/bIgE levels than partial and complete responders (p&lt;0.001). Non-response to omalizumab was best predicted by patients' w4IgE/bIgE ratios, significantly better than by bIgE levels (p=0.016). CONCLUSIONS: In CSU, total IgE levels and their change predict the response to treatment with omalizumab. The assessment of pre- and post-treatment IgE levels and their ratio may help to improve the management of CSU in patients who require omalizumab treatment. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171030IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Turkey -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13345</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29083482">PM:29083482</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171030-ErtasR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171030-ErtasR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171030, Ertas R</style></custom2><misc3><style face="normal" font="default">10.1111/all.13345</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86515</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Elieh Ali,K.D.</style></author><author><style face="normal" font="default"> Rambasek,T.</style></author><author><style face="normal" font="default"> Bielory,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</style></auth-address><titles><title><style face="normal" font="default">Clinical implications of mast cell involvement in allergic conjunctivitis</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">The conjunctiva is a common site for the allergic inflammatory response due to it being highly vascularized, having constant exposure to environmental pollutants and allergenic pollens and having a unique conjunctival associated lymphoid tissue. The primary morbidity of anterior surface conjunctival disorders that include allergic conjunctivitis and tear film disorders is associated with its high frequency of involvement rather than its severity, although the more chronic forms can involve the cornea and lead to sight threatening conditions. Ocular allergy is associated with IgE-mediated mast cell activation in conjunctival tissue leading to the release of preformed mediators including histamine and proteases and subsequent de novo formation of lipid-derived mediators and cytokines that trigger a cascade of cellular and molecular events leading to extensive migration and infiltration of inflammatory cells to the ocular surface. The trafficking of neutrophils, eosinophils, and lymphocytes to the ocular surface is due to establishing various chemokine gradients (mainly CCL11, CCL24, CCL5, MCP-3, and MCP-4), cell surface expression of adhesion molecules (such as VCAM-1 the ligand for VLA-4), and leukocyte adhesion to vascular endothelium. The release of preformed mediators underlies the acute ocular surface response while the secondary influx of inflammatory cells leading to the recruitment and activation of eosinophils and the subsequent activation of Th2 and Th1 lymphocytes at the level of the conjunctiva reflects the late-phase reaction. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Iran -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/all.13334</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29105783">PM:29105783</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171106-EliehAliKD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171106-EliehAliKD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Elieh Ali KD</style></custom2><misc3><style face="normal" font="default">10.1111/all.13334</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86516</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,Z.</style></author><author><style face="normal" font="default"> Zhao,J.</style></author><author><style face="normal" font="default"> Wei,N.</style></author><author><style face="normal" font="default"> Feng,M.</style></author><author><style face="normal" font="default"> Xian,M.</style></author><author><style face="normal" font="default"> Shi,X.</style></author><author><style face="normal" font="default"> Zheng,Z.</style></author><author><style face="normal" font="default"> Su,Q.</style></author><author><style face="normal" font="default"> Wong,G.W.K.</style></author><author><style face="normal" font="default"> Li,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy and Clinical Immunology, Guangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China</style></auth-address><titles><title><style face="normal" font="default">Cockroach is a major cross-reactive allergen source in shrimp-sensitized rural children in southern China</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">BACKGROUND: Little is known about the prevalence of food allergy (FA) in China. OBJECTIVE: To investigate the prevalence of FA and its disparity between urban and rural areas in southern China. METHODS: Europrevall questionnaire responses were obtained from 5,542 school-age-children in urban Guangzhou and 5,319 in rural Shaoguan. A case-control study enrolled 190 children with adverse reactions (ARs) after food intake as cases, and 212 controls in Guangzhou; 116 cases and 233 controls in Shaoguan. These subjects underwent skin-prick test (SPT) and serum IgE measurements to food and inhalant allergens. Allergen extracts from shrimp, house dust mite (HDM), and cockroach were prepared for IgE cross-relativity testing in 23 Guangzhou and 20 Shaoguan shrimp-sensitized subjects. RESULTS: The prevalence of ARs to shrimp was higher in Guangzhou than Shaoguan children (3.5% vs. 1.4%, p&lt;0.001). However, sensitization rate to shrimp (SPT: 3.7% vs. 11.2%, p=0.015; IgE: 12.6% vs. 36.2%, p&lt;0.001) and cockroach (SPT: 5.3% vs. 33.5%; IgE: 2.6% vs. 27.6%, p&lt;0.001) were lower in Guangzhou. A significant correlation between shrimp and HDM/cockroach IgE was found in Shaoguan children. The proportions of positive IgE to tropomyosin (Pen a 1, Der p 10) were lower than 7.4% in both areas. Cockroach allergen has a significantly higher inhibition rate of binding to IgE to house-dust-mite allergens in Shaoguan sera. CONCLUSIONS: Shrimp is a common allergic food in southern China. Higher proportion of shrimp sensitization in rural subjects could be explained by cross-reactive to cockroach. Tropomyosin was not a major allergen responding for the cross-reactivity. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171026IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - China -CO - Hong Kong -</style></notes><work-type><style face="normal" font="default">10.1111/all.13341</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29072879">PM:29072879</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171026-YangZ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171026-YangZ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171026, Yang Z</style></custom2><misc3><style face="normal" font="default">10.1111/all.13341</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86517</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Maio,S.</style></author><author><style face="normal" font="default"> Baldacci,S.</style></author><author><style face="normal" font="default"> Bresciani,M.</style></author><author><style face="normal" font="default"> Simoni,M.</style></author><author><style face="normal" font="default"> Latorre,M.</style></author><author><style face="normal" font="default"> Murgia,N.</style></author><author><style face="normal" font="default"> Spinozzi,F.</style></author><author><style face="normal" font="default"> Braschi,M.</style></author><author><style face="normal" font="default"> Antonicelli,L.</style></author><author><style face="normal" font="default"> Brunetto,B.</style></author><author><style face="normal" font="default"> Iacovacci,P.</style></author><author><style face="normal" font="default"> Roazzi,P.</style></author><author><style face="normal" font="default"> Pini,C.</style></author><author><style face="normal" font="default"> Pata,M.</style></author><author><style face="normal" font="default"> La Grasta,L.</style></author><author><style face="normal" font="default"> Paggiaro,P.</style></author><author><style face="normal" font="default"> Viegi,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pulmonary Environmental Epidemiology Unit, CNR Institute of Clinical Physiology, Pisa, Italy</style></auth-address><titles><title><style face="normal" font="default">RItA: The Italian severe/uncontrolled asthma registry</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">BACKGROUND: The Italian severe/uncontrolled asthma (SUA) web-based registry encompasses demographic, clinical, functional, inflammatory data; it aims to raise SUA awareness, identifying specific phenotypes and promoting optimal care. METHODS: 493 adult patients from 27 Italian centres (recruited in 2011-2014) were analyzed. RESULTS: Mean age was 53.8yrs. SUA patients were more frequently female (60.6%), with allergic asthma (83.1%). About 30% showed late onset of asthma diagnosis/symptoms (>40yrs); the mean age for asthma symptoms onset was 30.2yrs and for asthma diagnosis 34.4yrs. 97.1% used ICS (dose 2000 BDP), 93.6% LABA in association with ICS, 53.3% LTRAs, 64.1% anti-IgE, 10.7% theophylline, 16.0% oral corticosteroids. Mean FEV1 % pred of 75.1%, median values of 300/mm3 of blood eosinophil count, 323 kU/l of serum total IgE, 24 ppb of FENO were shown. Most common comorbidities were allergic rhinitis (62.4%), gastroesophageal reflux (42.1%), sinusitis (37.9%), nasal polyposis (30.2%), allergic conjunctivitis (30.2%). 55.7% of SUA patients had exacerbations in the last 12 months, 9.7% emergency department visits, 7.3% hospitalizations. Factors associated with exacerbation risk were: obesity (OR, 95%CI 2.46, 1.11-5.41), psychic disorders (2.87, 0.89-9.30 - borderline), nasal polyps (1.86, 0.88-3.89 - borderline), partial/poor asthma treatment adherence (2.54, 0.97-6.67 - borderline), anti-IgE use in a protective way (0.26, 0.12-0.53). Comparisons to severe asthma multicentre studies and available registries showed data consistency across European and American populations. CONCLUSIONS: An international effort in the implementation of SUA patients registries could help to better understand the clinical features and to manage severe asthma, representing a non negligible socio-economic burden for health services. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171026IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1111/all.13342</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29072882">PM:29072882</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171026-MaioS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171026-MaioS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171026, Maio S</style></custom2><misc3><style face="normal" font="default">10.1111/all.13342</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86518</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Eckl-Dorna,J.</style></author><author><style face="normal" font="default"> Froschl,R.</style></author><author><style face="normal" font="default"> Lupinek,C.</style></author><author><style face="normal" font="default"> Kiss,R.</style></author><author><style face="normal" font="default"> Gattinger,P.</style></author><author><style face="normal" font="default"> Marth,K.</style></author><author><style face="normal" font="default"> Campana,R.</style></author><author><style face="normal" font="default"> Blatt,K.</style></author><author><style face="normal" font="default"> Valent,P.</style></author><author><style face="normal" font="default"> Selb,R.</style></author><author><style face="normal" font="default"> Mayer,A.</style></author><author><style face="normal" font="default"> Gangl,K.</style></author><author><style face="normal" font="default"> Steiner,I.</style></author><author><style face="normal" font="default"> Gamper,J.</style></author><author><style face="normal" font="default"> Perkmann,T.</style></author><author><style face="normal" font="default"> Zieglmayer,P.</style></author><author><style face="normal" font="default"> Gevaert,P.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author><author><style face="normal" font="default"> Niederberger,V.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otorhinolaryngology, Medical University of Vienna, Wahringer Gurtel 18-20, A-1090, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Intranasal administration of allergen increases specific IgE whereas intranasal Omalizumab does not increase serum IgE levels - a pilot study</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">BACKGROUND: Administration of the therapeutic anti-IgE antibody omalizumab to patients induces strong increases of IgE antibody levels. OBJECTIVE: To investigate the effect of intranasal administration of major birch pollen allergen Bet v 1, omalizumab or placebo on the levels of total and allergen-specific IgE in patients with birch pollen allergy. METHODS: Based on the fact that intranasal allergen application induces rises of systemic allergen-specific IgE we performed a double-blind placebo-controlled pilot trial in which birch pollen allergic subjects were challenged intranasally with omalizumab, placebo or birch pollen allergen Bet v 1. Total and allergen-specific IgE, IgG and basophil sensitivity were measured before and 8 weeks after challenge. For control purposes, total, allergen-specific IgE levels and omalizumab-IgE complexes as well as specific IgG levels were studied in subjects treated subcutaneously with either omalizumab or placebo. Effects of omalizumab on IgE production by IL-4/anti-CD40-treated PBMCs from allergic patients were studied in vitro. RESULTS: Intranasal challenge with Bet v 1 induced increases of Bet v 1-specific IgE levels by a median of 59.2% and this change differed significantly from the other treatment groups (p=0.016). No relevant change of allergen-specific and total IgE levels were observed in subjects challenged with omalizumab. Addition of omalizumab did not enhance IL-4/anti-CD40-induced IgE production in vitro. Significant rises in total IgE (mean IgE before: 131.83 kU/L to mean IgE after: 505.23 kU/L) and the presence of IgE-omalizumab complexes were observed after subcutaneous administration of omalizumab. CONCLUSION: Intranasal administration of allergen induced rises of allergen-specific IgE levels whereas intranasal administration of omalizumab did not enhance systemic total or allergen-specific IgE levels. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171030IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1111/all.13343</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29083477">PM:29083477</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171030-EcklDornaJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171030-EcklDornaJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171030, Eckl-Dorna J</style></custom2><misc3><style face="normal" font="default">10.1111/all.13343</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86523</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Snast,I.</style></author><author><style face="normal" font="default"> Reiter,O.</style></author><author><style face="normal" font="default"> Hodak,E.</style></author><author><style face="normal" font="default"> Friedland,R.</style></author><author><style face="normal" font="default"> Mimouni,D.</style></author><author><style face="normal" font="default"> Leshem,Y.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Beilinson Hospital, Rabin Medical Center, 4941492, Petah Tikva, Israel</style></auth-address><titles><title><style face="normal" font="default">Are Biologics Efficacious in Atopic Dermatitis? A Systematic Review and Meta-Analysis</style></title><secondary-title><style face="normal" font="default">Am J Clin Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Clin Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">BACKGROUND: Current systemic treatments for atopic dermatitis (AD) offer limited efficacy and are often restricted by safety concerns. Biologics may address the unmet need for improved AD therapeutics. OBJECTIVE: The aim of this study was to evaluate the efficacy and safety of biologic agents in AD. METHODS: A systematic review and meta-analysis of studies evaluating AD patients treated with biologics was performed. The primary outcome was the Eczema Area and Severity Index (EASI)-75 response, while secondary outcomes were SCOring Atopic Dermatitis (SCORAD)-75, EASI-50, SCORAD-50, Investigator Global Assessment 0/1 responses, change in responses from baseline, and adverse events. RESULTS: We included 13 randomized controlled trials (RCTs) and 10 observational studies evaluating nine biologics. High-quality evidence was available for dupilumab, nemolizumab and ustekinumab. Pooling five studies, at weeks 12-16 dupilumab 300 mg every week to every 2 weeks achieved EASI-75 responses of 55%, superior to placebo [relative risk (RR) 3.3, 95% confidence interval (CI) 2.9-3.6]. Nemolizumab had similar EASI-75 responses as placebo, but significantly improved pruritus. In online reports, lebrikizumab demonstrated superior EASI-50 responses versus placebo (RR 1.3, 95% CI 1.04-1.7), while tralokinumab had superior SCORAD-50 responses versus placebo, with borderline significance (RR 1.7, 95% CI 0.97-3.1). In two RCTs each, omalizumab and ustekinumab were comparable with placebo, while antithymic stromal lymphopoietin receptor, infliximab, and rituximab lacked adequate evidence of efficacy. All medications had a comparable safety profile to placebo. LIMITATIONS: Lack of RCTs and the use of variable outcome measures limited conclusions. CONCLUSION: Dupilumab is currently the only biologic with robust evidence of efficacy in AD. Nemolizumab, lebrikizumab, and tralokinumab show promise but further data are needed. Longer follow-up and larger studies will establish their safety profile</style></abstract><notes><style face="normal" font="default">DA - 20171103IS - 1179-1888 (Electronic)IS - 1175-0561 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Israel -</style></notes><work-type><style face="normal" font="default">10.1007/s40257-017-0324-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29098604">PM:29098604</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Am J Clin Dermatol\20171103-SnastI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Am J Clin Dermatol\20171103-SnastI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171103, Snast I</style></custom2><misc3><style face="normal" font="default">10.1007/s40257-017-0324-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86524</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Singh,A.</style></author><author><style face="normal" font="default"> Shannon,C.P.</style></author><author><style face="normal" font="default"> Kim,Y.W.</style></author><author><style face="normal" font="default"> Yang,C.X.</style></author><author><style face="normal" font="default"> Balshaw,R.</style></author><author><style face="normal" font="default"> Cohen Freue,G.V.</style></author><author><style face="normal" font="default"> Gauvreau,G.M.</style></author><author><style face="normal" font="default"> Fitzgerald,J.M.</style></author><author><style face="normal" font="default"> Boulet,L.P.</style></author><author><style face="normal" font="default"> O'Byrne,P.M.</style></author><author><style face="normal" font="default"> Tebbutt,S.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of British Columbia, Surrey, British Columbia, Canada ; amrit.singh@hli.ubc.ca</style></auth-address><titles><title><style face="normal" font="default">Novel Blood-based Transcriptional Biomarker Panels Predict the Late Phase Asthmatic Response</style></title><secondary-title><style face="normal" font="default">Am J Respir Crit Care Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Respir Crit Care Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="31" Month="10" Year="2017">2017/10/31</year></dates><abstract><style face="normal" font="default">RATIONALE: The allergen inhalation challenge is used in clinical trials to test the efficacy of new treatments in attenuating the late phase asthmatic response (LAR) and associated airway inflammation in subjects with allergic asthma. However, not all subjects with allergic asthma develop the LAR after allergen inhalation. Blood-based transcriptional biomarkers that can identify such individuals may help in subject recruitment for clinical trials as well as provide novel molecular insights. OBJECTIVES: To identify blood-based transcriptional biomarker panels that can predict an individual's response to allergen inhalation challenge. METHODS: We applied RNA sequencing to total RNA from whole blood (n=36) collected before and after allergen challenge and generated both genome-guided and de novo datasets: UCSC genes, UCSC gene-isoforms, Ensembl and Trinity. Candidate biomarker panels were validated using the NanoString platform in an independent cohort of 33 subjects. MEASUREMENT AND MAIN RESULTS: The Trinity biomarker panel consisting of known and novel biomarker transcripts had an AUROC of greater than 0.70 in both the discovery and validation cohorts. The Trinity biomarker panel was useful in predicting the response of subjects that elicited different responses (accuracy between 0.65-0.71) and subjects that elicit a dual response (accuracy between 0.70-0.75) upon repeated allergen inhalation challenges. CONCLUSIONS: Interestingly, the biomarker panel containing novel transcripts successfully validated compared to panels with known, well-characterized genes. These biomarker-blood tests may be used to identify asthmatic subjects who develop the LAR, and may also represent members of novel molecular mechanisms that can be targeted for therapy</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1535-4970 (Electronic)IS - 1073-449X (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1164/rccm.201701-0110OC</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29087730">PM:29087730</url></web-urls><pdf-urls><url ppv-ref="no">amrit.singh@hli.ubc.ca</url><url ppv-ref="no">Scott.Tebbutt@hli.ubc.ca</url></pdf-urls><text-urls><url ppv-ref="no">researchgate</url></text-urls><related-urls><url ppv-ref="no">presto - 1 anno</url></related-urls></urls><custom2><style face="normal" font="default">20171031, Singh A</style></custom2><misc3><style face="normal" font="default">10.1164/rccm.201701-0110OC</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86525</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Panda,R.</style></author><author><style face="normal" font="default"> Boyer,M.</style></author><author><style face="normal" font="default"> Garber,E.A.E.</style></author></authors></contributors><titles><title><style face="normal" font="default">A multiplex competitive ELISA for the detection and characterization of gluten in fermented-hydrolyzed foods</style></title><secondary-title><style face="normal" font="default">Anal Bioanal Chem</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Anal Bioanal Chem</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1618-2650</style></isbn><abstract><style face="normal" font="default">A novel competitive ELISA was developed utilizing the G12, R5, 2D4, MIoBS, and Skerritt antibody-HRP conjugates employed in nine commercial ELISA test kits that are routinely used for gluten detection. This novel multiplex competitive ELISA simultaneously measures gliadin-, deamidated gliadin-, and glutenin-specific epitopes. The assay was used to evaluate 20 wheat beers, 20 barley beers, 6 barley beers processed to reduce gluten, 15 soy sauces, 6 teriyaki sauces, 6 Worcestershire sauces, 6 vinegars, and 8 sourdough breads. For wheat beers, the apparent gluten concentration values obtained by the G12 and Skerritt antibodies were typically higher than those obtained using the R5 antibodies. The sourdough bread samples resulted in higher apparent gluten concentration values with the Skerritt antibody, while the values generated by the G12 and R5 antibodies were comparable. Although the soy-based sauces showed non-specific inhibition with the multiple R5 and G12 antibodies, their overall profile was distinguishable from the other categories of fermented foods. Cluster analysis of the apparent gluten concentration values obtained by the multiplex competitive ELISA, as well as the relative response of the nine gluten-specific antibodies used in the assay to different gluten proteins/peptides, distinguishes among the different categories of fermented-hydrolyzed foods by recognizing the differences in the protein/peptide profiles characteristic of each product. This novel gluten-based multiplex competitive ELISA provides insight into the extent of proteolysis resulting from various fermentation processes, which is essential for accurate gluten quantification in fermented-hydrolyzed foods</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s00216-017-0677-z</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s00216-017-0677-z</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Anal Bioanal Chem\20171114-PandaR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Anal Bioanal Chem\20171114-PandaR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Panda R</style></custom2><misc3><style face="normal" font="default">10.1007/s00216-017-0677-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86526</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,H.</style></author><author><style face="normal" font="default"> Honda,M.</style></author><author><style face="normal" font="default"> Saito,A.</style></author><author><style face="normal" font="default"> Kajisa,T.</style></author><author><style face="normal" font="default"> Yanase,Y.</style></author><author><style face="normal" font="default"> Sakata,T.</style></author></authors></contributors><titles><title><style face="normal" font="default">Non-optical detection of allergic response with a cell-coupled gate field-effect transistor</style></title><secondary-title><style face="normal" font="default">Anal Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Anal Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">In this study, we report the label-free and reliable detection of allergic response using a cell-coupled gate field-effect transistor (cell-based FET). Rat basophilic leukemia (RBL-2H3) cells were cultured as a signal transduction interface to induce allergic reaction on the gate oxide surface of the FET, because IgE antibodies, which bind to Fcepsilon receptors at the RBL-2H3 cell membrane, are specifically cross-linked by allergens, resulting in the allergic response of RBL-2H3 cells. In fact, the surface potential at the FET gate decreased owing to secretions such as histamine from the IgE-bound RBL-2H3 cells, which reacted with the allergen. This is because histamine, as one of the candidate secretions, shows basicity, resulting in a change in pH around the cell/gate interface. That is, the RBL-2H3-cell-based FET used in this study was originally from an ion-sensitive FET (ISFET), whose oxide surface (Ta2O5) with hydroxyl groups is fully responsive to pH on the basis of the equilibrium reaction. The allergic response of RBL-2H3 cells on the gate was also confirmed by estimating the amount of beta-hexosaminidase released together with histamine and was analyzed using the electrical properties based on an inflammatory response of secreted histamine with the vascular endothelial cell-based FET. Thus, the allergic responses were monitored in a non-optical and real-time manner using the cell-based FETs with the cellular layers on the gate, which reproduced the in vivo system and were useful for the reliable detection of allergic reaction</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1520-6882 (Electronic)IS - 0003-2700 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1021/acs.analchem.7b03688</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29116752">PM:29116752</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Anal Chem\20171108-YangH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Anal Chem\20171108-YangH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Yang H</style></custom2><misc3><style face="normal" font="default">10.1021/acs.analchem.7b03688</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86527</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lang,D.M.</style></author><author><style face="normal" font="default"> Portnoy,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy and Clinical Immunology, Cleveland Clinic, Respiratory Institute, Cleveland, Ohio.</style></auth-address><titles><title><style face="normal" font="default">Allergy and immunology practice parameters and guidelines: The new normal</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29103800">PM:29103800</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-LangDM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-LangDM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Lang DM</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86528</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dykewicz,M.S.</style></author><author><style face="normal" font="default"> Wallace,D.V.</style></author><author><style face="normal" font="default"> Baroody,F.</style></author><author><style face="normal" font="default"> Bernstein,J.</style></author><author><style face="normal" font="default"> Craig,T.</style></author><author><style face="normal" font="default"> Finegold,I.</style></author><author><style face="normal" font="default"> Huang,F.</style></author><author><style face="normal" font="default"> Larenas-Linnemann,D.</style></author><author><style face="normal" font="default"> Meltzer,E.</style></author><author><style face="normal" font="default"> Steven,G.</style></author><author><style face="normal" font="default"> Bernstein,D.I.</style></author><author><style face="normal" font="default"> Blessing-Moore,J.</style></author><author><style face="normal" font="default"> Dinakar,C.</style></author><author><style face="normal" font="default"> Greenhawt,M.</style></author><author><style face="normal" font="default"> Horner,C.C.</style></author><author><style face="normal" font="default"> Khan,D.A.</style></author><author><style face="normal" font="default"> Lang,D.</style></author><author><style face="normal" font="default"> Oppenheimer,J.</style></author><author><style face="normal" font="default"> Portnoy,J.M.</style></author><author><style face="normal" font="default"> Randolph,C.R.</style></author><author><style face="normal" font="default"> Rank,M.A.</style></author><author><style face="normal" font="default"> Dykewicz,M.S.</style></author><author><style face="normal" font="default"> Wallace,D.V.</style></author></authors></contributors><titles><title><style face="normal" font="default">Treatment of seasonal allergic rhinitis: An evidence-based focused 2017 guideline update</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.012</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29103802">PM:29103802</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-DykewiczMS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-DykewiczMS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Dykewicz MS</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.012</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86529</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Elliott,T.</style></author><author><style face="normal" font="default"> Shih,J.</style></author><author><style face="normal" font="default"> Dinakar,C.</style></author><author><style face="normal" font="default"> Portnoy,J.</style></author><author><style face="normal" font="default"> Fineman,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">New York University Medical Center, New York, New York</style></auth-address><titles><title><style face="normal" font="default">American College of Allergy, Asthma &amp; Immunology Position Paper on the Use of Telemedicine for Allergists</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">The integration of telecommunications and information systems in health care first began 4 decades ago with 500 patient consultations performed via interactive television. The use of telemedicine services and technology to deliver health care at a distance is increasing exponentially. Concomitant with this rapid expansion is the exciting ability to provide enhancements in quality and safety of care. Telemedicine enables increased access to care, improvement in health outcomes, reduction in medical costs, better resource use, expanded educational opportunities, and enhanced collaboration between patients and physicians. These potential benefits should be weighed against the risks and challenges of using telemedicine. The American College of Allergy, Asthma, and Immunology advocates for incorporation of meaningful and sustained use of telemedicine in allergy and immunology practice. This article serves to offer policy and position statements of the use of telemedicine pertinent to the allergy and immunology subspecialty</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.052</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29103799">PM:29103799</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-ElliottT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-ElliottT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Elliott T</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.052</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86530</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Arkwright,P.D.</style></author><author><style face="normal" font="default"> Sharma,V.</style></author><author><style face="normal" font="default"> Ewing,C.I.</style></author><author><style face="normal" font="default"> Hughes,S.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Paediatric Allergy &amp; Immunology, University of Manchester, Manchester, United Kingdom; Royal Manchester Children's Hospital, Manchester, United Kingdom.</style></auth-address><titles><title><style face="normal" font="default">Home-based program of maintaining unresponsiveness in children with allergic reactions to larger amounts of peanuts</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="7" Month="11" Year="2017">2017/11/7</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171111IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.064</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29126711">PM:29126711</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171111ArkwrightPD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171111ArkwrightPD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171111, Arkwright PD</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.064</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86531</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Antico,A.</style></author><author><style face="normal" font="default"> Vegro,M.</style></author><author><style face="normal" font="default"> Rasio,G.</style></author><author><style face="normal" font="default"> Pasini,G.</style></author><author><style face="normal" font="default"> Curioni,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit, Ospedale Civile Srl, Volta Mantovana, Mantua, Italy.</style></auth-address><titles><title><style face="normal" font="default">Bee moth (Galleria mellonella) allergy: New insight from a case of monosensitization</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.057</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29107466">PM:29107466</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-AnticoA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-AnticoA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Antico A</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.057</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86532</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Blaiss,M.S.</style></author><author><style face="normal" font="default"> Castro,M.</style></author><author><style face="normal" font="default"> Chipps,B.E.</style></author><author><style face="normal" font="default"> Zitt,M.</style></author><author><style face="normal" font="default"> Panettieri,R.A.,Jr.</style></author><author><style face="normal" font="default"> Foggs,M.B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatrics, Medical College of Georgia at Augusta University, Augusta, Georgia.</style></auth-address><titles><title><style face="normal" font="default">Guiding principles for use of newer biologics and bronchial thermoplasty for patients with severe asthma</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">BACKGROUND: Severe asthma poses significant disease-related and economic burdens in the United States. Challenges in practice include how to define "severe asthma" for a given patient, knowing which are the right tests to perform and when, and having a better understanding of a patient's asthma phenotype. Furthermore, current guidelines do not address a clear, practical approach to treatment that is based on a patient's asthma phenotype. OBJECTIVE: To develop a consensus on the definition of severe asthma, the role of biomarkers and phenotyping severe asthma, and the use of newer biologic therapies and bronchial thermoplasty to help guide practicing clinicians. METHODS: A roundtable meeting was convened with a panel of severe asthma experts to discuss areas in practice that are not adequately addressed by current guidelines, specifically phenotype-guided treatment. RESULTS: We describe a consensus on the definition of severe asthma, asthma phenotyping with the use of available biomarkers, and guiding principles for newer biologic therapies and bronchial thermoplasty. CONCLUSION: To optimize therapy and improve outcomes such as daily symptoms, quality of life, exacerbations, and hospitalizations, a clear picture of a patient's asthma phenotype is needed to guide therapy. Determining asthma phenotypes is the foundation of precision medicine for this persistent, often difficult-to-treat disease</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.058</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29103801">PM:29103801</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-BlaissMS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171106-BlaissMS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Blaiss MS</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.058</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86533</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Alaya,S.</style></author><author><style face="normal" font="default"> Mofredj,A.</style></author><author><style face="normal" font="default"> Darmon,N.</style></author><author><style face="normal" font="default"> Tassaioust,K.</style></author><author><style face="normal" font="default"> Mrabet,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Anaphylactic Shock Following Repeated Rasburicase Treatment</style></title><secondary-title><style face="normal" font="default">Ann Pharmacother</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Pharmacother</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="1" Month="11" Year="2017">2017/11/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 1542-6270 (Electronic)IS - 1060-0280 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1177/1060028017740599</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29095045">PM:29095045</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Pharmacother\20171102-AlayaS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Pharmacother\20171102-AlayaS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Alaya S</style></custom2><misc3><style face="normal" font="default">10.1177/1060028017740599</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86534</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Van Hoang,V</style></author><author><style face="normal" font="default"> Ochi,T.</style></author><author><style face="normal" font="default"> Kurata,K.</style></author><author><style face="normal" font="default"> Arita,Y.</style></author><author><style face="normal" font="default"> Ogasahara,Y.</style></author><author><style face="normal" font="default"> Enomoto,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Environmental Science and Engineering, Kochi University of Technology, 185 Miyanokuchi, Tosayamada, Kami, Kochi, 782-8502, Japan</style></auth-address><titles><title><style face="normal" font="default">Nisin-induced expression of recombinant T cell epitopes of major Japanese cedar pollen allergens in Lactococcus lactis</style></title><secondary-title><style face="normal" font="default">Appl Microbiol Biotechnol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Appl Microbiol Biotechnol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">Japanese cedar pollinosis is a seasonal allergic disease caused by two major pollen allergens: Cry j 1 and Cry j 2 antigens. To develop an oral vaccine to treat pollinosis, we constructed recombinant Lactococcus lactis harboring the gene encoding fused T cell epitopes from the Cry j 1 and Cry j 2 antigens. The recombinant T cell epitope peptide was designed to contain the fused cholera toxin B subunit as an adjuvant and a FLAG tag at the C-terminus. An expression plasmid was constructed by inserting the T cell epitope peptide gene into the multiple cloning sites of plasmid pNZ8148, an Escherichia coli-L. lactis shuttle vector. The constructed plasmid was transformed into L. lactis NZ9000 for expression induced by nisin, an antibacterial peptide from L. lactis. The expression of the epitope peptide was induced with 10-40 ng/mL nisin, and the expressed T cell epitope peptide was detected by western blot analysis using an anti-FLAG antibody and an antibody against the T cell epitopes. The concentration of the epitope peptide was estimated to be ~ 22 mg/L of culture in the presence of 40 ng/mL nisin, although it varied depending on the nisin concentration, the culture time, and the bacterial concentration when nisin was added. The expression of the recombinant epitope peptide in L. lactis, an organism generally recognized as safe, as demonstrated in this study, may contribute to the development of an oral vaccine for the treatment of pollinosis</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 1432-0614 (Electronic)IS - 0175-7598 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1007/s00253-017-8579-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29094185">PM:29094185</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Appl Microbiol Biotechnol\20171102-VanHoangV.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Appl Microbiol Biotechnol\20171102-VanHoangV.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Van Hoang V</style></custom2><misc3><style face="normal" font="default">10.1007/s00253-017-8579-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86536</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,Y.</style></author><author><style face="normal" font="default"> Hwang,Y.H.</style></author><author><style face="normal" font="default"> Kim,K.J.</style></author><author><style face="normal" font="default"> Park,A.K.</style></author><author><style face="normal" font="default"> Paik,M.J.</style></author><author><style face="normal" font="default"> Kim,S.H.</style></author><author><style face="normal" font="default"> Lee,S.U.</style></author><author><style face="normal" font="default"> Yee,S.T.</style></author><author><style face="normal" font="default"> Son,Y.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon, Jeonnam, 57922, Korea</style></auth-address><titles><title><style face="normal" font="default">Proteomic and transcriptomic analysis of lung tissue in OVA-challenged mice</style></title><secondary-title><style face="normal" font="default">Arch Pharm Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arch Pharm Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">Asthma is a long term inflammatory disease of the airway of lungs characterized by variable airflow obstruction and bronchospasm. Asthma is caused by a complex combination of environmental and genetic interactions. In this study, we conducted proteomic analysis of samples derived from control and OVA challenged mice for environmental respiratory disease by using 2-D gel electrophoresis. In addition, we explored the genes associated with the environmental substances that cause respiratory disease and conducted RNA-seq by next-generation sequencing. Proteomic analysis revealed 7 up-regulated (keratin KB40, CRP, HSP27, chaperonin containing TCP-1, TCP-10, keratin, and albumin) and 3 down-regulated proteins (PLC-alpha, PLA2, and precursor ApoA-1). The expression diversity of many genes was found in the lung tissue of OVA challenged moue by RNA-seq. 146 genes were identified as significantly differentially expressed by OVA treatment, and 118 genes of the 146 differentially expressed genes were up-regulated and 28 genes were downregulated. These genes were related to inflammation, mucin production, and airway remodeling. The results presented herein enable diagnosis and the identification of quantitative markers to monitor the progression of environmental respiratory disease using proteomics and genomic approaches</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 0253-6269 (Print)IS - 0253-6269 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1007/s12272-017-0972-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29086354">PM:29086354</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Arch Pharm Res\20171031-LeeY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Arch Pharm Res\20171031-LeeY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Lee Y</style></custom2><misc3><style face="normal" font="default">10.1007/s12272-017-0972-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86545</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kleine-Tebbe,J.</style></author><author><style face="normal" font="default"> Jakob,T.</style></author></authors></contributors><titles><title><style face="normal" font="default">Molecular Allergy Diagnostics</style></title><secondary-title><style face="normal" font="default">Books</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Books</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">This book, based on a recent German publication, offers an overview of basic data and recent developments in the groundbreaking field of molecular allergology. It comprehensively explores the origin and structure of single allergen molecules ("components") and their utility in improving the management of type I, IgE-mediated allergic reactions and disorders like allergic respiratory diseases, food allergies, and anaphylaxis.</style></abstract><notes><style face="normal" font="default">LA - ENG</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://www.springer.com/gp/book/9783319424989</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Books\Molecular Allergy Diagnostics.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Books\Molecular Allergy Diagnostics.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, AA VV</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86547</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kudo,F.</style></author><author><style face="normal" font="default"> Ikutani,M.</style></author><author><style face="normal" font="default"> Iseki,M.</style></author><author><style face="normal" font="default"> Takaki,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immune Regulation, Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine, Chiba, Japan</style></auth-address><titles><title><style face="normal" font="default">Cyclosporin A indirectly attenuates activation of group 2 innate lymphoid cells in papain-induced lung inflammation</style></title><secondary-title><style face="normal" font="default">Cell Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Cell Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">Cyclosporin A (CsA) is a well-known immunosuppressant that is used against steroid-resistant asthma. Group 2 innate lymphoid cells (ILC2s) and type 2 helper T (Th2) cells produce Th2 cytokines including IL-5 and play important roles in asthma pathogenesis. Here, we studied the effects of CsA in allergen-induced lung inflammation in mice and found that CsA decreased the number of lung ILC2s and attenuated papain-induced activation of ILC2s accompanied with IL-5 expression. The ILC2 suppression mediated by CsA was not observed in culture or in lymphocyte-deficient Rag2-/- mice. Thus, we propose a new suppressive effect of CsA, i.e., administration of CsA indirectly suppresses maintenance and activation of lung ILC2s in addition to direct suppression of T-cell activation and cytokine production</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1090-2163 (Electronic)IS - 0008-8749 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.cellimm.2017.10.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108648">PM:29108648</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Cell Immunol\20171107-KudoF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Cell Immunol\20171107-KudoF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Kudo F</style></custom2><misc3><style face="normal" font="default">10.1016/j.cellimm.2017.10.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86548</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,X.M.</style></author><author><style face="normal" font="default"> Wang,Y.B.</style></author><author><style face="normal" font="default"> Wu,Q.</style></author><author><style face="normal" font="default"> Bian,Z.R.</style></author><author><style face="normal" font="default"> Che,X.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Geriatric Medicine, the Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Ji'nan, 250011, China</style></auth-address><titles><title><style face="normal" font="default">Effects of Ligustrazine on Airway Inflammation in A Mouse Model of Neutrophilic Asthma</style></title><secondary-title><style face="normal" font="default">Chin J Integr Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Chin J Integr Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To investigate the effects of ligustrazine (LTZ) on airway inflammation in a mouse model of neutrophilic asthma (NA). METHODS: Forty healthy C57BL/6 female mice were randomly divided into 4 groups using a random number table, including the normal control, NA, LTZ and dexamethasone (DXM) groups, with 10 rats in each group. The NA mice model was established by the method of ovalbumin combined with lipopolysaccharide sensitization. At 0.5 h before each challenge, LTZ and DXM groups were intraperitoneally injected with LTZ (80 mg/kg) or DXM (0.5 mg/kg) for 14 d, respectively, while the other two groups were given the equal volume of normal saline. After last challenge for 24 h, the aerosol inhalation of methacholine was performed and the airway reactivity was measured. The bronchoalveolar lavage fluid (BALF) was collected. The Wright-Giemsa staining was used for total white blood cells and differential counts. The levels of cytokines interleukin (IL)-17 and IL-10 were detected by enzyme-linked immunosorbent assay. The pathological change of lung tissue was observed by hematoxylin eosin staining. RESULTS: The airway responsiveness of the NA group was significantly higher than the normal control group (P&lt;0.05), while those in the LTZ and DXM groups were significantly lower than the NA group (P&lt;0.05). The neutrophil and eosinophil counts in the LTZ and DXM groups were significantly lower than the NA group (P&lt;0.05), and those in the LTZ group were significantly lower than the DXM group (P&lt;0.05). There were a large number of peribronchiolar and perivascular inflammatory cells in filtration in the NA group. The airway inflammation in the LTZ and DXM groups were significantly alleviated than the NA group. The infiltration in the LTZ group was significantly reduced than the DXM group. Compared with the normal control group, the IL-17 level in BALF was significantly increased and the IL-10 level in BALF was significantly decreased in the NA group (P&lt;0.05). LTZ and DXM treatment significantly decreased IL-17 levels and increased IL-10 levels compared with the NA group (P&lt;0.05), and the changes in the above indices were more significant in the LTZ group (P&lt;0.05). CONCLUSION: LTZ could alleviate the airway inflammation in the NA mice model through increasing the IL-10 level and decreasing the IL-17 level</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1672-0415 (Print)IS - 1672-0415 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s11655-017-2830-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29086220">PM:29086220</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Chin J Integr Med\20171031-LiuXM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Chin J Integr Med\20171031-LiuXM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Liu XM</style></custom2><misc3><style face="normal" font="default">10.1007/s11655-017-2830-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86549</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kitoko,J.Z.</style></author><author><style face="normal" font="default"> de Castro,L.L.</style></author><author><style face="normal" font="default"> Nascimento,A.P.</style></author><author><style face="normal" font="default"> Abreu,S.C.</style></author><author><style face="normal" font="default"> Cruz,F.F.</style></author><author><style face="normal" font="default"> Arantes,A.C.</style></author><author><style face="normal" font="default"> Xisto,D.G.</style></author><author><style face="normal" font="default"> Martins,M.A.</style></author><author><style face="normal" font="default"> Morales,M.M.</style></author><author><style face="normal" font="default"> Rocco,P.R.M.</style></author><author><style face="normal" font="default"> Olsen,P.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of Clinical Bacteriology and Immunology, Faculty of Pharmacy, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil</style></auth-address><titles><title><style face="normal" font="default">Therapeutic administration of bone marrow-derived mesenchymal stromal cells reduces airway inflammation without upregulating Tregs in experimental asthma</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">BACKGROUND: Prophylactic administration of mesenchymal stromal cells (MSCs) derived from adipose (AD-MSC) and bone marrow tissue (BM-MSC) in ovalbumin-induced asthma hinders inflammation in a Treg-dependent manner. It is uncertain whether MSCs act through Tregs when inflammation is already established in asthma induced by a clinically relevant allergen. OBJECTIVE: Evaluate the effect of therapeutic administration of MSCs on inflammation and Treg cells in house dust mite (HDM)-induced asthma. METHODS: BM-MSCs and AD-MSCs were administered intratracheally to C57BL/6 mice 1 day after the last HDM challenge. Lung function, remodeling and parenchymal inflammation, were assayed 3 or 7 days after MSCs treatment, through invasive plethysmography and histology, respectively. Bronchoalveolar lavage fluid (BALF) and mediastinal lymph nodes (mLNs) were assessed for lymphocyte phenotyping by flow cytometry. MSCs were studied regarding their potential to induce Treg cells from primed and unprimed lymphocytes in vitro. RESULTS: BM-MSCs, but not AD-MSCs, reduced lung influx of eosinophils and B cells and increased IL-10 levels in HDM-challenged mice. Neither BM-MSCs nor AD-MSCs reduced lung parenchymal inflammation, airway hyperresponsiveness or mucus hypersecretion. BM- and AD-MSCs did not upregulate Treg cell counts within the airways and mLNs, but BM-MSCs decreased the pro-inflammatory profile of alveolar macrophages. Co-culture of BM-MSCs and AD-MSCs with allergen-stimulated lymphocytes reduced Treg cell counts in a cell to cell contact independent manner, although co-culture of both MSCs with unprimed lymphocytes upregulated Treg cell counts. CONCLUSIONS: MSCs therapeutically administered exert anti-inflammatory effects in the airway of HDM-challenged mice, but do not ameliorate lung function or remodeling. Although MSC pre-treatment can increase Treg cell numbers, it is highly unlikely that the MSCs will induce Treg cell expansion when lymphocytes are allergenically primed in an established lung inflammation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171025IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13048</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29068567">PM:29068567</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171025-KitokoJZ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171025-KitokoJZ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171025, Kitiko JZ</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13048</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86550</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Geslewitz,W.E.</style></author><author><style face="normal" font="default"> Percopo,C.M.</style></author><author><style face="normal" font="default"> Rosenberg,H.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Inflammation Immunobiology Section, Laboratory of Allergic Diseases, NIAID, National Institutes of Health, Bethesda, Maryland</style></auth-address><titles><title><style face="normal" font="default">Eosinophil persistence in vivo and sustained viability ex vivo in response to respiratory challenge with fungal allergens</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">BACKGROUND: Eosinophils are immunomodulatory leukocytes that contribute to the pathogenesis of Th2 driven asthma and allergic lung diseases. OBJECTIVE: Our goal was to identify unique properties of eosinophils recruited to the lungs and airways of mice in response to challenge with asthma-associated fungal allergens. METHODS: Mice were challenged intranasally on days 0, 3 and 6 with a filtrate of Alternaria alternata. Recruited eosinophils were enumerated in bronchoalveolar lavage fluid. Eosinophils were also isolated from lungs of mice sensitized and challenged with Aspergillus fumigatus and evaluated ex vivo in tissue culture. RESULTS: Eosinophils persist in the airways for several weeks in response to brief provocation with A. alternata in wild-type, Gm-csf- and eotaxin-1-gene-deleted mice, while eosinophils are recruited but do not persist in the absence of IL-13. Eosinophils isolated from the lungs A. alternata-challenged mice are cytokine-enriched compared to those from IL5tg mice, including 800-fold higher levels of eotaxin-1. Furthermore, eosinophils from the lungs and spleen of fungal-challenged wild-type are capable of prolonged survival ex vivo, in contrast to eosinophils from both un-treated and fungal-allergen challenged IL5tg mice, which undergo rapid demise in the absence of exogenous cytokine support. TNFalpha (but not IL5, IL-3, eotaxin-1 or GM-CSF) was detected in supernatants of ex vivo eosinophil cultures from the lungs of fungal-allergen challenged wild-type mice. However, neither TNFalpha gene-deletion nor anti-TNFalpha neutralizing antibodies had any impact sustained eosinophil survival ex vivo. CONCLUSION AND CLINICAL RELEVANCE: Eosinophils are phenotypically and functionally heterogeneous. As shown here, eosinophils from fungal-allergen challenged wild-type mice maintain a distinct cytokine profile, and, unlike eosinophils isolated from IL5tg mice, they survive ex vivo in the absence of exogenous pro-survival cytokine support. As treatments for asthma currently in development focus on limiting eosinophil viability via strategic cytokine blockade, the molecular mechanisms underlying differential survival merit further investigation.</style></abstract><notes><style face="normal" font="default">DA - 20171025IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13050</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29068539">PM:29068539</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171025-GeslewitzWE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171025-GeslewitzWE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171025, Geslewitz WE</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13050</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86551</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rajakulasingam,R.K.</style></author><author><style face="normal" font="default"> Farah,N.</style></author><author><style face="normal" font="default"> Huber,P.A.J.</style></author><author><style face="normal" font="default"> Durham,S.R.</style></author><author><style face="normal" font="default"> Clark,A.T.</style></author><author><style face="normal" font="default"> Nasser,S.M.</style></author><author><style face="normal" font="default"> Krishna,M.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Medicine/Allergy, Homerton University Hospital NHS Foundation Trust, London, UK</style></auth-address><titles><title><style face="normal" font="default">Practice and Safety of Allergen Specific Immunotherapy for Allergic Rhinitis in the UK National Health Service: A report of 'real world' clinical practice</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">Allergen specific immunotherapy (SIT) alleviates symptoms, improves health-related quality of life and alters the natural course of the disease in patients suffering from allergic rhinitis. It is currently delivered in the UK National Health Service (NHS) via 2 modalities namely subcutaneous injection immunotherapy (SCIT) and sublingual immunotherapy (SLIT). The latter has a superior safety profile - anaphylaxis is a rare occurrence. Most vaccines currently employed for SIT in the UK NHS are unlicensed and available on a named-patient basis and prescribed in secondary care by a specialist. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - LetterCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13052</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108101">PM:29108101</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171106-RajakulasingamRK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171106-RajakulasingamRK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Rajakulasingam RK</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13052</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86553</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,M.C.</style></author><author><style face="normal" font="default"> Xiao,H.</style></author><author><style face="normal" font="default"> Breslin,L.</style></author><author><style face="normal" font="default"> Bochner,B.</style></author><author><style face="normal" font="default"> Schroeder,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Johns Hopkins University, School of Medicine</style></auth-address><titles><title><style face="normal" font="default">Enhanced Antigen-presenting and T-cell Functions During Late-phase Allergic Responses in the Lung</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergic inflammation is a common feature of asthma and may contribute to both development and perpetuation of disease. The interaction of antigen presenting cells (APC) with sensitized helper T lymphocytes (TC) producing Th2 cytokines may determine the inflammatory response. Recruitment of APC and TC to the lung during allergic responses has been demonstrated, but functional studies in humans have been limited. OBJECTIVE: This study examined the function of APC and TC accumulating at sites of inflammation after segmental allergen challenge (SAC). METHODS: 15 allergic patients underwent SAC, and cells from bronchoalveolar lavage (BAL) were collected after 24 hours. APC and TC from the blood and BAL were purified based on expression of the monocyte marker, CD14; the plasmacytoid dendritic cell (pDC) marker, BDCA4, identifying neuropilin 1 (NRP1); and the helper T cell marker, CD4. Functional activity was assessed using allergen-induced T cell proliferation. Flow-cytometry identified cells expressing CD14 and NRP1. RESULTS: SAC resulted in a 12-fold increase of mononuclear cells having the morphologic appearance of blood monocytes. Most of these cells co-expressed CD14 and NRP1. After saline challenge, BAL mononuclear cells demonstrated little APC function Following SAC, BAL mononuclear cells showed function equal to pDC from blood and greater than blood monocytes. Purified NRP1+ cells from BAL had even greater function than pDC cells from blood (p = .008). Using consistent sources of APC, enhanced proliferation of TC from lung compared to blood was also demonstrated (p = .002). CONCLUSIONS: The marked increase in APC function for allergen-specific TC proliferation during allergic inflammation is largely due to the recruitment of monocytes and dendritic cells. There is also an enhanced response in the lung TC population, consistent with recruitment of allergen-specific T cells. Interactions between recruited APC and TC may occur as an early event promoting allergic airway inflammation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13054</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29105205">PM:29105205</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171106-LiuMC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171106-LiuMC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Liu MC</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13054</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86554</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Asero,R.</style></author><author><style face="normal" font="default"> Piantanida,M.</style></author><author><style face="normal" font="default"> Pinter,E.</style></author><author><style face="normal" font="default"> Pravettoni,V.</style></author></authors></contributors><auth-address><style face="normal" font="default">Ambulatorio di Allergologia, Clinica San Carlo, Paderno Dugnano, MI, Italy</style></auth-address><titles><title><style face="normal" font="default">The clinical relevance of lipid transfer protein</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">Despite a huge number of studies, many aspects of the lipid transfer protein (LTP)-syndrome, the most frequent primary food allergy in Mediterranean countries, remain unclear. Its peculiar geographical distribution, along with the extreme variability of its clinical expression make this type of food allergy something unique in the panorama of IgE-mediated food-induced allergic reactions. The present review article tried to summarize the current knowledge about the most important aspects of LTP sensitization and allergy, along with the importance of positive and negative co-factors in the clinical expression of the syndrome as well as the issues regarding the cross-reactivity between LTPs present in botanically related and unrelated foods. Further, the possible absence of the protein from some plant foods is discussed. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13053</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29105202">PM:29105202</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171106-AseroR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171106-AseroR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Asero R</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13053</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86556</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lanser,B.J.</style></author><author><style face="normal" font="default"> Leung,D.Y.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Division of Allergy and Clinical Immunology, National Jewish Health, 1400 Jackson St, J322, Denver, CO, 80206, USA.</style></auth-address><titles><title><style face="normal" font="default">The Current State of Epicutaneous Immunotherapy for Food Allergy: a Comprehensive Review</style></title><secondary-title><style face="normal" font="default">Clin Rev Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Rev Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="28" Month="10" Year="2017">2017/10/28</year></dates><abstract><style face="normal" font="default">The food allergy epidemic of recent years has led to the search for safe and effective methods of immunotherapy for foods. Studies of epicutaneous immunotherapy (EPIT) in mice have shown promising safety and efficacy data. Murine models have also identified probable mechanisms for the development of tolerance to food allergens, including the induction of regulatory T cells. Clinical data is lacking, but relatively small and early studies among peanut and cow's milk allergic subjects suggest that EPIT has an excellent safety profile, particularly compared to other methods of specific allergen immunotherapy. Efficacy data are also promising for peanut allergy, among younger patients (ages 4-11 years of age), suggesting that a majority of young patients will experience an increase in reaction threshold with therapy. The goal of this therapy is the protection from accidental exposures to a known food allergen. Additional clinical data is needed to prove efficacy and further demonstrate the safety profile of EPIT for food allergy, prior to approval by the Food and Drug Administration</style></abstract><notes><style face="normal" font="default">DA - 20171029IS - 1559-0267 (Electronic)IS - 1080-0549 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s12016-017-8650-3</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29081025">PM:29081025</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Rev Allergy Immunol\20171029-LanserBJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Rev Allergy Immunol\20171029-LanserBJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171029, Lanser BJ</style></custom2><misc3><style face="normal" font="default">10.1007/s12016-017-8650-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86569</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Manohar,M.</style></author><author><style face="normal" font="default"> Verma,A.K.</style></author><author><style face="normal" font="default"> Upparahalli,V.S.</style></author><author><style face="normal" font="default"> Goyal,H.</style></author><author><style face="normal" font="default"> Mishra,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorders Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA</style></auth-address><titles><title><style face="normal" font="default">Food-Induced Acute Pancreatitis</style></title><secondary-title><style face="normal" font="default">Dig Dis Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Dig Dis Sci</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">Food allergy, a commonly increasing problem worldwide, defined as an adverse immune response to food. A variety of immune-related effector cells such as mast cells, eosinophils, neutrophils, and T cells are involved in food-related allergic responses categorized as IgE mediated, non-IgE mediated, and mixed (IgE and non-IgE) depending upon underlying immunological mechanisms. The dietary antigens mainly target the gastrointestinal tract including pancreas that gets inflamed due to food allergy and leads acute pancreatitis. Reports indicate several food proteins induce pancreatitis; however, detailed underlying mechanism of food-induced pancreatitis is unexplored. The aim of the review is to understand and update the current scenario of food-induced pancreatitis. A comprehensive literature search of relevant research articles has been performed through PubMed, and articles were chosen based on their relevance to food allergen-mediated pancreatitis. Several cases in the literature indicate that acute pancreatitis has been provoked after the consumption of mustard, milk, egg, banana, fish, and kiwi fruits. Food-induced pancreatitis is an ignored and unexplored area of research. The review highlights the significance of food in the development of pancreatitis and draws the attention of physicians and scientists to consider food allergies as a possible cause for initiation of pancreatitis pathogenesis</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1573-2568 (Electronic)IS - 0163-2116 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s10620-017-4817-2</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29086330">PM:29086330</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Dig Dis Sci\20171031-ManoharM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Dig Dis Sci\20171031-ManoharM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Manohar M</style></custom2><misc3><style face="normal" font="default">10.1007/s10620-017-4817-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86570</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Letner,D.</style></author><author><style face="normal" font="default"> Farris,A.</style></author><author><style face="normal" font="default"> Khalili,H.</style></author><author><style face="normal" font="default"> Garber,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Gastrointestinal Unit, Massachusetts General Hospital</style></auth-address><titles><title><style face="normal" font="default">Pollen-food allergy syndrome is a common allergic comorbidity in adults with eosinophilic esophagitis</style></title><secondary-title><style face="normal" font="default">Dis Esophagus</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Dis Esophagus</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">Eosinophilic esophagitis (EoE) is associated with atopic diseases including asthma, allergic rhinitis, and atopic dermatitis; however, limited data exist on the correlation between pollen-food allergy syndrome (PFAS) and EoE. We analyzed 346 adults with EoE treated at a single center between 2002 and 2016. Demographic and EoE-specific data including clinical features and measures of EoE disease severity and treatments were collected. The presence of other atopic diseases, family history, prevalence of peripheral eosinophilia and elevated IgE, and details of PFAS triggers were collected. Twenty six percent of the 346 subjects in our cohort had both EoE and PFAS (EoE-PFAS). Compared to subjects with EoE alone, subjects with EoE-PFAS had an increased frequency of allergic rhinitis (86.7% vs. 64.2%, P &lt; 0.001) and family history of allergies (71.1% vs. 53.3%, P = 0.003), and comprised a higher proportion of EoE diagnoses made in the spring (Chi2 &lt; 0.001). 43.3% of subjects with concurrent EoE and PFAS opted for treatment with elimination diet, and these measures failed to induce remission in 46.2% of cases. In most cases, elimination diet failed despite strict avoidance of PFAS trigger foods in addition to common EoE triggers including dairy, wheat, and eggs. EoE-PFAS was also associated with higher serum IgE at the time of EoE diagnosis (460.6 vs. 289.9, P &lt; 0.019). Allergic rhinitis and a family history of food allergy were independently associated with having EoE-PFAS. The most common triggers of PFAS in adults with EoE are apples (21.1%), carrots (15.5%), and peaches (15.5%). Along with asthma, allergic rhinitis and atopic dermatitis, PFAS is a common allergic comorbidity that is highly associated with EoE. Further studies aimed at understanding mechanistic similarities and differences of PFAS and EoE may shed light on the pathogenesis of these closely related food allergy syndromes</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1442-2050 (Electronic)IS - 1120-8694 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1093/dote/dox122</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29087472">PM:29087472</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Dis Esophagus\20171031-LetnerD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Dis Esophagus\20171031-LetnerD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Letner D</style></custom2><misc3><style face="normal" font="default">10.1093/dote/dox122</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86575</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pelaia,C.</style></author><author><style face="normal" font="default"> Vatrella,A.</style></author><author><style face="normal" font="default"> Lombardo,N.</style></author><author><style face="normal" font="default"> Terracciano,R.</style></author><author><style face="normal" font="default"> Navalesi,P.</style></author><author><style face="normal" font="default"> Savino,R.</style></author><author><style face="normal" font="default"> Pelaia,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Medical and Surgical Sciences , University "Magna Graecia" of Catanzaro , Catanzaro , Italy</style></auth-address><titles><title><style face="normal" font="default">Biological mechanisms underlying the clinical effects of allergen-specific immunotherapy in asthmatic children</style></title><secondary-title><style face="normal" font="default">Expert Opin Biol Ther</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Expert Opin Biol Ther</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Allergen-specific immunotherapy (AIT) is indicated for patients with allergic asthma and/or allergic rhinitis, and can be implemented by either subcutaneous injection (SCIT) or sublingual administration (SLIT). AIT reduces asthma symptoms, lowers the use of pharmacologic controller therapy, and decreases the need for rescue medications. SLIT appears to be safer than SCIT, but SCIT seems to be more efficacious and acts earlier in allergic asthmatic children. Areas covered: This review looks at the pathobiology of allergic asthma as well as the role of regulatory T and B cells in allergen tolerance. It also reviews the immunological mechanisms underlying the clinical effects induced by AIT in allergic asthmatic children. Expert opinion: AIT is very effective in allergic asthmatic children, who can significantly benefit from this particular type of immunotherapy in order to achieve a better control of their disease. AIT is also capable of modifying the natural history of allergic asthma. Furthermore, AIT can potentially represent a valuable therapeutic tool within the context of precision medicine, as recombinant allergen technology might allow the creation of targeted extracts able to be effective against specific proteins to which individual asthmatic children are allergic, thus helping to implement a personalized approach to treatment</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1744-7682 (Electronic)IS - 1471-2598 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1080/14712598.2018.1402003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29113525">PM:29113525</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Expert Opin Biol Ther\20171108-PelaiaC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Expert Opin Biol Ther\20171108-PelaiaC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Pelaia C</style></custom2><misc3><style face="normal" font="default">10.1080/14712598.2018.1402003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86576</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ridolo,E.</style></author><author><style face="normal" font="default"> Martignago,I.</style></author><author><style face="normal" font="default"> Riario-Sforza,G.G.</style></author><author><style face="normal" font="default"> Incorvaia,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Medicine and Surgery Department , University of Parma , Parma , Italy</style></auth-address><titles><title><style face="normal" font="default">Allergen immunotherapy in atopic dermatitis</style></title><secondary-title><style face="normal" font="default">Expert Rev Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Expert Rev Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="7" Month="11" Year="2017">2017/11/7</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Atopic dermatitis (AD) is a chronic relapsing skin disease, characterized by flare-up due to the exposure to allergens in patients sensitized to them. Currently, therapy of AD is mainly based on symptomatic treatment and avoidance of irritating/allergenic factors, house dust mites being particularly important. Allergen immunotherapy (AIT) is suggested to be the only etiologic treatment, to modify the natural history of the disease. Areas covered: The aim of this review is investigating the putative role of AIT in AD through the evaluation of the most recent scientific literature. Several studies have been conducted since 1970, with promising results in improving the clinical outcome of AD, but they often lack the necessary scientific rigorousness. Moreover, heterogeneity of the studies makes it very difficult to compare and to analyze data in a systematic review or meta-analysis. Expert commentary: As a result of the above-mentioned limitations, the treatment of AD with causative aeroallergen can nowadays be suggested only as an add-on therapy in selected patients who are non-responsive to the traditional therapy</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1744-8409 (Electronic)IS - 1744-666X (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1080/1744666X.2018.1401469</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29110542">PM:29110542</url></web-urls></urls><custom2><style face="normal" font="default">20171107, Ridolo E</style></custom2><misc3><style face="normal" font="default">10.1080/1744666X.2018.1401469</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86578</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Azdad,O.</style></author><author><style face="normal" font="default"> Mejrhit,N.</style></author><author><style face="normal" font="default"> El Kabbaoui,M.</style></author><author><style face="normal" font="default"> Chda,A.</style></author><author><style face="normal" font="default"> Ouahidi,I.</style></author><author><style face="normal" font="default"> Tazi,A.</style></author><author><style face="normal" font="default"> Bencheikh,R.</style></author><author><style face="normal" font="default"> Aarab,L.</style></author></authors></contributors><titles><title><style face="normal" font="default">Effect of heating and enzymatic hydrolysis on casein cow milk sensitivity in Moroccan population</style></title><secondary-title><style face="normal" font="default">Food Agric Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Food Agric Immunol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="24" Month="10" Year="2017">2017/10/24</year></dates><publisher><style face="normal" font="default">Taylor &amp; Francis</style></publisher><isbn><style face="normal" font="default">0954-0105</style></isbn><abstract><style face="normal" font="default">The objectives of the present work were first to evaluate the sensitivity to cow raw milk of the population of Fez, and then to study the effect of heating and pepsin hydrolysis on the allergenicity of casein. A cross-sectional study was carried out in Fez Hospitals, in which 1000 patients were recruited to establish a sera bank used to evaluate specific IgE to cow milk and to casein. Then, we evaluated the reaction of human IgE to heated and pepsin-hydrolysed casein. The results showed that 11.5% of the population studied self-reported reactions to foods. From them, 3.6% reported allergy to milk. Evaluation of specific IgE to cow raw milk showed that 11.9% of patients presented higher specific IgE levels. The treatments of casein indicated that both heating and pepsin hydrolysis totally decreased its binding on the human IgE</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Morocco -</style></notes><work-type><style face="normal" font="default">10.1080/09540105.2017.1391179</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.1080/09540105.2017.1391179</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Agric Immunol\20171114-AzdadO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Agric Immunol\20171114-AzdadO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Azdad O</style></custom2><misc3><style face="normal" font="default">10.1080/09540105.2017.1391179</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86579</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bobrus-Chociej,A.</style></author><author><style face="normal" font="default"> Daniluk,U.</style></author><author><style face="normal" font="default"> Alifier,M.</style></author><author><style face="normal" font="default"> Stasiak-Barmuta,A.</style></author><author><style face="normal" font="default"> Kaczmarski,M.G.</style></author></authors></contributors><titles><title><style face="normal" font="default">Alterations of lymphocyte subpopulations and TGF-+¦ in children with transient or persistent cow's milk allergy</style></title><secondary-title><style face="normal" font="default">Food Agric Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Food Agric Immunol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="24" Month="10" Year="2017">2017/10/24</year></dates><publisher><style face="normal" font="default">Taylor &amp; Francis</style></publisher><isbn><style face="normal" font="default">0954-0105</style></isbn><abstract><style face="normal" font="default">The aim of the study was to evaluate changes in surface receptor expression of B and T lymphocytes and concentration of TGF-? in children who either developed tolerance to cow?s milk protein (CMP) or manifested persistent cow?s milk allergy (CMA). The study involved 30 patients with CMA who underwent an open food challenge after 12 months of milk-free diet. After the milk challenge, decreased concentration of CD19+CD23+ was observed in children who acquired tolerance to CMP, in comparison with the test before cow?s milk (CM) challenge (42.2% vs. 29.1%, p?=?.006). The same group demonstrated lower concentration of TGF-? than patients with persistent allergy (median 37.9 pg/ml vs. 52.8 pg/ml, p?=?.003, respectively). Moreover, before CM challenge, higher percentage of CD3+CD8+CD28+CD152+ cells (median 2.88% vs. 1.2%, p?=?.03) and CD3+CD4+CD25+CD62L+ (median 42.3% vs. 13.4%, p?=?.032) was noted in children who acquired tolerance to CMP, in comparison with subjects who remained allergic to CMP</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1080/09540105.2017.1387234</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.1080/09540105.2017.1387234</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Agric Immunol\20171114-BobrusChociejA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Agric Immunol\20171114-BobrusChociejA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Bobrus-Chociej A</style></custom2><misc3><style face="normal" font="default">10.1080/09540105.2017.1387234</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86585</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,T.</style></author><author><style face="normal" font="default"> Wang,F.</style></author><author><style face="normal" font="default"> Wang,G.</style></author><author><style face="normal" font="default"> Mao,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Medicine, West China Hospital, Sichuan University, Chengdu, 610041, China</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of benralizumab in patients with eosinophilic asthma: a meta-analysis of randomized placebo-controlled trials</style></title><secondary-title><style face="normal" font="default">Front Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Front Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">Benralizumab is a monoclonal antibody that targets interleukin-5 receptor alpha to deplete blood eosinophils and improve the clinical outcomes of allergic asthma. We conducted a meta-analysis to evaluate the safety and efficacy of different doses of benralizumab in patients with eosinophilic asthma. All randomized controlled trials involving benralizumab treatment for patients with eosinophilic asthma, which were searched in PubMed, Embase, and the Cochrane Library published until January 2017, as well as the rate of asthmatic exacerbation, pulmonary functionality, asthma control, quality of life scores, and adverse events were included. Randomized-effect models were used in the meta-analysis to calculate the pooled mean difference, relative risks, and 95% confidence intervals. Five studies involving 1951 patients were identified. Compared with the placebo, benralizumab treatment demonstrated significant improvements in the forced expiratory volume in 1 s (FEV1), Asthma Quality of Life Questionnaire scores, decreased asthmatic exacerbation and Asthma Control Questionnaire-6 (ACQ-6) scores. Benralizumab treatment was also not associated with increased adverse events. These findings indicated that benralizumab can be safely used to improve FEV1, enhance patient symptom control and quality of life, and reduce the risk of exacerbations and ACQ-6 scores in patients with eosinophilic asthma. Furthermore, our meta-analysis showed that benralizumab with 30 mg (every eight weeks) dosage can improve the health-related quality of life and appear to be more effective than 30 mg (every four weeks) dosage. Overall, data indicated that the optimal dosing regimen for benralizumab was possibly 30 mg (every eight weeks)</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 2095-0225 (Electronic)IS - 2095-0217 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s11684-017-0565-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29086236">PM:29086236</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Med\20171031-LiuT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Med\20171031-LiuT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Liu T</style></custom2><misc3><style face="normal" font="default">10.1007/s11684-017-0565-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86586</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rotondo,F.</style></author><author><style face="normal" font="default"> Hong,S.G.</style></author><author><style face="normal" font="default"> Peever,T.</style></author><author><style face="normal" font="default"> Pryor,B.M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Molecular diversity and allergenic profiles of Alternaria spp. from desert environments in Arizona</style></title><secondary-title><style face="normal" font="default">Fungal Biol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Fungal Biol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Alternaria</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> AFLP</style></keyword><keyword><style face="normal" font="default"> desert</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1878-6146</style></isbn><abstract><style face="normal" font="default">This study examined the genetic diversity of small-spored Alternaria species in the southwest desert of the USA by sampling 552 isolates from different habitats (soil and plant debris) in different locations (urban and an undisturbed desert). To estimate the genetic diversity, Amplified Fragment Length Polymorphism (AFLP) fingerprinting analysis was performed for all isolates. Strains representative of the sampled genotypic diversity (n=125) were further characterized according their sporulation pattern and the capability to produce allergens. Morphological characterization assigned the majority of the strains to the A. alternata and A. tenuissima morpho-groups with only two isolates assigned to the A. arborescens morpho-group. AFLP fingerprinting differentiated the A. arborescens morpho-groups, but could not distinguish between the A. alternata and A. tenuissima morpho-groups. Western blot analysis showed that a large number of allergenic proteins were produced by strains. These proteins were not specific for any morpho-group nor source of isolation. A hierarchical analysis of molecular variance was performed on the AFLP data to quantify molecular variation and partition this variation among sampled locations and habitat. No statistically significant differentiation among locations and habitat was detected indicating a lack of population structure across environments</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Korea -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.funbio.2017.10.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29248116">PM:29248116</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Fungal Biol\20171114-RotondoF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Fungal Biol\20171114-RotondoF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Rotondo F</style></custom2><misc3><style face="normal" font="default">10.1016/j.funbio.2017.10.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86587</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Caniatti,M.C.D.C.</style></author><author><style face="normal" font="default"> Borelli,S.D.</style></author><author><style face="normal" font="default"> Guilherme,A.L.F.</style></author><author><style face="normal" font="default"> Franzener,S.B.</style></author><author><style face="normal" font="default"> Tsuneto,L.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Basic Health Sciences, Universidade Estadual de Maringa (UEM), Maringa, Parana, Brazil.</style></auth-address><titles><title><style face="normal" font="default">Association between KIR genes and dust mite sensitization in a Brazilian population</style></title><secondary-title><style face="normal" font="default">Hum Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Hum Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="31" Month="10" Year="2017">2017/10/31</year></dates><abstract><style face="normal" font="default">BACKGROUND: Killer cell immunoglobulin-like receptors (KIRs), found on the surface of natural killer (NK) cells, play a key role in controlling the innate response. Such response depends on a series of cellular interactions between these receptors and HLA activating/inhibiting ligands. Atopic diseases have been associated with genes that regulate cytokine production and HLA genes, which may either protect or predispose to hypersensitivity. OBJECTIVE: To verify an association study of KIR genes with sensitization to the following mites: Dermatophagoides farinae, Dermatophagoides pteronyssinus, and Blomia tropicalis. METHODS: A total of 341 children aged up to 14years, were classified as mite-sensitive or mite-insensitive after undergoing a skin prick test for immediate allergic reactions. The presence/absence of KIR genes and their human leukocyte antigen (HLA) ligands was determined by polymerase chain reaction-sequence specific oligonucleotide (PCR-SSO) with the commercial kit LabType using Luminex. RESULTS: The frequencies of KIR genes and their respective class I HLA ligands and the frequency of haplotypes were performed in sensitive and insensitive individuals, and no significant differences were found. CONCLUSION: Our results suggest no influence of KIR genes on resistance/susceptibility to sensitization to dust mites</style></abstract><notes><style face="normal" font="default">DA - 20171104IS - 1879-1166 (Electronic)IS - 0198-8859 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.humimm.2017.10.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29100942">PM:29100942</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Hum Immunol\20171104-CaniattiMC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Hum Immunol\20171104-CaniattiMC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171104, Caniatti MC</style></custom2><misc3><style face="normal" font="default">10.1016/j.humimm.2017.10.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86588</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bozek,A.</style></author><author><style face="normal" font="default"> Kolodziejczyk,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical Department of Internal Disease, Dermatology and Allergology in Zabrze , Medical University of Silesia , Katowice , Poland</style></auth-address><titles><title><style face="normal" font="default">Safety of specific immunotherapy using an ultra-rush induction regimen in bee and wasp allergy</style></title><secondary-title><style face="normal" font="default">Hum Vaccin Immunother</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Hum Vaccin Immunother</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Specific allergen immunotherapy to Hymenoptera venom (VIT) is a basic treatment for patients allergic to Hymenoptera venom. The aim of the study was to evaluate the safety of an ultra-rush regimen compared with the rush and conventional protocols. MATERIALS AND METHODS: In 31 patients with an allergy to bee venom and 82 with an allergy to wasp venom, the allergic adverse reactions during VIT were monitored. Patients were selected based on the criteria established by EAACI (European Academy of Allergy and Clinical Immunology) recommendations. Adverse reactions during the ultra-rush immunotherapy were measured, documented and classified according to the criteria of Mueller. Ultra-rush, rush or conventional protocols of the initial phase VIT using the Venomenhal vaccine (Hal Allergy, Leiden, Netherlands) were conducted. RESULTS: Six (13.7%) patients on the ultra-rush regimen, 5 (14.3%) patients on the rush regimen and 9 (26.5%) on conventional VIT experienced an allergic reaction. There were no associations between the adverse allergic reactions and the following factors: gender, total IgE and allergen-specific IgE to wasp or bee venom before the VIT and cardiological drugs that were used. CONCLUSION: We found that the ultra-rush protocol (similar to the rush protocol) using the Venomenhal vaccine is safer than the conventional protocol</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 2164-554X (Electronic)IS - 2164-5515 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1080/21645515.2017.1397245</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29106324">PM:29106324</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Hum Vaccin Immunother\20171106-BozekA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Hum Vaccin Immunother\20171106-BozekA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Bozek A</style></custom2><misc3><style face="normal" font="default">10.1080/21645515.2017.1397245</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86589</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yoshino,N.</style></author><author><style face="normal" font="default"> Takeshita,R.</style></author><author><style face="normal" font="default"> Kawamura,H.</style></author><author><style face="normal" font="default"> Sasaki,Y.</style></author><author><style face="normal" font="default"> Kagabu,M.</style></author><author><style face="normal" font="default"> Sugiyama,T.</style></author><author><style face="normal" font="default"> Muraki,Y.</style></author><author><style face="normal" font="default"> Sato,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Infectious Diseases and Immunology, Department of Microbiology, School of Medicine, Iwate Medical University, Iwate, Japan</style></auth-address><titles><title><style face="normal" font="default">Mast cells partially contribute to mucosal adjuvanticity of surfactin in mice</style></title><secondary-title><style face="normal" font="default">Immun Inflamm Dis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immun Inflamm Dis</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Surfactin (SF) is a cyclic lipopeptide that has potent mucosal adjuvant properties. However, immunological mechanisms of SF adjuvant action have not yet been elucidated. As some cyclic lipopeptides, such as polymyxin, can stimulate histamine release from mast cells, we hypothesized that mast cell activation is critical for SF adjuvanticity. METHODS/RESULTS: We observed that following intranasal immunization with ovalbumin (OVA) plus SF, the titers of the OVA-specific antibody (Ab) in the mucosal secretions and plasma of mast cell-deficient mice were significantly lower than those in congenic normal mice, although OVA-specific Ab did not entirely disappear from mast cell-deficient mice. SF induced degranulation of mast cells and release of histamine in vitro. To investigate whether SF stimulated mast cells in vivo, we measured body temperature of mice immunized intranasally with OVA plus SF because histamine level affects body temperature. Following immunizations, body temperature of immunized congenic normal mice transiently decreased, whereas body temperature of mast cell-deficient mice did not change. Plasma levels of OVA-specific IgE Ab were not significantly different in mast cell-deficient and congenic normal mice. These findings suggest that SF directly affected mast cells in an IgE Ab-independent fashion. Furthermore, we analyzed the effects of SF on MC/9 mast cells cultured in vitro. MC/9 cells stimulated by SF released not only histamine but also leukotriene B4 and prostaglandin D2 . Moreover, SF up-regulated mRNA expression levels of Tnf, Ccr5, and Il4 genes in mast cells. These cytokines may play a facilitating role in OVA-specific immune responses in mice. CONCLUSION: Overall, our results showed that mast cell activation partially mediated SF adjuvanticity</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 2050-4527 (Electronic)IS - 2050-4527 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1002/iid3.204</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29105371">PM:29105371</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immun Inflamm Dis\20171106-YoshinoN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immun Inflamm Dis\20171106-YoshinoN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Yoshino N</style></custom2><misc3><style face="normal" font="default">10.1002/iid3.204</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86590</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Klier,J.</style></author><author><style face="normal" font="default"> Geis,S.</style></author><author><style face="normal" font="default"> Steuer,J.</style></author><author><style face="normal" font="default"> Geh,K.</style></author><author><style face="normal" font="default"> Reese,S.</style></author><author><style face="normal" font="default"> Fuchs,S.</style></author><author><style face="normal" font="default"> Mueller,R.S.</style></author><author><style face="normal" font="default"> Winter,G.</style></author><author><style face="normal" font="default"> Gehlen,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre for Clinical Veterinary Medicine, Equine Clinic, Ludwig-Maximilians-University, Munich, Germany</style></auth-address><titles><title><style face="normal" font="default">A comparison of nanoparticullate CpG immunotherapy with and without allergens in spontaneously equine asthma-affected horses, an animal model</style></title><secondary-title><style face="normal" font="default">Immun Inflamm Dis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immun Inflamm Dis</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="11" Year="2017">2017/11/1</year></dates><abstract><style face="normal" font="default">INTRODUCTION: New therapeutic strategies to modulate the immune response of human and equine allergic asthma are still under extensive investigation. Immunomodulating agents stimulating T-regulatory cells offer new treatment options beyond conventional symptomatic treatment or specific immunotherapy for human and equine allergic airway diseases, with the goal of a homoeostatic T-helper cell balance. The aim of this study was to evaluate the effects of a nebulized gelatin nanoparticle-CpG formulation (CpG-GNP) with and without specific allergens for the treatment of spontaneous allergic equine asthma as a model for human asthma. METHODS: Twenty equine asthma-affected horses were treated either with CpG-GNP alone or CpG-GNP with allergens. Two specific allergens were selected for each horse based on history and an in-vitro test. Each horse received seven administrations of the respective nebulized composition and was examined before treatment, immediately after and 6 weeks after the treatment course. RESULTS: Clinical parameters such as breathing rate, indirect interpleural measurement, arterial blood gases, amount of tracheal mucus and percentage of neutrophils and cytokines in tracheal washes and serum samples were evaluated. Treatment with CpG-GNP alone as well as in combinations with relevant allergens resulted in clinical improvement of nasal discharge, breathing rate, amount of secretion and viscosity, neutrophil percentage and partial oxygen pressure directly after and 6 weeks after treatment. There were no significant differences between the two treatments in clinical parameters or local cytokine profiles in the tracheal wash fluid (IL-10, IFN-g, and IL-17). IL-4 concentrations decreased significantly in both groups. CONCLUSION: Nonspecific CpG-GNP-based immunotherapy shows potential as a treatment for equine and possibly also human allergic asthma</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 2050-4527 (Electronic)IS - 2050-4527 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1002/iid3.198</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29094511">PM:29094511</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immun Inflamm Dis\20171102-KlierJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immun Inflamm Dis\20171102-KlierJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Klier J</style></custom2><misc3><style face="normal" font="default">10.1002/iid3.198</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86591</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lin,J.</style></author><author><style face="normal" font="default"> Huang,N.</style></author><author><style face="normal" font="default"> Wang,H.</style></author><author><style face="normal" font="default"> Fu,Q.</style></author><author><style face="normal" font="default"> Wang,E.</style></author><author><style face="normal" font="default"> Li,P.</style></author><author><style face="normal" font="default"> Yang,L.</style></author><author><style face="normal" font="default"> Luo,X.</style></author><author><style face="normal" font="default"> Liu,X.</style></author><author><style face="normal" font="default"> Liu,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">State Key Laboratory of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China</style></auth-address><titles><title><style face="normal" font="default">Identification of a novel cofilin-related molecule (Der f 31) as an allergen from Dermatophagoides farinae</style></title><secondary-title><style face="normal" font="default">Immunobiology</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunobiology</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="5" Month="10" Year="2017">2017/10/5</year></dates><abstract><style face="normal" font="default">House dust mite (HDM) allergen is a major cause of allergic disease. In this study, two-dimensional immunoblot and Matrix-Assisted Laser Desorption Ionization tandem Time-of-flight mass spectrometry (MALDI-TOF-MS) were used to identify Der f 31. After Der f 31 was cloned, expressed and purified, skin prick test (SPT), Immune inhibitory assays, Western blot, ELISA and asthmatic mouse model were employed to examine the allergenicity of recombinant Der f 31. The gene of Der f 31 includes 447 bps, and encoded 148 amino acids. Positive responses of SPT to r-Der f 31 were 32.5% in 43 HDM-allergic patients. r-Der f 31 can induce allergic pulmonary inflammation in the mouse model. In conclusion, Der f 31 is a novel subtype of dust mite allergens</style></abstract><notes><style face="normal" font="default">DA - 20171105IS - 1878-3279 (Electronic)IS - 0171-2985 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.imbio.2017.10.013</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29102047">PM:29102047</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunobiology\20171105-LinJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunobiology\20171105-LinJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171105, Lin J</style></custom2><misc3><style face="normal" font="default">10.1016/j.imbio.2017.10.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86593</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hwang,S.H.</style></author><author><style face="normal" font="default"> Shin,M.S.</style></author><author><style face="normal" font="default"> Yoon,T.J.</style></author><author><style face="normal" font="default"> Shin,K.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Food Science and Biotechnology, Kyonggi University, 154-42 Gwanggyosan-ro, Yeongtong-gu, Suwon-si, Gyeonggi-do, 16227, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Immunoadjuvant activity in mice of polysaccharides isolated from the leaves of Panax ginseng C.A. Meyer</style></title><secondary-title><style face="normal" font="default">Int J Biol Macromol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Biol Macromol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">Our previous study showed polysaccharide (GS-P) isolated from the leaves of Panax ginseng C.A. Meyer possessed anti-tumor metastatic activity in mouse model. In this study, we evaluated the immunoadjuvant effect of GS-P on the induction of humoral and cellular immune responses against ovalbumin (OVA) in mice. When mice were immunized subcutaneously with OVA admixed with or without GS-P, the OVA+GS-P group showed significantly higher antibody production than the group immunized with OVA alone. This suggests that GS-P has the ability to enhance the adaptive immune response. In addition, the OVA+GS-P+FIA (Freund's incomplete adjuvant) group induced higher levels of antigen-specific IgG1 and IgG2b antibodies than the OVA+FIA group. The culture supernatant obtained from the splenocytes of mice immunized with OVA+GS-P+FIA showed higher levels of OVA-specific Th1-type (IL-2, IFN-gamma, GM-CSF) and Th2-type (IL-10) cytokines. Following in vitro analysis of T cell proliferation, the splenocytes of mice treated with OVA+GS-P+FIA showed significantly more proliferation than those treated with OVA+FIA. Further, the production of IgE antibody was dramatically reduced when OVA+GS-P+FIA was used to immunize mice rather than OVA+FIA or OVA+FCA (Freund's complete adjuvant). Collectively, these results suggest that GS-P may possess adjuvant activity that potentially enhances humoral as well as cellular immune responses</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1879-0003 (Electronic)IS - 0141-8130 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1016/j.ijbiomac.2017.10.160</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29107141">PM:29107141</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Biol Macromol\20171106-HwangSH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Biol Macromol\20171106-HwangSH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Hwang SH</style></custom2><misc3><style face="normal" font="default">10.1016/j.ijbiomac.2017.10.160</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86601</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ihuoma,H.</style></author><author><style face="normal" font="default"> Belgrave,D.C.</style></author><author><style face="normal" font="default"> Murray,C.S.</style></author><author><style face="normal" font="default"> Foden,P.</style></author><author><style face="normal" font="default"> Simpson,A.</style></author><author><style face="normal" font="default"> Custovic,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Infection, Immunity and Respiratory Medicine, Faculty of Biology, Medicine and Health, Manchester Academic Health Sciences Centre, University of Manchester and University Hospital of South Manchester NHS Foundation Trust, Manchester, UK</style></auth-address><titles><title><style face="normal" font="default">Cat ownership, cat allergen exposure, and trajectories of sensitization and asthma throughout childhood</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">Exposure to cat and/or cat allergens can confer either an increase in risk, or protection, or will have no effect, depending on the age of the assessment, study design and the choice of study population</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.030</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29111216">PM:29111216</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-IhuomaH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-IhuomaH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Ihuoma H</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.030</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86602</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Peng,H.</style></author><author><style face="normal" font="default"> Ning,H.</style></author><author><style face="normal" font="default"> Wang,Q.</style></author><author><style face="normal" font="default"> Lu,W.</style></author><author><style face="normal" font="default"> Chang,Y.</style></author><author><style face="normal" font="default"> Wang,T.T.</style></author><author><style face="normal" font="default"> Lai,J.</style></author><author><style face="normal" font="default"> Kolattukudy,P.E.</style></author><author><style face="normal" font="default"> Hou,R.</style></author><author><style face="normal" font="default"> Hoft,D.F.</style></author><author><style face="normal" font="default"> Dykewicz,M.S.</style></author><author><style face="normal" font="default"> Liu,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Infectious Diseases, Allergy and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis University, St. Louis, MO 63104</style></auth-address><titles><title><style face="normal" font="default">MCPIP1 controls allergic airway inflammation by suppressing IL-5-producing Th2 cells through Notch/Gata3 pathway</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">BACKGROUND: Asthmatic and allergic inflammation is mediated by Th2 cytokines (IL-4, IL-5 and IL-13). Though we have learned much about how Th2 cells are differentiated, the Th2 checkpoint mechanisms remain elusive. OBJECTIVES: In this study, we investigate how monocyte chemotactic protein induced protein-1 (MCPIP1, encoded by zc3h12a gene) regulates IL-5-producing Th2 cell differentiation and Th2-mediated inflammation. METHODS: The functions of zc3h12a-/- CD4 T cells were evaluated by checking the expression of Th2 cytokines and transcription factors in vivo and in vitro. Allergic airway inflammation of zc3h12a-/- mice was examined with murine asthma models. In addition, antigen-specific CD4 T cells deficient in MCPIP1 were transferred to WT recipient mice, challenged with OVA or HDM, and accessed for Th2 inflammation. RESULTS: Zc3h12a-/- mice spontaneously develop severe lung inflammation, with an increase mainly in IL-5- and IL-13-producing but not IL-4-producing Th2 cells in the lung. Mechanistically, the differentiation of IL-5-producing zc3h12a-/- Th2 cells is mediated through Notch signaling and Gata3 independent of IL-4. Gata3 mRNA is stabilized in zc3h12a-/- Th2 cells. MCPIP1 promotes Gata3 mRNA decay via the RNase domain. Furthermore, deletion of MCPIP1 in OVA- or HDM-specific T cells leads to significantly increased Th2-mediated airway inflammation in OVA or HDM murine models of asthma. CONCLUSIONS: Our study reveals that MCPIP1 regulates the development and functions of IL-5-producing Th2 cells through Notch/Gata3 pathway. MCPIP1 represents a new promising target for the treatments of asthma and other Th2-mediated diseases</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.031</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29111212">PM:29111212</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-PengH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-PengH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Peng H</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.031</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86603</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee-Sarwar,K.</style></author><author><style face="normal" font="default"> Hauser,R.</style></author><author><style face="normal" font="default"> Calafat,A.M.</style></author><author><style face="normal" font="default"> Ye,X.</style></author><author><style face="normal" font="default"> O'Connor,G.T.</style></author><author><style face="normal" font="default"> Sandel,M.</style></author><author><style face="normal" font="default"> Bacharier,L.B.</style></author><author><style face="normal" font="default"> Zeiger,R.S.</style></author><author><style face="normal" font="default"> Laranjo,N.</style></author><author><style face="normal" font="default"> Gold,D.R.</style></author><author><style face="normal" font="default"> Weiss,S.T.</style></author><author><style face="normal" font="default"> Litonjua,A.A.</style></author><author><style face="normal" font="default"> Savage,J.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.</style></auth-address><titles><title><style face="normal" font="default">Prenatal and Early Life Triclosan and Parabens Exposure and Allergic Outcomes</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">BACKGROUND: In cross-sectional studies, triclosan and parabens, ubiquitous ingredients in personal care and other products, are associated with allergic disease. OBJECTIVES: We investigated the association between prenatal and early life triclosan and parabens exposure and childhood allergic disease in a prospective, longitudinal study. METHODS: Subjects were enrollees in VDAART, the Vitamin D Antenatal Asthma Reduction Trial. Triclosan, methyl paraben and propyl paraben concentrations were quantified in maternal plasma samples pooled from first and third trimesters and urine samples from children at age 3 or 4 years. Outcomes were parental report of physician-diagnosed asthma or recurrent wheezing, and allergic sensitization to food or environmental antigens based on serum specific IgE levels at age 3 in high-risk children. RESULTS: Analysis included 467 mother-child pairs. Overall, there were no statistically significant associations of maternal plasma or child urine triclosan or parabens concentrations with asthma or recurrent wheeze, food or environmental sensitization at age 3. A trend toward an inverse association between triclosan and parabens exposure and allergic sensitization was observed. There was evidence of effect measure modification by sex, with higher odds of environmental sensitization associated with increasing concentrations of parabens in males compared to females. CONCLUSIONS: We did not identify a consistent association between prenatal and early life triclosan or parabens concentrations and childhood asthma, recurrent wheeze or allergic sensitization in the overall study population. The differential effects of triclosan or parabens exposure on allergic sensitization by sex observed in this study warrants further exploration</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.029</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29111213">PM:29111213</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-LeeSarwarK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-LeeSarwarK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Lee-Sarwar K</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.029</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86605</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shamji,M.H.</style></author><author><style face="normal" font="default"> Temblay,J.N.</style></author><author><style face="normal" font="default"> Cheng,W.</style></author><author><style face="normal" font="default"> Byrne,S.M.</style></author><author><style face="normal" font="default"> Macfarlane,E.</style></author><author><style face="normal" font="default"> Switzer,A.R.</style></author><author><style face="normal" font="default"> Francisco,N.D.C.</style></author><author><style face="normal" font="default"> Olexandra,F.</style></author><author><style face="normal" font="default"> Jacubczik,F.</style></author><author><style face="normal" font="default"> Durham,S.R.</style></author><author><style face="normal" font="default"> Ashton-Rickardt,P.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunomodulation and Tolerance Group; Allergy and Clinical Immunology, Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, SW3 6LY, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Anti-apoptotic Serine Protease Inhibitors contribute towards the survival of allergenic Th2 cells</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">BACKGROUND: The mechanisms regulating the maintenance of persistent Th2 cells that potentiate allergic inflammation are not well understood. OBJECTIVE: The function of Serine Protease Inhibitor 2A (Spi2A) was studied in mouse Th2 cells and Serine Protease Inhibitor (SERPIN) B3 and B4 genes were studied in Th2 cells from grass pollen allergic individuals. METHODS: Spi2A deficient Th2 cells were studied in vitro culture or in vivo after challenge of Spi2A Knock-Out (KO) mice with ovalbumin in alum. The expression of SERPIN B3 and B4 mRNA was measured in vitro cultured Th2 cell and in ex vivo CD27-CD4+ and ICL2 cells from grass pollen allergic individuals using quantitative PCR. SERPIN B3 and B4 mRNA levels were knocked down in cultured CD27-CD4+ cells with shRNA. RESULTS: There were lower levels of in vitro polarized Th2 cells from Spi2A KO mice (P&lt;0.005) and in vivo after OVA challenge (P&lt;0.05), higher levels of apoptosis (annexin V positivity P&lt;0.005) and less lung allergic inflammation (number of lung eosinophils P&lt;0.005). In vitro polarized Th2 cells from grass pollen allergic individuals expressed higher levels of both SERPIN B3 and B4 (both P&lt;0.05) mRNA compared to un- polarized CD4 T cells. CD27-CD4+ from grass pollen allergic individuals expressed higher levels of both SERPIN B3 and B4 (both P&lt;0.0005) mRNA compared to CD27+CD4+ cells. ICL2 cells expressed higher levels of both SERPIN B3 and B4 (both P&lt;0.0005) mRNA compared to ICL1 cells. Knock-down of either SERPIN B3 or B4 (both P &lt;0.005) mRNA levels resulted in decreased viability of CD27-CD4+ compared to control transduced cells. CONCLUSION: The serpins Spi2A in mice and Serpin B3 and B4 in allergic individuals, control viability of Th2 cells. This provides proof-of-principle for a therapeutic approach for allergic disease through the ablation of allergic memory Th2 cells through mRNA SERPIN B3 and B4 down-regulation</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.07.055</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29106998">PM:29106998</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171106-ShamjiMH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171106-ShamjiMH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Shamji MH</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.07.055</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86606</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Grattan,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Guy's Hospital, London, United Kingdom. Electronic address: clive.e.grattan@gstt.nhs.uk</style></auth-address><titles><title><style face="normal" font="default">Autoimmune chronic spontaneous urticaria</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171105IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - LetterCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.014</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29102068">PM:29102068</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171105-GrattanC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171105-GrattanC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171105, Grattan C</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.014</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86608</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hoyt,A.E.W.</style></author><author><style face="normal" font="default"> Chapman,M.D.</style></author><author><style face="normal" font="default"> King,E.M.</style></author><author><style face="normal" font="default"> Platts-Mills,T.A.E.</style></author><author><style face="normal" font="default"> Steinke,J.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, University of Virginia Health System, Charlottesville, Va; Department of Pediatrics, University of Virginia Health System, Charlottesville, Va</style></auth-address><titles><title><style face="normal" font="default">Food allergen component proteins are not detected in early-childhood vaccines</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Vaccines</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword></keywords><dates><year Day="31" Month="10" Year="2017">2017/10/31</year></dates><abstract><style face="normal" font="default">Limited studies have explored the potential impact of vaccines on food allergy development. This study investigates and does not support the theory that earlychildhood vaccines contain specific food allergens that induce sensitization.</style></abstract><notes><style face="normal" font="default">DA - 20171104IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.09.023</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29100866">PM:29100866</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171104-HoytAE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171104-HoytAE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171104, Hoyt AE</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.09.023</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86609</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,Y.</style></author><author><style face="normal" font="default"> Koplin,J.J.</style></author><author><style face="normal" font="default"> Ho,M.H.K.</style></author><author><style face="normal" font="default"> Wong,W.H.S.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Murdoch Childrens Research Institute, Parkville, Victoria, Australia; Department of Paediatrics, University of Melbourne, Parkville, Victoria, Australia</style></auth-address><titles><title><style face="normal" font="default">Increasing hospital presentations for anaphylaxis in the pediatric population in Hong Kong</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - Australia -CO - Hong Kong -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.09.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29109048">PM:29109048</url></web-urls><pdf-urls><url ppv-ref="no">katrina.allen@mcri.edu.au</url></pdf-urls><text-urls><url ppv-ref="no">researchgate</url></text-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171107, Wang Y</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.09.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86610</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Meyer,R.</style></author><author><style face="normal" font="default"> Groetch,M.</style></author><author><style face="normal" font="default"> Venter,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Imperial College, Department of Paediatrics, London, United Kingdom.</style></auth-address><titles><title><style face="normal" font="default">When Should Infants with Cow's Milk Protein Allergy Use an Amino Acid Formula? A Practical Guide</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">Cow's milk protein allergy (CMPA) is the most common food allergy in childhood and its prevalence ranges between 1.9% and 4.9%. Most children present with CMPA at age less than 1 year and therefore may require a hypoallergenic formula in the absence of breast milk. Hypoallergenic formulas include both extensively hydrolyzed formula (EHF) and amino acid formula (AAF). For most children with a CMPA, an EHF will be sufficient for symptom resolution, as reflected in current guidelines, but there is a subset of children with CMPA where an AAF may be indicated. The appropriate use of an AAF is a highly debated topic, because there is a significant fiscal burden to either the health care system or the parents. From the literature, the following themes were identified as possible reasons for choosing an AAF: (1) symptoms not fully resolved on EHF, (2) faltering growth/failure to thrive, (3) multiple food eliminations, (4) severe complex gastrointestinal food allergies, (5) eosinophilic esophagitis, (6) food protein-induced enterocolitis syndrome, (7) severe eczema, and (8) symptoms while breast-feeding. Each of these themes was critically reviewed using all available published data and found that using an AAF in height growth faltering may be indicated. In addition, patients who end up on an AAF often present with multisystem involvement, requiring multiple food eliminations and fall within the more severe spectrum of gastrointestinal allergies. In eosinophilic esophagitis, all current recommendations support the use of an AAF as first-line approach, and in children with anaphylaxis, despite limited evidence an AAF is recommended because of the potential risk for a severe reaction. The use of an AAF in children who are breast-fed remains a highly controversial topic and at all times breast-feeding should be supported in children with CMPA. This article provides a practical guide that is evidence based for health care professionals to the use of AAF</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United Kingdom -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.09.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29109046">PM:29109046</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171107, Meyer R</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.09.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86611</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kolkhir,P.</style></author><author><style face="normal" font="default"> Church,M.K.</style></author><author><style face="normal" font="default"> Weller,K.</style></author><author><style face="normal" font="default"> Metz,M.</style></author><author><style face="normal" font="default"> Schmetzer,O.</style></author><author><style face="normal" font="default"> Maurer,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Venereology, I.M. Sechenov First Moscow State Medical University, Moscow, Russia</style></auth-address><titles><title><style face="normal" font="default">Reply (Refers To: Autoimmune chronic spontaneous urticaria)</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171105IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - LetterCO - Russia -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29102069">PM:29102069</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-KolkhirP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-KolkhirP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171105, Kolkhir P</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86612</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Qian,X.</style></author><author><style face="normal" font="default"> Aboushousha,R.</style></author><author><style face="normal" font="default"> van de,Wetering C.</style></author><author><style face="normal" font="default"> Chia,S.B.</style></author><author><style face="normal" font="default"> Amiel,E.</style></author><author><style face="normal" font="default"> Schneider,R.W.</style></author><author><style face="normal" font="default"> van der Velden,J.L.</style></author><author><style face="normal" font="default"> Lahue,K.G.</style></author><author><style face="normal" font="default"> Hoagland,D.A.</style></author><author><style face="normal" font="default"> Casey,D.T.</style></author><author><style face="normal" font="default"> Daphtary,N.</style></author><author><style face="normal" font="default"> Ather,J.L.</style></author><author><style face="normal" font="default"> Randall,M.J.</style></author><author><style face="normal" font="default"> Aliyeva,M.</style></author><author><style face="normal" font="default"> Black,K.E.</style></author><author><style face="normal" font="default"> Chapman,D.G.</style></author><author><style face="normal" font="default"> Lundblad,L.K.A.</style></author><author><style face="normal" font="default"> McMillan,D.H.</style></author><author><style face="normal" font="default"> Dixon,A.E.</style></author><author><style face="normal" font="default"> Anathy,V.</style></author><author><style face="normal" font="default"> Irvin,C.G.</style></author><author><style face="normal" font="default"> Poynter,M.E.</style></author><author><style face="normal" font="default"> Wouters,E.F.M.</style></author><author><style face="normal" font="default"> Vacek,P.M.</style></author><author><style face="normal" font="default"> Henket,M.</style></author><author><style face="normal" font="default"> Schleich,F.</style></author><author><style face="normal" font="default"> Louis,R.</style></author><author><style face="normal" font="default"> van der Vliet,A.</style></author><author><style face="normal" font="default"> Janssen-Heininger,Y.M.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, VT</style></auth-address><titles><title><style face="normal" font="default">Interleukin-1/inhibitory kappa B kinase epsilon-induced glycolysis augment epithelial effector function and promote allergic airways disease</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">BACKGROUND: Emerging studies suggest that enhanced glycolysis accompanies inflammatory responses. Virtually nothing is known about the relevance of glycolysis in allergic asthma. OBJECTIVES: Here we sought to determine if glycolysis is altered in allergic asthma and to address its importance in the pathogenesis of allergic asthma. METHODS: We examined alterations in glycolysis in sputum samples from asthmatics and primary human nasal cells, and used murine models of allergic asthma as well as primary mouse tracheal epithelial cells to evaluate the relevance of glycolysis. RESULTS: In a murine model of allergic asthma, glycolysis was induced in the lungs in an IL-1-dependent manner. Furthermore, administration of IL-1beta into airways stimulated lactate production and expression of glycolytic enzymes, with notable expression of lactate dehydrogenase A occurring in the airway epithelium. Indeed, exposure of mouse tracheal epithelial cells to IL-1beta or IL-1alpha resulted in increased glycolytic flux, glucose usage, expression of glycolysis genes, and lactate production. Enhanced glycolysis was required for IL-1beta- or IL-1alpha-mediated pro-inflammatory responses and the stimulatory effects of IL-1beta on HDM-induced release of TSLP, and GM-CSF from tracheal epithelial cells. Inhibitor of kappaB kinase epsilon was downstream of house dust mite (HDM) or IL-1beta, and was required for HDM-induced glycolysis and the pathogenesis of allergic airways disease. SiRNA-ablation of lactate dehydrogenase A attenuated HDM-induced increases in lactate and attenuated HDM-induced disease. Primary nasal epithelial cells from asthmatics intrinsically produced more lactate as compared to cells from healthy subjects. Lactate content was significantly higher in sputum supernatants from asthmatics, notably those patients with >61% neutrophils. A positively correlation was observed between sputum lactate and IL-1beta, and lactate content negatively correlated with lung function. CONCLUSIONS: Collectively, these findings demonstrate that IL-1beta/IKKepsilon signaling plays an important role in HDM-induced glycolysis and the pathogenesis of allergic airways disease</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Belgium -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.08.043</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108965">PM:29108965</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-QianX.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-QianX.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Qian X</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.08.043</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86614</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fraczek,M.G.</style></author><author><style face="normal" font="default"> Chishimba,L.</style></author><author><style face="normal" font="default"> Niven,R.M.</style></author><author><style face="normal" font="default"> Bromley,M.</style></author><author><style face="normal" font="default"> Simpson,A.</style></author><author><style face="normal" font="default"> Smyth,L.</style></author><author><style face="normal" font="default"> Denning,D.W.</style></author><author><style face="normal" font="default"> Bowyer,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Manchester, Faculty of Biology, Medicine and Health, Manchester Fungal Infection Group, Institute of Inflammation and Repair, Core Technology Facility, Manchester, UK</style></auth-address><titles><title><style face="normal" font="default">Corticosteroid treatment is associated with increased filamentous fungal burden in allergic fungal disease</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergic diseases caused by fungi are common. The best understood conditions are allergic bronchopulmonaryaspergillosis (ABPA) and severe asthma with fungal sensitisation (SAFS). Our knowledge of the fungal microbiome (mycobiome) is limited to a few studies involving healthy individuals, asthmatics and smokers. No study has yet examined the mycobiome in fungal lung disease. OBJECTIVES: The main aim of this study was to determine the mycobiome in lungs of individuals with well characterised fungal disease. A secondary objective was to determine possible effects of treatment on the mycobiome. METHODS: After bronchoscopy, ITS1 DNA was amplified and sequenced and fungal load determined by RT-PCR. Clinical and treatment variables were correlated with the main species identified. ABPA (n=16), SAFS (n=16), severe asthma not sensitised to fungi, (n=9), mild asthma patients(n=7) and 10 healthy controls were studied. RESULTS: The mycobiome was highly varied with severe asthmatics carrying higher loads of fungus. Healthy individuals had low fungal loads, mostly poorly characterised Malasezziales.The most common fungus in asthmatics was Aspergillus fumigatus complex and this taxon accounted for the increased burden of fungus in the high level samples. Corticosteroid treatment was significantly associated with increased fungal load (p&lt;0.01). CONCLUSIONS: The mycobiome is highly variable. Highest loads of fungus are observed in severe asthmatics and the most common fungus is Aspergillusfumigatus complex. Individuals receiving steroid therapy had significantly higher levels of Aspergillus and total fungus in their BAL</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.039</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122659">PM:29122659</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171110-FraczekMG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171110-FraczekMG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Fraczek MG</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.039</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86616</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">du Toit,G.</style></author><author><style face="normal" font="default"> Sayre,P.H.</style></author><author><style face="normal" font="default"> Roberts,G.</style></author><author><style face="normal" font="default"> Lawson,K.</style></author><author><style face="normal" font="default"> Sever,M.L.</style></author><author><style face="normal" font="default"> Bahnson,H.T.</style></author><author><style face="normal" font="default"> Fisher,H.R.</style></author><author><style face="normal" font="default"> Feeney,M.</style></author><author><style face="normal" font="default"> Radulovic,S.</style></author><author><style face="normal" font="default"> Basting,M.</style></author><author><style face="normal" font="default"> Plaut,M.</style></author><author><style face="normal" font="default"> Lack,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Paediatric Allergy, Division of Asthma, Allergy and Lung Biology, King's College London and Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">The allergen-specificity of early peanut consumption and the impact on the development of allergic disease in the LEAP Study Cohort</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">BACKGROUND: Early introduction of dietary peanut in high-risk infants with severe eczema and/or egg allergy prevented peanut allergy at 5 years of age in the LEAP Study; the protective effect persisted after 12 months of avoiding peanuts in the LEAP-On Study. It is unclear whether this benefit is allergen and allergic-disease specific. OBJECTIVE: To assess the impact of early introduction of peanut on the development of allergic disease, food sensitization and aeroallergen sensitization. METHODS: Asthma, eczema and rhinoconjunctivitis were diagnosed by clinical assessment. Reported allergic reactions and consumption of tree nuts and sesame were recorded by questionnaire. Sensitization to food and aeroallergens was determined by skin prick testing and specific IgE measurement. RESULTS: A high and increasing burden of food and aeroallergen sensitization and allergic disease was noted across study time points; 76% of LEAP participants had at least one allergic disease at 60 months of age. There were no differences in allergic disease between LEAP groups. There were small differences in sensitization and reported allergic reactions for select tree nuts; levels were higher in the LEAP consumption group. Significant resolution of eczema and sensitization to egg and milk occurred in LEAP participants; this was not affected by peanut consumption. CONCLUSION: Early consumption of peanut in infants at high risk of peanut allergy is allergen-specific and does not prevent the development of other allergic disease, sensitization to other foods and aeroallergens, or reported allergic reactions to tree nuts and sesame. Furthermore, peanut consumption does not hasten the resolution of eczema or egg allergy</style></abstract><notes><style face="normal" font="default">DA - 20171103IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.034</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29097103">PM:29097103</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171103-duToitG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171103-duToitG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171103, du Toit G</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.034</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86617</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bird,J.A.</style></author><author><style face="normal" font="default"> Spergel,J.M.</style></author><author><style face="normal" font="default"> Jones,S.M.</style></author><author><style face="normal" font="default"> Rachid,R.</style></author><author><style face="normal" font="default"> Assa'ad,A.H.</style></author><author><style face="normal" font="default"> Wang,J.</style></author><author><style face="normal" font="default"> Leonard,S.A.</style></author><author><style face="normal" font="default"> Laubach,S.S.</style></author><author><style face="normal" font="default"> Kim,E.H.</style></author><author><style face="normal" font="default"> Vickery,B.P.</style></author><author><style face="normal" font="default"> Davis,B.P.</style></author><author><style face="normal" font="default"> Heimall,J.</style></author><author><style face="normal" font="default"> Cianferoni,A.</style></author><author><style face="normal" font="default"> MacGinnitie,A.J.</style></author><author><style face="normal" font="default"> Crestani,E.</style></author><author><style face="normal" font="default"> Burks,A.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy &amp; Immunology, University of Texas Southwestern Medical Center, Dallas, Tex.</style></auth-address><titles><title><style face="normal" font="default">Efficacy and Safety of AR101 in Oral Immunotherapy for Peanut Allergy: Results of ARC001, a Randomized, Double-Blind, Placebo-Controlled Phase 2 Clinical Trial</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">BACKGROUND: Peanut oral immunotherapy, using a variety of approaches, has been previously shown to induce desensitization in peanut-allergic subjects, but no products have been approved for clinical use by regulatory agencies. OBJECTIVE: We performed the first phase 2 multicentered study to assess the safety and efficacy of AR101, a novel oral biologic drug product. METHODS: A randomized, double-blind, placebo-controlled trial was conducted at 8 US centers. Eligible subjects were 4 to 26 years old, sensitized to peanut, and had dose-limiting symptoms to &lt;/=143 mg of peanut protein in a screening double-blind, placebo-controlled food challenge (DBPCFC). Subjects were randomized 1:1 to daily AR101 or placebo and gradually up-dosed from 0.5 to 300 mg/day. The primary endpoint was the proportion of subjects in each arm able to tolerate >/=443 mg (cumulative peanut protein) at exit DBPCFC with no or mild symptoms. RESULTS: Fifty-five subjects (29 AR101, 26 placebo) were enrolled. In the intention-to-treat analysis, 23 of 29 (79%) and 18 of 29 (62%) AR101 subjects tolerated >/=443 mg and 1043 mg at exit DBPCFC, respectively, versus 5 of 26 (19%) and 0 of 26 (0%) placebo subjects (both P &lt; .0001). Compared with placebo, AR101 significantly reduced symptom severity during exit DBPCFCs and modulated peanut-specific cellular and humoral immune responses. Gastrointestinal (GI) symptoms were the most common treatment-related adverse events (AEs) in both groups, with 6 AR101 subjects (21%) withdrawing, 4 of those due primarily to recurrent GI AEs. CONCLUSIONS: In this study, AR101 demonstrated an acceptable safety profile and demonstrated clinical activity as a potential immunomodulatory treatment option in peanut-allergic children over the age of 4, adolescents, and young adults</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.09.016</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29092786">PM:29092786</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171102-BirdJA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171102-BirdJA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Bird JA</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.09.016</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86618</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Stokholm,J.</style></author><author><style face="normal" font="default"> Chawes,B.L.</style></author><author><style face="normal" font="default"> Vissing,N.</style></author><author><style face="normal" font="default"> Bonnelykke,K.</style></author><author><style face="normal" font="default"> Bisgaard,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">COPSAC, Copenhagen Prospective Studies on Asthma in Childhood, Herlev and Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark</style></auth-address><titles><title><style face="normal" font="default">Cat exposure in early life decreases asthma risk from the 17q21 high-risk variant</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="14" Month="10" Year="2017">2017/10/14</year></dates><abstract><style face="normal" font="default">BACKGROUND: Early-life exposure to cats and dogs has shown diverging associations with childhood asthma risk, and gene-environment interaction is one possible explanation. OBJECTIVES: We investigated interactions between cat and dog exposure and single nucleotide polymorphism rs7216389 variants in the chromosome 17q21 locus, the strongest known genetic risk factor for childhood asthma. METHODS: Genotyping was performed in 377 children from the at-risk Copenhagen Prospective Studies on Asthma in Childhood2000. The primary end point was the development of asthma until age 12 years. The secondary end point was the number of episodes with pneumonia and bronchiolitis from 0 to 3 years of age. Exposures included cat and dog ownership from birth and cat and dog allergen levels in bedding at age 1 year. Replication was performed in the unselected COPSAC2010 cohort with follow-up until 5 years of age. RESULTS: Cat and/or dog exposure from birth was associated with a lower prevalence of asthma among children with the rs7216389 high-risk TT genotype (adjusted hazard ratio, 0.16; 95% CI, 0.04-0.71; P = .015), with no effect in those with the CC/CT genotype (adjusted P = .283), demonstrating interaction between cat and dog exposure and the rs7216389 genotype (adjusted P = .044). Cat allergen levels were inversely associated with asthma development in children with the TT genotype (adjusted hazard ratio, 0.83; 95% CI, 0.71-0.97; P = .022), supporting the cat-rs7216389 genotype interaction (adjusted P = .008). Dog allergen exposure did not show such interaction. Furthermore, the TT genotype was associated with higher risk of pneumonia and bronchiolitis, and this increased risk was likewise decreased in children exposed to cat. Replication showed similar effects on asthma risk. CONCLUSION: The observed gene-environment interaction suggests a role of early-life exposure, especially to cat, for attenuating the risk of childhood asthma, pneumonia, and bronchiolitis in genetically susceptible subjects</style></abstract><notes><style face="normal" font="default">DA - 20171105IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.07.044</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29102067">PM:29102067</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171105-StokholmJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171105-StokholmJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171105, Stokholm J</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.07.044</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86619</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">KleinJan,A.</style></author><author><style face="normal" font="default"> Tindemans,I.</style></author><author><style face="normal" font="default"> Montgomery,J.E.</style></author><author><style face="normal" font="default"> Lukkes,M.</style></author><author><style face="normal" font="default"> de Bruijn,M.J.W.</style></author><author><style face="normal" font="default"> van Nimwegen,M.</style></author><author><style face="normal" font="default"> Bergen,I.</style></author><author><style face="normal" font="default"> Moellering,R.E.</style></author><author><style face="normal" font="default"> Hoogsteden,H.C.</style></author><author><style face="normal" font="default"> Boon,L.</style></author><author><style face="normal" font="default"> Amsen,D.</style></author><author><style face="normal" font="default"> Hendriks,R.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pulmonary Medicine, Erasmus MC Rotterdam, PO Box 2040, NL 3000CA Rotterdam, The Netherlands.</style></auth-address><titles><title><style face="normal" font="default">The Notch Pathway Inhibitor SAHM1 Abrogates the Hallmarks of Allergic Asthma</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">BACKGROUND: The Notch signaling pathway has been implicated in the pathogenesis of allergic airway inflammation. Targeting the active Notch transactivation complex by the cell-permeable, hydrocarbon-stapled synthetic peptide SAHM1 was results in genome-wide suppression of Notch-activated genes in leukemic cells and other models. However, efficacy of SAHM1 in allergic asthma models has remained unexplored. OBJECTIVE: We aimed to investigate therapeutic efficacy of SAHM1 in a house dust mite (HDM)-driven asthma model. METHODS: Topical therapeutic intervention with SAHM1 or a control peptide was performed during sensitization and/or challenge with HDM in mice. Airway inflammation was assessed by multi-color flow cytometry and bronchial hyperreactivity (BHR) was studied. Additionally, SAHM1 therapy was investigated in established asthma and in a model in which we neutralized IFNgamma during HDM challenge to support the Th2 response and exacerbate asthma. RESULTS: SAHM1 treatment during the challenge phase led to a marked reduction of eosinophils and T-cells in bronchoalveolar lavage (BAL), compared with diluent-treated or control peptide-treated mice. Likewise, T-cell cytokine content and BHR were reduced. SAHM1 treatment dampened Th2-inflammation during ongoing HDM challenge and enhanced recovery following established asthma. Additionally, in the presence of anti-IFNgamma antibodies, SAHM1 downregulated expression of the key Th2 transcription factor (TF) GATA3 and intracellular IL-4 in BAL T-cells, but expression of the Th17 TF RORgammat or intracellular IL-17 was not affected. SAHM1 therapy also reduced serum IgE levels. CONCLUSIONS: Therapeutic intervention of Notch signaling by SAHM1 inhibits allergic airway inflammation in mice and is therefore an interesting new topical treatment opportunity in asthma</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Netherlands -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.08.042</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29111218">PM:29111218</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-KleinJanA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-KleinJanA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, KleinJan A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.08.042</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86620</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Feichtner,C.R.</style></author><author><style face="normal" font="default"> Arlian,L.G.</style></author><author><style face="normal" font="default"> Morgan,M.S.</style></author><author><style face="normal" font="default"> Vyszenski-Moher,D.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biological Sciences, Wright State University, Dayton, OH 45435</style></auth-address><titles><title><style face="normal" font="default">Home freezers kill house dust mites</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.028</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29111219">PM:29111219</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-FeichtnerCR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171107-FeichtnerCR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Feichtner CR</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.028</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86621</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Di Berardino,F.</style></author><author><style face="normal" font="default"> Zanetti,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Audiology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Department of Clinical Sciences and Community Health , University of Milan , Milan , Italy</style></auth-address><titles><title><style face="normal" font="default">Delayed Immunomodulatory Effect of Cow Milk-Free Diet in Meniere's Disease</style></title><secondary-title><style face="normal" font="default">J Am Coll Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Coll Nutr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="31" Month="10" Year="2017">2017/10/31</year></dates><abstract><style face="normal" font="default">OBJECTIVE: Since 1930, dietary modification has been proposed as adjunct treatment in Meniere's disease (MD) with different and controversial results. We report the case of a 42-year-old female suffering from definite MD and intermittent seasonal allergic rhino-conjunctivitis because it highlights the importance of evaluating the different combinations of defined causative elements in an atopic patient with MD. METHODS: An immunological and audiological evaluation was performed, including pure-tone, speech, and immittance audiometry; glycerol dehydration test; bithermal caloric testing; video head impulse test; cervical vestibular evoked myogenic potentials; static posturography; and Dizziness Handicap Inventory questionnaire. RESULTS: A milk-free diet was crucial to relief from MD symptoms and a cow's milk challenge test was able to evoke them but vestibukar symptoms persist. CONCLUSIONS: The effect of dietary modification was evident only after specific immunotherapies against other allergens. This highlights the importance of evaluating different combinations of defined causative elements in the allergic treatment of MD</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1541-1087 (Electronic)IS - 0731-5724 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1080/07315724.2017.1364181</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29087236">PM:29087236</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Coll Nutr\20171031-DiBerardinoF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Coll Nutr\20171031-DiBerardinoF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Di Berardino F</style></custom2><misc3><style face="normal" font="default">10.1080/07315724.2017.1364181</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86623</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Morschheuser,L.</style></author><author><style face="normal" font="default"> Mink,K.</style></author><author><style face="normal" font="default"> Horst,R.</style></author><author><style face="normal" font="default"> Kallinich,C.</style></author><author><style face="normal" font="default"> Rohn,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Hamburg, Hamburg School of Food Science, Institute of Food Chemistry, Grindelallee 117, D-20146 Hamburg, Germany</style></auth-address><titles><title><style face="normal" font="default">Immunological analysis of food proteins using high-performance thin-layer chromatography-immunostaining</style></title><secondary-title><style face="normal" font="default">J Chromatogr A</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Chromatogr A</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="20" Month="10" Year="2017">2017/10/20</year></dates><abstract><style face="normal" font="default">The chromatographic analysis of intact proteins is still challenging, especially when biological functions as antigenicity of proteins or peptides are in the focus. Traditional immunoassays provide information about the entirety of antigenic proteins/peptides, e.g., in ELISA assays. On the other hand, when focusing on the investigation of (cross) reactivity of antibodies, Western blot following gel-electrophoresis represents the method of choice. However, gel-electrophoresis is limited by the molecular weight and therefore, not suitable for peptides &lt;/=3kDa or proteins >/=250kDa. Furthermore, for gaining detailed information about the protein sequence (e.g., via mass spectrometric analysis), a so called in-gel digest needs to be performed following electrophoretic separation and is therefore elaborate and accompanied by a significant loss of structural, and even more severe, conformational information. Here, protein analysis using HPTLC seems to be a promising alternative due to the high level of variability regarding the chromatographic system (multiple mobile and stationary phases, even mixed) and manifold detection as well as hyphenation possibilities. This study exemplarily focused on the immunological investigation of proteins in milk following thin-layer chromatographic separation. The detection of these antigens is mandatory, as they might trigger allergenic reactions in sensitized people. Besides the proof of its applicability on different stationary phase materials, the newly developed immunoassay can be used as an approach for semi-quantitative estimation of antigenic proteins. In addition to the analysis of intact food allergens, also analyzing peptides thereof is worth considering which can be realized using HPTLC-immunostaining as well</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1873-3778 (Electronic)IS - 0021-9673 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.chroma.2017.10.046</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29106961">PM:29106961</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Chromatogr A\20171106-MorschheuserL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Chromatogr A\20171106-MorschheuserL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Morschheuser L</style></custom2><misc3><style face="normal" font="default">10.1016/j.chroma.2017.10.046</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86624</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yatagai,T.</style></author><author><style face="normal" font="default"> Shimauchi,T.</style></author><author><style face="normal" font="default"> Yamaguchi,H.</style></author><author><style face="normal" font="default"> Sakabe,J.I.</style></author><author><style face="normal" font="default"> Aoshima,M.</style></author><author><style face="normal" font="default"> Ikeya,S.</style></author><author><style face="normal" font="default"> Tatsuno,K.</style></author><author><style face="normal" font="default"> Fujiyama,T.</style></author><author><style face="normal" font="default"> Ito,T.</style></author><author><style face="normal" font="default"> Ojima,T.</style></author><author><style face="normal" font="default"> Tokura,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Hamamatsu University School of Medicine, Hamamatsu, Japan.</style></auth-address><titles><title><style face="normal" font="default">Sensitive skin is highly frequent in extrinsic atopic dermatitis and correlates with disease severity markers but not necessarily with skin barrier impairment</style></title><secondary-title><style face="normal" font="default">J Dermatol Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Dermatol Sci</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">BACKGROUND: Sensitive skin is a condition of cutaneous hypersensitivity to environmental factors. Lactic acid stinging test (LAST) is commonly used to assess sensitive skin and composed of four distinct sensations (pain, burning sensation, itch, and crawly feeling). A link between sensitive skin and barrier dysfunction has been proposed in atopic dermatitis (AD) patients. However, clinical and laboratory factors that are associated with sensitive skin remain unelucidated. OBJECTIVE: To investigate relationship between sensitive skin and AD-associated markers. METHODS: Forty-two Japanese AD patients and 10 healthy subjects (HS) were enrolled. AD patients were divided into extrinsic (EAD; high IgE levels) and intrinsic (IAD; normal IgE levels) types. We conducted 1% LAST by assessing the four distinct sensations and calculated the frequencies of sensitive skin in EAD, IAD, and HS. We also performed clinical AD-related tests, including transepidermal water loss (TEWL), visual analogue scale (VAS) of pruritus, and quality of life, and measured laboratory markers, including blood levels of IgE, CCL17/TARC, lactate dehydrogenase (LDH) and eosinophil counts, and concentration levels of serum Th1/Th2 cytokines. Filaggrin (FLG) mutations were examined in 21 patients. These values were subjected to correlation analyses with each of the four sensation elements. RESULTS: According to the standard criteria for LAST positivity, the frequencies of LAST-positive subjects were 54.8% and 10.0% in AD and HS, respectively (P=0.014). EAD patients showed a significantly (P=0.026) higher frequency of positive LAST (65.6%) than did IAD patients (20.0%). Among the four LAST sensation elements, the crawly feeling and pain scores positively correlated with VAS of pruritus, total serum IgE, mite-specific IgE, CCL17/TARC, and/or LDH. There was no association of the LAST scores with serum Th1/Th2 cytokine levels. Notably, neither TEWL nor FLG mutations correlated with LAST positivity or any sensation scores. CONCLUSIONS: The frequency of sensitive skin is higher in EAD than in IAD. Sensitive skin is associated with AD severity, but not necessarily with barrier condition</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 1873-569X (Electronic)IS - 0923-1811 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.jdermsci.2017.10.011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122406">PM:29122406</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Dermatol Sci\20171110-YatagaiT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Dermatol Sci\20171110-YatagaiT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Yatagai T</style></custom2><misc3><style face="normal" font="default">10.1016/j.jdermsci.2017.10.011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86625</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,H.J.</style></author><author><style face="normal" font="default"> Lee,S.H.</style></author><author><style face="normal" font="default"> Go,H.N.</style></author><author><style face="normal" font="default"> Ahn,J.R.</style></author><author><style face="normal" font="default"> Kim,H.J.</style></author><author><style face="normal" font="default"> Hong,S.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Veterinary Internal Medicine, College of Veterinary Medicine, Chonnam National University, Gwangju, South Korea</style></auth-address><titles><title><style face="normal" font="default">Effects of kestose on gut mucosal immunity in an atopic dermatitis mouse model</style></title><secondary-title><style face="normal" font="default">J Dermatol Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Dermatol Sci</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="18" Month="10" Year="2017">2017/10/18</year></dates><abstract><style face="normal" font="default">BACKGROUND: Atopic dermatitis (AD) is recently increasing among populations, but the underlying mechanisms remain controversial. Interactions between the gut microbiota and mucosal immunity are considered to be a crucial etiology. Fructooligosaccharide (FOS), prebiotics have been reported as activators of the gut microbiota. OBJECTIVE: The aim of this study was to investigate the effects of kestose, the smallest FOS and FOS on atopic dermatitis in mice. METHODS: An AD mouse model was developed by (ovalbumin) epidermal sensitization using BALB/c mice. Kestose (1%, 5%, and 10%) or FOS (5%, positive control) was orally administered throughout the study. RESULTS: In comparison with the values observed for the control AD mice, transepidermal water loss (TEWL), clinical score, and skin inflammation on histopathology were significantly decreased by the oral administration of kestose. Total IgE, thymic stromal lymphopoietin (TSLP) in skin, and IL-4 were also suppressed by this administration. In addition, the population of CD4+Foxp3+ cells in mesenteric lymph nodes (MLNs) and acetate concentrations in feces were significantly increased by kestose treatment. CONCLUSIONS: These findings suggest that kestose activates the gut immune system to induce the tolerance against allergic skin inflammations in AD</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1873-569X (Electronic)IS - 0923-1811 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1016/j.jdermsci.2017.10.006</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29111180">PM:29111180</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Dermatol Sci\20171107-KimHJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Dermatol Sci\20171107-KimHJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Kim HJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.jdermsci.2017.10.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86626</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Singh,P.B.</style></author><author><style face="normal" font="default"> Pua,H.H.</style></author><author><style face="normal" font="default"> Happ,H.C.</style></author><author><style face="normal" font="default"> Schneider,C.</style></author><author><style face="normal" font="default"> von Moltke,J.</style></author><author><style face="normal" font="default"> Locksley,R.M.</style></author><author><style face="normal" font="default"> Baumjohann,D.</style></author><author><style face="normal" font="default"> Ansel,K.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA</style></auth-address><titles><title><style face="normal" font="default">MicroRNA regulation of type 2 innate lymphoid cell homeostasis and function in allergic inflammation</style></title><secondary-title><style face="normal" font="default">J Exp Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Exp Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">MicroRNAs (miRNAs) exert powerful effects on immunity through coordinate regulation of multiple target genes in a wide variety of cells. Type 2 innate lymphoid cells (ILC2s) are tissue sentinel mediators of allergic inflammation. We established the physiological requirements for miRNAs in ILC2 homeostasis and immune function and compared the global miRNA repertoire of resting and activated ILC2s and T helper type 2 (TH2) cells. After exposure to the natural allergen papain, mice selectively lacking the miR-17 approximately 92 cluster in ILC2s displayed reduced lung inflammation. Moreover, miR-17 approximately 92-deficient ILC2s exhibited defective growth and cytokine expression in response to IL-33 and thymic stromal lymphopoietin in vitro. The miR-17 approximately 92 cluster member miR-19a promoted IL-13 and IL-5 production and inhibited expression of several targets, including SOCS1 and A20, signaling inhibitors that limit IL-13 and IL-5 production. These findings establish miRNAs as important regulators of ILC2 biology, reveal overlapping but nonidentical miRNA-regulated gene expression networks in ILC2s and TH2 cells, and reinforce the therapeutic potential of targeting miR-19 to alleviate pathogenic allergic responses</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 1540-9538 (Electronic)IS - 0022-1007 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1084/jem.20170545</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122948">PM:29122948</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Exp Med\20171110-SinghPB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Exp Med\20171110-SinghPB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Singh PB</style></custom2><misc3><style face="normal" font="default">10.1084/jem.20170545</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86627</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vanga,S.K.</style></author><author><style face="normal" font="default"> Raghavan,V.</style></author></authors></contributors><titles><title><style face="normal" font="default">How well do plant based alternatives fare nutritionally compared to cow</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖs milk?</style></title><secondary-title><style face="normal" font="default">J Food Sci Technol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Food Sci Technol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0975-8402</style></isbn><abstract><style face="normal" font="default">Due to the issues like lactose intolerance and milk allergy arising from the consumption of cow</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖs milk, there has been an increased demand in the plant based alternative milks around the world. Food industry has addressed these demands by introducing various milk beverages which are promoted as alternatives coming from plant sources which include almond milk and soy milk. Though they are popularly advertised as healthy and wholesome, little research has been done in understanding the nutritional implications of consuming these milk beverages in short term and long term. Further, consumers associate these alternatives to be a direct substitute of cow</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖs milk which might not be true in all cases. This review tries to address the issue by outlining the differences between cow</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖs milk and commercially available alternative milks in terms of their nutrient content. Though various plant based alternate milks have been studied, only the four most consumed milk beverages are presented in this review which are consumed widely around the world. A complete nutritional outline and the corresponding health benefits of consuming these plant based milk beverages have been discussed in detail which could help the consumers make an informed decision</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1007/s13197-017-2915-y</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s13197-017-2915-y</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Food Sci Technol\20171114-VangaSK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Food Sci Technol\20171114-VangaSK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Vanga SK</style></custom2><misc3><style face="normal" font="default">10.1007/s13197-017-2915-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86628</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lindner,J.</style></author><author><style face="normal" font="default"> Rausch,S.</style></author><author><style face="normal" font="default"> Treptow,S.</style></author><author><style face="normal" font="default"> Geldmeyer-Hilt,K.</style></author><author><style face="normal" font="default"> Krause,T.</style></author><author><style face="normal" font="default"> St-Arnaud,R.</style></author><author><style face="normal" font="default"> Arabian,A.</style></author><author><style face="normal" font="default"> Radbruch,A.</style></author><author><style face="normal" font="default"> Hartmann,S.</style></author><author><style face="normal" font="default"> Worm,M.</style></author><author><style face="normal" font="default"> Heine,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Klinik fur Dermatologie, Venerologie und Allergologie, Allergie-Centrum-Charite, Campus Charite Mitte, Charite - Universitatsmedizin Berlin, D-10117 Berlin, Germany</style></auth-address><titles><title><style face="normal" font="default">Endogenous Calcitriol Synthesis Controls the Humoral IgE Response in Mice</style></title><secondary-title><style face="normal" font="default">J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">The vitamin D receptor participates in the control of IgE class-switch recombination in B cells. The physiologic vitamin D receptor agonist, 1,25(OH)2D3 (calcitriol), is synthesized by the essential enzyme 25-hydroxyvitamin D3-1alpha-hydroxylase (CYP27B1), which can be expressed by activated immune cells. The role of endogenous calcitriol synthesis for the regulation of IgE has not been proven. In this study, we investigated IgE-responses in Cyp27b1-knockout (KO) mice following sensitization to OVA or intestinal infection with Heligmosomoides polygyrus Specific Igs and plasmablasts were determined by ELISA and ELISpot, Cyp27b1 expression was measured by quantitative PCR. The data show elevated specific IgE and IgG1 concentrations in the blood of OVA-sensitized Cyp27b1-KO mice compared with wild-type littermates (+898 and +219%). Accordingly, more OVA-specific IgG1-secreting cells are present in spleen and fewer in the bone marrow of Cyp27b1-KO mice. Ag-specific mechanisms are suggested as the leucopoiesis is in general unchanged and activated murine B and T lymphocytes express Cyp27b1 Accordingly, elevated specific IgE concentrations in the blood of sensitized T cell-specific Cyp27b1-KO mice support a lymphocyte-driven mechanism. In an independent IgE-inducing model, i.e., intestinal infection with H. polygyrus, we validated the increase of total and specific IgE concentrations of Cyp27b1-KO compared with wild-type mice, but not those of IgG1 or IgA. We conclude that endogenous calcitriol has an impact on the regulation of IgE in vivo. Our data provide genetic evidence supporting previous preclinical and clinical findings and suggest that vitamin D deficiency not only promotes bone diseases but also type I sensitization</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1550-6606 (Electronic)IS - 0022-1767 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Canada -</style></notes><work-type><style face="normal" font="default">10.4049/jimmunol.1602080</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29109124">PM:29109124</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol\20171107-LindnerJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol\20171107-LindnerJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Lindner J</style></custom2><misc3><style face="normal" font="default">10.4049/jimmunol.1602080</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86631</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shin,H.S.</style></author><author><style face="normal" font="default"> Eom,J.E.</style></author><author><style face="normal" font="default"> Shin,D.U.</style></author><author><style face="normal" font="default"> Yeon,S.H.</style></author><author><style face="normal" font="default"> Lim,S.I.</style></author><author><style face="normal" font="default"> Lee,S.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Research Group of Gut Microbiome, Korea Food Research Institute, Sungnam-Si, Gyeonggi-Do 13539, Korea</style></auth-address><titles><title><style face="normal" font="default">Preventive effects of a probiotic mixture in an ovalbumin-induced food allergy model</style></title><secondary-title><style face="normal" font="default">J Microbiol Biotechnol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Microbiol Biotechnol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">Although there has been a steady increase in the prevalence of food allergies worldwide in recent decades, no effective therapeutic strategies have been developed. Modulation of the gut microbiota composition and/or function through probiotics has been highlighted as a promising target for protection against food allergies. In this study, we aimed to investigate the allergy-reducing effects of a probiotic mixture (P5: Lactococcus lactis KF140, Pediococcus pentosaceus KF159, Lactobacillus pentosus KF340, Lactobacillus paracasei 698, and Bacillus amyloliquefaciens 26N) in mice with ovalbumin (OVA)-induced food allergy. Administration of P5 significantly suppressed the oral OVA challenge-induced anaphylactic response and rectal temperature decline, reduced diarrhea symptoms. Moreover, P5 also significantly inhibited the secretion of IgE, Th2 cytokines (interleukin [IL]-4, IL-5, IL-10, and IL-13), and Th17 cytokines (IL-17), which were increased in mice with OVA-induced food allergy, and induced generation of CD4+Foxp3+ regulatory T cells. These results revealed that P5 may have applications as a preventive agent for food allergy</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 1738-8872 (Electronic)IS - 1017-7825 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4014/jmb.1708.08051</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29121702">PM:29121702</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Microbiol Biotechnol\20171109-ShinHS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Microbiol Biotechnol\20171109-ShinHS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Shin HS</style></custom2><misc3><style face="normal" font="default">10.4014/jmb.1708.08051</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86632</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Trablesi,H.</style></author><author><style face="normal" font="default"> Hadrich,I.</style></author><author><style face="normal" font="default"> Neji,S.</style></author><author><style face="normal" font="default"> Fendri,N.</style></author><author><style face="normal" font="default"> Ghorbel,D.</style></author><author><style face="normal" font="default"> Makni,F.</style></author><author><style face="normal" font="default"> Ayadi,H.</style></author><author><style face="normal" font="default"> Kammoun,S.</style></author><author><style face="normal" font="default"> Ayadi,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of Fungal and Parasitic Molecular Biology, School of Medicine, University of Sfax, Sfax, Tunisia</style></auth-address><titles><title><style face="normal" font="default">Environmental and molecular study of fungal flora in asthmatic patients</style></title><secondary-title><style face="normal" font="default">J Mycol Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Mycol Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">The aim of the present study was to investigate the epidemiological and fungal environmental profile in asthmatic patients. We conducted a prospective study involving 49 patients with allergic asthma. One hundred and forty-five clinical samples and 289 environmental samples were performed. Only 30 patients accepted to participate to the environmental study at their home. For specific IgE antibodies, ELISA assay was conducted for 21 patients. Molecular ITS sequencing was performed for 37 isolates. The frequency of attacks was significantly associated with the seasonality, which was closely related to climate (P=0.024), exposure to animals (cats, P=0.025), plants (olive, P=0.018), physical effort (P=0.04) and the number of permanent occupants in house (>6) (P=0.026). Fungal contaminants were detected from 78.6% of biological samples and 97.8% of environmental samples. Antibodies corresponding to the studied allergens were detected in 10 patients (10/21). PCR sequencing allowed as rectified morphological identification for 27.02% (10/37) strains of Aspergillus. The allergy in molds is an indisputable reality that is necessary to look for in front of any severe asthma. So, it is important to establish clearly a relationship between exposure to fungi and health disorders in order to set up specific and effective preventive measures</style></abstract><notes><style face="normal" font="default">DA - 20171105IS - 1773-0449 (Electronic)IS - 1156-5233 (Linking)LA - engPT - Journal ArticleCO - Tunisia -</style></notes><work-type><style face="normal" font="default">10.1016/j.mycmed.2017.09.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29102311">PM:29102311</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Mycol Med\20171105-TrablesiH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Mycol Med\20171105-TrablesiH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171105, Trablesi H</style></custom2><misc3><style face="normal" font="default">10.1016/j.mycmed.2017.09.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86633</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bozicevic,A.</style></author><author><style face="normal" font="default"> De Mieri,M.</style></author><author><style face="normal" font="default"> Nassenstein,C.</style></author><author><style face="normal" font="default"> Wiegand,S.</style></author><author><style face="normal" font="default"> Hamburger,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pharmaceutical Biology, University of Basel , Klingelbergstrasse 50, CH-4056 Basel, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Secondary Metabolites in Allergic Plant Pollen Samples Modulate Afferent Neurons and Murine Tracheal Rings</style></title><secondary-title><style face="normal" font="default">J Nat Prod</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Nat Prod</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="7" Month="11" Year="2017">2017/11/7</year></dates><abstract><style face="normal" font="default">Plant pollens are strong airborne elicitors of asthma. Their proteinaceous allergens have been studied intensively, but little is known about a possible contribution of pollen secondary metabolites to the nonallergic exacerbation of asthma. Pollen samples originating from 30 plant species were analyzed by HPLC coupled to PDA, ESIMS, and ELSD detectors and off-line NMR spectroscopy. Polyamine conjugates, flavonoids, and sesquiterpene lactones were identified. Polyamine conjugates were characteristic of all Asteraceae species. The presence of sesquiterpene lactones in Asteraceae pollen varied between species and pollen lots. All plant pollen, including those from non-Asteraceae species, contained to some extent electrophiles as determined by their reaction with N-acetyl-l-cysteine. Selected pollen extracts and pure compounds were tested in murine afferent neurons and in murine tracheal preparations. Tetrahydrofuran extracts of Ambrosia artemisiifolia and Ambrosia psilostachya pollen and a mixture of sesquiterpene lactones coronopilin/parthenin increased the intracellular Ca2+ concentration in 15%, 32%, and 37% of cinnamaldehyde-responsive neurons, respectively. In organ bath experiments, only the sesquiterpene lactones tested induced a weak dilatation of naive tracheas and strongly lowered the maximal methacholine-induced tracheal constriction. A tetrahydrofuran extract of A. psilostachya and coronopilin/parthenin led to a time-dependent relaxation of the methacholine-preconstricted trachea. These results provide the first evidence for a potential role of pollen secondary metabolites in the modulation of the tracheal tone</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1520-6025 (Electronic)IS - 0163-3864 (Linking)LA - engPT - Journal ArticleCO - Switzerland -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1021/acs.jnatprod.7b00495</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29112407">PM:29112407</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Nat Prod\20171107-BozicevicA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Nat Prod\20171107-BozicevicA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Bozicevic A</style></custom2><misc3><style face="normal" font="default">10.1021/acs.jnatprod.7b00495</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86634</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mullins,R.J.</style></author><author><style face="normal" font="default"> Turner,P.J.</style></author><author><style face="normal" font="default"> Barnes,E.H.</style></author><author><style face="normal" font="default"> Campbell,D.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">John James Medical Centre, University of Sydney, Canberra, Australian Capital Territory, Australia</style></auth-address><titles><title><style face="normal" font="default">Allergic gastroenteritis hospital admission time trends in Australia and New Zealand</style></title><secondary-title><style face="normal" font="default">J Paediatr Child Health</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Paediatr Child Health</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="31" Month="10" Year="2017">2017/10/31</year></dates><abstract><style face="normal" font="default">AIM: Recent epidemiological studies indicate increases in hospital food allergy-related anaphylaxis admission rates in Australian and New Zealand. The aim of the study was to examine whether non-IgE-mediated food allergy might have increased in parallel. METHODS: We analysed childhood hospital admissions rates by ICD 10 codes for allergic gastroenteritis (AG) and infective gastroenteritis in Australia and New Zealand between June 1998 and July 2014. RESULTS: In Australia, most AG-related admissions (73%) occurred in those aged &lt;1 year and increased by 7.3%/year (95% confidence interval (CI) 5.5-9.3, P &lt; 0.0001) from 6.8 to 26.5/105 population. Similar trends were observed for New Zealand; 81% of admissions occurred in those aged &lt;1 year and increased by 9.4%/year (95% CI 5.5-9.3, P &lt; 0.0001) from 7.2 to 30.7/105 population. By contrast there were no significant changes in AG-related admission rates in the older patients and infective gastroenteritis admissions fell in both countries in those aged &lt;1 year; Australia by 4.4%/year (95% CI 4.3-4.6, P &lt; 0.0001) and in New Zealand by 5.8%/year (95% CI 5.4-6.2, P &lt; 0.0001). CONCLUSION: We observed a fourfold increase in AG-related admission rates in two countries with known high rates of IgE-mediated food allergy/anaphylaxis. If confirmed by other studies, it will be of interest to determine if factors thought to contribute to the increase in IgE-mediated food allergy might also play a role in non-IgE-mediated gastroenterological food allergy syndromes</style></abstract><notes><style face="normal" font="default">DA - 20171101IS - 1440-1754 (Electronic)IS - 1034-4810 (Linking)LA - engPT - Journal ArticleCO - Australia -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/jpc.13767</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29090503">PM:29090503</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Paediatr Child Health\20171101-MullinsRJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Paediatr Child Health\20171101-MullinsRJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171101, Mullins RJ</style></custom2><misc3><style face="normal" font="default">10.1111/jpc.13767</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86635</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Navarro-Lopez,V.</style></author><author><style face="normal" font="default"> Ramirez-Bosca,A.</style></author><author><style face="normal" font="default"> Ramon-Vidal,D.</style></author><author><style face="normal" font="default"> Ruzafa-Costas,B.</style></author><author><style face="normal" font="default"> Genoves-Martinez,S.</style></author><author><style face="normal" font="default"> Chenoll-Cuadros,E.</style></author><author><style face="normal" font="default"> Carrion-Gutierrez,M.</style></author><author><style face="normal" font="default"> Horga de la Parte,J.</style></author><author><style face="normal" font="default"> Prieto-Merino,D.</style></author><author><style face="normal" font="default"> Codoner-Cortes,F.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical Microbiology and Infectious Disease Unit, Hospital Universitario Vinalopo, Elche, Spain</style></auth-address><titles><title><style face="normal" font="default">Effect of Oral Administration of a Mixture of Probiotic Strains on SCORAD Index and Use of Topical Steroids in Young Patients With Moderate Atopic Dermatitis: A Randomized Clinical Trial</style></title><secondary-title><style face="normal" font="default">JAMA Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">JAMA Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">Importance: Oral intake of new probiotic formulations may improve the course of atopic dermatitis (AD) in a young population. Objective: To determine whether a mixture of oral probiotics is safe and effective in the treatment of AD symptoms and to evaluate its influence on the use of topical steroids in a young population. Design, Setting, and Participants: A 12-week randomized, double-blind, placebo-controlled intervention trial, from March to June 2016, at the outpatient hospital Centro Dermatologico Estetico de Alicante, Alicante, Spain. Observers were blinded to patient groupings. Participants were children aged 4 to 17 years with moderate atopic dermatitis. The groups were stratified and block randomized according to sex, age, and age of onset. Patients were ineligible if they had used systemic immunosuppressive drugs in the previous 3 months or antibiotics in the previous 2 weeks or had a concomitant diagnosis of intestinal bowel disease or signs of bacterial infection. Interventions: Twelve weeks with a daily capsule containing freeze-dried powder with 109 total colony-forming units of the probiotic strains Bifidobacterium lactis CECT 8145, B longum CECT 7347, and Lactobacillus casei CECT 9104 and maltodextrin as a carrier, or placebo (maltodextrin-only capsules). Main Outcomes and Measures: SCORAD index score and days of topical steroid use were analyzed. Results: Fifty children (26 [50%] female; mean [SD] age, 9.2 [3.7] years) participated. After 12 weeks of follow-up, the mean reduction in the SCORAD index in the probiotic group was 19.2 points greater than in the control group (mean difference, -19.2; 95% CI, -15.0 to -23.4). In relative terms, we observed a change of -83% (95% CI, -95% to -70%) in the probiotic group and -24% (95% CI, -36% to -11%) in the placebo group (P &lt; .001). We found a significant reduction in the use of topical steroids to treat flares in the probiotic arm (161 of 2084 patient-days [7.7%]) compared with the control arm (220 of 2032 patient-days [10.8%]; odds ratio, 0.63; 95% CI, 0.51 to 0.78). Conclusions and Relevance: The mixture of probiotics was effective in reducing SCORAD index and reducing the use of topical steroids in patients with moderate AD. Trial Registration: clinicaltrials.gov Identifier: NCT02585986</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 2168-6084 (Electronic)IS - 2168-6068 (Linking)LA - engPT - Journal ArticleCO - Spain -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1001/jamadermatol.2017.3647</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29117309">PM:29117309</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\JAMA Dermatol\20171108-NavarroLopezV.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\JAMA Dermatol\20171108-NavarroLopezV.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Navarro-Lopez V</style></custom2><misc3><style face="normal" font="default">10.1001/jamadermatol.2017.3647</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86638</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Roth-Walter,F.</style></author><author><style face="normal" font="default"> Pacios,L.F.</style></author><author><style face="normal" font="default"> Bianchini,R.</style></author><author><style face="normal" font="default"> Jensen-Jarolim,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Comparative Medicine, at the Interuniversity Messerli Research Institute, University of Veterinary Medicine Vienna, Medical University of Vienna and University of Vienna, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Linking iron-deficiency with allergy: role of molecular allergens and the microbiome</style></title><secondary-title><style face="normal" font="default">Metallomics</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Metallomics</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">Atopic individuals tend to develop a Th2 dominant immune response, resulting in hyperresponsiveness to harmless antigens, termed allergens. In the last decade, epidemiological studies have emerged that connected allergy with a deficient iron-status. Immune activation under iron-deficient conditions results in the expansion of Th2-, but not Th1 cells, can induce class-switching in B-cells and hampers the proper activation of M2, but not M1 macrophages. Moreover, many allergens, in particular with the lipocalin and lipocalin-like folds, seem to be capable of binding iron indirectly via siderophores harboring catechol moieties. The resulting locally restricted iron-deficiency may then lead during immune activation to the generation of Th2-cells and thus prepare for allergic sensitization. Moreover, iron-chelators seem to also influence clinical reactivity: mast cells accumulate iron before degranulation and seem to respond differently depending on the type of the encountered siderophore. Whereas deferoxamine triggers degranulation of connective tissue-type mast cells, catechol-based siderophores reduce activation and degranulation and improve clinical symptoms. Considering the complex interplay of iron, siderophores and immune molecules, it remains to be determined whether iron-deficiencies are the cause or the result of allergy</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 1756-591X (Electronic)IS - 1756-5901 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Austria -CO - Spain -</style></notes><work-type><style face="normal" font="default">10.1039/c7mt00241f</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29120476">PM:29120476</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Metallomics\20171109-RothWalterF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Metallomics\20171109-RothWalterF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Roth-Walter F</style></custom2><misc3><style face="normal" font="default">10.1039/c7mt00241f</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86643</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cheng,Q.</style></author><author><style face="normal" font="default"> Shang,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Pulmonology Department, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China</style></auth-address><titles><title><style face="normal" font="default">ORMDL3 may participate in the pathogenesis of bronchial epithelialmesenchymal transition in asthmatic mice with airway remodeling</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">Asthma is a common chronic respiratory disease in children that is caused by a complex interaction between genetic and environmental factors. Orosomucoidlike 3 (ORMDL3) is a candidate gene that has been strongly associated with asthma; however, the underlying mechanisms are unknown. ORMDL3 regulates the expression of metalloproteinases and transforming growth factorbeta, and ORMDL3 transgenic mice exhibit increased airway remodeling. Therefore, ORMDL3 may be associated with airway remodeling. The present study attempted to examine the associations between ORMDL3 and the severity of airway remodeling in asthmatic mice, and also to determine whether ORMDL3 induces epithelialmesenchymal transition (EMT) in the bronchial epithelium. For this purpose, BALB/c mice were randomly assigned to control and asthma groups. Lung tissues were collected on days 3, 7 and 14 of the ovalbumin (OVA) challenge. Airway remodeling in asthmatic mice was then observed by hematoxylin and eosin, and Masson staining. Morphological changes in the bronchial epithelium were assessed by transmission electron microscopy. The EMTassociated indicators Ecadherin (Ecad), fibroblastspecific protein 1 (FSP1) and Vimentin (VIM) were assessed by western blotting and reverse transcriptionquantitative polymerase chain reaction (RTqPCR) at different time points of airway remodeling in asthmatic mice to detect the trend in EMT. Then, the localization of ORMDL3 was observed by immunohistochemistry, and its protein and mRNA expression was examined by western blotting and RTqPCR, respectively. Furthermore, the bronchial epithelial cell line 16HBE14owas transfected with an ORMDL3expressing plasmid, and the differences in Ecad, FSP1 and VIM expression were detected by immunofluorescence, western blotting and RTqPCR; the cell invasive ability was assessed by microscopy. The results revealed that ORMDL3 expression in the bronchial epithelium was associated with airway remodeling and EMT progression in vivo. Transfection of ORMDL3 into 16HBE 14ocells in vitro induced EMT. Taken together, these findings suggest that ORMDL3 may regulate EMT in the bronchial epithelium, thereby affecting airway remodeling in asthma</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.7972</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29115563">PM:29115563</url></web-urls><pdf-urls><url ppv-ref="no">yunxiaoshang0523@163.com</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171108, Cheng Q</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.7972</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86644</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kong,R.</style></author><author><style face="normal" font="default"> Kang,O.H.</style></author><author><style face="normal" font="default"> Seo,Y.S.</style></author><author><style face="normal" font="default"> Zhou,T.</style></author><author><style face="normal" font="default"> Kim,S.A.</style></author><author><style face="normal" font="default"> Shin,D.W.</style></author><author><style face="normal" font="default"> Kwon,D.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Oriental Pharmacy, College of Pharmacy, Wonkwang Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk 54538, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">MAPKs and NFkappaB pathway inhibitory effect of bisdemethoxycurcumin on phorbol12myristate13acetate and A23187induced inflammation in human mast cells</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="20" Month="10" Year="2017">2017/10/20</year></dates><abstract><style face="normal" font="default">Inflammationassociated damage may occur in any tissue following infection, exposure to toxins, following ischemia, and in allergic and autoimmune reactions. Inflammation may also result from mast cell degranulation induced by the intracellular calcium concentration. The inflammatory process may be inhibited by compounds that affect mast cells. Bisdemethoxycurcumin [1,7bis(4hydroxyphenyl) hepta1,6diene3,5dione, BDCM] is the active component of turmeric. It has anticancer, antioxidant and antibacterial properties. To investigate the molecular mechanism associated with the antiinflammatory activity of BDCM, human mast cell line 1 (HMC1) cells were treated with phorbol12myristate13acetate (PMA) and calcium ionophore A23187 (A23187) to induce the inflammatory process. Various HMC1 cells were pretreated with BDCM prior to stimulation of inflammation. BDCM inhibited the inflammationtriggered production of cytokines including interleukin (IL)6, IL8, and tumor necrosis factor (TNF)alpha. BDCM inhibition extended to the gene level. In activated HMC1 cells, phosphorylation levels of extracellular signalregulated kinase, cjun Nterminal kinase and p38 mitogenactivated protein kinase were decreased by treatment with BDCM. BDCM also inhibited nuclear factor(NF)kappaB activation and IkappaB degradation. In conclusion, BDCM suppresses the expression of TNFalpha, IL8, and IL6 by inhibiting the NFkappaB and mitogen activated protein kinase signaling pathways</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.7852</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29115448">PM:29115448</url></web-urls><pdf-urls><url ppv-ref="no">sssimi@wku.ac.kr</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171108, Kong R</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.7852</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86645</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,S.Y.</style></author><author><style face="normal" font="default"> Bae,C.S.</style></author><author><style face="normal" font="default"> Seo,J.H.</style></author><author><style face="normal" font="default"> Cho,S.S.</style></author><author><style face="normal" font="default"> Bae,M.S.</style></author><author><style face="normal" font="default"> Oh,D.S.</style></author><author><style face="normal" font="default"> Park,D.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">College of Oriental Medicine, Dongshin University, Naju, Jeollanamdo 58245, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Mycoleptodonoides aitchisonii suppresses asthma via Th2 and Th1 cell regulation in an ovalbumininduced asthma mouse model</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">Asthma is a chronic respiratory disease related to hyperresponsiveness. The majority of patients suffer mild symptoms, however, some cases, especially in the young and the elderly, can lead to death by apnea. Mycoleptodonoides atichisonii (M. atichisonii) is an edible mushroom that has previously been reported to possess several bioactive properties, such as the synthesis of nerve growth factors, antiobesity effects and the ability to prevent cell death. In the current study, the authors evaluated the antiasthmatic effects of M. atichisonii using an ovalbumininduced asthma mouse model. M. atichisonii dosedependently suppressed the levels of white blood cells, eosinophils and immunoglobulin (Ig)E in BALB/c mice, resulting from ovalbumininduced asthma. M. atichisonii recovered the typical asthmatic morphological changes in lungs, such as mucous hypersecretion, epithelial layer hyperplasia, eosinophil infiltration and various cell surface molecules, such as CD3, CD4, CD8, CD19 and major histocompatibility complex class II. With the exception of CD19+ cells and IL12p40, M. atichisonii affected almost all factors related to asthma induction including the T helper (Th)1/Th2 transcription factors, Tbet and GATA3, Th1related cytokines, Th2related cytokines and proinflammatory cytokines. In addition, M. atichisonii significantly inhibited the expression of IL5, IL13 and IL6. The authors concluded that M. atichisonii may be a promising drug candidate against asthma</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.7901</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29115454">PM:29115454</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Med Rep\20171108-LeeSY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Med Rep\20171108-LeeSY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Lee SY</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.7901</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86646</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shen,Y.</style></author><author><style face="normal" font="default"> Ke,X.</style></author><author><style face="normal" font="default"> Yun,L.</style></author><author><style face="normal" font="default"> Hu,G.H.</style></author><author><style face="normal" font="default"> Kang,H.Y.</style></author><author><style face="normal" font="default"> Hong,S.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Decreased expression of interleukin37 and its antiinflammatory effect in allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">Interleukin37 (IL37), a novel member of the IL1 cytokine family has been identified as a natural suppressor of innate immunity and inflammatory responses. The present study aimed to determine the expression of IL37 in peripheral blood mononuclear cells (PBMCs) from patients with allergic rhinitis (AR), and examine the possible immunosuppressive effect of IL37 on inflammatory mediators and CD4+ T cells in the pathogenesis of AR. The expression levels of IL37 were determined in PBMCs from 39 patients with AR and 43 controls using reverse transcriptionquantitative polymerase chain reaction (RTqPCR) analysis and flow cytometry. Cytokines in the supernatants of the PBMCs and CD4+ T cells, which were stimulated with lipopolysaccharide in the presence or absence of IL37, were assayed using enzymelinked immunosorbent assays and RTqPCR analysis. The results showed that the patients with AR exhibited significantly decreased expression of IL37, and increased expression levels of interleukin (IL)1beta and IL6 in PBMCs. Recombinant IL37 (rIL37) inhibited the production of IL1p and IL6, and enhanced the production of IL27 in PBMCs from the patients with AR and the control individuals. rIL37 also markedly decreased the expression of IL17 by CD4+ T cells in the patients with AR and controls. These results suggested that IL37 may be an important cytokine in the pathogenesis of AR. It may have a protective role in AR by inhibiting the production of proinflammatory cytokines and through suppressive regulation of the Th17 response</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.7988</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29115624">PM:29115624</url></web-urls><pdf-urls><url ppv-ref="no">khy_cq@sina.com</url><url ppv-ref="no">hsl_prof@sina.cn</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171108, Shen Y</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.7988</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86647</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,D.W.</style></author><author><style face="normal" font="default"> Ni,W.W.</style></author><author><style face="normal" font="default"> Zhou,Y.J.</style></author><author><style face="normal" font="default"> Huang,W.</style></author><author><style face="normal" font="default"> Cao,M.D.</style></author><author><style face="normal" font="default"> Meng,L.</style></author><author><style face="normal" font="default"> Wei,J.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Research Division of Clinical Pharmacology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Expression, purification and epitope analysis of Pla a 2 allergen from Platanus acerifolia pollen</style></title><secondary-title><style face="normal" font="default">Mol Med Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Med Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="26" Month="10" Year="2017">2017/10/26</year></dates><abstract><style face="normal" font="default">Platanus acerifolia is one of the major sources of outdoor allergens to humans, and can induce allergic asthma, rhinitis, dermatitis and other allergic diseases. Pla a 2 is a polygalacturonase and represents the major allergen identified in P. acerifolia pollen. The aim of the present study was to express and purify Pla a 2, and to predict B and T cell epitopes of Pla a 2. The gene encoding Pla a 2 was cloned into the pET28a vector and subsequently transfected into ArcticExpress (DE3) Escherichia coli cells; purified Pla a 2 was analyzed by western blot analysis. The results of the present study revealed that the Pla a 2 allergen has the ability to bind immunoglobulin E within the sera of patients allergic to P. acerifolia pollen. In addition, the B cell epitopes of Pla a 2 were predicted using the DNAStar Protean system, Bioinformatics Predicted Antigenic Peptides and BepiPred 1.0 software; T cell epitopes were predicted using NetMHCIIpan 3.0 and 2.2. In total, eight B cell epitopes (1524, 6066, 7886, 109124, 232240, 260269, 298306 and 315322) and five T cell epitopes (6267, 8691, 125132, 217222 and 343350) were predicted in the present study. These findings may be used to improve allergen immunotherapies and reduce the frequency of pollenassociated allergic reactions</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1791-3004 (Electronic)IS - 1791-2997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/mmr.2017.7883</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29115430">PM:29115430</url></web-urls><pdf-urls><url ppv-ref="no">weijifu@hotmail.com</url><url ppv-ref="no">mengling-ml@163.com</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171108, Wang DW</style></custom2><misc3><style face="normal" font="default">10.3892/mmr.2017.7883</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86650</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Palomares,F.</style></author><author><style face="normal" font="default"> Gomez,F.</style></author><author><style face="normal" font="default"> Bogas,G.</style></author><author><style face="normal" font="default"> Paloma,C.</style></author><author><style face="normal" font="default"> Perkins,J.R.</style></author><author><style face="normal" font="default"> Diaz-Perales,A.</style></author><author><style face="normal" font="default"> Rodriguez,M.J.</style></author><author><style face="normal" font="default"> Prieto,A.</style></author><author><style face="normal" font="default"> Barber,D.</style></author><author><style face="normal" font="default"> Torres,M.J.</style></author><author><style face="normal" font="default"> Mayorga,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Research Laboratory, IBIMA-Regional University Hospital of Malaga-UMA, Malaga, Spain</style></auth-address><titles><title><style face="normal" font="default">Immunological Changes Induced in Peach Allergy Patients with Systemic Reactions by Pru p 3 Sublingual Immunotherapy</style></title><secondary-title><style face="normal" font="default">Mol Nutr Food Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Nutr Food Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">SCOPE: Sublingual immunotherapy using peach extract enriched in Pru p 3 (Pru p 3-enriched-SLIT) brings a new perspective to treating patients with allergy to lipid transfer proteins. We evaluated the immunological changes induced by Pru p 3-enriched-SLIT during one year. METHODS AND RESULTS: Three groups were included: peach allergic patients who received Pru p 3-enriched-SLIT, peach allergic untreated patients and controls. Peripheral blood mononuclear cells were obtained before treatment and different time-points. Monocyte-derived dendritic cells (moDCs) maturation and lymphocyte proliferation were assessed by flow cytometry. Data showed a significant reduction of moDCs maturation status during one year of treatment and an increase in PD-L1. Moreover, we observed a significant decrease of the Pru p 3-specific proliferation of effector cells and an increase in Treg cells with higher PD-L1 expression and IL-10 production. These were observed in patients treated only. CONCLUSION: Successful Pru p 3-enriched-SLIT is linked to an important immunosuppression of allergen-specific effector T cells maybe the increase of allergen-specific Treg cells. These cellular changes are orchestrated by the activity of moDCs promoting the expression PD-L1 that will participate in the regulatory response. These changes may serve as biomarkers during SLIT alongside other features such as IgE/IgG4 ratio. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1613-4133 (Electronic)IS - 1613-4125 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1002/mnfr.201700669</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29105313">PM:29105313</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Nutr Food Res\20171106-PalomaresF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Nutr Food Res\20171106-PalomaresF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Palomares F</style></custom2><misc3><style face="normal" font="default">10.1002/mnfr.201700669</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86652</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tremlett,H.</style></author><author><style face="normal" font="default"> Rodney,R.</style></author><author><style face="normal" font="default"> Lucas,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">Can falling infection rates in one country explain rising incidence of autoimmune and allergic diseases in other countries? Caution when (over) interpreting ecological data from disparate areas</style></title><secondary-title><style face="normal" font="default">Mult Scler Relat Disord</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Mult Scler Relat Disord</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">multiple sclerosis</style></keyword><keyword><style face="normal" font="default"> autoimmune diseases</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> ecological studies</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2211-0348</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Canada -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.msard.2017.11.001</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.msard.2017.11.001</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mult Scler Relat Disord\20171114-TremlettH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mult Scler Relat Disord\20171114-TremlettH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Tremlett H</style></custom2><misc3><style face="normal" font="default">10.1016/j.msard.2017.11.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86653</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hoenigl,M.</style></author><author><style face="normal" font="default"> Prattes,J.</style></author><author><style face="normal" font="default"> Neumeister,P.</style></author><author><style face="normal" font="default"> Wolfler,A.</style></author><author><style face="normal" font="default"> Krause,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Section of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Medical University Graz, Austria</style></auth-address><titles><title><style face="normal" font="default">Real world challenges and unmet needs in the diagnosis and treatment of suspected invasive pulmonary aspergillosis in patients with hematological diseases: an illustrative case study</style></title><secondary-title><style face="normal" font="default">Mycoses</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mycoses</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="7" Month="11" Year="2017">2017/11/7</year></dates><abstract><style face="normal" font="default">Recent years have seen important advances in the diagnosis of invasive pulmonary aspergillosis (IPA), complemented by the introduction of new therapies. Despite this, IPA remains a major cause of infection-related mortality in patients with hematological diseases. There are two main reasons for this. First, diagnosis of IPA remains a challenge, since risk factors and the clinical, radiological and mycological presentations vary not only by fungal disease stage, but also by patient group (e.g. neutropenic versus non-neutropenic patients). Diagnosis is particularly challenging in patients receiving mold-active prophylactic or empirical treatment, which reduces the sensitivity of all diagnostic tests for IPA. Second, treatment of IPA is complex due to unpredictable pharmacokinetic profiles of antifungal agents, small therapeutic window in terms of exposure and adverse events, and multiple drug-drug interactions through the CYP450 system. Here we report a case of a 23-year-old male with severe aplastic anaemia and subpleural nodules. Diagnostic tests for IPA obtained during ongoing mold-active empirical treatment were negative. Intravenous voriconazole was stopped after visual disturbances and hallucinations. The patient then had an anaphylactic reaction to liposomal amphotericin B and was switched to intravenous posaconazole, which had to be discontinued due to a significant increase in transaminase levels. He was treated with oral isavuconazole with reduced dosage, triggered by increasing transaminases under the standard dosage. Even under reduced dosage, blood concentrations of isavuconazole were high and treatment was successful. The case illustrates real-world challenges and unmet needs in the diagnosis and treatment of IPA in patients with hematological diseases. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1439-0507 (Electronic)IS - 0933-7407 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/myc.12727</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29112326">PM:29112326</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mycoses\20171107-HoeniglM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mycoses\20171107-HoeniglM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Hoenigl M</style></custom2><misc3><style face="normal" font="default">10.1111/myc.12727</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86654</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gupta,A.</style></author><author><style face="normal" font="default"> Singh,M.</style></author><author><style face="normal" font="default"> Chakrabarti,A.</style></author><author><style face="normal" font="default"> Mathew,J.L.</style></author><author><style face="normal" font="default"> Rawat,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, India</style></auth-address><titles><title><style face="normal" font="default">Correlation between Fungal Sensitization in Childhood Persistent Asthma and Disease Severity</style></title><secondary-title><style face="normal" font="default">Mycoses</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mycoses</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Fungal sensitization in adults is associated with severe asthma but prevalence and clinical significance of fungal sensitization remains unclear in paediatric population. OBJECTIVE: To study association of fungal sensitization with disease severity in children with persistent asthma PATIENTS AND METHODS: One hundred children with persistent asthma in age group 7-15 years, symptom duration >2 years and forced expiratory volume in first second >50% of expected were enrolled. Skin prick test (SPT) to 8 fungal antigens and total serum IgE were done. Fungal sensitization was described as positive SPT (wheel diameter more than 3mm larger than the negative control) to any of the fungal antigens and total serum IgE >200ng/ml. RESULTS: Seventeen patients showed evidence of fungal sensitization, of which, six demonstrated sensitization to multiple fungi. 17.6% patients with fungal sensitization had severe asthma as compared to 2.4% patients without fungal sensitization (p value 0.032). Significant increase in family history of allergic comorbidities was noted among patients with fungal sensitization (47.1% vs 21.7%, p value 0.03). The most common implicated organism in fungal sensitized patients was Aspergillus flavus (47.1%). CONCLUSION: The results of this study, a first among Indian children with asthma, suggest that children with fungal sensitization have more severe asthma as compared to children without fungal sensitization. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1439-0507 (Electronic)IS - 0933-7407 (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.1111/myc.12726</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29110335">PM:29110335</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mycoses\20171107-GuptaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mycoses\20171107-GuptaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Gupta A</style></custom2><misc3><style face="normal" font="default">10.1111/myc.12726</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86655</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dong,J.J.</style></author><author><style face="normal" font="default"> Shen,J.J.</style></author><author><style face="normal" font="default"> Lee,Y.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Family Medicine, Yonsei University College of Medicine, Seoul, Korea</style></auth-address><titles><title><style face="normal" font="default">Dose-dependent effect of cotinine-verified tobacco smoking on serum immunoglobulin E levels in Korean adult males</style></title><secondary-title><style face="normal" font="default">Nicotine Tob Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nicotine Tob Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">Background: Smoking is one of the risk factors to exacerbate allergic diseases, and it may affect serum immunoglobulin E (IgE) levels. However, few studies have relied on an objective biomarker to examine the effect of tobacco smoking on serum IgE levels. Method: A nationwide cross-sectional study was conducted to examine the relationship between urinary cotinine (Ucot) concentrations and IgE levels in 973 males using data from the 2010 Korean National Health and Nutrition Examination Survey (KNHANES). Ucot was classified into four groups based on concentration (ng/mL) as follows: nonsmoker group (Ucot &lt;50 ng/mL) and three tertile groups in smokers (T1 [Ucot: 50.00-921.28 ng/mL]; T2 [Ucot: 921.29-1,869.36 ng/mL]; and T3 [Ucot >/=1,869.37 ng/mL]). The dose-response relationships between Ucot concentrations and total serum IgE level were estimated using analysis of covariance (ANCOVA) and multiple linear regression analysis after adjusting for confounding variables. Results: We found a significant and positive dose-related effect of cigarette smoking as measured by Ucot concentrations on total serum IgE level. The multivariate adjusted means of total serum IgE levels (SE) were 321.0 (36.3), 404.4 (102.7), 499.2 (79.2), and 534.7 (82.7) IU/mL, after adjusting for age, body mass index, alcohol ingestion, physical exercise, job, and household income. The regression coefficient beta for total serum IgE was beta = 68.6 with increasing level of Ucot group after adjusting for the same co-variables (P = 0.009). Conclusion: These findings suggest that the amount of smoking may have a dose-dependent effect on total serum IgE levels. Implication: Smoking is one of the risk factors to exacerbate allergic diseases, and it may affect serum immunoglobulin E (IgE) levels, which is closely related to type 1 mediated allergic diseases. However, few studies have relied on an objective biomarker to examine the effect of tobacco smoking on serum IgE levels. We found that tobacco exposure, as measured by Ucot concentrations, increased the serum IgE levels in a dose-response manner in a representative sample of Korean adult males</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 1469-994X (Electronic)IS - 1462-2203 (Linking)LA - engPT - Journal ArticleCO - South Korea -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1093/ntr/ntx247</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29126169">PM:29126169</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nicotine Tob Res\20171110-DongJJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nicotine Tob Res\20171110-DongJJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Dong JJ</style></custom2><misc3><style face="normal" font="default">10.1093/ntr/ntx247</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86660</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ohnishi,T.</style></author><author><style face="normal" font="default"> Kubo,A.</style></author><author><style face="normal" font="default"> Yoshinari,T.</style></author><author><style face="normal" font="default"> Watanabe,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Microbiology, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya, Tokyo, 158-8501, Japan.</style></auth-address><titles><title><style face="normal" font="default">A Kudoa septempunctata antigen induces production of IgE in BALB/c mice</style></title><secondary-title><style face="normal" font="default">Parasitol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Parasitol Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">Kudoa septempunctata, a myxosporean parasite, is the causative agent of a foodborne illness associated with consumption of raw Paralichthys olivaceus (olive flounder). Because the lag phase of this illness is short (from 1 to 12 h), it is possible that an allergic response is relevant to this illness. To test whether a K. septempunctata antigen is the possible allergen, we injected a myxospore extract into BALB/c mice and measured IgE levels in serum. When the mice were injected with the myxospore extract, the total serum IgE concentration increased significantly after the second immunization as compared to the negative control. After the third immunization, total IgE concentration in the immunized mice reached 26.5 ng/ml and was almost equivalent to that of egg albumin-injected mice. Western blot analysis revealed that IgE antibodies-in serum samples that were collected from myxospore extract-injected mice-bound to at least two Kudoa proteins with molecular weight between 28 and 36 kDa. These results suggested that a K. septempunctata antigen is the allergen. Further studies are needed to clarify the contribution of allergy to the foodborne illness caused by K. septempunctata</style></abstract><notes><style face="normal" font="default">DA - 20171104IS - 1432-1955 (Electronic)IS - 0932-0113 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1007/s00436-017-5665-x</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29101472">PM:29101472</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Parasitol Res\20171104-OhnishiT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Parasitol Res\20171104-OhnishiT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171104, Ohnishi T</style></custom2><misc3><style face="normal" font="default">10.1007/s00436-017-5665-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86662</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tham,E.H.</style></author><author><style face="normal" font="default"> Shek,L.P.</style></author><author><style face="normal" font="default"> Van Bever,H.P.</style></author><author><style face="normal" font="default"> Vichyanond,P.</style></author><author><style face="normal" font="default"> Ebisawa,M.</style></author><author><style face="normal" font="default"> Wong,G.W.K.</style></author><author><style face="normal" font="default"> Lee,B.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore</style></auth-address><titles><title><style face="normal" font="default">Early Introduction of Allergenic Foods for the Prevention of Food Allergy from an Asian Perspective - An APAPARI Consensus Statement</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">Emerging evidence for the early introduction of allergenic foods for the prevention of food allergies, such as peanut allergy in Western populations, has led to the recent publication of guidelines in the US and Europe recommending early peanut introduction for high-risk infants with severe eczema or egg allergy. Peanut allergy is, however, much less prevalent in Asia compared to the West. Varying patterns of food allergy are seen even within Asian countries - such as a predominance of wheat allergy in Japan and Thailand and shellfish allergy in Singapore and the Philippines. Customs and traditions, such as diet and infant feeding practices, also differ between Asian populations. Hence, there are unique challenges in adapting guidelines on early allergenic food introduction to the Asian setting. In this paper, we review the evidence and discuss the possible approaches to guide the timely introduction of allergenic food in high-risk infants in Asia. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171025IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Singapore -CO - Hong Kong -CO - Thailand -CO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12820</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29068090">PM:29068090</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171025-ThamEH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171025-ThamEH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171025, Tham EH</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12820</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86663</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wahn,U.</style></author><author><style face="normal" font="default"> Matricardi,P.M.</style></author><author><style face="normal" font="default"> Bieber,T.</style></author><author><style face="normal" font="default"> Bousquet,J.</style></author><author><style face="normal" font="default"> Grattan,C.</style></author><author><style face="normal" font="default"> Simon,H.U.</style></author><author><style face="normal" font="default"> Muraro,A.</style></author><author><style face="normal" font="default"> Agache,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Department, Charite, Berlin, GermanyAG Molecular Allergology and Immunomodulation, Department of Pediatric Pneumology and Immunology, Charite Medical University, Berlin, GermanyDepartment of Dermatology and Allergy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, GermanyMACVIA-France, Contre les MAladies Chroniques pour un VIeillissement Actif en France European Innovation Partnership on Active and Healthy Ageing Reference Site, Montpellier, FranceINSERM U 1168, VIMA: Ageing and chronic diseases Epidemiological and public health approaches, Villejuif, Universite Versailles St-Quentin-en-Yvelines UMR-S 1168, Montigny le Bretonneux, France and EuforeaBrussels, BelgiumDermatology Centre, Norfolk&amp; Norwich University Hospital, Norwich, United KingdomInstitute of Pharmacology, University of Bern, Bern, SwitzerlandFood Allergy Referral Centre Veneto Region, Department of Women and Child Health, Padua General University Hospital, Padua, ItalyFaculty of Medicine, Transylvania University, Brasov, Romania</style></auth-address><titles><title><style face="normal" font="default">Food allergy in EAACI journals (2016)</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">The European Academy of Allergy and Clinical Immunology (EAACI) owns three journals: Allergy, Pediatric Allergy and Immunology and Clinical and Translational Allergy. One of the major goals of EAACI is to understand and better manage food allergy, and to disseminate the knowledge of allergy to all stakeholders including the EAACI junior members (1). The European Symposium on Precision Medicine in Allergy and Airways Diseases at the European Union Parliament (October 14, 2015) stressed that the socioeconomic impact of food allergy (2). This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171025IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Germany -CO - France -CO - Belgium -CO - United Kingdom -CO - switzerland -CO - Italy -CO - Romania -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12830</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29067711">PM:29067711</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171025-WahnU.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171025-WahnU.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171025, Wahn U</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12830</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86664</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bakel,L.A.</style></author><author><style face="normal" font="default"> Hamid,J.</style></author><author><style face="normal" font="default"> Ewusie,J.</style></author><author><style face="normal" font="default"> Liu,K.</style></author><author><style face="normal" font="default"> Mussa,J.</style></author><author><style face="normal" font="default"> Straus,S.</style></author><author><style face="normal" font="default"> Parkin,P.</style></author><author><style face="normal" font="default"> Cohen,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">International Variation in Asthma and Bronchiolitis Guidelines</style></title><secondary-title><style face="normal" font="default">Pediatrics</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Pediatrics</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">BACKGROUND AND OBJECTIVES: Guideline recommendations for the same clinical condition may vary. The purpose of this study was to determine the degree of agreement among comparable asthma and bronchiolitis treatment recommendations from guidelines.METHODS: National and international guidelines were searched by using guideline databases (eg, National Guidelines Clearinghouse: December 16</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô17, 2014, and January 9, 2015). Guideline recommendations were categorized as (1) recommend, (2) optionally recommend, (3) abstain from recommending, (4) recommend against a treatment, and (5) not addressed by the guideline. The degree of agreement between recommendations was evaluated by using an unweighted and weighted +¦ score. Pairwise comparisons of the guidelines were evaluated similarly.RESULTS: There were 7 guidelines for asthma and 4 guidelines for bronchiolitis. For asthma, there were 166 recommendation topics, with 69 recommendation topics given in </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ2 guidelines. For bronchiolitis, there were 46 recommendation topics, with 21 recommendation topics provided in </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ2 guidelines. The overall +¦ for asthma was 0.03, both unweighted (95% confidence interval [CI]: </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">êÆ0.01 to 0.07) and weighted (95% CI: </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">êÆ0.01 to 0.10); for bronchiolitis, it was 0.32 unweighted (95% CI: 0.16 to 0.52) and 0.15 weighted (95% CI: </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">êÆ0.01 to 0.5).CONCLUSIONS: Less agreement was found in national and international guidelines for asthma than for bronchiolitis. Additional studies are needed to determine if differences are based on patient preferences and values and economic considerations or if other recommendation-level, guideline-level, and condition-level factors are driving these differences</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -CO - Canada -</style></notes><work-type><style face="normal" font="default">10.1542/peds.2017-0092</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1542/peds.2017-0092</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatrics\20171114-BakelLA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatrics\20171114-BakelLA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Bakel LA</style></custom2><misc3><style face="normal" font="default">10.1542/peds.2017-0092</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86665</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shumoy,H.</style></author><author><style face="normal" font="default"> Raes,K.</style></author></authors></contributors><titles><title><style face="normal" font="default">Tef: The Rising Ancient Cereal: What do we know about its Nutritional and Health Benefits?</style></title><secondary-title><style face="normal" font="default">Plant Foods Hum Nutr</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Plant Foods Hum Nutr</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-9104</style></isbn><abstract><style face="normal" font="default">This review covers the nutritional significance of tef cereal as compared to other common cereals with emphasis on carbohydrate content and starch digestibility, protein content, iron and zinc bioavailability and antioxidant potentials. Tef is a gluten free cereal and contains the highest iron and calcium among other cereals. It has high micro- and macro- nutritional profile and is becoming globally popular in the healthy grain food chain. Tef starch has a high gelatinization temperature, an essential precondition in the preparation of low glycemic index foods. There are significantly conflicting reports of iron content of tef ranging from 5 to 150-ámg/100-ág-ádm. The traditional fermentation of injera reduced majority of the phytic acid but no significant change to mineral bioavailability was observed. This review indicated that studies on starch digestibility, protein characterization, amylase and protease inhibitors, mineral bioavailability and antioxidant potentials are needed to further explore the nutritional and health benefits of tef</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1007/s11130-017-0641-2</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29098639">PM:29098639</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Plant Foods Hum Nutr\20171114-ShumoyH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Plant Foods Hum Nutr\20171114-ShumoyH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Shumoy H</style></custom2><misc3><style face="normal" font="default">10.1007/s11130-017-0641-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86674</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Beaudouin,E.</style></author><author><style face="normal" font="default"> Lavaud,F.</style></author></authors></contributors><titles><title><style face="normal" font="default">Cofactors in food allergy</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> ACE inhibitors</style></keyword><keyword><style face="normal" font="default"> Betablockers</style></keyword><keyword><style face="normal" font="default"> NSAID</style></keyword><keyword><style face="normal" font="default"> Estrogens</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> Mastocytosis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">The cofactors of anaphylaxis, seen in up to 30% of cases, require screening for any of the aggravating circumstances that can cause the most severe clinical reactions. Drugs play a key role in this respect, with the following having all been incriminated: NSAIDs, beta-blockers, ACE inhibitors, sartans; and more recently, proton-pump inhibitors and statins. Certain situations such as acute infections, exercise, alcohol consumption and patients comorbidities (e.g. asthma, cardiovascular disease, mastocytosis) constitute further identified cofactors. Finally, the effect of certain hormones such as estrogens has recently been highlighted as an instrumental factor in the severity of anaphylaxis</style></abstract><notes><style face="normal" font="default">LA - FRECO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.09.002</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.09.002</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\20171114-BeaudouinE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\20171114-BeaudouinE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Beaudouin E</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.09.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86675</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Renaudin,J.M.</style></author><author><style face="normal" font="default"> Beaumont,P.</style></author><author><style face="normal" font="default"> Sabouraud,D.</style></author><author><style face="normal" font="default"> Dumond,P.</style></author><author><style face="normal" font="default"> Liabeuf,V.</style></author><author><style face="normal" font="default"> Tscheiller,S.</style></author><author><style face="normal" font="default"> Drouet,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Severe food anaphylaxis: Data from the Réseau d'Allergo-Vigilance® (2002-2017) and emerging allergens</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">Since 2002, cases of severe food anaphylaxis are collected within the Allergy-Vigilance-« Network (AVN), an associative network of French-speaking allergists, mainly located in France and Belgium. The objective of this work is to analyze the cases recorded over the last 15years in order to improve the knowledge on the etiologies of this rare pathology and to identify emerging food allergens</style></abstract><notes><style face="normal" font="default">LA - FRECO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.10.005</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.10.005</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\20171114-RenaudinJM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\20171114-RenaudinJM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Renaudin JM</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.10.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86676</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Drouet,M.</style></author><author><style face="normal" font="default"> Hoppe,A.</style></author><author><style face="normal" font="default"> Moreau,A.S.</style></author><author><style face="normal" font="default"> Bonneau,J.C.</style></author><author><style face="normal" font="default"> Leclere,J.M.</style></author><author><style face="normal" font="default"> Le,Sellin J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Unite d'allergologie generale, departement de pneumologie, oncologie thoracique et allergologie, CHU, 4, rue Larrey, 49933 Angers cedex 09, France.</style></auth-address><titles><title><style face="normal" font="default">Cannabis and crossed allergy with food</style></title><secondary-title><style face="normal" font="default">Rev Pneumol Clin</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Pneumol Clin</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="11/16/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">Cannabis use has increased over the last decade. At the same time, we see cannabis allergies appearing, ranging from simple rhinoconjunctivitis to anaphylactic-type reactions, some of which are severe since fatal cases have been described, but we also see allergic-induced food allergies cross-linked in the family of lipid transfer proteins (LTP). Indeed, cannabis contains an LTP called Can s 3. The LT are very widespread in the vegetable kingdom and are present in many vegetables and fruits. LTPs have a similar chemical structure and therefore cross-allergy is common. Thus, by becoming aware of the LTP of cannabis, it is possible to become allergic by a mechanism of cross-allergy to the other LTPs present in fruits and vegetables. This syndrome is referred to as cannabis-fruit-vegetable syndrome</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 0761-8417 (Print)IS - 0761-8417 (Linking)LA - frePT - English AbstractPT - Journal ArticlePT - ReviewCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.pneumo.2017.09.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122396">PM:29122396</url></web-urls><pdf-urls><url ppv-ref="no">madrouet@chu-angers.fr</url></pdf-urls></urls><custom2><style face="normal" font="default">20171110, Drouet M</style></custom2><misc3><style face="normal" font="default">10.1016/j.pneumo.2017.09.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86677</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Galvao,C.E.S.</style></author><author><style face="normal" font="default"> Graudenz,G.S.</style></author><author><style face="normal" font="default"> Kalil,J.</style></author><author><style face="normal" font="default"> Castro,F.F.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">MD, PhD. Attending Physician, Clinical Immunology and Allergy Service, Hospital das Clinicas, Universidade de Sao Paulo (HCFMUSP), Sao Paulo (SP), BrazilMD, PhD. Allergogist, Clinical Immunology and Allergy Service, Hospital das Clinicas, Universidade de Sao Paulo, Sao Paulo (SP), BrazilMD. Full Professor, Clinical Immunology and Allergy Service, Hospital das Clinicas, Universidade de Sao Paulo, Sao Paulo (SP), BrazilMD, PhD. Attending Physician and Clinical Supervisor, Clinical Immunology and Allergy Service, Hospital das Clinicas, Universidade de Sao Paulo, Sao Paulo (SP), Brazil</style></auth-address><titles><title><style face="normal" font="default">Sensitization to cat allergen and its association with respiratory allergies: cross-sectional study</style></title><secondary-title><style face="normal" font="default">Sao Paulo Med J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sao Paulo Med J</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">Cats are a significant source of allergens that contribute towards worsening of allergic diseases. The aim of this study was to investigate the association between sensitization to cat allergens and allergic respiratory diseases.This was an observational retrospective study based on the skin pricktests results of patients at a tertiary-level hospital in Sao Paulo. A total of 1,985 test results were assessed. The prevalence of sensitization to cat allergen was 20% (399 patients). Our data indicated that in this population of atopic patients, a positive skin prick test result for cat allergen was not associated significantly with a diagnosis of respiratory allergy</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1806-9460 (Electronic)IS - 1516-3180 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1590/1516-3180.2017.0072170617</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29116310">PM:29116310</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sao Paulo Med J\20171108-GalvaoCE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sao Paulo Med J\20171108-GalvaoCE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Galvao CE</style></custom2><misc3><style face="normal" font="default">10.1590/1516-3180.2017.0072170617</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86684</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Janssen,M.P.</style></author><author><style face="normal" font="default"> van Tilborgh,A.J.W.</style></author><author><style face="normal" font="default"> de Vooght,K.M.K.</style></author><author><style face="normal" font="default"> Bokhorst,A.G.</style></author><author><style face="normal" font="default"> Wiersum-Osselton,J.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Transfusion Technology Assessment Unit, Sanquin Research, Amsterdam, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">Direct costs of transfusion reactions - an expert judgement approach</style></title><secondary-title><style face="normal" font="default">Vox Sang</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Vox Sang</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">BACKGROUND AND OBJECTIVES: Despite increasingly meticulous haemovigilance reporting throughout the world, a systematic assessment of the cost of transfusion reactions is still lacking. This is partly caused by the fact that such an assessment requires a subjective expert assessment of the additional costs linked to the adverse reaction. Data on the cost of transfusion reactions could support decision-making regarding blood transfusion safety measures. MATERIALS AND METHODS: Thirteen experts from nine hospitals were asked to estimate the additional care required following various types of transfusion reactions. Additional care was quantified as the proportion of reactions requiring care, and the amount of care required (e.g. hospitalization days, additional physician's time). Experts were also asked to provide, per type of transfusion reaction, an estimate of the proportion of transfusion reactions preventable. Structured quantitative expert elicitation methods were applied to obtain and combine expert estimates. RESULTS: The estimated annual in-hospital cost of transfusion reactions in the Netherlands is euro933 356 per year (euro1.52 per transfusion). Two-thirds (64%) of these are incurred by non-serious transfusion reactions. Circulatory overload, TRALI and anaphylaxis clearly dominate the costs of serious adverse transfusion reactions (66% in total); non-haemolytic transfusion reactions incur 46% of the cost of non-serious transfusion reactions. Additional safety measures targeting circulatory overload and new antibody formation potentially offer the highest cost reduction. CONCLUSION: In-hospital costs of transfusion reactions are substantial but contribute to less than 1% of the total cost of transfusion in the Netherlands. A considerable part of these costs (24%) might be preventable</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 1423-0410 (Electronic)IS - 0042-9007 (Linking)LA - engPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1111/vox.12614</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29124766">PM:29124766</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Vox Sang\20171110-JanssenMP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Vox Sang\20171110-JanssenMP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Janssen MP</style></custom2><misc3><style face="normal" font="default">10.1111/vox.12614</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86685</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pant,M.</style></author><author><style face="normal" font="default"> Dubey,S.</style></author><author><style face="normal" font="default"> Varghese,E.</style></author><author><style face="normal" font="default"> Kumar,N.</style></author><author><style face="normal" font="default"> Naik,S.N.</style></author><author><style face="normal" font="default"> Patanjali,P.K.</style></author></authors></contributors><titles><title><style face="normal" font="default">Efficacy of Waste Biomass Based Tablet Formulation for Cockroach Control</style></title><secondary-title><style face="normal" font="default">Waste Biomass Valorization</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Waste Biomass Valorization</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1877-265X</style></isbn><abstract><style face="normal" font="default">The current paper has elaborated the efficient utilization of house hold botanical waste like OP (orange peel), UTL (used tea leaves) and industrial waste i.e., KCP and JCP (non-edible oil seed cakes of Karanja and jatropha) for developing a herbal tablet formulation for cockroach control. The percentage mortality and KD50 values recorded with and without KCP and JCP were 25.9597, 100% (after 96-áh) and 50.6697, 90% (After 96-áh). Analysis with ATR-FTIR also confirmed the presence of presence of OP; KCP&amp; JCP in tablet composition. SEM analysis generated the morphological details for the tablet containing active and other inert ingredients</style></abstract><notes><style face="normal" font="default">LA - ENGCO - India -</style></notes><work-type><style face="normal" font="default">10.1007/s12649-017-0111-y</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s12649-017-0111-y</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Waste Biomass Valorization\20171114-PantM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Waste Biomass Valorization\20171114-PantM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Pant M</style></custom2><misc3><style face="normal" font="default">10.1007/s12649-017-0111-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86688</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,J.</style></author><author><style face="normal" font="default"> Li,Y.C.</style></author><author><style face="normal" font="default"> Zhang,Z.</style></author><author><style face="normal" font="default"> Li,Y.</style></author><author><style face="normal" font="default"> Wang,C.Y.</style></author></authors></contributors><titles><title><style face="normal" font="default">The dispersion characteristics of airborne pollen in the Shijiazhuang (China) urban area and its relationship with meteorological factors</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">In this study, a Tauber pollen trap was used in the urban area of Shijiazhuang to monitor continuously the outdoor air pollen from 2007 to 2011. The trap was emptied at regular intervals (typically 15-ádays). The results show that airborne pollen assemblages are generally similar each year among 2007</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô2011 and are responsive to the flowering times of plants, being dominated by pollen from woody plants in the spring and by pollen from herbaceous plants in summer and autumn. Two peak pollen influx periods, especially for the main allergenic pollen taxa, are seen, one between early March to early June and a second between late August to early October. During the four seasons, the main pollen taxa are Juglans, Artemisia, Platanus, Populus, Chenopodiaceae, Urtica-á+-áHumulus, Rosaceae, Pinus, Poaceae, Cereals, Quercus, and Betula, and all taxa other than Rosaceae were confirmed by relevant studies to be allergenic pollen taxa. RDA analysis of pollen influx and meteorological factors shows that in spring, temperature and humidity have significant effects on the pollen influx of woody plants; in summer, humidity and precipitation have significant negative effects on pollen influx of herbaceous plants; in autumn, temperature, water vapor pressure, and precipitation have a significant positive influence on herbaceous pollen influx; in winter, there were no significant correlations between airborne pollen influx and meteorological factors. The results reveal the dispersion patterns of airborne pollen and provide an important reference to appropriate construction of urban green systems and the reliable reduction in regional pollinosis</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-017-9501-7</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-017-9501-7</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20171120-LiJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20171120-LiJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Li J</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-017-9501-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86689</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Manikpuri,M.</style></author><author><style face="normal" font="default"> Tiwari,K.L.</style></author><author><style face="normal" font="default"> Tiwary,B.N.</style></author></authors></contributors><titles><title><style face="normal" font="default">Effect of seasonal variation on aeromycoflora of Bilaspur, Chhattisgarh, involved in allergic reactions</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Alternaria</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">The biotic (bacteria, fungi, pollen grains, algae) and abiotic (dust mites) factors present in the atmosphere are responsible for the common allergic reactions in humans. Fungi are one of the major biotic factors resulting in allergic conditions and sometimes lead to fatal diseases affecting vital organs. A detailed survey was carried out for 2-áyears (from May 2014 to April 2016) to assess the seasonal distribution and comparative diversity of aeromycoflora present in the urban and rural areas of Bilaspur, Chhattisgarh (India). During the survey, a marked variation in the types of fungal isolates and their colonies were observed in the samples collected at study sites. The maximum number of fungal colonies was obtained in the month of October and November during the first and second year, respectively. Among the isolates, Aspergillus and Curvularia sp. were found with the highest percent frequency and percent contribution. The predominant fungal species observed during the survey were Aspergillus fumigatus, Aspergillus niger, Aspergillus flavus, Penicillium sp. and Alternaria alternata which are known to cause different types of diseases including allergy in human beings, suggesting the possibility of occurrence of fungal allergy in the human population of Bilaspur</style></abstract><notes><style face="normal" font="default">LA - ENGCO - India -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-017-9500-8</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-017-9500-8</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20171120-ManikpuriM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20171120-ManikpuriM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Manikpuri M</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-017-9500-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86690</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gebarowska,E.</style></author><author><style face="normal" font="default"> Pusz,W.</style></author><author><style face="normal" font="default"> Kucinska,J.</style></author><author><style face="normal" font="default"> Kita,W.</style></author></authors></contributors><titles><title><style face="normal" font="default">Comparative analysis of airborne bacteria and fungi in two salt mines in Poland</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">The aim of this work was to determine the genera or species composition and the number of colony forming units of airborne bacteria and fungi, respectively, in two salt mines in Poland </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Wieliczka</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ (Lesser Poland) and </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Polkowice</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇôSieroszowice</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ (Lower Silesia). Both of them are working environments characterized by extreme conditions, and additionally </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Wieliczka,</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ officially placed on the UNESCO World Heritage Sites</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖ list, plays a role of tourist attraction. There are also some curative chambers located in this mine. Air samples were taken once in December 2015, between 6:00 a.m. and 9:00 a.m. There were nine measurement points located about 200-ám underground in </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Wieliczka</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ and six measurement points located in the working shafts about 400-ám underground in </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Polkowice</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇôSieroszowice.</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ The total volume of each air sample was 150-áL. Air samples, collected in individual measurement points of both salt mines, were inoculated on two microbiological media: potato dextrose agar and tryptic soy agar using the impact method. We identified 10 and 3 fungal genera in the </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Wieliczka</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ Salt Mine and in </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Polkowice</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇôSieroszowice,</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ respectively. The most common were fungi of the Penicillium genus. In both mines, the Gram-positive bacteria of genus Micrococcus were detected most frequently. Among identified microorganisms, there were neither pathogenic fungi nor bacteria. The most prevalent microorganisms detected in indoor air were Gram-positive cocci, which constituted up to 80% of airborne microflora. Our results showed that microorganisms recorded in the air samples are not a threat to workers, tourists or patients. Neither pathogens nor potentially pathogenic microorganisms, listed as BSL-2, BSL-3 or BSL-4, were detected. The microbes identified during our analysis commonly occur in such environments as the soil, water and air. Some of the detected bacteria are component of natural microflora of human skin and mucous membranes, and they can cause only opportunistic infections in individuals depending on their health condition</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-017-9502-6</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-017-9502-6</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20171120-GebarowskaE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20171120-GebarowskaE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Gebarowska E</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-017-9502-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86695</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Erban,T.</style></author><author><style face="normal" font="default"> Klubal,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Crop Research Institute, 507/73, Prague 6-Ruzyne, CZ-16106, Czech Republic.</style></auth-address><titles><title><style face="normal" font="default">Non-protease native allergens partially purified from bodies of eight domestic mites using p-aminobenzamidine ligand</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: Optimised purification steps for concentrating trace target native antigens are needed. Combining the p-aminobenzamidine ligand with protease inactivation enables partial purification of mite non-protease allergens lacking proteases. OBJECTIVE: We sought to analyse in detail proteins obtained using this method from eight species of synanthropic acaridid mites and tested IgE reactivity using pooled human sera. MATERIALS AND METHODS: Proteins affinity bound to p-aminobenzamidine as a ligand were identified by MALDI TOF/TOF. After electroblotting, the proteins were visualised using the fluorescent SYPRO-Ruby protein blot stain, and IgE reactivity was further analysed using pooled human sera collected from patients allergic to house dust mites. RESULTS: MS/MS identification confirmed previous results that no proteases were purified. Protein patterns corresponding to the allergens Der f 7, Der f 30 and actins indicated that these proteins are purified using p-aminobenzamidine and are present across a wide spectrum of acaridid mites. When using Dermatophagoides farinae, apolipophorins (Der f 14), chitinase-like Der f 15 and 18, 70-kDa heat shock protein, and a Der f Alt a10 allergen homolog (gi|37958173) were also detected. The target antigens tropomyosins and paramyosins showed similar IgE binding among the mite species tested. IgE reactivity with miscellaneous D. farinae antigen was also observed. CONCLUSIONS: Partial purification of mite non-protease antigens using a strategy combining p-aminobenzamidine with protease inactivation was verified by 1D-E and 2D-E analyses. IgE binding to p-aminobenzamidine-purified native non-protease mite antigens was tested using pooled sera. This preliminary study allows for further work on individual serum samples, allowing confirmation of immunoreactivity</style></abstract><notes><style face="normal" font="default">DA - 20171112IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Czechia -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.07.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29128091">PM:29128091</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171112-ErbanT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171112-ErbanT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171112, Erban T</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.07.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86699</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ohta,K.</style></author><author><style face="normal" font="default"> Adachi,M.</style></author><author><style face="normal" font="default"> Tohda,Y.</style></author><author><style face="normal" font="default"> Kamei,T.</style></author><author><style face="normal" font="default"> Kato,M.</style></author><author><style face="normal" font="default"> Mark Fitzgerald,J.</style></author><author><style face="normal" font="default"> Takanuma,M.</style></author><author><style face="normal" font="default"> Kakuno,T.</style></author><author><style face="normal" font="default"> Imai,N.</style></author><author><style face="normal" font="default"> Wu,Y.</style></author><author><style face="normal" font="default"> Aurivillius,M.</style></author><author><style face="normal" font="default"> Goldman,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">National Hospital Organization, Tokyo National Hospital, Tokyo, Japan.</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of benralizumab in Japanese patients with severe, uncontrolled eosinophilic asthma</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: In the Phase III CALIMA trial, benralizumab significantly reduced asthma exacerbations, increased lung function, and alleviated symptoms for patients with severe, uncontrolled eosinophilic asthma. The aim of this subgroup analysis was to evaluate the efficacy and safety of benralizumab for Japanese patients in the CALIMA trial. METHODS: CALIMA was a randomised, controlled trial of 1306 patients (aged 12-75 years; registered at ClinicalTrials.gov: NCT01914757) with severe asthma uncontrolled by medium- to high-dosage inhaled corticosteroids and long-acting beta2-agonists (ICS/LABA). Patients received 56 weeks' benralizumab 30 mg either every 4 weeks (Q4W) or every 8 weeks (Q8W; first three doses Q4W), or placebo Q4W. The primary analysis population was patients receiving high-dosage ICS/LABA with blood eosinophils >/=300 cells/muL. This subgroup analysis covered Japanese patients from this group. RESULTS: Of 83 patients randomised in Japan, 46 were receiving high-dosage ICS/LABA and had blood eosinophils >/=300 cells/muL. Compared with placebo, benralizumab reduced the annual rate of asthma exacerbations by 66% (Q4W; rate ratio 0.34, 95% CI, 0.11-0.99) and 83% (Q8W; rate ratio 0.17, 95% CI, 0.05-0.60); increased prebronchodilator FEV1 by 0.334 L (Q4W; 95% CI, 0.020-0.647) and 0.198 L (Q8W; 95% CI, -0.118 to 0.514); and decreased total asthma symptom score by 0.17 (Q4W; 95% CI, -0.82 to 0.48) and 0.24 (Q8W; 95% CI, -0.87 to 0.40). Percentages of adverse events were consistent with the overall CALIMA group. CONCLUSIONS: Benralizumab reduced annual asthma exacerbations and symptoms, increased lung function, and was well-tolerated by Japanese patients with severe, uncontrolled eosinophilic asthma</style></abstract><notes><style face="normal" font="default">DA - 20171112IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - Journal ArticleCO - Japan -CO - United States -CO - Canada -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.10.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29128192">PM:29128192</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171112-OhtaK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171112-OhtaK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171112, Ohta K</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.10.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86700</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Burkhardt,J.G.</style></author><author><style face="normal" font="default"> Chapa-Rodriguez,A.</style></author><author><style face="normal" font="default"> Bahna,S.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy&amp; Immunology Section, Louisiana State University Health Sciences Center, Shreveport, Louisiana, USA</style></auth-address><titles><title><style face="normal" font="default">Gluten sensitivities and the allergist: Threshing the grain from the husks</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> ASIA</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="13" Month="11" Year="2017">2017/11/13</year></dates><abstract><style face="normal" font="default">"Gluten sensitivity" has become commonplace among the public. Wheat allergy (WA) and celiac disease (CD) are well-defined entities, but are becoming a fraction of individuals following a gluten-free diet. WA has a prevalence of &lt;0.5%. Wheat, specifically its omega-5 gliadin fraction, is the most common allergen implicated in food-dependent, exercise-induced anaphylaxis. CD is a non-IgE hypersensitivity to certain cereal proteins: gluten in wheat, secalin in rye, hordein in barley, and to a lesser extent avenin in oat. It is a rare disease, with an estimated prevalence that varied widely geographically, being higher in Northern Europe and the African Saharawi region than in Southeast Asia. In addition to suggestive symptoms, serologic testing has high diagnostic reliability and biopsy is a confirmatory procedure. CD patients have extra-intestinal autoimmune comorbid conditions more frequently than expected. A third entity is non-celiac gluten sensitivity, which has been created because of the increasing number of subjects who claim a better quality of life or improvement of their variety of symptoms on switching to a gluten-free diet. The phenomenon is being fueled by the media and exploited by the industry. The lack of a specific objective test has been raising substantial controversy about this entity. Allergists and gastroenterologists need to pay attention to the multitudes of individuals who elect to follow a gluten-free diet. Many such subjects might have WA, CD, or another illness. Providing them with appropriate evaluation and specific management would be of great advantages, medically and economically. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/all.13354</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29131356">PM:29131356</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171113-BurkhardtJG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171113-BurkhardtJG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Burkhardt JG</style></custom2><misc3><style face="normal" font="default">10.1111/all.13354</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86701</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bonertz,A.</style></author><author><style face="normal" font="default"> Roberts,G.</style></author><author><style face="normal" font="default"> Slater,J.E.</style></author><author><style face="normal" font="default"> Bridgewater,J.</style></author><author><style face="normal" font="default"> Rabin,R.L.</style></author><author><style face="normal" font="default"> Hoefnagel,M.</style></author><author><style face="normal" font="default"> Timon,M.</style></author><author><style face="normal" font="default"> Pini,C.</style></author><author><style face="normal" font="default"> Pfaar,O.</style></author><author><style face="normal" font="default"> Sheikh,A.</style></author><author><style face="normal" font="default"> Ryan,D.</style></author><author><style face="normal" font="default"> Akdis,C.</style></author><author><style face="normal" font="default"> Goldstein,J.</style></author><author><style face="normal" font="default"> Poulsen,L.K.</style></author><author><style face="normal" font="default"> van Ree,R.</style></author><author><style face="normal" font="default"> Rhyner,C.</style></author><author><style face="normal" font="default"> Barber,D.</style></author><author><style face="normal" font="default"> Palomares,O.</style></author><author><style face="normal" font="default"> Pawankar,R.</style></author><author><style face="normal" font="default"> Hamerlijnk,D.</style></author><author><style face="normal" font="default"> Klimek,L.</style></author><author><style face="normal" font="default"> Agache,I.</style></author><author><style face="normal" font="default"> Angier,E.</style></author><author><style face="normal" font="default"> Casale,T.</style></author><author><style face="normal" font="default"> Fernandez-Rivas,M.</style></author><author><style face="normal" font="default"> Halken,S.</style></author><author><style face="normal" font="default"> Jutel,M.</style></author><author><style face="normal" font="default"> Lau,S.</style></author><author><style face="normal" font="default"> Pajno,G.</style></author><author><style face="normal" font="default"> Sturm,G.</style></author><author><style face="normal" font="default"> Varga,E.M.</style></author><author><style face="normal" font="default"> van Wijk,R.G.</style></author><author><style face="normal" font="default"> Bonini,S.</style></author><author><style face="normal" font="default"> Muraro,A.</style></author><author><style face="normal" font="default"> Vieths,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Paul-Ehrlich-Institut, Langen, Germany</style></auth-address><titles><title><style face="normal" font="default">Allergen manufacturing and quality aspects for allergen immunotherapy in Europe and the United States: An analysis from the EAACI AIT Guidelines Project</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">Adequate quality is essential for any medicinal product to be eligible for marketing. Quality includes verification of the identity, content and purity of a medicinal product in combination with a specified production process and its control. Allergen products derived from natural sources require particular considerations to ensure adequate quality. Here, we describe key aspects of the documentation on manufacturing and quality aspects for allergen immunotherapy products in the European Union and the United States. In some key parts, requirements in these areas are harmonized while other fields are regulated separately between both regions. Essential differences are found in the use of Reference Preparations, or the requirement to apply standardized assays for potency determination. Since the types of products available are different in specific regions, regulatory guidance for such products may also be available in one specific region only, such as for allergoids in the European Union. Region-specific issues and priorities are a result of this. As allergen products derived from natural sources are inherently variable in their qualitative and quantitative composition, these products present special challenges to balance the variability and ensuring batch-to-batch consistency. Advancements in scientific knowledge on specific allergens and their role in allergic disease will consequentially find representation in future regulatory guidelines. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Germany -CO - United Kingdom -CO - United States -CO - Netherlands -CO - Italy -CO - Switzerland -CO - Denmark -CO - Spain -CO - Japan -CO - Romania -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.1111/all.13357</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150848">PM:29150848</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171118-BonertzA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171118-BonertzA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Bonertz A</style></custom2><misc3><style face="normal" font="default">10.1111/all.13357</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86702</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mosges,R.</style></author><author><style face="normal" font="default"> Kasche,E.M.</style></author><author><style face="normal" font="default"> Raskopf,E.</style></author><author><style face="normal" font="default"> Singh,J.</style></author><author><style face="normal" font="default"> Sohlich,L.</style></author><author><style face="normal" font="default"> Astvatsatourov,A.</style></author><author><style face="normal" font="default"> Shah-Hosseini,K.</style></author><author><style face="normal" font="default"> Pirotton,S.</style></author><author><style face="normal" font="default"> Haazen,L.</style></author><author><style face="normal" font="default"> Durham,S.R.</style></author><author><style face="normal" font="default"> Legon,T.</style></author><author><style face="normal" font="default"> Zadoyan,G.</style></author><author><style face="normal" font="default"> Shamji,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Medical Statistics, Informatics and Epidemiology (IMSIE), Faculty of Medicine, University of Cologne, Cologne, Germany</style></auth-address><titles><title><style face="normal" font="default">A randomized, double-blind, placebo-controlled, dose-finding trial with Lolium perenne peptide immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="18" Month="11" Year="2017">2017/11/18</year></dates><abstract><style face="normal" font="default">BACKGROUND: A novel subcutaneous allergen immunotherapy formulation (gpASIT+ ) containing Lolium perenne peptides (LPP) and having a short up-dosing phase has been developed to treat grass pollen-induced seasonal allergic rhinoconjunctivitis. We investigated peptide immunotherapy containing the hydrolysate from perennial ryegrass allergens for the optimum dose in terms of clinical efficacy, immunogenicity, and safety. METHODS: This prospective, double-blind, placebo-controlled, phase IIb, parallel, four-arm, dose-finding study randomized 198 grass pollen-allergic adults to receive placebo or cumulative doses of 70, 170, or 370 mug LPP. All patients received weekly subcutaneous injections, with the active treatment groups reaching assigned doses within 2, 3, and 4 weeks, respectively. Efficacy was assessed by comparing conjunctival provocation test (CPT) reactions at baseline, after 4 weeks, and after completion. Grass pollen-specific immunoglobulins were analysed before and after treatment. RESULTS: CPT response thresholds improved from baseline to V7 by at least one concentration step in 51.2% (170 mug; P = .023), 46.3% (370 mug), and 38.6% (70 mug) of patients receiving LPP versus 25.6% of patients receiving placebo (modified per protocol set). Also, 39% of patients in the 170 mug-group became non-reactive to CPT versus 18% in the placebo group. Facilitated allergen-binding assays revealed a highly significant (P &lt; .001) dose-dependent reduction in IgE allergen binding across all treatment groups (70 mug: 17.1%; 170 mug: 18.8%; 370 mug: 26.4%). Specific IgG4 levels increased to 1.6-fold (70 mug), 3.1-fold (170 mug), and 3.9-fold (370 mug) (mPP). CONCLUSION: Three-week immunotherapy with 170 mug LPP reduced CPT reactivity significantly and increased protective specific antibodies. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Belgium -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/all.13358</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150857">PM:29150857</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171118-MosgesR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171118-MosgesR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Mosges R</style></custom2><misc3><style face="normal" font="default">10.1111/all.13358</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86703</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lund,G.</style></author><author><style face="normal" font="default"> Brand,S.</style></author><author><style face="normal" font="default"> Ramos,T.</style></author><author><style face="normal" font="default"> Jimeno,L.</style></author><author><style face="normal" font="default"> Boissy,P.</style></author><author><style face="normal" font="default"> Vega,F.</style></author><author><style face="normal" font="default"> Arina,M.</style></author><author><style face="normal" font="default"> Christensen,L.H.</style></author><author><style face="normal" font="default"> Hoof,I.</style></author><author><style face="normal" font="default"> Meno,K.H.</style></author><author><style face="normal" font="default"> Barber,D.</style></author><author><style face="normal" font="default"> Blanco,C.</style></author><author><style face="normal" font="default"> Wurtzen,P.A.</style></author><author><style face="normal" font="default"> Andersen,P.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Global Research, ALK-Abello, 2970, Horsholm, Denmark</style></auth-address><titles><title><style face="normal" font="default">Strong and frequent T-cell responses to the minor allergen Phl p 12 in Spanish patients IgE-sensitized to Profilins</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: Profilins are dominant pan-allergens known to cause cross-sensitization, leading to clinical symptoms such as the pollen food syndrome. This study aims to determine the T-cell response to Phl p 12 in profilin-sensitized patients, by measuring the prevalence, strength and cross-reactivity to clinically relevant profilins. METHODS: The release of Phl p allergens from pollen was determined by mass spectrometry and immunochemistry. T-cell responses, epitope mapping and cross-reactivity to profilins (Phl p 12, Ole e 2, Bet v 2, and Mal d 4) were measured in-vitro using PBMCs from 26 Spanish grass allergic donors IgE-sensitized to profilin. Cross-reactivity was addressed in-vivo using two different mouse strains (BALB/c and C3H). RESULTS: Phl p 12 and Phl p 1 are released from pollen simultaneously and in similar amounts. Both T cell response frequency (17/26 donors) and strength were comparable between Phl p 12 and Phl p 1. T-cell cross-reactivity to other profilins correlated with overall sequence homology, and two immunodominant epitope regions of Phl p 12 were identified. Data from mice immunized with Phl p 12 showed that cross-reactivity to Bet v 2 was mediated by conserved epitopes, and further influenced by additional genetic factors, likely to be MHC II. CONCLUSION: The strength, prevalence and cross reactivity of T-cell responses towards Phl p 12 is comparable to the major allergen Phl p 1, which supports the hypothesis that T-cells to Phl p 12 can play an important role in development of allergic symptoms, such as those associated with the pollen-food syndrome. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Denmark -CO - Spain -</style></notes><work-type><style face="normal" font="default">10.1111/all.13351</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29121407">PM:29121407</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171109-LundG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171109-LundG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Lund G</style></custom2><misc3><style face="normal" font="default">10.1111/all.13351</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86704</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Krohn,I.K.</style></author><author><style face="normal" font="default"> Callebaut,I.</style></author><author><style face="normal" font="default"> Alpizar,Y.A.</style></author><author><style face="normal" font="default"> Steelant,B.</style></author><author><style face="normal" font="default"> Van Gerven,L.</style></author><author><style face="normal" font="default"> Skov,P.S.</style></author><author><style face="normal" font="default"> Kasran,A.</style></author><author><style face="normal" font="default"> Talavera,K.</style></author><author><style face="normal" font="default"> Wouters,M.M.</style></author><author><style face="normal" font="default"> Ceuppens,J.L.</style></author><author><style face="normal" font="default"> Seys,S.F.</style></author><author><style face="normal" font="default"> Hellings,P.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of Clinical Immunology, Dpt. Microbiology &amp; Immunology, KU Leuven, Leuven, Belgium</style></auth-address><titles><title><style face="normal" font="default">MP29-02 reduces nasal hyperreactivity and nasal mediators in patients with house dust mite allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: Nasal hyperreactivity (NHR) is an important clinical feature of allergic rhinitis (AR). The efficacy of MP29-02 (azelastine hydrochloride (AZE) and fluticasone propionate (FP)) nasal spray on local inflammatory mediators and NHR in AR is unknown. We tested if MP29-02 decreases inflammatory mediators and NHR in AR and if this effect is due to restoration of nasal epithelial barrier function. METHODS: A 4-week double-blinded placebo-controlled trial with MP29-02 treatment was conducted in 28 patients with house dust mite (HDM) AR. The presence of NHR was evaluated by measuring reduction of nasal flow upon cold dry air exposure. The effects of AZE+/-FP on barrier integrity and airway inflammation were studied in a murine model of HDM induced NHR and on reduced activation of murine sensory neurons and human mast cells. RESULTS: MP29-02 but not placebo reduced NHR (p&lt;0.0001 vs. p=0.21), levels of substance P (p=0.026 vs. p=0.941) and beta-hexosaminidase (p=0.036 vs. p=0.632) in human nasal secretions. In wild type C57BL6 mice, the reduction of beta-hexosaminidase levels (p&lt;0.0001) by AZE+FP treatment upon HDM challenge was found in parallel with a decreased transmucosal passage (p=0.0012) and completely reversed eosinophilic inflammation (p=0.0013). In vitro, repeated applications of AZE+FP desensitized sensory neurons expressing the transient receptor potential channels TRPA1 and TRPV1. AZE+FP reduced MC degranulation to the same extent as AZE alone. CONCLUSION: MP29-02 treatment reduces inflammatory mediators and NHR in AR. The effects of AZE+FP on MC degranulation, nasal epithelial barrier integrity and TRP channels provide novel insights into the pathophysiology of allergic rhinitis. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Belgium -CO - Denmark -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1111/all.13349</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29121401">PM:29121401</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171109-KrohnIK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171109-KrohnIK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Krohn IK</style></custom2><misc3><style face="normal" font="default">10.1111/all.13349</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86705</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Elizur,A.</style></author><author><style face="normal" font="default"> Appel,M.Y.</style></author><author><style face="normal" font="default"> Nachshon,L.</style></author><author><style face="normal" font="default"> Levy,M.B.</style></author><author><style face="normal" font="default"> Epstein-Rigby,N.</style></author><author><style face="normal" font="default"> Golobov,K.</style></author><author><style face="normal" font="default"> Goldberg,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Allergy, Immunology and Pediatric Pulmonology, Assaf-Harofeh Medical Center, Israel</style></auth-address><titles><title><style face="normal" font="default">NUT Co Reactivity - Acquiring Knowledge for Elimination Recommendations (NUT CRACKER) Study</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="11" Month="11" Year="2017">2017/11/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Ambiguities exist regarding the diagnosis of tree-nut allergy, necessitating either elimination or performance of oral food challenges (OFC). OBJECTIVE: To examine the co-incidences of allergies among tree-nuts and improve diagnostic testing to minimize the need for OFC. METHODS: Eighty three patients prospectively evaluated for walnut, pecan, cashew, pistachio, hazelnut and almond allergy. A history of previous reactions was obtained and standardized skin prick tests (SPT) using finely ground tree-nut solution and basophil activation tests (BAT) were performed. Patients underwent OFC for each tree-nut they eliminated and to which a reaction in the previous 2 years was not documented. RESULTS: While most patients were sensitized to 5-6 tree-nuts, over 50% were allergic to only 1-2 tree-nuts. The highest rate of allergy in sensitized patients was observed for walnut (74.6%) and cashew (65.6%). The rate of co-allergy for most tree-nuts was &lt; 30%. Two thirds of walnut- and cashew-allergic patients were also allergic to pecan and pistachio, respectively, while all pecan- and pistachio-allergic patients were allergic to walnut and cashew, respectively. Receiver operating characteristic analysis for SPT and BAT was tree-nut dependent and yielded area under the curve (AUC) values ranging from 0.75-0.94. Knowledge of co-incident allergies in these pairs along with the combination of SPT and BAT correctly distinguished allergic from tolerant patients for walnut (87%), pecan (66%), cashew (71%) and pistachio (79%). CONCLUSION: The data presented here should assist in differentiating between allergic and tolerant patients, decrease the need for OFC and allow for appropriate elimination recommendations. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171111IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Israel -</style></notes><work-type><style face="normal" font="default">10.1111/all.13353</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29127694">PM:29127694</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171111-ElizurA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171111-ElizurA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171111, Elizur A</style></custom2><misc3><style face="normal" font="default">10.1111/all.13353</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86706</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Glatstein,M.</style></author><author><style face="normal" font="default"> Carbell,G.</style></author><author><style face="normal" font="default"> Scolnik,D.</style></author><author><style face="normal" font="default"> Rimon,A.</style></author><author><style face="normal" font="default"> Hoyte,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Denver Health and Hospital Authority, Rocky Mountain Poison and Drug Center, Denver, CO, USA; Department of Emergency Medicine, University of Colorado School of Medicine at Anschutz Medical Center, Aurora, CO, USA</style></auth-address><titles><title><style face="normal" font="default">Treatment of pediatric black widow spider envenomation: A national poison center's experience</style></title><secondary-title><style face="normal" font="default">Am J Emerg Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Emerg Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Black widow species (Latrodectus species) envenomation can produce a syndrome characterized by painful muscle rigidity and autonomic disturbances. Symptoms tend to be more severe in young children and adults. We describe black widow spider exposures and treatment in the pediatric age group, and investigate reasons for not using antivenom in severe cases. METHODS: All black widow exposures reported to the Rocky Mountain Poison Center between January 1, 2012, and December 31, 2015, were reviewed. Demographic data were recorded. Patients were divided into 2 groups. Group 1: contact through families from their place of residence, public schools and/or cases where patients were not referred to healthcare facilities. Group 2: patient contact through healthcare facilities. RESULTS: 93 patients were included. Forty (43%) calls were in Group 1 and 53 (57%) in Group 2. Symptoms were evident in all victims; 43 (46.2%) were grade 1, 16 (17.2%) grade 2 and 34 (36.5%) grade 3, but only 14 patients (41.1%) of this group received antivenom. Antivenom use was associated with improvement of symptoms within minutes, and all treated patients were discharged within hours, without an analgesic requirement or any complications. Reasons for not receiving antivenom included: skin test positive (2/20), strong history of asthma or allergies (2/20), physician preference (2/20), non-availability of the antivenom at the health care facility (14/20). CONCLUSION: In our study, most symptomatic black widow envenomations were minor. Relatively few patients received antivenom, but antivenom use was associated with shorter symptom duration among moderate and major outcome groups</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1532-8171 (Electronic)IS - 0735-6757 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Canada -CO - Israel -</style></notes><work-type><style face="normal" font="default">10.1016/j.ajem.2017.11.011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29133072">PM:29133072</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Am J Emerg Med\20171114-GlatsteinM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Am J Emerg Med\20171114-GlatsteinM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Glatstein M</style></custom2><misc3><style face="normal" font="default">10.1016/j.ajem.2017.11.011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86707</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tse,R.</style></author><author><style face="normal" font="default"> Garland,J.</style></author><author><style face="normal" font="default"> Ahn,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">From the *Department of Forensic Pathology, LabPLUS, Auckland City Hospital, Auckland, New Zealand</style></auth-address><titles><title><style face="normal" font="default">Decline in 2 Serial Postmortem Tryptase Measurements Beyond 72 Hours After Death in an Antibiotic-Related Anaphylactic Death</style></title><secondary-title><style face="normal" font="default">Am J Forensic Med Pathol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Forensic Med Pathol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">Anaphylaxis can be difficult to diagnose in the postmortem setting. Postmortem tryptase is a widely used ancillary test in aiding the diagnosis in which an elevation supports a death from anaphylaxis. Postmortem tryptase can be difficult to interpret, and the effects of postmortem kinetics are not fully understood. Clinically, mast cell tryptase returns to baseline 24 to 72 hours after an anaphylactic stimulus. We report another anaphylactic death from antibiotic administration in which 2 serial postmortem total tryptase measurements at 3 days (72 hours) and 6 days (144 hours) after death declined from 522 mug/L to 300 mug/L (baseline, 5.6 mug/L). The declination appears to be slower than what is expected in the clinical setting. This case highlights yet another example of the difficult and complex interaction of postmortem interval on postmortem tryptase, especially in an anaphylactic death. We suggest that early blood sampling and serial tests be performed if possible in suspected anaphylactic death</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1533-404X (Electronic)IS - 0195-7910 (Linking)LA - engPT - Journal ArticleCO - New Zealand -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1097/PAF.0000000000000363</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29135492">PM:29135492</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Am J Forensic Med Pathol\20171114-TseR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Am J Forensic Med Pathol\20171114-TseR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Tse R</style></custom2><misc3><style face="normal" font="default">10.1097/PAF.0000000000000363</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86708</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zoltowska Nilsson,A.M.</style></author><author><style face="normal" font="default"> Lei,Y.</style></author><author><style face="normal" font="default"> Adner,M.</style></author><author><style face="normal" font="default"> Nilsson,G.P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Karolisnska Institutet</style></auth-address><titles><title><style face="normal" font="default">Mast cell dependent IL-33/ST2 signaling is protective against the development of airway hyperresponsiveness in a house dust mite mouse model of asthma</style></title><secondary-title><style face="normal" font="default">Am J Physiol Lung Cell Mol Physiol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Physiol Lung Cell Mol Physiol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="16" Month="11" Year="2017">2017/11/16</year></dates><abstract><style face="normal" font="default">Interleukin-33 (IL-33) and its receptor ST2 have been influentially associated to the pathophysiology of asthma. Due to the divergent roles of IL-33 in regulating mast cell functions, there is a need to further characterize IL-33/ST2-dependent mast cell responses and their significance in the context of asthma. This study aimed to investigate how IL-33/ST2-dependent mast cell responses contribute to the development of airway hyperresponsiveness (AHR) and airway inflammation in a mouse model of house dust mite (HDM) induced asthma. Mast cell deficient C57BL/6-KitW-sh (Wsh) mice engrafted with either wild-type (Wsh+MC-WT) or ST2 deficient bone marrow derived mast cells (Wsh+MC-ST2KO) were exposed to HDM delivered intranasally. An exacerbated development of AHR in response to HDM was seen in Wsh+MC-ST2KO compared to Wsh+MC-WT mice. The contribution of this IL-33/ST2-dependent mast cell response to AHR seems to reside within the smaller airways in the peripheral parts of the lung, as suggested by the isolated yet marked effect on tissue resistance. Considering the absence of a parallel increase in cellular inflammation in BALF and lung, the aggravated AHR in Wsh+MC-ST2KO mice, seems to be independent of cellular inflammation. We observed an association between the elevated AHR and reduced PGE2 levels in bronchoalveolar lavage fluid. Due to the protective properties of PGE2 in airway responses, it is conceivable that IL-33/ST2-dependent mast cell induction of PGE2 could be responsible for the dampening effect on AHR. In conclusion, we reveal that IL-33/ST2-dependent mast cell responses can have a protective, rather than causative role in the development of AHR</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1522-1504 (Electronic)IS - 1040-0605 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1152/ajplung.00270.2017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29146574">PM:29146574</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171117, Zoltowska Nilsson AM</style></custom2><misc3><style face="normal" font="default">10.1152/ajplung.00270.2017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86710</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nimata,M.</style></author><author><style face="normal" font="default"> Okada,H.</style></author><author><style face="normal" font="default"> Kurihara,K.</style></author><author><style face="normal" font="default"> Sugimoto,T.</style></author><author><style face="normal" font="default"> Honjoh,T.</style></author><author><style face="normal" font="default"> Kuroda,K.</style></author><author><style face="normal" font="default"> Yano,T.</style></author><author><style face="normal" font="default"> Tachibana,H.</style></author><author><style face="normal" font="default"> Shoji,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Morinaga Institute of Biological Science, Inc., 2-1-16 Sachiura, Kanazawa-ku, Yokohama, 236-0003, Japan</style></auth-address><titles><title><style face="normal" font="default">A harmonized immunoassay with liquid chromatography-mass spectrometry analysis in egg allergen determination</style></title><secondary-title><style face="normal" font="default">Anal Bioanal Chem</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Anal Bioanal Chem</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">Food allergy is a serious health issue worldwide. Implementing allergen labeling regulations is extremely challenging for regulators, food manufacturers, and analytical kit manufacturers. Here we have developed an "amino acid sequence immunoassay" approach to ELISA. The new ELISA comprises of a monoclonal antibody generated via an analyte specific peptide antigen and sodium lauryl sulfate/sulfite solution. This combination enables the antibody to access the epitope site in unfolded analyte protein. The newly developed ELISA recovered 87.1%-106.4% ovalbumin from ovalbumin-incurred model processed foods, thereby demonstrating its applicability as practical egg allergen determination. Furthermore, the comparison of LC-MS/MS and the new ELISA, which targets the amino acid sequence conforming to the LC-MS/MS detection peptide, showed a good agreement. Consequently the harmonization of two methods was demonstrated. The complementary use of the new ELISA and LC-MS analysis can offer a wide range of practical benefits in terms of easiness, cost, accuracy, and efficiency in food allergen analysis. In addition, the new assay is attractive in respect to its easy antigen preparation and predetermined specificity. Graphical abstract The ELISA composing of the monoclonal antibody targeting the amino acid sequence conformed to LC-MS detection peptide, and the protein conformation unfolding reagent was developed. In ovalbumin determination, the developed ELISA showed a good agreement with LC-MS analysis. Consequently the harmonization of immunoassay with LC-MS analysis by using common target amino acid sequence was demonstrated</style></abstract><notes><style face="normal" font="default">DA - 20171115IS - 1618-2650 (Electronic)IS - 1618-2642 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1007/s00216-017-0721-z</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29138881">PM:29138881</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Anal Bioanal Chem\20171115-NimataM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Anal Bioanal Chem\20171115-NimataM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171115, Nimata M</style></custom2><misc3><style face="normal" font="default">10.1007/s00216-017-0721-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86716</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Garcia,M.S.S.M.</style></author><author><style face="normal" font="default"> Ordonez,M.D.C.L.</style></author><author><style face="normal" font="default"> Diaz-Zorita,B.</style></author><author><style face="normal" font="default"> Baeza,M.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Service, Hospital General Universitario Gregorio Maranon,Madrid, Spain</style></auth-address><titles><title><style face="normal" font="default">An infrequent case of anaphylaxis</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.012</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132686">PM:29132686</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171114-GarciaMS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171114-GarciaMS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Garcia MS</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.012</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86727</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vanshylla,K.</style></author><author><style face="normal" font="default"> Opazo,F.</style></author><author><style face="normal" font="default"> Gronke,K.</style></author><author><style face="normal" font="default"> Wienands,J.</style></author><author><style face="normal" font="default"> Engels,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Cellular &amp; Molecular Immunology, Unversity Medical Center Gottingen, Humboldtallee 34, 37073, Gottingen, Germany</style></auth-address><titles><title><style face="normal" font="default">The extracellular membrane-proximal domain of membrane-bound IgE restricts B cell activation by limiting B cell antigen receptor surface expression</style></title><secondary-title><style face="normal" font="default">Eur J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Amino Acids</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">Immunoglobulin E (IgE) antibodies are key mediators of allergic reactions. Due to their potentially harmful anaphylactic properties their production is tightly regulated. The membrane-bound isoform of IgE (mIgE), which is an integral component of the B cell antigen receptor, has been shown to be critical for the regulation of IgE responses in mice. In primate species including humans, mIgE can be expressed in two isoforms that are produced by alternative splicing of the primary epsilon Ig heavy chain transcript, and differ in the absence or presence of an extracellular membrane-proximal domain (EMPD) consisting of 52 amino acids. However, the function of the EMPD remains unclear. Here, we demonstrate that the EMPD restricts surface expression of mIgE-containing BCRs in human and murine B cells. The EMPD does not interfere with BCR assembly but acts as an autonomous endoplasmic reticulum retention domain. Limited surface expression of EMPD-containing mIgE-BCRs caused impaired activation of intracellular signaling cascades and hence represents a regulatory mechanism that may control the production of potentially anaphylactic IgE antibodies in primate species. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1521-4141 (Electronic)IS - 0014-2980 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1002/eji.201747196</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150831">PM:29150831</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur J Immunol\20171118-VanshyllaK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur J Immunol\20171118-VanshyllaK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Vanshylla K</style></custom2><misc3><style face="normal" font="default">10.1002/eji.201747196</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86729</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,Y.</style></author><author><style face="normal" font="default"> Wang,W.</style></author><author><style face="normal" font="default"> Zhou,R.</style></author><author><style face="normal" font="default"> Yang,J.</style></author><author><style face="normal" font="default"> Sheng,W.</style></author><author><style face="normal" font="default"> Guo,J.</style></author><author><style face="normal" font="default"> Wang,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Effects of heating, autoclaving and ultra-high pressure on the solubility, immunoreactivity and structure of major allergens in egg</style></title><secondary-title><style face="normal" font="default">Food Agric Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Food Agric Immunol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><publisher><style face="normal" font="default">Taylor &amp; Francis</style></publisher><isbn><style face="normal" font="default">0954-0105</style></isbn><abstract><style face="normal" font="default">Ovotransferrin (OVT) and ovomucoid (OVM) were treated, respectively by different food processing conditions. The protein recovery and immunoreactivity of OVT significantly decreased during heat treatment (P?&lt;?.05), and aggregates appeared after dry heating at 150-¦C or 200-¦C or boiling at 100-¦C. OVM appeared more stable than OVT under the same treatment. Greatly reduced solubility occurred only after dry heating at 200-¦C. The immunoreactivity increased after dry heating at 100-¦C or 150-¦C or moist heating (60-¦C, boiling). Autoclave sterilization had a strong effect on the characteristics of both OVT and OVM. Ultra-high pressure had very little effect on OVT and OVM, except at 600?MPa in the moist treatment. Results showed that temperature synergistic processing with water and high pressure had the greatest impact on the characteristics, which could be a potential strategy for mitigating the negative effects of allergens in egg</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1080/09540105.2017.1387520</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.1080/09540105.2017.1387520</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto - 18 mesi</url></related-urls></urls><custom2><style face="normal" font="default">20171119, Zhang Y</style></custom2><misc3><style face="normal" font="default">10.1080/09540105.2017.1387520</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86753</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Devdas,J.M.</style></author><author><style face="normal" font="default"> Mckie,C.</style></author><author><style face="normal" font="default"> Fox,A.T.</style></author><author><style face="normal" font="default"> Ratageri,V.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Father Muller Medical College, Mangalore, India</style></auth-address><titles><title><style face="normal" font="default">Food Allergy in Children: An Overview</style></title><secondary-title><style face="normal" font="default">Indian J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Indian J Pediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Diagnosis of food allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">The estimated prevalence of food allergy amongst children in the west is around 6-8% but there is paucity of data in the Indian population. There is a complex interplay of environmental influences and genetic factors in the immuno-pathogenesis and manifestations of food allergy. A reliable thorough clinical history, combined with positive skin prick tests or food-specific IgE, is essential for a more precise diagnosis of food allergy. Currently there is no cure for food allergy. The management of food allergy usually includes strict avoidance, patient education and provision of emergency medication (adrenaline-autoinjectors). Emerging therapies based on evolving research are focused on a more active approach to management which includes early introduction of potentially allergenic foods, anticipatory testing and desensitisation to food allergens. Lack of food labelling policy and non availability of adrenaline auto-injectors is a huge limiting factor for effective management of food allergy among children in India. The present review focuses on IgE mediated food allergy</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 0973-7693 (Electronic)IS - 0019-5456 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - India -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1007/s12098-017-2535-6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29147890">PM:29147890</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Indian J Pediatr\20171117-DevdasJM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Indian J Pediatr\20171117-DevdasJM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Devdas JM</style></custom2><misc3><style face="normal" font="default">10.1007/s12098-017-2535-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86754</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Campo,P.</style></author><author><style face="normal" font="default"> Del Carmen Plaza-Seron,M.</style></author><author><style face="normal" font="default"> Eguiluz-Gracia,I.</style></author><author><style face="normal" font="default"> Verge,J.</style></author><author><style face="normal" font="default"> Galindo,L.</style></author><author><style face="normal" font="default"> Barrionuevo,E.</style></author><author><style face="normal" font="default"> Fernandez,J.</style></author><author><style face="normal" font="default"> Jurado,R.</style></author><author><style face="normal" font="default"> Mayorga,C.</style></author><author><style face="normal" font="default"> Torres,M.J.</style></author><author><style face="normal" font="default"> Rondon,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit, Instituto de Investigacion Biomedica de Malaga (IBIMA)-Regional University Hospital of Malaga, Malaga, Spain</style></auth-address><titles><title><style face="normal" font="default">Direct intranasal application of the solid phase of ImmunoCAP(R) increases nasal specific immunoglobulin E detection in local allergic rhinitis patients</style></title><secondary-title><style face="normal" font="default">Int Forum Allergy Rhinol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Forum Allergy Rhinol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">BACKGROUND: The measurement of nasal specific IgE (NsIgE) in local allergic rhinitis (LAR) patients is challenging and shows variability. The objective of this work was to evaluate a minimally-invasive method of direct detection of NsIgE in patients with LAR to Dermatophagoides pteronyssinus (DP) using an automated immunoassay. METHODS: Fifty patients participated (LAR, n = 14; allergic rhinitis (AR), n = 20; healthy controls [HC], n = 16). Detection of NsIgE was performed by direct application of the solid phase of a commercial DP ImmunoCAP(R) test 24 hours after DP nasal provocation. RESULTS: There was no difference in the median volume of secretion absorbed by the solid phase of the ImmunoCAP test in the 3 studied groups (p = 0.17). According to receiver operating characteristic (ROC) curve analysis, NsIgE >/=0.1450 was the optimal cutoff point, obtaining in LAR patients 42.86% sensitivity with the highest specificity (100%), and 75% sensitivity and 100% specificity for AR. CONCLUSION: This study demonstrates the detection of NsIgE to DP in LAR by using a simple, commercial device with high specificity</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 2042-6984 (Electronic)IS - 2042-6976 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1002/alr.22039</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29136342">PM:29136342</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171114-CampoP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171114-CampoP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Campo P</style></custom2><misc3><style face="normal" font="default">10.1002/alr.22039</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86755</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Patel,V.S.</style></author><author><style face="normal" font="default"> Choby,G.</style></author><author><style face="normal" font="default"> Shih,L.C.</style></author><author><style face="normal" font="default"> Patel,Z.M.</style></author><author><style face="normal" font="default"> Nayak,J.V.</style></author><author><style face="normal" font="default"> Hwang,P.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Rhinology, Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, CA</style></auth-address><titles><title><style face="normal" font="default">Equivalence in outcomes between Draf 2B vs Draf 3 frontal sinusotomy for refractory chronic frontal rhinosinusitis</style></title><secondary-title><style face="normal" font="default">Int Forum Allergy Rhinol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Forum Allergy Rhinol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">methods</style></keyword></keywords><dates><year Day="13" Month="11" Year="2017">2017/11/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: Endoscopic Draf 2B and Draf 3 frontal sinusotomies are frequently performed for chronic refractory frontal rhinosinusitis. The purpose of this study was to compare outcomes between Draf 2B and Draf 3 procedures. METHODS: A retrospective cohort study was conducted comparing patients undergoing bilateral Draf 2B vs Draf 3 procedures from 2000 to 2016. Patients with neoplasia, dysplasia, mucocele, cystic fibrosis, or ciliary dyskinesia were excluded. Preoperative disease parameters included number of prior surgeries, presence of polyps, preoperative 22-item Sino-Nasal Outcome Test (SNOT-22) score, frontal Lund-Mackay score, anterior-posterior diameter of the frontal ostium, and Global Osteitis Scoring Scale (GOSS). Postoperative outcomes included SNOT-22 score, neo-ostium patency, surgical revision rates, and complications. RESULTS: A total of 21 patients with bilateral Draf 2B and 17 patients with Draf 3 surgeries were compared. Mean follow-up time was 15.6 months. No significant differences were seen between groups for any preoperative disease parameter. Both cohorts showed statistically significant (p = 0.0001 [Draf 2B]; p = 0.0001 [Draf 3]) and clinically meaningful (Delta = 24.1; Delta = 24.9) improvements in SNOT-22 at last follow-up vs preoperatively. The Draf 2B group had greater improvement in SNOT-22 score than the Draf 3 group at 1 to 3 months (p = 0.003), but the magnitude of improvement equalized at 5 to 9 months (p = 0.66) and last follow-up (p = 0.90). No significant differences were noted between groups regarding patency, revision rates, or complications. CONCLUSION: Both Draf 2B and Draf 3 procedures offer durable symptomatic improvement for patients with refractory frontal CRS. The Draf 2B is associated with earlier postoperative symptom improvement and overall shows comparable long-term outcomes to the Draf 3 sinusotomy</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 2042-6984 (Electronic)IS - 2042-6976 (Linking)LA - engPT - Journal ArticleCO - Taiwan -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/alr.22032</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29131540">PM:29131540</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171113-PatelVS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171113-PatelVS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Patel VS</style></custom2><misc3><style face="normal" font="default">10.1002/alr.22032</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86757</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gao,Y.</style></author><author><style face="normal" font="default"> Liu,Q.</style></author><author><style face="normal" font="default"> Liu,B.</style></author><author><style face="normal" font="default"> Xie,C.L.</style></author><author><style face="normal" font="default"> Cao,M.J.</style></author><author><style face="normal" font="default"> Yang,X.W.</style></author><author><style face="normal" font="default"> Liu,G.M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Inhibitory activities of compounds from the marine actinomycete Williamsia sp. MCCC 1A11233 variant on IgE-mediated mast cells and passive cutaneous anaphylaxis</style></title><secondary-title><style face="normal" font="default">J Agric Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Agric Food Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">Compounds of the deep-sea-derived marine Williamsia sp. MCCC 1A11233 (CDMW), which are secondary metabolites of the actinomycetes, were isolated. In this study, seven kinds of CDMW were found to decrease degranulation and histamine release in immunoglobulin E (IgE)-mediated rat basophilic leukemia (RBL)-2H3 cells. The production of cytokines (tumor necrosis factor-alpha and interleukin-4) was inhibited by these CDMW in RBL-2H3 cells, and their chemical structures were established mainly based on detailed analysis of their NMR spectra. CDMW-3, CDMW-5, and CDMW-15 were further demonstrated to block mast cell-dependent passive cutaneous anaphylaxis in IgE-sensitized mice. Bone marrow mononuclear cells (BMMCs) were established to clarify the effect of CDMW-3, CDMW-5, and CDMW-15 on mast cells. The seven kinds of CDMW decreased the degranulation and histamine release of BMMCs. Furthermore, flow cytometry results indicated that CDMW-3, CDMW-5, and CDMW-15 increased the annexin+ cell population of BMMCs. In conclusion, CDMW-3, CDMW-5, and CDMW-15 have obvious anti-allergic activity due to induction of the apoptosis of mast cells</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1520-5118 (Electronic)IS - 0021-8561 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1021/acs.jafc.7b04314</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29148756">PM:29148756</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Agric Food Chem\20171117-GaoY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Agric Food Chem\20171117-GaoY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Gao Y</style></custom2><misc3><style face="normal" font="default">10.1021/acs.jafc.7b04314</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86758</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Katayama,S.</style></author><author><style face="normal" font="default"> Ohno,F.</style></author><author><style face="normal" font="default"> Mitani,T.</style></author><author><style face="normal" font="default"> Akiyama,H.</style></author><author><style face="normal" font="default"> Nakamura,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Rutinosylated ferulic acid attenuates food allergic response and colitis by up-regulating regulatory T cells in mouse models</style></title><secondary-title><style face="normal" font="default">J Agric Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Agric Food Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="15" Month="11" Year="2017">2017/11/15</year></dates><abstract><style face="normal" font="default">The purpose of this study was to screen the phytochemicals capable of inducing immune tolerance via enhanced TGF-beta1 secretion and investigate their effects in a mouse model of food allergy and colitis. In a screening test using THP-1-derived dendritic cells, a significant increase in TGF-beta1 levels was observed upon treatment with ferulic acid (FA) and its glycosides, of which FA rutinoside (FAR) induced the highest level of TGF-beta1 secretion. Oral administration of FAR suppressed serum levels of IgE and histamine in ovalbumin-sensitized mice and triggered the differentiation of regulatory T (Treg) cells. Compared with the control, FAR treatment also induced stronger TGF-beta1 secretion from splenic dendritic cells. FAR treatment attenuated dextran sulfate sodium-induced colitis in model mice and induced Treg differentiation. These results suggest that FAR exerts potent immunomodulatory effects against allergic and intestinal inflammatory responses by inducing Treg differentiation</style></abstract><notes><style face="normal" font="default">DA - 20171116IS - 1520-5118 (Electronic)IS - 0021-8561 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1021/acs.jafc.7b03933</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29141406">PM:29141406</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Agric Food Chem\20171116-KatayamaS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Agric Food Chem\20171116-KatayamaS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171116, Katayama S</style></custom2><misc3><style face="normal" font="default">10.1021/acs.jafc.7b03933</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86759</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Renand,A.</style></author><author><style face="normal" font="default"> Shamji,M.H.</style></author><author><style face="normal" font="default"> Harris,K.M.</style></author><author><style face="normal" font="default"> Qin,T.</style></author><author><style face="normal" font="default"> Wambre,E.</style></author><author><style face="normal" font="default"> Scadding,G.W.</style></author><author><style face="normal" font="default"> Wurtzen,P.A.</style></author><author><style face="normal" font="default"> Till,S.J.</style></author><author><style face="normal" font="default"> Togias,A.</style></author><author><style face="normal" font="default"> Nepom,G.T.</style></author><author><style face="normal" font="default"> Kwok,W.W.</style></author><author><style face="normal" font="default"> Durham,S.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Benaroya Research Institute at Virginia Mason, Seattle, WA, USA</style></auth-address><titles><title><style face="normal" font="default">Synchronous Immune Alterations Mirror Clinical Response During Allergen Immunotherapy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Nasal allergen challenge</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: Three years treatment with either sublingual or subcutaneous allergen immunotherapy has been shown to be effective and to induce long-term tolerance. The GRASS * trial demonstrated that two years treatment via either route was effective in suppressing the response to nasal allergen challenge, although was insufficient for inhibition one year after discontinuation. OBJECTIVE: To examine in the GRASS trial the time-course of immunologic changes during two years sublingual and subcutaneous immunotherapy and for one year after treatment discontinuation. METHODS: We performed multi-modal immunomonitoring to assess allergen-specific CD4 T cell properties, in parallel with analysis of local mucosal cytokine responses induced by nasal allergen exposure and humoral immune responses that included IgE-dependent basophil activation and measurement of serum inhibitory activity for allergen-IgE binding to B cells (IgE-Facilitated Allergen Binding). RESULTS: All three of these distinct arms of the immune response displayed significant and coordinate alterations during 2 years allergen desensitization, followed by reversal at 3 years, reflecting a lack of a durable immunological effect. Whereas frequencies of antigen-specific Th2 cells in peripheral blood determined by HLA class II tetramer analysis most closely paralleled clinical outcomes, IgE-antibody dependent functional assays remained partially inhibited one year following discontinuation. CONCLUSION: Two years of allergen immunotherapy were effective but insufficient for long-term tolerance. Allergen-specific Th2 cells most closely paralleled the transient clinical outcome and it is likely that recurrence of the T cell 'drivers' of allergic immunity abrogated the potential for durable tolerance. On the other hand, persistence of IgE-blocking antibody one year after discontinuation may be an early indicator of a pro-tolerogenic mechanism</style></abstract><notes><style face="normal" font="default">DA - 20171112IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - United States -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.041</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29128670">PM:29128670</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171112-RenandA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171112-RenandA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171112, Renand A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.041</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86760</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Amoah,A.S.</style></author><author><style face="normal" font="default"> Asuming-Brempong,E.K.</style></author><author><style face="normal" font="default"> Obeng,B.B.</style></author><author><style face="normal" font="default"> Versteeg,S.A.</style></author><author><style face="normal" font="default"> Larbi,I.A.</style></author><author><style face="normal" font="default"> Aryeetey,Y.</style></author><author><style face="normal" font="default"> Platts-Mills,T.A.E.</style></author><author><style face="normal" font="default"> Mari,A.</style></author><author><style face="normal" font="default"> Brzezicka,K.</style></author><author><style face="normal" font="default"> Gyan,B.A.</style></author><author><style face="normal" font="default"> Mutocheluh,M.</style></author><author><style face="normal" font="default"> Boakye,D.A.</style></author><author><style face="normal" font="default"> Reichardt,N.C.</style></author><author><style face="normal" font="default"> van Ree,R.</style></author><author><style face="normal" font="default"> Hokke,C.H.</style></author><author><style face="normal" font="default"> van Diepen,A.</style></author><author><style face="normal" font="default"> Yazdanbakhsh,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Parasitology, Noguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Accra, Ghana</style></auth-address><titles><title><style face="normal" font="default">Identification of dominant anti-glycan IgE responses in school-children by glycan microarray</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171112IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Ghana -CO - Netherlands -CO - Italy -CO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.040</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29128671">PM:29128671</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171112-AmoahAS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171112-AmoahAS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171112, Amoah AS</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.040</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86761</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Israel,E.</style></author><author><style face="normal" font="default"> Panettieri,R.A.,Jr.</style></author></authors></contributors><auth-address><style face="normal" font="default">Divisions of Pulmonary and Critical Care Medicine and Allergy, Immunology and Rheumatology, Department of Medicine, Harvard Medical School, Brigham &amp; Women's Hospital, Boston, Mass</style></auth-address><titles><title><style face="normal" font="default">Anti-IgE or Anti-IL5: That Is the Question</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 2213-2201 (Electronic)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.025</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150253">PM:29150253</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171118, Israel E</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.025</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86762</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bellach,J.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatric Pneumology and Immunology, Charite-Universitatsmedizin, Berlin, Germany</style></auth-address><titles><title><style face="normal" font="default">Reply (Refers To: Timing of regular egg intake for prevention of egg allergy)</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - LetterCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.020</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29146010">PM:29146010</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-BellachA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-BellachA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Bellach J</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.020</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86763</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Traidl,S.</style></author><author><style face="normal" font="default"> Kienlin,P.</style></author><author><style face="normal" font="default"> Begemann,G.</style></author><author><style face="normal" font="default"> Jing,L.</style></author><author><style face="normal" font="default"> Koelle,D.M.</style></author><author><style face="normal" font="default"> Werfel,T.</style></author><author><style face="normal" font="default"> Roesner,L.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Allergy, Division of Immunodermatology and Allergy Research, Hannover Medical School, Hannover, Germany</style></auth-address><titles><title><style face="normal" font="default">Patients with atopic dermatitis and history of eczema herpeticum elicit HSV-specific type 2 immune responses</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword></keywords><dates><year Day="15" Month="11" Year="2017">2017/11/15</year></dates><abstract><style face="normal" font="default">An increased type 2 and in parallel decreased type 1 T cell immune response to herpes simplex virus 1 may lead to the clinical phenotype of eczema herpeticum</style></abstract><notes><style face="normal" font="default">DA - 20171120IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.048</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29155096">PM:29155096</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-TraidlS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-TraidlS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Traidl S</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.048</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86764</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vermeulen,E.M.</style></author><author><style face="normal" font="default"> Koplin,J.J.</style></author><author><style face="normal" font="default"> Dharmage,S.C.</style></author><author><style face="normal" font="default"> Gurrin,L.C.</style></author><author><style face="normal" font="default"> Peters,R.L.</style></author><author><style face="normal" font="default"> McWilliam,V.</style></author><author><style face="normal" font="default"> Ponsonby,A.L.</style></author><author><style face="normal" font="default"> Dwyer,T.</style></author><author><style face="normal" font="default"> Lowe,A.J.</style></author><author><style face="normal" font="default"> Tang,M.L.K.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Murdoch Children's Research Institute, Parkville, Victoria, Australia</style></auth-address><titles><title><style face="normal" font="default">Food Allergy Is an Important Risk Factor for Childhood Asthma, Irrespective of Whether It Resolves</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="15" Month="11" Year="2017">2017/11/15</year></dates><abstract><style face="normal" font="default">BACKGROUND: The risk of developing asthma in those with early food allergy is unknown, particularly when early life food allergy has resolved. OBJECTIVE: To understand whether challenge-proven food allergy in infancy increases the risk of asthma at age 4 years, using data from a population-based cohort. METHODS: A total of 5,276 12-month-old infants were recruited using a population-based sampling frame. Infants underwent skin prick test to egg, peanut, and sesame and those with a detectable skin prick test result had oral food challenges. At age 4 years, food challenges were repeated to determine persistence or resolution of food allergy. The association between food allergy and doctor-diagnosed asthma was examined using binomial regression in 2,789 participants. RESULTS: Children with food allergy at age 1 year had an increased risk of asthma (1 food allergy: relative risk [RR], 1.69; 95% CI, 1.29-2.21; 2 or more food allergies: RR, 2.76; 95% CI, 1.94-3.92). The risk of asthma was highest in children with food allergy and coexistent eczema in infancy (RR, 2.87; 95% CI, 2.22-3.70). Transient food allergy and persistent food allergy were both associated with an increased risk of asthma (transient egg allergy: RR, 1.92; 95% CI, 1.46-2.51; persistent egg allergy: RR, 2.60; 95% CI, 1.76-3.85). CONCLUSIONS: Asthma at age 4 years is twice as common in those with challenge-proven food allergy at age 1 year, irrespective of whether the food allergy subsequently resolves. Children with 2 or more food allergies and those with coexistent eczema were almost 3 times as likely to develop asthma compared with those with no food allergies</style></abstract><notes><style face="normal" font="default">DA - 20171120IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.019</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29153880">PM:29153880</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171120-VermeulenEM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171120-VermeulenEM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Vermeulen EM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.019</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86765</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Maurer,M.</style></author><author><style face="normal" font="default"> Kaplan,A.</style></author><author><style face="normal" font="default"> Rosen,K.</style></author><author><style face="normal" font="default"> Holden,M.</style></author><author><style face="normal" font="default"> Iqbal,A.</style></author><author><style face="normal" font="default"> Trzaskoma,B.L.</style></author><author><style face="normal" font="default"> Yang,M.</style></author><author><style face="normal" font="default"> Casale,T.B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Allergy, Allergie-Centrum-Charite, Charite-Universitatsmedizin Berlin, Berlin, Germany. Electronic address: Marcus.Maurer@charite.deThe Medical University of South Carolina, Charleston, SCGenentech, Inc., South San Francisco, Calif</style></auth-address><titles><title><style face="normal" font="default">The XTEND-CIU study: long term use of Omalizumab in Chronic Idiopathic Urticaria</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">These data support omalizumab safety and efficacy in patients with antihistamine-resistant CIU/CSU to 48 weeks and provide evidence of omalizumab re-treatment efficacy and safety</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132956">PM:29132956</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-MaurerM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-MaurerM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Maurer M</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86766</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Martin,L.J.</style></author><author><style face="normal" font="default"> He,H.</style></author><author><style face="normal" font="default"> Collins,M.H.</style></author><author><style face="normal" font="default"> Abonia,J.P.</style></author><author><style face="normal" font="default"> Biagini Myers,J.M.</style></author><author><style face="normal" font="default"> Eby,M.</style></author><author><style face="normal" font="default"> Johansson,H.E.</style></author><author><style face="normal" font="default"> Kottyan,L.C.</style></author><author><style face="normal" font="default"> Khurana Hershey,G.K.</style></author><author><style face="normal" font="default"> Rothenberg,M.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Human Genetics, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OHry; Department of Pediatrics, University of Cincinnati Medical School, Cincinnati, OH</style></auth-address><titles><title><style face="normal" font="default">EoE genetic susceptibility is mediated by synergistic interactions between EoE-specific and general atopic disease loci</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">methods</style></keyword></keywords><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: Eosinophilic esophagitis (EoE) is an esophageal inflammatory disease associated with atopic diseases. TSLP and CAPN14 genetic variation contribute to EoE, but how this relates to atopy is unclear. The purpose of this study was to explore the relationship between EoE, atopy and genetic risk. METHODS: EoE-atopy enrichment was tested using 700 EoE cases and 801 community controls. Probing 372 SNPs in 63 atopy-genes, we evaluated EoE associations using 412 non-atopic and 868 atopic disease controls. Interaction and stratified analyses of EoE-specific and atopy SNPs were performed. RESULTS: Atopic disease was enriched in EoE (p &lt; 0.0001). Comparing EoE and non-atopic controls, EoE associated strongly with IL4/KIF3A (p = 2.8x10-6; odds ratio (OR) = 1.85), moderately with TSLP (p = 1.5x10-4; OR = 1.43), and nominally with CAPN14 (p = 0.029; OR = 1.35). Comparing EoE to atopic disease controls, EoE associated strongly with ST2 (p = 3.5x10-6; OR = 1.79) and nominally with IL4/KIF3A (p = 0.019, OR = 1.25); TSLP's association persisted (p = 4.7x10-5; OR = 1.37), and CAPN14's association strengthened (p = 0.0001; OR = 1.71). Notably, there was gene-gene interaction between TSLP and IL4 SNPs (p = 0.0074). Children with risk alleles for both genes were at higher risk for EoE (p = 2.0x10-10; OR = 3.67). CONCLUSIONS: EoE genetic susceptibility is mediated by EoE-specific and general atopic disease loci which may have synergistic effects. These results may aid in identifying potential therapeutics and predicting EoE susceptibility. CLINICAL IMPLICATIONS: EoE susceptibility is mediated by multiple genes, which have synergistic effects. These genes include both EoE-specific and general atopic disease loci. Identifying these effects may help customize treatments</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.046</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129581">PM:29129581</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171113-MartinLJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171113-MartinLJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Martin LJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.046</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86767</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rosa,N.</style></author><author><style face="normal" font="default"> Triffaux,E.</style></author><author><style face="normal" font="default"> Robert,V.</style></author><author><style face="normal" font="default"> Mars,M.</style></author><author><style face="normal" font="default"> Klein,M.</style></author><author><style face="normal" font="default"> Bouchaud,G.</style></author><author><style face="normal" font="default"> Canivet,A.</style></author><author><style face="normal" font="default"> Magnan,A.</style></author><author><style face="normal" font="default"> Guery,J.C.</style></author><author><style face="normal" font="default"> Pelletier,L.</style></author><author><style face="normal" font="default"> Savignac,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Center of Physiopathology Toulouse Purpan, University Paul Sabatier Toulouse III, INSERM U1043, CNRS UMR 5282, 31024 Toulouse, France</style></auth-address><titles><title><style face="normal" font="default">The beta and alpha2delta auxiliary subunits of Cav1 channels are required for Th2-lymphocyte function and acute allergic airway inflammation</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: T-lymphocytes express not only the cell membrane calcium ORAI1 but also voltage-dependent Cav1 channels. In excitable cells, these channels are composed of the ion forming pore alpha1 and auxiliary subunits (beta and alpha2delta) needed for proper trafficking and activation of the channel. We previously disclosed the role of Cav1.2 alpha1 in mouse and human Th2- but not Th1-cell functions and showed that knocking-down Cav1 alpha1 prevents experimental asthma OBJECTIVE: We investigated the role of beta and alpha2delta auxiliary subunits on Cav1 alpha1 function in Th2 lymphocytes and on the development of acute allergic airway inflammation. METHODS: We used antisense oligonucleotides (CavbetaAS) to knockdown Cavbeta and gabapentin, a drug that binds to and inhibits alpha2delta1 and alpha2delta2, to test their effects on Th2 functions and their capacity to reduce allergic airway inflammation. RESULTS: Mouse and human Th2-cells express mainly Cavbeta1, beta3 and alpha2delta2 subunits. CavbetaAS reduces TCR-driven calcium responses and cytokine production by mouse and human Th2, with no effect on Th1-cells. Cavbeta is mainly involved in restraining Cav1.2 alpha1 degradation through the proteasome as a proteasome inhibitor partially restores the alpha1 protein level. Gabapentin impairs TCR-driven calcium response and cytokine production associated with the loss of alpha2delta2 protein in Th2-cells. CONCLUSIONS: These results stress the role of Cavbeta and alpha2delta2 auxiliary subunits in the stability and activation of Cav1.2 channels in Th2 lymphocytes both in vitro and in vivo as demonstrated by the beneficial effect of CavbetaAS and gabapentin in allergic airway inflammation. CLINICAL IMPLICATIONS: The demonstration that auxiliary subunits are involved in calcium signaling through Cav1 channels and function of mouse and human Th2-lymphocytes supports their potential beneficial effect on allergic asthma</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.045</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129580">PM:29129580</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171113-RosaN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171113-RosaN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Rosa N</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.045</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86768</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Skevaki,C.</style></author><author><style face="normal" font="default"> Hudemann,C.</style></author><author><style face="normal" font="default"> Matrosovich,M.</style></author><author><style face="normal" font="default"> Mobs,C.</style></author><author><style face="normal" font="default"> Paul,S.</style></author><author><style face="normal" font="default"> Wachtendorf,A.</style></author><author><style face="normal" font="default"> Alhamwe,B.A.</style></author><author><style face="normal" font="default"> Potaczek,D.P.</style></author><author><style face="normal" font="default"> Hagner,S.</style></author><author><style face="normal" font="default"> Gemsa,D.</style></author><author><style face="normal" font="default"> Garn,H.</style></author><author><style face="normal" font="default"> Sette,A.</style></author><author><style face="normal" font="default"> Renz,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Laboratory Medicine, Philipps University Marburg, 35043 Marburg, Germany</style></auth-address><titles><title><style face="normal" font="default">Influenza-derived peptides cross-react with allergens and provide asthma protection</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: The hygiene hypothesis is the leading concept to explain the current asthma epidemic, which is built on the observation that a lack of bacterial contact early in life induces allergic Th2 immune responses. OBJECTIVE: Since little is known about the contribution of respiratory viruses in this context, we evaluated the effect of prior influenza-infection on the development of allergic asthma. METHODS: Mice were infected with influenza and once recovered, subjected to an ovalbumin or house dust mite-induced experimental asthma protocol. Influenza-polarized T effector memory cells (Tem) were adoptively transferred to allergen sensitized animals prior to allergen challenge. A comprehensive in silico analysis assessed homologies between virus- and allergen- derived proteins. Influenza-polarized Tem cells were stimulated ex vivo with candidate peptides. Mice were immunized with a pool of virus-derived T-cell epitopes. RESULTS: We found in two murine models a long-lasting preventive effect against experimental asthma features. Protection could be attributed about equally to CD4+ and CD8+ T-effector memory (Tem) cells from influenza-infected mice. An in silico bioinformatic analysis identified four influenza and three allergen-derived MHC-class I and -class II candidate T-cell epitopes with potential antigen-specific cross-reactivity between influenza and allergens. Lymphocytes from influenza-infected mice produced IFNgamma and IL-2 but not IL-5 upon stimulation with the aforementioned peptides. Immunization with a mixture of the influenza-peptides conferred asthma protection, and peptide immunized mice transferred protection via CD4+ and CD8+ Tem cells. CONCLUSION: Our results illustrate for the first time heterologous immunity of virus-infected animals towards allergens. This finding extends the original hygiene hypothesis</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.07.056</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132960">PM:29132960</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-SkevakiC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-SkevakiC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Skevaki C</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.07.056</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86769</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Park,C.O.</style></author><author><style face="normal" font="default"> Fu,X.</style></author><author><style face="normal" font="default"> Jiang,X.</style></author><author><style face="normal" font="default"> Pan,Y.</style></author><author><style face="normal" font="default"> Teague,J.E.</style></author><author><style face="normal" font="default"> Collins,N.</style></author><author><style face="normal" font="default"> Tian,T.</style></author><author><style face="normal" font="default"> O'Malley,J.T.</style></author><author><style face="normal" font="default"> Emerson,R.O.</style></author><author><style face="normal" font="default"> Kim,J.H.</style></author><author><style face="normal" font="default"> Jung,Y.</style></author><author><style face="normal" font="default"> Watanabe,R.</style></author><author><style face="normal" font="default"> Fuhlbrigge,R.C.</style></author><author><style face="normal" font="default"> Carbone,F.R.</style></author><author><style face="normal" font="default"> Gebhardt,T.</style></author><author><style face="normal" font="default"> Clark,R.A.</style></author><author><style face="normal" font="default"> Lin,C.P.</style></author><author><style face="normal" font="default"> Kupper,T.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA</style></auth-address><titles><title><style face="normal" font="default">Staged development of long lived TCRalphabeta Th17 resident memory T cell population to Candida albicans after skin infection</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">methods</style></keyword></keywords><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: Candida albicans is a dimorphic fungus to which humans are exposed early in life and by adulthood it is part of the mycobiome of skin and other tissues. Neonatal skin lacks resident memory T (TRM) cells, but in adults the C. albicans skin test is a surrogate for immunocompetence. Young adult mice raised under SPF conditions are naive to C. albicans, and have recently been shown to have an immune system resembling that of neonatal humans. OBJECTIVE: We studied the evolution of the adaptive cutaneous immune response to Candida. METHODS: We examined both human skin T cells and the de novo and memory immune responses in a mouse model of C. albicans skin infection. RESULTS: In mice, the initial IL-17 producing cells after C. albicans infection were dermal gammadelta T cells, but by day 7 alphabeta Th17 T effector cells were predominant. By day 30, the majority of C. albicans reactive IL-17 producing T cells were CD4 TRM cells. Intravital microscopy showed that CD4 effector T cells were recruited to the site of primary infection and were highly motile 10 days post infection. Between 30-90 days post infection, these CD4 T cells became increasingly sessile, acquired expression of CD69 and CD103, and localized to the papillary dermis. These established TRM produced IL-17 upon challenge, while motile migratory memory T (TMM) cells did not. TRM rapidly clear an infectious challenge with C. albicans more effectively than re-circulating T cells, though both populations participate. We found that in normal human skin, IL-17 producing CD4+ TRM that responded to C. albicans in an MHC Class II restricted fashion could be readily identified. CONCLUSIONS: These studies demonstrate that C. albicans infection of skin preferentially generates CD4+ IL-17 producing TRM, which mediate durable protective immunity</style></abstract><notes><style face="normal" font="default">DA - 20171112IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Korea -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.042</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29128674">PM:29128674</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171112-ParkCO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171112-ParkCO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171112, Park CO</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.042</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86770</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Verma,M.</style></author><author><style face="normal" font="default"> Liu,S.</style></author><author><style face="normal" font="default"> Michalec,L.</style></author><author><style face="normal" font="default"> Sripada,A.</style></author><author><style face="normal" font="default"> Gorska,M.M.</style></author><author><style face="normal" font="default"> Alam,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">National Jewish Health, Department of Medicine, Division of Allergy &amp; Immunology, Denver, Colorado</style></auth-address><titles><title><style face="normal" font="default">Title: Experimental Asthma Persists in IL33 Receptor Knockout Mice Due to the Emergence of a TSLP-driven IL9+ and IL13+ ILC2 subpopulations</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: IL33 plays an important role in development of experimental asthma. OBJECTIVE: To study the role of the IL33 receptor (ST2) in persistence of asthma in a mouse model. METHODS: We studied allergen-induced experimental asthma in ST2 knockout (KO) and wild-type control mice. We measured airway hyperresponsiveness (AHR) by flexivent, inflammatory indices by ELISA, histology and real-time PCR, and ILC2s in lung single cell preparations by flow cytometry. RESULTS: The AHR level was elevated in allergen-treated ST2 KO mice and was comparable to that from allergen-treated WT controls. Peribronchial and perivascular inflammation and mucus production were largely similar in both groups. Persistence of experimental asthma in ST2 KO mice was associated with an increase in the level of TSLP, IL9 and IL13 but not IL5 in bronchoalveolar lavage (BAL). ST2 deletion expectedly caused a reduction in IL13+ CD4 T cells, Foxp3+ Tregs and IL5+ ILC2s. Unexpectedly, ST2 deletion led to an overall increase in ILCs (CD45+lin-CD25+ cells), IL13+ ILC2s, the emergence of a TSLP-R+ IL9+ ILC2 population and an increase in intraepithelial mast cells in the lung. An anti-TSLP antibody abrogated AHR, inflammation and mucus production in allergen-treated ST2 KO mice. It also caused a reduction in ILCs, ILC2s, and IL9+ and IL13+ ILC2s in the lung. CONCLUSIONS: Genetic deletion of the IL33 receptor paradoxically increases TSLP production, which stimulates the emergence of IL9+ and IL13+ ILC2s and mast cells, and leads to the development of chronic experimental asthma. An anti-TSLP antibody abrogates all pathologic features of asthma in this model</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.020</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132961">PM:29132961</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-VermaM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-VermaM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Verma M</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.020</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86771</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Paternoster,L.</style></author><author><style face="normal" font="default"> Savenije,O.E.M.</style></author><author><style face="normal" font="default"> Heron,J.</style></author><author><style face="normal" font="default"> Evans,D.M.</style></author><author><style face="normal" font="default"> Vonk,J.M.</style></author><author><style face="normal" font="default"> Brunekreef,B.</style></author><author><style face="normal" font="default"> Wijga,A.H.</style></author><author><style face="normal" font="default"> Henderson,A.J.</style></author><author><style face="normal" font="default"> Koppelman,G.H.</style></author><author><style face="normal" font="default"> Brown,S.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">MRC Integrative Epidemiology Unit, School of Social &amp; Community Medicine, University of Bristol, Bristol, UK.</style></auth-address><titles><title><style face="normal" font="default">Identification of atopic dermatitis subgroups in children from two longitudinal birth cohorts</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">BACKGROUND: Atopic dermatitis (AD) is a prevalent disease with variable natural history. Longitudinal birth cohort studies provide an opportunity to define subgroups based on disease trajectories, which may represent different genetic and environmental pathomechanisms. OBJECTIVE: To investigate the existence of distinct longitudinal phenotypes of AD and test whether these findings are reproducible in two independent cohorts. METHODS: The presence of AD was examined in two birth cohort studies including 9,894 children from the UK (ALSPAC) and 3,652 from the Netherlands (PIAMA). AD was defined by parental report of a typical itchy and/or flexural rash. Longitudinal latent class analysis was used to investigate patterns of AD from birth to the age of 11 to 16 years. We investigated associations with known AD risk factors, including FLG null mutations, 23 other established AD-genetic risk variants and atopic comorbidity. RESULTS: Six latent classes were identified, representing subphenotypes of AD, with remarkable consistency between the two cohorts. The most prevalent class was early-onset-early-resolving AD, which was associated with male gender. Two classes of persistent disease were identified (early-onset-persistent and early-onset-late-resolving); these were most strongly associated with the AD-genetic risk score as well as personal and parental history of atopic disease. A yet unrecognised class of mid-onset-resolving AD, not associated with FLG mutations, but strongly associated with asthma, was identified. CONCLUSION: Six classes based on temporal trajectories of rash were consistently identified in two population-based cohorts. The differing risk factor profiles and diverse prognoses demonstrate the potential importance of a stratified medicine approach for AD. CLINICAL IMPLICATIONS: Atopic dermatitis ranges from a transient condition to lifelong morbidity. This study has identified distinct subphenotypes of atopic dermatitis in children, which could indicate the importance of a stratified approach to management of this complex disease</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Netherlands -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.044</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129583">PM:29129583</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171113-PaternosterL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171113-PaternosterL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Paternoster L</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.044</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86772</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jiang,W.H.</style></author><author><style face="normal" font="default"> Deng,L.</style></author><author><style face="normal" font="default"> Ye,Q.J.</style></author><author><style face="normal" font="default"> Cai,J.R.</style></author><author><style face="normal" font="default"> Cai,X.R.</style></author><author><style face="normal" font="default"> Li,X.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiration, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, People's Republic of China</style></auth-address><titles><title><style face="normal" font="default">Timing of regular egg intake for prevention of egg allergy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - LetterCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29146009">PM:29146009</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-JiangWH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-JiangWH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Jiang WH</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86773</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Levin,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Cape Town, Cape Town</style></auth-address><titles><title><style face="normal" font="default">Allergy terminology: towards a common language and shared understanding</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">Terminology that is used in an inconsistent and ambiguous way by allergists includes the term "cross reactivity" and the use of the word "positive" when referring to allergy tests. This may have serious potential for miscommunication and adversely affect patient care</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - South Africa -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.021</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132957">PM:29132957</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-LevinM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171114-LevinM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Levin M</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.021</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86775</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tran,M.M.</style></author><author><style face="normal" font="default"> Lefebvre,D.L.</style></author><author><style face="normal" font="default"> Dharma,C.</style></author><author><style face="normal" font="default"> Dai,D.</style></author><author><style face="normal" font="default"> Lou,W.Y.W.</style></author><author><style face="normal" font="default"> Subbarao,P.</style></author><author><style face="normal" font="default"> Becker,A.B.</style></author><author><style face="normal" font="default"> Mandhane,P.J.</style></author><author><style face="normal" font="default"> Turvey,S.E.</style></author><author><style face="normal" font="default"> Sears,M.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, McMaster University, Hamilton, Ontario, Canada</style></auth-address><titles><title><style face="normal" font="default">Predicting the atopic march: Results from the Canadian Healthy Infant Longitudinal Development Study</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="1" Month="11" Year="2017">2017/11/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: The atopic march describes the progression from atopic dermatitis during infancy to asthma and allergic rhinitis in later childhood. In a Canadian birth cohort we investigated whether concomitant allergic sensitization enhances subsequent development of these allergic diseases at age 3 years. METHODS: Children completed skin prick testing at age 1 year. Children were considered sensitized if they produced a wheal 2 mm or larger than that elicited by the negative control to any of 10 inhalant or food allergens. Children were also assessed for atopic dermatitis by using the diagnostic criteria of the UK Working Party. At age 3 years, children were assessed for asthma, allergic rhinitis, food allergy, and atopic dermatitis. Data from 2311 children were available. RESULTS: Atopic dermatitis without allergic sensitization was not associated with an increased risk of asthma at age 3 years after adjusting for common confounders (relative risk [RR], 0.46; 95% CI, 0.11-1.93). Conversely, atopic dermatitis with allergic sensitization increased the risk of asthma more than 7-fold (RR, 7.04; 95% CI, 4.13-11.99). Atopic dermatitis and allergic sensitization had significant interactions on both the additive (relative excess risk due to interaction, 5.06; 95% CI, 1.33-11.04) and multiplicative (ratio of RRs, 5.80; 95% CI, 1.20-27.83) scales in association with asthma risk. There was also a positive additive interaction between atopic dermatitis and allergic sensitization in their effects on food allergy risk (relative excess risk due to interaction, 15.11; 95% CI, 4.19-35.36). CONCLUSIONS: Atopic dermatitis without concomitant allergic sensitization was not associated with an increased risk of asthma. In combination, atopic dermatitis and allergic sensitization had strong interactive effects on both asthma and food allergy risk at age 3 years</style></abstract><notes><style face="normal" font="default">DA - 20171120IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.08.024</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29153857">PM:29153857</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-TranMM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-TranMM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Tran MM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.08.024</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86776</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Neeland,M.R.</style></author><author><style face="normal" font="default"> Koplin,J.J.</style></author><author><style face="normal" font="default"> Dang,T.D.</style></author><author><style face="normal" font="default"> Dharmage,S.C.</style></author><author><style face="normal" font="default"> Tang,M.L.</style></author><author><style face="normal" font="default"> Prescott,S.L.</style></author><author><style face="normal" font="default"> Saffery,R.</style></author><author><style face="normal" font="default"> Martino,D.J.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Murdoch Childrens Research Institute, Parkville, VIC, Australia</style></auth-address><titles><title><style face="normal" font="default">Early life innate immune signatures of persistent food allergy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">BACKGROUND: Food allergy naturally resolves in a proportion of food allergic children without intervention, however the underlying mechanisms governing the persistence or resolution of food allergy in childhood are not understood. OBJECTIVES: This study aimed to define the innate immune profiles associated with egg allergy at one year of age, determine the phenotypic changes that occur with the development of natural tolerance in childhood and explore the relationship between early life innate immune function and serum vitamin D. METHODS: This study used longitudinally collected PBMC samples from a population-based cohort of challenge-confirmed egg allergic infants with either persistent or transient egg allergy outcomes in childhood to phenotype and quantify the functional innate immune response associated with clinical phenotypes of egg allergy. RESULTS: We show that infants with persistent egg allergy exhibit a unique innate immune signature, characterised by increased numbers of circulating monocytes and dendritic cells that produce more inflammatory cytokines both at baseline and following endotoxin exposure when compared to infants with transient egg allergy. Follow up analysis revealed that this unique innate immune signature continues into childhood in those with persistent egg allergy and that increased serum vitamin D levels correlate with changes in innate immune profiles observed in children who developed natural tolerance to egg. CONCLUSION: Early life innate immune dysfunction may represent a key immunological driver and predictor of persistent food allergy in childhood. Serum vitamin D may play an immune-modulatory role in the development of natural tolerance</style></abstract><notes><style face="normal" font="default">DA - 20171120IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.024</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29154959">PM:29154959</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-NeelandMR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-NeelandMR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Neeland MR</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.024</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86778</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Choi,S.P.</style></author><author><style face="normal" font="default"> Oh,H.N.</style></author><author><style face="normal" font="default"> Choi,C.Y.</style></author><author><style face="normal" font="default"> Ahn,H.</style></author><author><style face="normal" font="default"> Yun,H.S.</style></author><author><style face="normal" font="default"> Chung,Y.M.</style></author><author><style face="normal" font="default"> Kim,B.</style></author><author><style face="normal" font="default"> Lee,S.J.</style></author><author><style face="normal" font="default"> Chun,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Oral administration of Lactobacillus plantarum CJLP133 and CJLP243 alleviates birch pollen induced allergic rhinitis in mice</style></title><secondary-title><style face="normal" font="default">J Appl Microbiol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Appl Microbiol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="12" Month="11" Year="2017">2017/11/12</year></dates><abstract><style face="normal" font="default">AIMS: In this study, we evaluated the therapeutic efficacy of selected probiotics in a mouse model of birch pollen (BP)-induced allergic rhinitis. METHODS AND RESULTS: Oral administration of lactobacillus plantarum CJLP133 and CJLP243 ameliorated the symptoms of BP-induced allergic rhinitis by reducing airway hyperresponsiveness (AHR), and both the histological scores and the number of infiltrated cells in the nasal cavities and lungs. Compared with those from vehicle-treated mice, bronchoalveolar lavage (BAL) fluid and draining lymph node samples from CJLP133 and CJLP243-administrated mice showed diminished numbers of immune cells, increased secretion of a Th1-type cytokine (IFN-gamma), and decreased production of Th2-type cytokines (IL-4, IL-5 and IL-13). Consistent with these results, levels of IL-4, IL-5, IL-13, serum IgE, and BP-specific serum IgG1 were decreased, whereas secretion of IFN-gamma and BP-specific serum IgG2a were augmented upon administration of CJLP133 and CJLP243 in mice. CONCLUSION: Oral administration of lactobacillus plantarum CJLP133 and CJLP243 alleviates symptoms of BP-induced allergic rhinitis in mice by recovering Th1/Th2 balance via enhancement of the Th1-type immune response. SIGNIFICANCE AND IMPACT OF THE STUDY: Lactobacillus plantarum CJLP133 and CJLP243 have therapeutic effects on BP-induced allergic rhinitis in an animal model. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1365-2672 (Electronic)IS - 1364-5072 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1111/jam.13635</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130606">PM:29130606</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Appl Microbiol\20171113-ChoiSP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Appl Microbiol\20171113-ChoiSP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Choi SP</style></custom2><misc3><style face="normal" font="default">10.1111/jam.13635</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86784</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Brooks,J.F.</style></author><author><style face="normal" font="default"> Davies,J.M.</style></author><author><style face="normal" font="default"> Wells,J.W.</style></author><author><style face="normal" font="default"> Steptoe,R.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">The University of Queensland, Translational Research Institute, University of Queensland Diamantina Institute, Level 6, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia</style></auth-address><titles><title><style face="normal" font="default">Re-educating immunity in respiratory allergies: the potential for hematopoietic stem cell-mediated gene therapy</style></title><secondary-title><style face="normal" font="default">J Mol Med (Berl)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Mol Med (Berl)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Autoimmunity</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">Respiratory allergies represent a significant disease burden worldwide affecting up to 300 million people globally. Medication and avoidance of known triggers do not address the underlying pathology. Traditional immunotherapies for allergy aim to reinstate immune homeostasis but require years of treatment and have poor long-term efficacy. Novel approaches, such as gene-engineered hematopoietic stem cell transplantation, induce profound antigen-specific tolerance in autoimmunity. Recent evidence shows this approach may also have therapeutic utility for allergy. Here, we review the mechanisms of antigen-specific tolerance and the potential of stem cell-mediated gene therapy to induce tolerance in allergic respiratory diseases</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1432-1440 (Electronic)IS - 0946-2716 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1007/s00109-017-1611-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150718">PM:29150718</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Mol Med (Berl)\20171118-BrooksJF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Mol Med (Berl)\20171118-BrooksJF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Brooks JF</style></custom2><misc3><style face="normal" font="default">10.1007/s00109-017-1611-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86786</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Valle,E.</style></author><author><style face="normal" font="default"> Pozzo,L.</style></author><author><style face="normal" font="default"> Giribaldi,M.</style></author><author><style face="normal" font="default"> Bergero,D.</style></author><author><style face="normal" font="default"> Gennero,M.S.</style></author><author><style face="normal" font="default"> Dezzutto,D.</style></author><author><style face="normal" font="default"> McLean,A.</style></author><author><style face="normal" font="default"> Borreani,G.</style></author><author><style face="normal" font="default"> Coppa,M.</style></author><author><style face="normal" font="default"> Cavallarin,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dipartimento di Scienze Veterinarie, Universita di Torino, Largo P. Braccini 2, 10095, Grugliasco, Turin, Italy</style></auth-address><titles><title><style face="normal" font="default">Effect of farming system on donkey milk composition</style></title><secondary-title><style face="normal" font="default">J Sci Food Agric</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Sci Food Agric</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword></keywords><dates><year Day="13" Month="11" Year="2017">2017/11/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: Donkey milk is considered a functional food for sensitive consumers, such as children allergic to cow milk. No information is available regarding the effect of farming systems on the quality of donkey milk. The study was aimed at evaluating the effect of the farming system and lactation stage on gross composition, fat-soluble vitamins and fatty acids (FA) in donkey milk. RESULTS: Individual milk samples were collected from lactating jennies (n=53) on the six of the largest farms located in North West Italy. The performance of lactating jennies, the herd characteristics, and feeding strategies were recorded at each milk sampling. The gross composition of the milk along with the fat-soluble vitamin content differed according to the farming system. The lactation stage had limited effects on milk quality. A higher milk fat content corresponded to a higher amount of fresh herbage proportion in the diet, with the highest polyunsaturated (PUFA) FA, C18:1c9, C18:3n-3, n-3 FA, retinol and alpha-tocopherol content and the lowest concentrations of the FA less favorable for human health in the milk of animals fed on only forage diets. CONCLUSIONS: Extensive farming of dairy donkeys increased fat content and fat-soluble vitamin concentration of milk and altered the FA composition to a more favorable profile for human nutrition</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1097-0010 (Electronic)IS - 0022-5142 (Linking)LA - engPT - Journal ArticleCO - Italy -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/jsfa.8777</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29131337">PM:29131337</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Sci Food Agric\20171113-ValleE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Sci Food Agric\20171113-ValleE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Valle E</style></custom2><misc3><style face="normal" font="default">10.1002/jsfa.8777</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86797</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nguyen,H.M.T.</style></author><author><style face="normal" font="default"> Bala,A.</style></author><author><style face="normal" font="default"> Gabrielson,A.T.</style></author><author><style face="normal" font="default"> Hellstrom,W.J.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Urology, Tulane University School of Medicine, New Orleans, LA, USA</style></auth-address><titles><title><style face="normal" font="default">Post-Orgasmic Illness Syndrome: A Review</style></title><secondary-title><style face="normal" font="default">Sex Med Rev</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sex Med Rev</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">methods</style></keyword></keywords><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Post-orgasmic illness syndrome (POIS) is a rare but debilitating cluster of postejaculatory symptoms affecting men. It is a chronic disorder manifesting as a constellation of flulike and allergic symptoms within seconds, minutes, or hours after ejaculation. POIS can be followed by mental sequelae such as diminished concentration and irritability. POIS negatively affects the life of patients by limiting sexual encounters, dampening romantic prospects, creating internal struggles to avoid eroticism, and affecting patients' schedules. First described in 2002, the prevalence and incidence of POIS are still unknown owing to a paucity of studies but is likely under-reported. There are approximately 50 cases of POIS in the literature. Despite the debilitating effects of POIS, the pathophysiology of POIS is still not well elucidated. AIM: To provide an update on the current literature on POIS, provide updated information on the pathophysiology of POIS, and discuss potential management options. METHODS: Comprehensive review of literature pertaining to POIS. MAIN OUTCOME MEASURES: The symptoms, classification, pathophysiology, diagnostic considerations, and management of POIS were reviewed. RESULTS: There are 5 preliminary diagnostic criteria for diagnosing this condition. POIS is categorized as primary or secondary. The autoimmune-allergy hypothesis is the most accepted hypothesis explaining the pathogenesis of POIS. A competing hypothesis involves a disorder involving endogenous mu-opioid receptors. Another hypothesis invokes impairment of the cytokine and neuroendocrine responses. There are no known treatment modalities for POIS; patients have been symptomatically treated with antihistamines, selective serotonin reuptake inhibitors, and benzodiazepines. A trial of hyposensitization therapy with autologous semen was successful. A trial of non-steroidal anti-inflammatory medication helped 1 patient described in a single case report, but failed to successfully treat other patients. CONCLUSIONS: POIS is a rare condition that is underdiagnosed and under-reported. Further studies are warranted to investigate the prevalence, pathophysiology, and treatment of this debilitating condition. Nguyen HMT, Bala A, Gabrielson AT, Hellstrom WJG. Post-Orgasmic Illness Syndrome: A Review. Sex Med Rev 2017;X:XXX-XXX</style></abstract><notes><style face="normal" font="default">DA - 20171112IS - 2050-0521 (Electronic)IS - 2050-0521 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.sxmr.2017.08.006</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29128269">PM:29128269</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171112, Nguyen HM</style></custom2><misc3><style face="normal" font="default">10.1016/j.sxmr.2017.08.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86798</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">McCarthy,A.J.</style></author><author><style face="normal" font="default"> Sheahan,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Histopathology, St. Vincent's University Hospital, Elm Park, Dublin 4, Ireland.</style></auth-address><titles><title><style face="normal" font="default">Classification of eosinophilic disorders of the small and large intestine</style></title><secondary-title><style face="normal" font="default">Virchows Arch</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Virchows Arch</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Eosinophil</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">Eosinophilic gastrointestinal diseases (EGIDs), including eosinophilic gastroenteritis and eosinophilic colitis, have been increasing in prevalence in Western countries in recent years. Eosinophils are normally scanty in the gastrointestinal tract, and increased numbers of eosinophils can denote pathology. Normal values for tissue eosinophils vary widely between different segments of the colon, thus location of the biopsy is critically important for the interpretation of findings. However, no standard diagnostic criteria have been proposed for the diagnosis of eosinophilic gastroenteritis or eosinophilic colitis. Gut eosinophilia encompasses entitites that are predominantly immunoglobulin E (IgE)-mediated, the primary EGIDs and those that are secondary and not IgE-mediated. A final diagnosis of eosinophilic gastrointestinal diseases requires careful pathological assessment, clinical correlation and exclusion of several differential diagnoses</style></abstract><notes><style face="normal" font="default">DA - 20171111IS - 1432-2307 (Electronic)IS - 0945-6317 (Linking)LA - engPT - Journal ArticleCO - Ireland -</style></notes><work-type><style face="normal" font="default">10.1007/s00428-017-2249-1</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29127496">PM:29127496</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Virchows Arch\20171111-McCarthyAJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Virchows Arch\20171111-McCarthyAJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171111, McCarthy AJ</style></custom2><misc3><style face="normal" font="default">10.1007/s00428-017-2249-1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86777</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Palmer,D.J.</style></author><author><style face="normal" font="default"> Prescott,S.L.</style></author><author><style face="normal" font="default"> Makrides,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Medicine, University of Western Australia, Crawley, Australia; Telethon Kids Institute, University of Western Australia, Subiaco, Australia.</style></auth-address><titles><title><style face="normal" font="default">Reply (Refers To: Timing of regular egg intake for prevention of egg allergy)</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - LetterCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.021</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29146011">PM:29146011</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-PalmerDJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-PalmerDJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Palmer DJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.021</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86802</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hoebeke,L.</style></author><author><style face="normal" font="default"> Bruffaerts,N.</style></author><author><style face="normal" font="default"> Verstraeten,C.</style></author><author><style face="normal" font="default"> Delcloo,A.</style></author><author><style face="normal" font="default"> De Smedt,T.</style></author><author><style face="normal" font="default"> Packeu,A.</style></author><author><style face="normal" font="default"> Detandt,M.</style></author><author><style face="normal" font="default"> Hendrickx,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Thirty-four years of pollen monitoring: an evaluation of the temporal variation of pollen seasons in Belgium</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">For the first time in Belgium, fluctuations in airborne pollen quantities over a 34-áyears period have been analyzed. Seven pollen types have been selected comprising the most clinically relevant in Belgium nowadays (birch, alder, hazel and grasses) and others that are known to be allergenic in other European countries and frequently found in Belgium (plane, ash and mugwort). Pollen monitoring was performed with a seven-day recording volumetric spore trap placed in Brussels. We measured increasing airborne pollen for four trees, namely alder, hazel, ash and plane. Although the total pollen index for birch has not increased significantly, an increasing trend in the annual amount of days above the concentration threshold of 80 pollen grains/m3 was clearly observed. Concerning temporal variations, the pollen season has tended to end earlier for birch, ash and plane and the peak concentration of the pollen of plane has been appearing earlier in the year. In the investigated period, the pollen seasons of grasses and mugwort have tended to become less severe. Furthermore, we reported a temporal shift of the grass pollen season, beginning and ending earlier, together with an advance of the annual peak date</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-017-9503-5</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-017-9503-5</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20171201-HoebekeL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20171201-HoebekeL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Hoebeke L</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-017-9503-5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86803</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hajkova,L.</style></author><author><style face="normal" font="default"> Hubalek,Z.</style></author><author><style face="normal" font="default"> Koznarova,V.</style></author><author><style face="normal" font="default"> Bartosova,L.</style></author><author><style face="normal" font="default"> Mozny,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Flowering of allergenically important plant species in relation to the North Atlantic Oscillation system and thermal time in the Czech Republic</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">This paper analyses long-term (1960</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô2015) onset of flowering in 16 native terrestrial plants (11 of them produce important allergens) recorded in different parts of the Czech Republic (southern, central and northern part) in relation to the North Atlantic Oscillation (NAO) index of the preceding winter and thermal data</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çögrowing degree-days (GDD) and soil temperature. Flowering occurred significantly earlier following positive winter NAO phases (causing spring to be warmer than normal in Central Europe) in nearly all early-flowering (February, March, April) species; high Pearson correlation values were recorded in, e.g. wood anemone, common snowdrop, goat willow, common hazel and common alder. There was found a difference between the southern and northern part of the country, e.g. in silver birch and pedunculate oak. Out of the later-flowering (May</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇôJuly) plant species, black elder and meadow foxtail also significantly correlated with the winter NAO index, lime tree correlated less markedly. The best results of a threshold for calculation of GDD to onset of beginning of flowering were found in lime tree</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çöit was 5-á-¦C at all three stations. Results of other taxa were more variable (e.g. 4</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô7-á-¦C in goat willow; 6</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô10-á-¦C in silver birch). Pearson correlation coefficients between NAO index and GDD were negative in lime tree at all thresholds (5, 6, 7, 8, 9, 10-á-¦C), while goat willow and silver birch were not so uniform (both positive and negative values). Correlation coefficients between phenophase onset and soil temperature (10-ácm depth) had the highest values in silver birch, European larch and wood anemone. Stations situated at higher elevation showed negative correlation coefficient with soil temperature in common snowdrop, pedunculate oak, meadow foxtail and lime tree; other values were positive</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Czechia -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-017-9504-4</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-017-9504-4</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20171202-HajkovaL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20171202-HajkovaL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Hajkova L</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-017-9504-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86808</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ozkars,M.Y.</style></author><author><style face="normal" font="default"> Keskin,O.</style></author><author><style face="normal" font="default"> Tokur,M.</style></author><author><style face="normal" font="default"> Ulasli,M.</style></author><author><style face="normal" font="default"> Gogebakan,B.</style></author><author><style face="normal" font="default"> Ciralik,H.</style></author><author><style face="normal" font="default"> Kucukosmanoglu,E.</style></author><author><style face="normal" font="default"> Demirel,C.</style></author><author><style face="normal" font="default"> Oztuzcu,S.</style></author><author><style face="normal" font="default"> Kahraman,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatric Allergy and Immunology, Gaziantep University School of Medicine, Gaziantep, Turkey.</style></auth-address><titles><title><style face="normal" font="default">Comparing the effects of fluticasone, anti-IgE and anti-TNF treatments in a chronic asthma model</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">BACKGROUND: Corticosteroids are used in the treatment of asthma. The aim of this study was to determine the efficacy of anti-IgE and anti-TNF alpha as asthma treatments. METHODS: A mouse model of chronic asthma was developed. The fluticasone group was exposed to fluticasone and the anti-IgE and anti-TNF groups were administered anti-IgE or anti-TNF. IL-4, and IgE levels were measured, and histological analysis, pathological analysis and miRNA-126, miRNA-133a analyses were applied. RESULTS: The cell concentration in the BAL fluid decreased in all the treatment groups. The rate of perivascular and peribronchial cell infiltration decreased in the lung in the high-dose anti-IgE and anti-TNF groups. Smooth muscle thickness decreased in the lung tissue in the low-dose anti-IgE and anti-TNF groups. Bronchial wall thickness decreased in the lung tissue in the fluticasone+anti-IgE group. The IL-4 level in BAL fluid decreased in the high-dose anti-IgE, fluticasone+anti-IgE and anti-TNF groups. IgE levels increased in the BAL fluid in the high-dose anti-IgE and anti-TNF groups. The lymphocyte level increased in the BAL fluid in the high-dose anti-IgE group. The macrophage level decreased in the BAL fluid in the anti-TNF group. The relative expression of miRNA-126 increased in all groups. The relative expression of miRNA-133a decreased in the placebo and fluticasone groups. The relative expression of miRNA-133a increased in the low-dose anti-IgE, high-dose anti-IgE, fluticasone+anti-IgE and anti-TNF groups. CONCLUSIONS: The results showed that anti-IgE is successful as a treatment. Fluticasone+anti-IgE and anti-TNF were seen to be superior to other therapeutic modalities when used for prophylaxis</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Turkey -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.07.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29191361">PM:29191361</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171129-OzkarsMY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171129-OzkarsMY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Ozkars MY</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.07.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86809</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Malaquias,M.A.S.</style></author><author><style face="normal" font="default"> Oyama,L.A.</style></author><author><style face="normal" font="default"> Jerico,P.C.</style></author><author><style face="normal" font="default"> Costa,I.</style></author><author><style face="normal" font="default"> Padilha,G.</style></author><author><style face="normal" font="default"> Nagashima,S.</style></author><author><style face="normal" font="default"> Lopes-Pacheco,M.</style></author><author><style face="normal" font="default"> Rebelatto,C.L.K.</style></author><author><style face="normal" font="default"> Michelotto,P.V.</style></author><author><style face="normal" font="default"> Xisto,D.G.</style></author><author><style face="normal" font="default"> Brofman,P.R.S.</style></author><author><style face="normal" font="default"> Rocco,P.R.M.</style></author><author><style face="normal" font="default"> de Noronha,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pathology Experimental Laboratory, School of Medicine, Pontifical Catholic University of Parana, Curitiba, Brazil.</style></auth-address><titles><title><style face="normal" font="default">Effects of mesenchymal stromal cells play a role the oxidant/antioxidant balance in a murine model of asthma</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">Asthma is a heterogeneous disease characterised by chronic airway inflammation. One of the most devastating consequences of this inflammatory process is the generation of reactive oxygen and nitrogen species responsible for oxidative stress. The aim of this study is to analyse the efficiency of treatment with human bone marrow-derived mesenchymal stromal cells (hMSC) in maintaining the oxidative balance in a murine model of allergic asthma by quantifying nitrotyrosine in lung tissues. After confirmation of asthma in the experimental model, samples of lung parenchyma were submitted to immunohistochemical assessment. Intravenous administration of hMSC reduced the levels of nitrotyrosine in the ASTHMA-hMSC group compared to those in the ASTHMA-SAL group. In conclusion, therapeutic administration of hMSC had a beneficial effect on oxidative stress, reducing the levels of nitrotyrosine in lung tissues in a model of allergic asthma</style></abstract><notes><style face="normal" font="default">IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.06.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29174587">PM:29174587</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171123-MalaquiasMA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\20171123-MalaquiasMA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, Malaquias MA</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.06.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86810</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Inomata,N.</style></author><author><style face="normal" font="default"> Miyakawa,M.</style></author><author><style face="normal" font="default"> Aihara,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Environmental Immuno-Dermatology, Yokohama City University School of Medicine, Yokohama, Japan.</style></auth-address><titles><title><style face="normal" font="default">Surfing as a risk factor for sensitization to poly(gamma-glutamic acid) in fermented soybeans, natto, allergy</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">BACKGROUND: Poly(gamma-glutamic acid) (PGA) is an allergen in natto, fermented soybeans, which causes late-onset anaphylaxis. We hypothesized that jellyfish stings sensitize adults to PGA because a surfer had allergies to both natto and jellyfish, whose sting contains PGA. The aim of the study was to identify behavioral factors, such as marine sports, associated with PGA sensitization. METHODS: Outpatients diagnosed with food allergies based on relevant clinical history, positive skin test and/or food challenge test answered a questionnaire during a regular visit in 2016. RESULTS: Questionnaire data from 140 outpatients were analyzed. These patients were divided into two groups: natto allergy group (13 patients, M:F = 10:3, mean age 40.6 years) and non-natto allergy group (127 patients, M:F = 46:81, mean age 44.5 years). All patients with natto allergy had positive results in skin prick test and basophil activation test with PGA. Of these, 92.3% had a marine sport hobby, especially surfing (84.6%). PGA sensitization was independently associated with marine sports (odds ratio, 278.0, 95 percent confidence interval, 36.9-6315.9, p &lt; 0.001) adjusted for male sex and sea bathing, but not with male sex or sea bathing. In addition, although there was no significant difference in the experience of marine sports between natto and non-natto allergy groups, the natto allergy group participated significantly more frequently in marine sports than the non-natto allergy group (p &lt; 0.001). There was no significant difference between natto consumption amount and PGA sensitization. CONCLUSIONS: Surfing is a risk factor for PGA sensitization in those with allergy to natto</style></abstract><notes><style face="normal" font="default">IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.11.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29175280">PM:29175280</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171124-InomataN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171124-InomataN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Inomata N</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.11.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86811</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hayashi,H.</style></author><author><style face="normal" font="default"> Fukutomi,Y.</style></author><author><style face="normal" font="default"> Mitsui,C.</style></author><author><style face="normal" font="default"> Watai,K.</style></author><author><style face="normal" font="default"> Tomita,Y.</style></author><author><style face="normal" font="default"> Kamide,Y.</style></author><author><style face="normal" font="default"> Sekiya,K.</style></author><author><style face="normal" font="default"> Tsuburai,T.</style></author><author><style face="normal" font="default"> Horita,A.</style></author><author><style face="normal" font="default"> Saito,I.</style></author><author><style face="normal" font="default"> Hasegawa,Y.</style></author><author><style face="normal" font="default"> Taniguchi,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical Research Center for Allergy and Rheumatology, Sagamihara National Hospital, Sagamihara, Japan</style></auth-address><titles><title><style face="normal" font="default">Th1-related disease development during omalizumab treatment: Two cases with severe asthma</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - LetterCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.10.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29191372">PM:29191372</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171127-HayashiH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171127-HayashiH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171127, Hayashi H</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.10.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86812</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Inuo,C.</style></author><author><style face="normal" font="default"> Ando,H.</style></author><author><style face="normal" font="default"> Tanaka,K.</style></author><author><style face="normal" font="default"> Nakajima,Y.</style></author><author><style face="normal" font="default"> Tsuge,I.</style></author><author><style face="normal" font="default"> Urisu,A.</style></author><author><style face="normal" font="default"> Kondo,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, School of Medicine, Fujita Health University, Toyoake, Japan</style></auth-address><titles><title><style face="normal" font="default">Long-term immunological effects of Japanese cedar pollen-based subcutaneous immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - LetterCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.11.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29198713">PM:29198713</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171129-InuoC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171129-InuoC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171229, Inuo C</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.11.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86813</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sander,I.</style></author><author><style face="normal" font="default"> Lotz,A.</style></author><author><style face="normal" font="default"> Neumann,H.D.</style></author><author><style face="normal" font="default"> Czibor,C.</style></author><author><style face="normal" font="default"> Flagge,A.</style></author><author><style face="normal" font="default"> Zahradnik,E.</style></author><author><style face="normal" font="default"> Raulf,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute for Prevention and Occupational Medicine, German Social Accident Insurance, Institute of the Ruhr-Universitat Bochum (IPA), Bochum, Germany</style></auth-address><titles><title><style face="normal" font="default">Indoor allergen levels in settled airborne dust are higher in day-care centres than at home</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">BACKGROUND: Early life sensitization to indoor allergens predicts asthma development. Aim of study was to compare allergen concentrations in day-care centres (DCC) to those in private homes. METHODS: Settled airborne dust was collected four times a year from 20 German DCC (620 samples), and from the homes of children and day-care workers (602 samples) using electrostatic dust collectors (EDC). The samples were analysed with fluorescence-enzyme-immunoassays recognising domestic mite allergens (DM), Fel d 1, Can f 1 and Mus m 1. Pet allergen thresholds that discriminate samples from homes with cats or dogs to those without were calculated using receiver-operator characteristics. Influences on allergen levels were analysed using multilevel models. RESULTS: Allergen loads were on average higher in DCC than in homes. In DCC, 96% of the samples were positive for DM, 95% for Can f 1, 90% for Fel d 1, and 83% for Mus m 1. In homes, 84% contained DM, 48.5% Can f 1, 33% Fel d 1, and 43% Mus m 1. The threshold level for homes with dogs was 75 ng/m(2) Can f 1 (96.8% sensitivity, 96% specificity), and 46 ng/m(2) Fel d 1 for homes with cats (92% sensitivity, 94.9% specificity). In DCC, Can f 1 and Fel d 1 loads were higher than these thresholds in 37% and 54% of the samples, respectively. Allergen levels were significantly influenced by the season and room type; however, carpets on floors had no influence. CONCLUSIONS: Mite, mouse, cat and dog allergens were mostly higher in DCC than in homes. Exposure to dog and cat allergens in DCC often reached levels of households with pets. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13371</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29193190">PM:29193190</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171129-SanderI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171129-SanderI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Sander I</style></custom2><misc3><style face="normal" font="default">10.1111/all.13371</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86814</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vizzardelli,C.</style></author><author><style face="normal" font="default"> Gindl,M.</style></author><author><style face="normal" font="default"> Roos,S.</style></author><author><style face="normal" font="default"> Mobs,C.</style></author><author><style face="normal" font="default"> Nagl,B.</style></author><author><style face="normal" font="default"> Zimmann,F.</style></author><author><style face="normal" font="default"> Sexl,V.</style></author><author><style face="normal" font="default"> Kenner,L.</style></author><author><style face="normal" font="default"> Neunkirchner,A.</style></author><author><style face="normal" font="default"> Zlabinger,G.J.</style></author><author><style face="normal" font="default"> Pickl,W.F.</style></author><author><style face="normal" font="default"> Pfutzner,W.</style></author><author><style face="normal" font="default"> Bohle,B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Pathophysiology and Allergy Research, Medical University of Vienna, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Blocking antibodies induced by allergen-specific immunotherapy ameliorate allergic airway disease in a human/mouse chimeric model</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergen-specific immunotherapy (AIT) induces specific blocking antibodies (Ab) which are claimed to prevent IgE-mediated reactions to allergens. Additionally, AIT modulates cellular responses to allergens, e.g. by desensitizing effector cells, inducing regulatory T and B lymphocytes and immune deviation. It is still enigmatic which of these mechanisms mediate(s) clinical tolerance. We sought to address the role of AIT-induced blocking Ab separately from cellular responses in a chimeric human/mouse model of respiratory allergy. METHODS: Non-obese diabetic severe combined immunodeficient gammac(-/-) (NSG) mice received intraperitoneally allergen-reactive PBMC from birch pollen-allergic patients together with birch pollen extract and human IL-4. Engraftment was assessed by flow cytometry. Airway hyperresponsiveness (AHR) and bronchial inflammation were analyzed after intranasal challenges with allergen or PBS. Sera collected from patients before and during AIT with birch pollen were added to the allergen prior to intranasal challenge. The IgE-blocking activity of post-AIT sera was assessed in vitro. RESULTS: Human cells were detected in cell suspensions of murine lungs and spleens indicating successful humanization. Humanized mice displayed a more pronounced AHR and bronchial inflammation when challenged with allergen compared to negative controls. Post-AIT sera excerted IgE-blocking activity. In contrast to pre-AIT sera, the presence of heterologous and autologous post-AIT sera significantly reduced the allergic airway inflammation and matched their IgE-blocking activity determined in vitro. CONCLUSION: Our data demonstrate that post-AIT sera with IgE-blocking activity ameliorate allergic airway inflammation in a human/mouse chimeric model of respiratory allergy independently of AIT-induced cellular changes. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13363</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29159964">PM:29159964</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171121-VizzardelliC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171121-VizzardelliC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Vizzardelli C</style></custom2><misc3><style face="normal" font="default">10.1111/all.13363</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86816</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gerlich,J.</style></author><author><style face="normal" font="default"> Benecke,N.</style></author><author><style face="normal" font="default"> Peters-Weist,A.S.</style></author><author><style face="normal" font="default"> Heinrich,S.</style></author><author><style face="normal" font="default"> Roller,D.</style></author><author><style face="normal" font="default"> Genuneit,J.</style></author><author><style face="normal" font="default"> Weinmayr,G.</style></author><author><style face="normal" font="default"> Windstetter,D.</style></author><author><style face="normal" font="default"> Dressel,H.</style></author><author><style face="normal" font="default"> Range,U.</style></author><author><style face="normal" font="default"> Nowak,D.</style></author><author><style face="normal" font="default"> von Mutius,E.</style></author><author><style face="normal" font="default"> Radon,K.</style></author><author><style face="normal" font="default"> Vogelberg,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute and Clinic for Occupational, Social, and Environmental Medicine, University Hospital, LMU Munich, Germany</style></auth-address><titles><title><style face="normal" font="default">Pregnancy and perinatal conditions and atopic disease prevalence in childhood and adulthood</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">BACKGROUND: Previous studies showed controversial results for the influence of pregnancy-related and perinatal factors on subsequent respiratory and atopic diseases in children. The aim of this study was to assess the association between perinatal variables and the prevalence of asthma, bronchial hyperreactivity, flexural eczema, allergic rhinitis, and sensitization in childhood and early adulthood. METHODS: The studied population was first examined in Munich and Dresden in 1995/1996 at age 9-11 yrs. Participants were followed until age 19-24 yrs. using questionnaires and clinical examinations. Associations between perinatal data and subsequent atopic diseases were examined using logistic regression analyses adjusting for potential confounders. RESULTS: Cesarean section was statistically significantly associated with BHR in early adulthood (Odds Ratio 4.8, 95% confidence interval 1.5-15.2), while assisted birth was associated with presence of asthma symptoms in childhood (2.2, 1.2-3.9), flexural eczema symptoms (2.2, 1.2-4.3) and doctor's diagnosis of atopic dermatitis (1.9, 1.0-3.4) in childhood, and sensitization in early adulthood (2.2, 1.1-4.3). Lower birth length (1.9, 1.1-3.2), lower birth weight (0.5, 0.3-0.9) and higher birth weight (0.6 (0.4-1.0)) were predictive of sensitization in early adulthood compared to average birth length and birth weight, respectively. None of the other perinatal factors showed statistically significant associations with the outcomes. CONCLUSIONS: Our results indicate that children, who are born by Cesarean section and especially by assisted birth, might be at greater risk for developing asthma, flexural eczema and sensitization and should hence be monitored. Prenatal maternal stress might partly explain these associations, which should be further investigated. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/all.13372</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29193127">PM:29193127</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171129-GerlichJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171129-GerlichJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Gerlich J</style></custom2><misc3><style face="normal" font="default">10.1111/all.13372</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86817</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pinzer,T.C.</style></author><author><style face="normal" font="default"> Tietz,E.</style></author><author><style face="normal" font="default"> Waldmann,E.</style></author><author><style face="normal" font="default"> Schink,M.</style></author><author><style face="normal" font="default"> Neurath,M.F.</style></author><author><style face="normal" font="default"> Zopf,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine 1, Hector Center for Nutrition, Exercise and Sports, Friedrich-Alexander-University Erlangen-Nuremberg, Ulmenweg 18, 91054, Erlangen, Germany</style></auth-address><titles><title><style face="normal" font="default">Circadian profiling reveals higher histamine plasma levels and lower diamine oxidase serum activities in 24% of patients with suspected histamine intolerance compared to food allergy and controls</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">BACKGROUND: Histamine intolerance is thought to trigger manifold clinical symptoms after ingesting histamine-rich food due to reduced activity of diamine oxidase (DAO). No study has hitherto systematically assessed daily fluctuations of histamine levels and DAO activities in symptomatic patients. The aim of the study was to investigate the presence of histamine intolerance, to therefore establish day profiles of histamine levels and DAO activities, and to compare the results between patients with suspected histamine intolerance, food allergy and healthy controls. METHODS: We determined day profiles of histamine plasma levels and DAO serum activities in 33 patients with suspected histamine intolerance, in 21 patients with proven food allergy and in 10 healthy control patients. Clinical symptoms, food intolerances and further clinical and laboratory-chemical parameters were evaluated. RESULTS: 24% (8 of 33) suspected histamine intolerant patients showed elevated histamine levels during the day. That might be caused by constantly and significantly reduced DAO activities in these patients compared to food allergy and control patients. The remaining 25 patients presented normal histamine levels and DAO activities, but an increased prevalence of multiple food intolerances compared to the other subgroup of suspected histamine intolerants. There was no correlation between subjective complaints and serological histamine parameters in patients with suspected histamine intolerance. CONCLUSIONS: We determined by daily profiling that decreased DAO activities correlated with elevated histamine levels in a subgroup of suspected histamine intolerants. This finding discriminates these patients from food intolerant individuals with similar clinical symptoms, and strongly suggests the presence of histamine intolerance. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13361</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29154390">PM:29154390</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171120-PinzerTC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171120-PinzerTC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Pinzer TC</style></custom2><misc3><style face="normal" font="default">10.1111/all.13361</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86818</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Brier,S.</style></author><author><style face="normal" font="default"> Le Mignon,M.</style></author><author><style face="normal" font="default"> Jain,K.</style></author><author><style face="normal" font="default"> Lebrun,C.</style></author><author><style face="normal" font="default"> Peurois,F.</style></author><author><style face="normal" font="default"> Kellenberger,C.</style></author><author><style face="normal" font="default"> Bordas-Le Floch,V.</style></author><author><style face="normal" font="default"> Mascarell,L.</style></author><author><style face="normal" font="default"> Nony,E.</style></author><author><style face="normal" font="default"> Moingeon,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Stallergenes Greer, 6 rue Alexis de Tocqueville, 92183, Antony, cedex, France</style></auth-address><titles><title><style face="normal" font="default">Characterization of epitope specificities of reference antibodies used for the quantification of the birch pollen allergen Bet v 1</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">BACKGROUND: Accurate allergen quantification is needed to document the consistency of allergen extracts used for immunotherapy. Herein, we characterize the epitope specificities of two monoclonal antibodies used in an ELISA for the quantification of the major birch pollen allergen Bet v 1, established as a reference by the BSP090 European project. METHODS: The ability of mAbs 5B4 and 6H4 to recognize Bet v 1 isoforms was addressed by immunochromatography. The capacity of each mAb to compete with patients' IgE for binding to Bet v 1 was measured by ELISA inhibition. Epitope mapping was performed by pepscan analysis, site-directed mutagenesis and hydrogen/deuterium exchange-mass spectrometry. RESULTS: The 5B4 epitope corresponds to a peptide sequence (I56-K68) overlapping with the binding sites of patients' serum IgEs. Mutation of residues P59, E60 and K65 abolishes 5B4 binding to Bet v 1 and reduces the level of IgE recognition. In contrast, 6H4 recognizes a conformational epitope lying opposite to the 5B4 binding site, involving residues located in segments I44-K55 and R70-F79. Substitution of E45 reduces the binding capacity of 6H4, confirming that it is critical for the interaction. Both mAbs interact with >90% of Bet v 1 content present in the birch pollen extract, while displaying a weak cross-reactivity with other allergens of the PR-10 family. CONCLUSIONS: MAbs 5B4 and 6H4 recognize structurally distinct epitopes present in the vast majority of Bet v 1 isoforms. These results support the relevance as a reference method of the Bet v 1-specific quantitative ELISA adopted by the European Pharmacopoeia. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1111/all.13364</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29171882">PM:29171882</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171124-BrierS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171124-BrierS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Brier S</style></custom2><misc3><style face="normal" font="default">10.1111/all.13364</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86819</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pfaar,O.</style></author><author><style face="normal" font="default"> Bonini,S.</style></author><author><style face="normal" font="default"> Cardona,V.</style></author><author><style face="normal" font="default"> Demoly,P.</style></author><author><style face="normal" font="default"> Jakob,T.</style></author><author><style face="normal" font="default"> Jutel,M.</style></author><author><style face="normal" font="default"> Kleine-Tebbe,J.</style></author><author><style face="normal" font="default"> Klimek,L.</style></author><author><style face="normal" font="default"> Klysner,S.</style></author><author><style face="normal" font="default"> Kopp,M.V.</style></author><author><style face="normal" font="default"> Kuna,P.</style></author><author><style face="normal" font="default"> Larche,M.</style></author><author><style face="normal" font="default"> Muraro,A.</style></author><author><style face="normal" font="default"> Schmidt-Weber,C.B.</style></author><author><style face="normal" font="default"> Shamji,M.</style></author><author><style face="normal" font="default"> Simonsen,K.</style></author><author><style face="normal" font="default"> Somoza,C.</style></author><author><style face="normal" font="default"> Valovirta,E.</style></author><author><style face="normal" font="default"> Zieglmayer,P.</style></author><author><style face="normal" font="default"> Zuberbier,T.</style></author><author><style face="normal" font="default"> Wahn,U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otorhinolaryngology Head and Neck Surgery, Universitatsmedizin Mannheim Medical Faculty Mannheim Heidelberg University Mannheim</style></auth-address><titles><title><style face="normal" font="default">Perspectives in allergen immunotherapy: 2017 and beyond</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">The Future of the Allergists and Specific Immunotherapy (FASIT) workshop provides a regular platform for global experts from academia, allergy clinics, regulatory authorities and industry to review developments in the field of allergen immunotherapy (AIT). The most recent meeting, held in February 2017, had two main themes: advances in AIT and hot topics in AIT from the regulatory point of view. The first theme covered opportunities for personalised AIT, advances in adjuvants and delivery systems, and the development of new molecules and future vaccines for AIT. Key topics in the second part of the meeting were the effects of the enactment of European Directive 2001/83 on the availability of allergens for therapy and diagnosis across the EU, the challenges of conducting Phase III studies in the field, the future role of allergen exposure chambers in AIT-studies, and specific considerations in performing AIT-studies in the paediatric population. Finally, the group highlighted the forthcoming EAACI guidelines and their particular importance for the standardisation of practice in the treatment of allergies. This supplement presents a comprehensive insight into those panel discussions and highlights unmet needs and also possible solutions to them for the future. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Germany -CO - Italy -CO - United Kingdom -CO - Spain -CO - France -CO - Poland -CO - Denmark -CO - Canada -CO - Switzerland -CO - Switzerland -CO - Finland -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.1111/all.13355</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29171712">PM:29171712</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171124-PfaarO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171124-PfaarO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Pfaar O</style></custom2><misc3><style face="normal" font="default">10.1111/all.13355</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86820</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Baek,J.O.</style></author><author><style face="normal" font="default"> Lee,J.R.</style></author><author><style face="normal" font="default"> Roh,J.Y.</style></author><author><style face="normal" font="default"> Jung,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Gachon University Gil Medical Center, Incheon, Korea</style></auth-address><titles><title><style face="normal" font="default">Oral tolerance modulates the skin transcriptome in mice with induced atopic dermatitis</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">Defective gut immune reactions have been implicated in the development of atopic dermatitis (AD), whereas oral tolerance (OT), i.e., the immune unresponsiveness induced by oral antigen administration, protects mice against AD. To investigate this protective role of OT, the transcriptomic profiles of skin were obtained by RNA sequencing from mice that were epicutaneously sensitized, orally tolerized prior to epicutaneous sensitization, or neither (control). OT inhibited the upregulation of keratin- and allergic inflammation-associated genes that occurred in the epicutaneously sensitized group. Compared to the controls, mice that were orally tolerized and epicutaneously sensitized showed an upregulation of genes that regulate inflammation or keratinocyte differentiation. Knocking down two of those genes, SCGB1A1 and TSC22D3, upregulated Th2 inflammatory mediators and downregulated a cornified cell envelope-related gene. Based on our findings, OT may protect skin against allergic inflammation by promoting the expression of genes that regulate Th2 inflammatory responses and skin barrier function. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1111/all.13367</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29168893">PM:29168893</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171123-BaekJO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171123-BaekJO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, Baek JO</style></custom2><misc3><style face="normal" font="default">10.1111/all.13367</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86821</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Carter,M.C.</style></author><author><style face="normal" font="default"> Ruiz-Esteves,K.N.</style></author><author><style face="normal" font="default"> Workman,L.</style></author><author><style face="normal" font="default"> Lieberman,P.</style></author><author><style face="normal" font="default"> Platts-Mills,T.A.</style></author><author><style face="normal" font="default"> Metcalfe,D.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA</style></auth-address><titles><title><style face="normal" font="default">Identification of alpha-gal sensitivity in patients with a diagnosis of idiopathic anaphylaxis</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Mastocytosis</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">IgE antibodies (Ab) specific to galactose-alpha-1,3-galactose (alpha-gal) are responsible for a delayed form of anaphylaxis that occurs 3 to 6 hours after red meat ingestion. In a unique prospective study of seventy participants referred with a diagnosis of idiopathic anaphylaxis (IA), six (9%) were found to have IgE to alpha-gal. Upon institution of a diet free of red meat, all patients had no further episodes of anaphylaxis. Two of these individuals had indolent systemic mastocytosis (ISM). Those with ISM had more severe clinical reactions but lower specific IgE to alpha-gal and higher serum tryptase levels, reflective of the mast cell burden. The identification of alpha-gal syndrome in patients with IA supports the need for routine screening for this sensitivity as a cause of anaphylaxis, where reactions to alpha-gal are delayed and thus may be overlooked. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/all.13366</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29161766">PM:29161766</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171121-CarterMC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171121-CarterMC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Carter MC</style></custom2><misc3><style face="normal" font="default">10.1111/all.13366</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86822</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Arzt,L.</style></author><author><style face="normal" font="default"> Bokanovic,D.</style></author><author><style face="normal" font="default"> Schrautzer,C.</style></author><author><style face="normal" font="default"> Laipold,K.</style></author><author><style face="normal" font="default"> Mobs,C.</style></author><author><style face="normal" font="default"> Pfutzner,W.</style></author><author><style face="normal" font="default"> Herzog,S.A.</style></author><author><style face="normal" font="default"> Vollmann,J.</style></author><author><style face="normal" font="default"> Reider,N.</style></author><author><style face="normal" font="default"> Bohle,B.</style></author><author><style face="normal" font="default"> Aberer,W.</style></author><author><style face="normal" font="default"> Sturm,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Venerology, Medical University of Graz, Austria</style></auth-address><titles><title><style face="normal" font="default">Immunological differences between insect venom-allergic patients with and without immunotherapy and asymptomatically sensitized subjects</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">BACKGROUND: Currently available tests are unable to distinguish between asymptomatic sensitization and clinically relevant Hymenoptera venom allergy. A reliable serological marker to monitor venom immunotherapy (VIT) does also not exist. Our aim was to find reliable serological markers to predict tolerance to bee and vespid stings. METHODS: We included 77 asymptomatically-sensitized subjects, 85 allergic-patients with acute systemic sting reactions, and 61 allergic-patients currently treated with VIT. Levels of sIgE and sIgG4 to bee and vespid venom, rApi-m-1 and rVes-v-5 were measured immediately after allergic sting-reactions or before sting-challenges and four weeks later. All sting challenges were tolerated. The inhibitory activity was determined using BAT-inhibition and ELIFAB-assay. RESULTS: Median sIgG4 levels were 96-fold higher in VIT patients (p&lt;0.001) while sIgE/sIgG4 ratios were consistently lower (p&lt;0.001). The ELIFAB-assay was paralleled by low sIgE/sIgG4 ratios in VIT-patients, showing markedly higher allergen-blocking capacity (p&lt;0.001). An almost complete inhibition of the basophil response was seen in all patients treated with vespid venom, but not in those treated with bee venom. Four weeks after the sting, sIgE and sIgG4 levels were increased in allergic and asymptomatically-sensitized patients, but not in VIT-patients. CONCLUSION: Immunological responses after stings varied in bee and vespid venom allergic patients. In patients under VIT, sIgE and sIgG4 remained completely stable after sting-challenges. Monitoring VIT efficacy was only possible in vespid venom allergy and the sIgG4 threshold for rVes-v-5 had the highest sensitivity to confirm tolerance. The BAT-inhibition test was the most reliable tool to confirm tolerance on an individual basis. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13368</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29171032">PM:29171032</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171123-ArztL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171123-ArztL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, Arzt L</style></custom2><misc3><style face="normal" font="default">10.1111/all.13368</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86833</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Djukanovic,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Southampton University , is Clinical and Experimental Science, Faculty of > Medicine, Southampton, United Kingdom of Great Britain and Northern IrelandNIHR Southampton Biomedical Research Centre , Southampton, United Kingdom of Great Britain and Northern Ireland ; R.Djukanovic@soton.ac.uk</style></auth-address><titles><title><style face="normal" font="default">Predicting Asthmatic Responses to Inhaled Allergen Using an Unbiased Transcriptomics Approach</style></title><secondary-title><style face="normal" font="default">Am J Respir Crit Care Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Respir Crit Care Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/14/2017" status="on-request"/><keywords/><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1535-4970 (Electronic)IS - 1073-449X (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Ireland -</style></notes><work-type><style face="normal" font="default">10.1164/rccm.201711-2237ED</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29182887">PM:29182887</url></web-urls><pdf-urls><url ppv-ref="no">R.Djukanovic@soton.ac.uk</url></pdf-urls><text-urls><url ppv-ref="no">researchgate</url></text-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171128, Djukanovic R</style></custom2><misc3><style face="normal" font="default">10.1164/rccm.201711-2237ED</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86834</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gastaminza,G.</style></author><author><style face="normal" font="default"> Lafuente,A.</style></author><author><style face="normal" font="default"> Goikoetxea,M.J.</style></author><author><style face="normal" font="default"> D'Amelio,C.M.</style></author><author><style face="normal" font="default"> Bernad-Alonso,A.</style></author><author><style face="normal" font="default"> Vega,O.</style></author><author><style face="normal" font="default"> Martinez-Molina,J.A.</style></author><author><style face="normal" font="default"> Ferrer,M.</style></author><author><style face="normal" font="default"> Nunez-Cordoba,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">From the Departments of Allergology and Clinical Immunology, Anaesthesia, and Research Support Service, Central Clinical Trials Unit, Clinica Universidad de Navarra, Pamplona, Spain</style></auth-address><titles><title><style face="normal" font="default">Improvement of the Elevated Tryptase Criterion to Discriminate IgE- From Non-IgE-Mediated Allergic Reactions</style></title><secondary-title><style face="normal" font="default">Anesth Analg</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Anesth Analg</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">BACKGROUND: Differentiating between immunoglobulin E (IgE)-dependent and IgE-independent hypersensitivity reactions may improve the etiologic orientation and clinical management of patients with allergic reactions in the anesthesia setting. Serum tryptase levels may be useful to discriminate the immune mechanism of allergic reactions, but the diagnostic accuracy and optimal cutpoint remain unclear.We aimed to compare the diagnostic accuracy of tryptase during reaction (TDR) alone and the TDR/basal tryptase (TDR/BT) ratio for discriminating IgE- from non-IgE-mediated allergic reactions, and to estimate the best cut point for these indicators. METHODS: We included 111 patients (45% men; aged 3-99 years) who had experienced an allergic reaction, even though the allergic reaction could be nonanaphylactic. Allergy tests were performed to classify the reaction as an IgE- or non-IgE-mediated one. The area under the curve (AUC) of the receiver operating characteristic analysis was performed to estimate the discriminative ability of TDR and TDR/BT ratio. RESULTS: An IgE-mediated reaction was diagnosed in 49.5% of patients, of whom 56% met anaphylaxis criteria. The median (quartiles) TDR for the IgE-mediated reactions was 8.0 (4.9-19.6) and 5.1 (3.5-8.1) for the non-IgE-mediated (P = .022). The median (quartiles) TDR/BT ratio was 2.7 (1.7-4.5) in IgE-mediated and 1.1 (1.0-1.6) in non-IgE-mediated reactions (P &lt; .001). The TDR/BT ratio showed the greatest ability to discriminate IgE- from non-IgE-mediated reactions compared to TDR (AUC TDR/BT = 0.79 [95% confidence interval (CI), 1.1-2.2] and AUC TDR = 0.66 [95% CI, 1.1-2.2]; P = .003). The optimal cut point for TDR/BT (maximization of the sum of the sensitivity and specificity) was 1.66 (95% CI, 1.1-2.2). CONCLUSIONS: The TDR/BT ratio showed a significantly better discriminative ability than TDR to discriminate IgE- from non-IgE-mediated allergic reactions. An optimal TDR/BT ratio threshold of approximately 1.66 may be useful in clinical practice to classify allergic reactions as IgE- or non-IgE-mediated</style></abstract><notes><style face="normal" font="default">IS - 1526-7598 (Electronic)IS - 0003-2999 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1213/ANE.0000000000002656</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29189281">PM:29189281</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Anesth Analg\20171117-GastaminzaG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Anesth Analg\20171117-GastaminzaG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Gastaminza G</style></custom2><misc3><style face="normal" font="default">10.1213/ANE.0000000000002656</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86836</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Foong,R.X.</style></author><author><style face="normal" font="default"> Brough,H.A.</style></author><author><style face="normal" font="default"> Chan,S.</style></author><author><style face="normal" font="default"> Fox,A.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Asthma, Allergy and Lung Biology, Department of Paediatric Allergy, King's College London and Guy's and St. Thomas' NHS Foundation Trust, London, UK</style></auth-address><titles><title><style face="normal" font="default">US guidelines for the prevention of peanut allergy 2017</style></title><secondary-title><style face="normal" font="default">Arch Dis Child Educ Tract Ed</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arch Dis Child Educ Tract Ed</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1743-0593 (Electronic)IS - 1743-0585 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1136/archdischild-2017-313094</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29175880">PM:29175880</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Arch Dis Child Educ Tract Ed\20171124-FoongRX.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Arch Dis Child Educ Tract Ed\20171124-FoongRX.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Foong RX</style></custom2><misc3><style face="normal" font="default">10.1136/archdischild-2017-313094</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86837</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dupont,C.</style></author><author><style face="normal" font="default"> Soulaines,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Service d'explorations fonctionnelles digestives et allergie alimentaire, hopital Necker, 149, rue de Sevres, 75015 Paris, France. Electronic address: christophe.dupont@aphp.frService d'explorations fonctionnelles digestives et allergie alimentaire, hopital Necker, 149, rue de Sevres, 75015 Paris, France</style></auth-address><titles><title><style face="normal" font="default">[Update on dietary management of cow's milk allergy]</style></title><secondary-title><style face="normal" font="default">Arch Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arch Pediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Amino Acids</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">Dietary management of cow's milk allergy is based on the elimination of all cow's milk proteins from the diet. For non-breastfed infants, the main dietetic move is the replacement of the standard infant formula with a formula for which the protein fraction has been modified. This formula can be based on hydrolyzed cow's milk proteins, rice proteins or amino acids. Monitoring the growth of these children is essential. The reintroduction of cow's milk, raw or heated, should always be made carefully and gradually. As the child grows and remains allergic, the use of heated (baked) milk substantially eases his/her feeding</style></abstract><notes><style face="normal" font="default">IS - 1769-664X (Electronic)IS - 0929-693X (Linking)LA - frePT - English AbstractPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.arcped.2017.09.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29169718">PM:29169718</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Arch Pediatr\20171121-DupontC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Arch Pediatr\20171121-DupontC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Dupont C</style></custom2><misc3><style face="normal" font="default">10.1016/j.arcped.2017.09.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86838</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wu,G.</style></author><author><style face="normal" font="default"> Yang,L.</style></author><author><style face="normal" font="default"> Xu,Y.</style></author><author><style face="normal" font="default"> Jiang,X.</style></author><author><style face="normal" font="default"> Jiang,X.</style></author><author><style face="normal" font="default"> Huang,L.</style></author><author><style face="normal" font="default"> Mao,L.</style></author><author><style face="normal" font="default"> Cai,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory and Critical Care Medicine, Chronic Airways Diseases Laboratory, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China</style></auth-address><titles><title><style face="normal" font="default">FABP4 induces asthmatic airway epithelial barrier dysfunction via ROS-activated FoxM1</style></title><secondary-title><style face="normal" font="default">Biochem Biophys Res Commun</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biochem Biophys Res Commun</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Glucose</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">Functional abnormal airway epithelial cells, along with activated inflammatory cells, resulting in chronic airway inflammation, are considered as the characteristic of asthma. Fatty Acid Binding Protein 4 (FABP4) takes part in glucose and lipid homeostasis, and also have an important role in allergic airway inflammation. However, whether FABP4 influence barrier function of airway epithelial cells is unknown. In vivo, a HDM-induced murine model of asthma was obtained to assessed airway inflammation and protein expression of E-cadherin and Forkhead Box M1 (FoxM1). In vitro, 16-HBE was cultured and was treated with hrFABP4, siFABP4, FABPF4 inhibitor BMS, or FoxM1 inhibitor RCM-1. IL-4, IL-5, and IL-13 level was determined by ELISA. Transepithelial electrical resistance (TER), paracellular permeability and E-cadherin-special immunofluorescence were measured to value airway epithelial barrier function. Intracellular ROS production was determined by DCF-DA fluorescence. FABP4 inhibitor BMS alleviate airway inflammation and destruction of E-cad in allergic mouse. Treatment with HDM or hrFABP4 aggravated inflammatory response, damaged airway epithelial barrier, which could be inhibited by siFABP4 and BMS. Treatment with HDM or hrFABP4 also enhanced levels of FoxM1, and Inhibited FoxM1 suppressed HDM- and hrFABP4-induced inflammation and airway epithelial barrier dysfunction. In addition, H2O2 promoted FoxM1 expression, HDM and hrFABP4 induced-FoxM1 could be inhibited by NAC, leading to decreased inflammation and improved airway epithelial barrier. Upregulated ROS induced by FABP4 was of significance in activating FoxM1 leading to airway inflammation and epithelial barrier dysfunction</style></abstract><notes><style face="normal" font="default">IS - 1090-2104 (Electronic)IS - 0006-291X (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.bbrc.2017.11.106</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29158087">PM:29158087</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biochem Biophys Res Commun\20171120-WuG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biochem Biophys Res Commun\20171120-WuG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Wu G</style></custom2><misc3><style face="normal" font="default">10.1016/j.bbrc.2017.11.106</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86840</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liang,P.</style></author><author><style face="normal" font="default"> Peng,S.</style></author><author><style face="normal" font="default"> Zhang,M.</style></author><author><style face="normal" font="default"> Ma,Y.</style></author><author><style face="normal" font="default"> Zhen,X.</style></author><author><style face="normal" font="default"> Li,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Rd., Zhengzhou, 450052, People's Republic of China</style></auth-address><titles><title><style face="normal" font="default">Huai Qi Huang corrects the balance of Th1 /Th2 and Treg /Th17 in an ovalbumin -induced asthma mouse model</style></title><secondary-title><style face="normal" font="default">Biosci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biosci Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">This study is designed to determine whether Huai Qi Huang has immuno-regulatory effects on the Th1/Th2 and Treg/Th17 balance in ovalbumin (OVA)-induced asthma model mice. Asthma model mice were constructed by OVA treatment and Huai Qi Huang was administrated. The amount of migrated in fl ammatory cells in the bronchoalveolar lavage fl uid (BALF) from the OVA mice was counted. The total immunoglobulin E (IgE) in the sera was detected by the IgE ELISA kit. Cell suspensions from the lung were stained with antibodies speci fi c for CD4 and the master transcription factors for Th1 (T-bet), Th2 (Gata-3), Th17 (RORgammat), and Treg (Foxp3). The left lobe of the lung was used to prepare a single-cell suspension for fl ow cytometry to determine whether Huai Qi Huang in fl uenced CD4(+) T-cell subsets. Histological analyses were performed by using hematoxylin and eosin staining. The mRNA expression levels of the transcription factors were detected by using qRT-PCR. Huai Qi Huang inhibited in fi ltration of in fl ammatory cells into the lung, reduced in fl ux of eosinophils (EOS), lymphocytes (LYM), neutrophils (NEU) and macrophages (MAC) in the BALF, and decreased IgE in the serum in OVA-treated mice. Huai Qi Huang could regulate Th1/Th2 and Treg/Th17 via the re-balance of cytokine pro fi les and change the mRNA expression levels of the transcription factors, T-bet/Gata-3 and Foxp3/RORgammat in OVA-treated mice. Our results showed that Huai Qi Huang could correct the imbalance of Th1/Th2 and Treg/Th17 in OVA-induced asthma model mice, indicating its effects on inhibiting the development and severity of asthma</style></abstract><notes><style face="normal" font="default">IS - 1573-4935 (Electronic)IS - 0144-8463 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1042/BSR20171071</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29162668">PM:29162668</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biosci Rep\20171121-LiangP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biosci Rep\20171121-LiangP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Liang P</style></custom2><misc3><style face="normal" font="default">10.1042/BSR20171071</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86844</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Totte,J.E.E.</style></author><author><style face="normal" font="default"> Pardo,L.M.</style></author><author><style face="normal" font="default"> Fieten,K.B.</style></author><author><style face="normal" font="default"> de Wit,J.</style></author><author><style face="normal" font="default"> de Boer,D.V.</style></author><author><style face="normal" font="default"> van Wamel,W.J.</style></author><author><style face="normal" font="default"> Pasmans,S.G.M.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Erasmus MC University Medical Centre Rotterdam, Rotterdam, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">The IgG response against Staphylococcus aureus is associated with severe atopic dermatitis in children</style></title><secondary-title><style face="normal" font="default">Br J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="30" Month="11" Year="2017">2017/11/30</year></dates><abstract><style face="normal" font="default">BACKGROUND: An altered immune response against Staphylococcus (S.) aureus might contribute to inflammation and barrier damage in atopic dermatitis (AD). OBJECTIVES: We profiled IgG antibodies against 55 S. aureus antigens in sera of children with mild to severe AD using a Luminex assay. Additionally, we evaluated the association between IgG levels and disease severity. METHODS: In this cross-sectional study, we included children with AD of two interventional study cohorts, namely SMA (n= 131) and the older DAVOS cohort (n= 76). AD severity was assessed using the Self Administrated-Eczema Area and Severity Index (SA-EASI) and levels of thymus and activation-regulated chemokine (TARC) in serum. IgG antibody levels against 55 S. aureus antigens were quantified simultaneously using a Luminex assay. Pair-wise correlations were calculated between the 55 IgG levels using the Spearman rank correlation test. A linear regression analysis was performed to test for associations between 55 IgG levels and SA-EASI and TARC adjusting for age, sex and S. aureus colonisation. RESULTS: In the SMA cohort 16 antigens were associated with SA-EASI and 12 antigens were associated with TARC (10 overlapping antigens; P-values from 0.001 to 0.044). The associated IgG antibodies targeted mainly secreted proteins with immune-modulatory functions. In the DAVOS study, IgG levels against only four and one S. aureus antigen(s) were associated with SA-EASI and TARC, respectively (no overlap). CONCLUSIONS: In young children, severity of AD is associated with an IgG response directed against S. aureus antigens with mainly immune-modulatory functions. These findings encourage further evaluation of the role of S. aureus in AD pathogenesis. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2133 (Electronic)IS - 0007-0963 (Linking)LA - engPT - Journal ArticleCO - Netherlands -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/bjd.16153</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29194572">PM:29194572</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Dermatol\20171204-TotteJE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Dermatol\20171204-TotteJE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Totte JE</style></custom2><misc3><style face="normal" font="default">10.1111/bjd.16153</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86847</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pyrhonen,K.</style></author><author><style face="normal" font="default"> Kulmala,P.</style></author><author><style face="normal" font="default"> Nayha,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Center for Life Course Health Research, University of Oulu, Oulu, Finland</style></auth-address><titles><title><style face="normal" font="default">Coincidence of pollen season with the first fetal trimester together with early pet exposure is associated with sensitisation to cat and dog allergens in early childhood: a Finnish population-based study</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">BACKGROUND: Children whose 11(th) fetal week falls in pollen season (spring) reportedly have an increased risk of sensitisation to food allergens. No such finding has been reported for pet allergens. OBJECTIVE: The aim of the study was to 1) evaluate the incidence of pet (dog and cat) sensitisation according to the season of the 11(th) fetal week and 2) whether the association between pet exposure and respective sensitisation is modified by the coincidence of the 11(th) fetal week with pollen season. METHODS: The study population comprised all children (born between 2001 and 2006) in the province of South Karelia, Finland (N=5920). Their data of IgE and skin prick tests to pet allergens (N=538) were collected from patient records and linked with questionnaire data on pet exposure. RESULTS: The seasonal incidence peak of cat sensitisation was observed in children whose 11(th) fetal week occurred in June (7.4%) and that of dog sensitisation in April (3.8%) and June (4.7%). The relative rate (RR) for cat sensitisation was 2.92 (95% CI 1.40-6.08) in children with cat exposure alone, 8.53 (4.07-17.86) in children with cat and fetal pollen exposures, and 0.61 (0.20-1.83) in children exposed to pollen alone, compared with children without these exposures. The respective RRs for dog sensitisation were 2.17 (1.13-4.19), 4.40 (2.19-8.83) and 1.65 (0.77-3.53). CONCLUSIONS AND CLINICAL RELEVANCE: Coincidence of the first fetal trimester with pollen season strengthens the association between pet exposure and respective sensitisation. Pollen exposure at early pregnancy may deviate immune system towards Th2 type reactivity promoting development of specific allergy in case allergen exposure occurred. Therefore, primary prevention of allergic diseases may need to begin during early pregnancy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Finland -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13067</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29171126">PM:29171126</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171124-PyrhonenK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171124-PyrhonenK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Pyrhonen K</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13067</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86848</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jorg,L.</style></author><author><style face="normal" font="default"> Pecaric-Petkovic,T.</style></author><author><style face="normal" font="default"> Reichenbach,S.</style></author><author><style face="normal" font="default"> Coslovsky,M.</style></author><author><style face="normal" font="default"> Stalder,O.</style></author><author><style face="normal" font="default"> Pichler,W.</style></author><author><style face="normal" font="default"> Hausmann,O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Rheumatology, Immunology and Allergology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Double-blind placebo-controlled trial of the effect of omalizumab on basophils in chronic urticaria patients</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="22" Month="11" Year="2017">2017/11/22</year></dates><abstract><style face="normal" font="default">BACKGROUND: Omalizumab has been shown to be effective in treating chronic spontaneous urticaria (CSU). The reduction of FcepsilonRI receptor density on the surface of basophils and mast cells is thought to play a major role in its effectiveness. We conducted a double-blind, randomized, placebo-controlled trial to investigate the mode of action of omalizumab in patients with antihistamine-resistant CSU. METHODS: Thirty patients were randomized in a 2:1 ratio to receive either 300 mg omalizumab or placebo. Four monthly applications of omalizumab/placebo were followed up with a visit 2 months after the last injection. The primary endpoint was the FcepsilonRI receptor density change on basophils. RESULTS: OMALIZUMAB LED TO A SIGNIFICANT REDUCTION OF FCEpsilonRI RECEPTOR DENSITY ON: basophils as soon as 1 week after the first injection: baseline omalizumab vs. placebo group, 80.31 +/- 47.18x10(3) vs. 78.29 +/- 45.09x10(3) receptors/basophil +/- SD; 1 week, 72.89 +/- 47.79x10(3) vs. 27.83 +/- 20.87x10(3), p=0.001. This effect continued during the treatment phase and persisted for 2 months after the last injection: 93.81 +/- 56.50x10(3) vs. 21.09 +/- 15.23x10(3), p=0.002. Values for basophil "releasability" and the basophil activation test (CU-BAT) of patient serum using donor basophils were unchanged despite treatment: CU-BAT, CD63 10.75% (7.35) in the placebo group vs. 8.35% (15.20) in the omalizumab group, p=0.778. CONCLUSION: We demonstrated a rapid reduction of FcepsilonRI receptor density on basophils following treatment with omalizumab. Because CU-BAT using well-characterized, omalizumab-naive donor basophils did not change during the treatment phase, autoreactive serum factors seem to remain unaltered. This points towards a cellular effect of omalizumab on basophils. To predict the omalizumab response time and to monitor disease, FcepsilonRI density and CU-BAT might be promising cellular-based assays. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13066</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29164723">PM:29164723</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171122-Jorg L.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171122-Jorg L.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171122, Jorg L</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13066</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86849</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ruethers,T.</style></author><author><style face="normal" font="default"> Raith,M.</style></author><author><style face="normal" font="default"> Sharp,M.F.</style></author><author><style face="normal" font="default"> Koeberl,M.</style></author><author><style face="normal" font="default"> Stephen,J.N.</style></author><author><style face="normal" font="default"> Nugraha,R.</style></author><author><style face="normal" font="default"> Le,T.T.K.</style></author><author><style face="normal" font="default"> Quirce,S.</style></author><author><style face="normal" font="default"> Nguyen,H.X.M.</style></author><author><style face="normal" font="default"> Kamath,S.D.</style></author><author><style face="normal" font="default"> Mehr,S.S.</style></author><author><style face="normal" font="default"> Campbell,D.E.</style></author><author><style face="normal" font="default"> Bridges,C.R.</style></author><author><style face="normal" font="default"> Taki,A.C.</style></author><author><style face="normal" font="default"> Swoboda,I.</style></author><author><style face="normal" font="default"> Lopata,A.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Molecular Allergy Research Laboratory, Division of Tropical Health and Medicine, James Cook University, Townsville, Australia</style></auth-address><titles><title><style face="normal" font="default">Characterisation of Ras k 1 a novel major allergen in Indian mackerel and identification of parvalbumin as the major fish allergen in 33 Asia-Pacific fish species</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> ASIA</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">BACKGROUND: Fish is a well-recognised cause of food allergy and anaphylaxis. The evolutionary and taxonomic diversity of the various consumed fish species poses a challenge in the identification and characterisation of the major fish allergens critical for reliable diagnostics. Globally, fish is a rising cause of food allergy complicated by a large under-investigated variety of species as well as increasing global tourism and trade. This is the first comprehensive study on allergen profiles of heat-processed fish from Vietnam. OBJECTIVE: The aim of this study was to identify the major heat-stable allergens from frequently exported Asia-Pacific freshwater and marine fish, and characterise the major allergen parvalbumin (PV) from one of the most consumed and exported fish species from Asia, the Indian mackerel (Rastrelliger kanagurta). METHODS: Heated protein extracts from 33 fish species were separated by gel-electrophoresis. PV isoforms were identified by immunoblotting utilising three different PV-specific monoclonal and polyclonal antibodies and further characterised by mass spectrometry. IgE reactivity was investigated using sera from 21 patients with confirmed fish allergy. RESULTS: Heat stable IgE-reactive PVs, with up to five isoforms per species, were identified in all 33 analysed fish species. In the Indian mackerel, seven PV isoforms were identified by 2D-gel electrophoresis combined with mass spectrometric analyses. The amino acid sequence deduced from cDNA of the most expressed isoform showed a high identity (>90%) to PVs from two other mackerel species. CONCLUSIONS &amp; CLINICAL RELEVANCE: Different PVs were identified as the major heat-stable allergens in all 33 analysed freshwater and marine fish species from Vietnam, many of which are exported worldwide and 21 species that have never been investigated before. The Indian mackerel PV represents a novel fish allergen, now officially registered as Ras k 1. Improved diagnostics for fish allergy against Asia-Pacific species should be developed with focus on PV. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Australia -CO - Austria -CO - Spain -CO - Viet Nam -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13069</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29193486">PM:29193486</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171128-RuethersT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171128-RuethersT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171128, Ruethers T</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13069</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86850</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Geiselhart,S.</style></author><author><style face="normal" font="default"> Nagl,C.</style></author><author><style face="normal" font="default"> Dubiela,P.</style></author><author><style face="normal" font="default"> Pedersen,A.C.</style></author><author><style face="normal" font="default"> Bublin,M.</style></author><author><style face="normal" font="default"> Radauer,C.</style></author><author><style face="normal" font="default"> Bindslev-Jensen,C.</style></author><author><style face="normal" font="default"> Hoffmann-Sommergruber,K.</style></author><author><style face="normal" font="default"> Mortz,C.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pathophysiology and Allergy Research, Medical University of Vienna, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Concomitant sensitization to legumin, Fag e 2 and Fag e 5 predicts buckwheat allergy</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">BACKGROUND: Buckwheat (Fagopyrum esculentum) has become increasingly popular as a healthy food in Europe. However, for sensitized individuals, consumption can cause anaphylactic reactions. The aim of this study was to identify individual well-characterized buckwheat allergens for component resolved diagnosis. METHODS: Patients were selected by positive skin prick test to buckwheat and divided into two groups: (1) sensitized to buckwheat without clinical symptoms and (2) buckwheat allergy. Buckwheat proteins were extracted from raw buckwheat seeds, purified applying a combination of protein precipitation and chromatographic methods and analyzed by IgE immunoblotting and ELISA. RESULTS: Buckwheat-allergic patients had a significantly larger median skin prick test wheal diameter for buckwheat than the sensitized group and the positive control. Also, IgE-immunoblotting clearly showed a distinct pattern in sera from allergic patients when compared to sensitized individuals. Several IgE-reactive proteins were purified from crude buckwheat extract, namely legumin (Fag e 1 plus its large subunit), Fag e 2 (2S albumin), and newly identified Fag e 5 (vicilin-like) as well as hevein-like antimicrobial peptides, designated Fag e 4. All four allergens showed superior diagnostic precision compared to extract-based ImmunoCAP with high sensitivity as well as high specificity. CONCLUSIONS: Patients with clinical symptoms clearly show a distinct allergen recognition pattern. We characterized a buckwheat vicilin-like protein as a new relevant marker allergen, designated Fag e 5. Additionally, another new allergen, Fag e 4, potentially important for cross-reactivity to latex was added to the allergen panel of buckwheat. Further, our data show that the full-length legumin comprising both, large and small subunit should be applied for component resolved diagnosis. Our data indicate that concomitant sensitization to legumin, Fag e 2 and Fag e 5 predicts buckwheat allergy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13068</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29171912">PM:29171912</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171124-GeiselhartS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171124-GeiselhartS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Geiselhart S</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13068</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86851</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shimizu,S.</style></author><author><style face="normal" font="default"> Takezawa-Yasuoka,K.</style></author><author><style face="normal" font="default"> Ogawa,T.</style></author><author><style face="normal" font="default"> Tojima,I.</style></author><author><style face="normal" font="default"> Kouzaki,H.</style></author><author><style face="normal" font="default"> Shimizu,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otorhinolaryngology, Shiga University of Medical Science, Otsu, Shiga, Japan.</style></auth-address><titles><title><style face="normal" font="default">The epidermal growth factor receptor inhibitor AG1478 inhibits eosinophilic inflammation in upper airways</style></title><secondary-title><style face="normal" font="default">Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="25" Month="11" Year="2017">2017/11/25</year></dates><abstract><style face="normal" font="default">Mucus hypersecretion and eosinophil infiltration are important characteristics of eosinophilic inflammation in upper airways, such as allergic rhinitis and chronic rhinosinusitis with nasal polyp. EGFR transactivation induces mucus and inflammatory cytokine secretion from airway epithelial cells. However, the roles of EGFR in eosinophilic inflammation in upper airways are still unknown. The purpose of the study is to elucidate the effects of the EGFR inhibitor AG1478 on eosinophilic airway inflammation. AG1478 significantly inhibited thrombin-induced GM-CSF secretion from nasal epithelial cells and thrombin-induced secretion of eotaxin-1 and RANTES from nasal fibroblasts. Intranasal instillation of AG1478 inhibited OVA-induced goblet cell metaplasia, mucus production and eosinophil/neutrophil infiltration in rat nasal epithelium, as did intraperitoneal injection of AG1478. These results indicate that EGFR transactivation plays an important role in eosinophilic airway inflammation. Intranasal instillation of an EGFR inhibitor may be a new therapeutic approach for the treatment of intractable eosinophilic inflammation in upper airways</style></abstract><notes><style face="normal" font="default">IS - 1521-7035 (Electronic)IS - 1521-6616 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.clim.2017.11.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29183867">PM:29183867</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Immunol\20171125-ShimizuS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Immunol\20171125-ShimizuS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171125, Shimizu S</style></custom2><misc3><style face="normal" font="default">10.1016/j.clim.2017.11.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86857</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Calzada,D.</style></author><author><style face="normal" font="default"> Baos,S.</style></author><author><style face="normal" font="default"> Cremades,L.</style></author><author><style face="normal" font="default"> Cardaba,B.O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunology Department, IIS-Fundacion Jimenez Diaz, UAM, Madrid. Spain</style></auth-address><titles><title><style face="normal" font="default">New treatments for allergy: Advances in peptide immunotherapy</style></title><secondary-title><style face="normal" font="default">Curr Med Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Med Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="30" Month="11" Year="2017">2017/11/30</year></dates><abstract><style face="normal" font="default">BACKGROUND: Nowadays, allergen-specific immunotherapy (AIT) is the only treatment able to modulate the course of allergic diseases. Although it has been applied for the last 100 years, treatment with whole allergen extracts is not without its drawbacks: AIT can cause local and systemic adverse events and may produce new IgE sensitization against other allergens present in the extract. Furthermore, the lengthy treatment duration (3-5 years), frequent administration, and high cost of treatment are other disadvantages. For these reasons, there is a need for safer and more effective AIT strategies. One promising approach is the use of synthetic peptides representing the B- or T-cell epitopes of allergens. OBJECTIVE: This review summarizes the main advances in peptide immunotherapy, from preclinical models to early clinical trials, focusing on house dust mite, bee venom, cat allergy, and Oleaceae pollinosis. RESULTS: Following an extensive review of the relevant literature, we summarize how peptide therapies may change the course of allergic diseases and promote allergen tolerance, thereby ameliorating the main disadvantages of AIT. Although the molecular mechanisms involved are not yet fully defined, they seem to depend on structure, length, peptide sequence, and route of administration. This novel immunotherapy has been demonstrated to modulate the immune system, promoting regulatory T-cell induction and Th2 inhibition. This tolerance-inducing potential has led this therapy to be termed SPIRE (synthetic peptide immuno-regulatory epitopes). CONCLUSION: Experimental models and clinical trials have demonstrated the usefulness of SPIRE treatment to cure these diseases, opening a new era in allergen therapeutics</style></abstract><notes><style face="normal" font="default">IS - 1875-533X (Electronic)IS - 0929-8673 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.2174/0929867325666171201114353</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29205109">PM:29205109</url></web-urls></urls><custom2><style face="normal" font="default">20171130, Calzada D</style></custom2><misc3><style face="normal" font="default">10.2174/0929867325666171201114353</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86860</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Heidinger,A.</style></author><author><style face="normal" font="default"> Rabensteiner,D.F.</style></author><author><style face="normal" font="default"> Rabensteiner,J.</style></author><author><style face="normal" font="default"> Kieslinger,P.</style></author><author><style face="normal" font="default"> Horwath-Winter,J.</style></author><author><style face="normal" font="default"> Stabentheiner,E.</style></author><author><style face="normal" font="default"> Riedl,R.</style></author><author><style face="normal" font="default"> Wedrich,A.</style></author><author><style face="normal" font="default"> Schmut,O.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Ophthalmology , Medical University of Graz , Auenbruggerplatz 4 , 8036 Graz , Austria</style></auth-address><titles><title><style face="normal" font="default">Decreased viability and proliferation of Chang conjunctival epithelial cells after contact with ultraviolet light-irradiated pollen</style></title><secondary-title><style face="normal" font="default">Cutan Ocul Toxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Cutan Ocul Toxicol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">Context - Contact with pollen is the major reason for the development of allergic symptoms on the ocular surface leading to a significant increase of allergic diseases worldwide. Environmental changes such as increased ultraviolet (UV) radiation and air pollution are discussed as contributory causes for this increase. Objective - We investigated the effect of ultraviolet (UV) light on the histamine content of pollen and examined if an irradiation of pollen affects the viability and proliferation of conjunctival cells. Materials and Methods - Alder (Alnus glutinosa) and hazel (Corylus avellana) pollen were irradiated for different time periods with sunlight, UV-A or UV-B light and the histamine content was analysed and compared with non-irradiated pollen. Conjunctival epithelial cells (CHANG cells) were exposed to irradiated and non-irradiated pollen followed by an assessment of cell viability with the colorimetric MTS test and the impedance based measurement of cell proliferation using the xCELLigence real time analysis system. Results - UV light irradiation increased the histamine level of alder and hazelnut pollen in a dose dependent manner. CHANG cells treated with irradiated pollen induced a statistically significant higher decrease of cell viability than treatment with non-irradiated pollen. Discussion and conclusion - Our results indicate that UV light is able to alter pollen thus making them more harmful for conjunctival cells</style></abstract><notes><style face="normal" font="default">IS - 1556-9535 (Electronic)IS - 1556-9527 (Linking)LA - engPT - Journal ArticleCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1080/15569527.2017.1414226</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29216751">PM:29216751</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Cutan Ocul Toxicol\20171207-HeidingerA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Cutan Ocul Toxicol\20171207-HeidingerA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Heidinger A</style></custom2><misc3><style face="normal" font="default">10.1080/15569527.2017.1414226</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86861</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Castillo,E.F.</style></author><author><style face="normal" font="default"> Zheng,H.</style></author><author><style face="normal" font="default"> Yang,X.O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, USA.</style></auth-address><titles><title><style face="normal" font="default">Orchestration of epithelial-derived cytokines and innate immune cells in allergic airway inflammation</style></title><secondary-title><style face="normal" font="default">Cytokine Growth Factor Rev</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Cytokine Growth Factor Rev</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">Allergic asthma, a chronic respiratory disease, is a leading worldwide health problem, which inflames and constricts the airways, leading to breathing difficulty. Many studies have focused on the pathogenesis contributed by the adaptive immune system, including CD4(+) T lymphocytes in delayed type hypersensitivity and B cell-produced IgE in anaphylaxis. More recently, a focus on the airway mucosal barrier and the innate immune system has highlighted, in coordination with T and B cells, to initiate and establish disease. This review highlights the impacts of epithelial-derived cytokines and innate immune cells on allergic airway reactions</style></abstract><notes><style face="normal" font="default">IS - 1879-0305 (Electronic)IS - 1359-6101 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.cytogfr.2017.11.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29169815">PM:29169815</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Cytokine Growth Factor Rev\20171121-CastilloEF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Cytokine Growth Factor Rev\20171121-CastilloEF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Castillo EF</style></custom2><misc3><style face="normal" font="default">10.1016/j.cytogfr.2017.11.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86865</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Incorvaia,C.</style></author><author><style face="normal" font="default"> Martignago,I.</style></author><author><style face="normal" font="default"> Ridolo,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Can the Pattern of Early Sensitization to Allergen Molecules Drive a New Approach for Prevention of Allergy?</style></title><secondary-title><style face="normal" font="default">EBioMedicine</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">EBioMedicine</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2352-3964</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.ebiom.2017.11.016</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29257749">PM:29257749</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\EBioMedicine\20171122-IncorvaiaC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\EBioMedicine\20171122-IncorvaiaC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171122, Incorvaia C</style></custom2><misc3><style face="normal" font="default">10.1016/j.ebiom.2017.11.016</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86866</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wickman,M.</style></author><author><style face="normal" font="default"> Lupinek,C.</style></author><author><style face="normal" font="default"> Andersson,N.</style></author><author><style face="normal" font="default"> Belgrave,D.</style></author><author><style face="normal" font="default"> Asarnoj,A.</style></author><author><style face="normal" font="default"> Benet,M.</style></author><author><style face="normal" font="default"> Pinart,M.</style></author><author><style face="normal" font="default"> Wieser,S.</style></author><author><style face="normal" font="default"> Garcia-Aymerich,J.</style></author><author><style face="normal" font="default"> Baar,A.</style></author><author><style face="normal" font="default"> Pershagen,G.</style></author><author><style face="normal" font="default"> Simpson,A.</style></author><author><style face="normal" font="default"> Kull,I.</style></author><author><style face="normal" font="default"> Bergstrom,A.</style></author><author><style face="normal" font="default"> Melen,E.</style></author><author><style face="normal" font="default"> Hamsten,C.</style></author><author><style face="normal" font="default"> Anto,J.M.</style></author><author><style face="normal" font="default"> Bousquet,J.</style></author><author><style face="normal" font="default"> Custovic,A.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author><author><style face="normal" font="default"> van Hage,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Detection of IgE Reactivity to a Handful of Allergen Molecules in Early Childhood Predicts Respiratory Allergy in Adolescence</style></title><secondary-title><style face="normal" font="default">EBioMedicine</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">EBioMedicine</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Prediction</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2352-3964</style></isbn><abstract><style face="normal" font="default">Sensitization in early childhood may precede respiratory allergy in adolescence. IgE reactivity against 132 allergen molecules was evaluated using the MeDALL micro-array in sera obtained from a random sample of 786 children at the age of 4, 8 and 16years in a population based birth cohort (BAMSE). Symptoms were analyzed by questionnaire at ages 4, 8 and 16years. Clinically and independent relevant allergen molecules accounting for </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ90% of IgE reactivities in sensitized individuals and at all time-points were identified as risk molecules and used to predict respiratory allergy. The data was replicated in the Manchester Asthma and Allergy Study (MAAS) birth cohort by studying IgE reactivity with the use of a commercial IgE micro-array. Sera was obtained from children at the ages of 3, 5, 8 and 11years (N=248) and the outcome was studied at 11years. In the BAMSE cohort 4 risk molecules could be identified, i.e.: Ara h 1 (peanut), Bet v 1 (birch), Fel d 1 (cat), Phl p 1 (grass). For MAAS the corresponding number of molecules was 5: Der p 1 (dust mite), Der f 2 (dust mite), Phlp 1 (grass), Phl p 5 (grass), Fel d 1 (cat). In BAMSE, early IgE reactivity to </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ3 of 4 allergen molecules at four years predicted incident and persistent asthma and/or rhinitis at 16years (87%, and 95%, respectively). The corresponding proportions in the MAAS cohort, 16years were 100% and 100%, respectively for IgE reactivity to </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ3 of 5 risk molecules. IgE reactivity to a few allergen molecules early in life identifies children with a high risk of asthma and/or rhinitis at 16years. These findings will be of importance for developing preventive strategies for asthma and rhinitis in children</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Sweden -CO - Austria -CO - United Kingdom -CO - Spain -CO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.ebiom.2017.11.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29221963">PM:29221963</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\EBioMedicine\20171114-WickmanM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\EBioMedicine\20171114-WickmanM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Wickman M</style></custom2><misc3><style face="normal" font="default">10.1016/j.ebiom.2017.11.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86867</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Buquicchio,R.</style></author><author><style face="normal" font="default"> Ventura,M.T.</style></author><author><style face="normal" font="default"> Traetta,P.L.</style></author><author><style face="normal" font="default"> Nenna,S.</style></author><author><style face="normal" font="default"> Iadarola,G.</style></author><author><style face="normal" font="default"> Magrone,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dermatological Clinic, Department of Biomedical Science and Human Oncology, University of Bari Medical School, Policlinico, Bari. Italy</style></auth-address><titles><title><style face="normal" font="default">IgE sensitization to Anisakis simplex and diet recommendation in a polycentric study</style></title><secondary-title><style face="normal" font="default">Endocr Metab Immune Disord Drug Targets</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Endocr Metab Immune Disord Drug Targets</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergy to Anisakis simplex (s.) is spreading due to the increased consumption of raw, smoked or marinated fish. In humans, Anisakis s. can directly attack the gastrointestinal mucosa, provoking a parasitosis known as anisakiasis, or giving rise to the formation of IgE and, finally, inducing IgE-mediated reactions like urticaria, angioedema and anaphylactic shock. During recent years, a dietary approach to Anisakis s. infestation has also been addressed. METHODS: A total of 620 patients with urticaria, angioedema, or both and a history of anaphylaxis following consumption of raw, smoked or marinated fish were recruited, evaluated for specific IgE levels to Anisakis s. and subjected to skin prick test. Following 18 month fish-free diet, patients were re-evaluated at 6, 12 and 18 months, respectively. RESULTS: After 6-month fish-free diet, we recorded an improvement of symptoms and a remarkable reduction of specific IgE levels. The extension of the diet over 6 months in some cases resulted in a further reduction of specific IgE levels. CONCLUSION: Data obtained confirm the importance of a fish-free diet in patients with severe symptoms since a new antigenic exposure coincides with a relapse of symptoms and increased IgE levels. This last point should be kept in mind and carefully evaluated in patients at risk for anaphylaxis or angioedema</style></abstract><notes><style face="normal" font="default">IS - 2212-3873 (Electronic)IS - 1871-5303 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.2174/1871530318666171129211350</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29189183">PM:29189183</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171129, Buquicchio R</style></custom2><misc3><style face="normal" font="default">10.2174/1871530318666171129211350</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86868</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sowiak,M.</style></author><author><style face="normal" font="default"> Kozajda,A.</style></author><author><style face="normal" font="default"> Jezak,K.</style></author><author><style face="normal" font="default"> Szadkowska-Stanczyk,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Nofer Institute of Occupational Medicine, 8 Teresy Str, 91-348, Lodz, Poland</style></auth-address><titles><title><style face="normal" font="default">Does the air condition system in busses spread allergic fungi into driver space?</style></title><secondary-title><style face="normal" font="default">Environ Sci Pollut Res Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Environ Sci Pollut Res Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">The aim of this study was to establish whether the air-conditioning system in buses constitutes an additional source of indoor air contamination with fungi, and whether or not the fungi concentration depends on the period from the last disinfection of the system, combined with replacement of the cabin dust particle filter. The air samples to fungi analysis using impact method were taken in 30 buses (20 with an air-conditioning system, ACS; 10 with a ventilation system, VS) in two series: 1 and 22 weeks after cabin filter replacement and disinfection of the air-conditioning system. During one test in each bus were taken two samples: before the air-conditioning or ventilation system switched on and 6 min after operating of these systems. The atmospheric air was the external background (EB). After 1 week of use of the system, the fungi concentrations before starting of the ACS and VS system were 527.8 and 1053.0 cfu/m(3), respectively, and after 22 weeks the concentrations were 351.9 and 1069.6 cfu/m(3), respectively. While in the sample after 6 min of ACS and VS system operating, the fungi concentration after 1 week of use was 127.6 and 233.7 cfu/m(3), respectively, and after 22 weeks it was 113.3 and 324.9 cfu/m(3), respectively. Results do not provide strong evidence that air-conditioning system is an additional source of indoor air contamination with fungi. A longer operation of the system promoted increase of fungi concentration in air-conditioned buses only</style></abstract><notes><style face="normal" font="default">IS - 1614-7499 (Electronic)IS - 0944-1344 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1007/s11356-017-0830-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29209965">PM:29209965</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Environ Sci Pollut Res Int\20171205-SowiakM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Environ Sci Pollut Res Int\20171205-SowiakM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Sowiak M</style></custom2><misc3><style face="normal" font="default">10.1007/s11356-017-0830-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86871</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Purschke,B.</style></author><author><style face="normal" font="default"> Meinlschmidt,P.</style></author><author><style face="normal" font="default"> Horn,C.</style></author><author><style face="normal" font="default"> Rieder,O.</style></author><author><style face="normal" font="default"> Jager,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Improvement of techno-functional properties of edible insect protein from migratory locust by enzymatic hydrolysis</style></title><secondary-title><style face="normal" font="default">Eur Food Res Technol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Eur Food Res Technol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Flour</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1438-2385</style></isbn><abstract><style face="normal" font="default">Enzymatic hydrolysis of migratory locust (Locusta migratoria L.) protein flour (MLPF) was investigated as a method to improve the techno-functional properties. Experiments were conducted under variation of the applied proteases (Alcalase, Neutrase, Flavourzyme, Papain) or combinations thereof, enzyme</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çôsubstrate ratio (0.05</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô1.0% w/w), heat pre-treatment (60</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô80-á-¦C; 15</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô60-ámin), and hydrolysis time (0</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô24-áh). Protein degradation was monitored in terms of degree of hydrolysis (DH) and SDS-PAGE. Solubility, emulsifying, foaming and water/oil binding properties of the hydrolysates were determined. In comparison to the control (DH</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë=</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë5%), hydrolysis resulted in considerably higher DH values up to 42%. SDS-PAGE profiles revealed a steady decrease of bands between 25 and 75-ákDa and an increase of low molecular weight bands (10</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô15-ákDa). However, different heat pre-treatments resulted in impaired hydrolytic cleavage as evidenced by lower DH values. Protein solubility of MLPF hydrolysates was improved over a broad pH range from initially 10</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô22% up to 55% at alkaline conditions. Furthermore, hydrolysis resulted in enhanced emulsifying activity (54%) at pH 7, improved foamability (326%) at pH 3 and advanced oil binding capacity. The results of this study have clearly demonstrated the potential of targeted enzymatic degradation to improve the techno-functionality of migratory locust protein in order to produce tailored insect-based ingredients for the use in food applications</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1007/s00217-017-3017-9</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s00217-017-3017-9</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Food Res Technol\20171202-PurschkeB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Food Res Technol\20171202-PurschkeB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Purschke B</style></custom2><misc3><style face="normal" font="default">10.1007/s00217-017-3017-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86872</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kalogianni Despina,P.</style></author></authors></contributors><titles><title><style face="normal" font="default">DNA-based analytical methods for milk authentication</style></title><secondary-title><style face="normal" font="default">Eur Food Res Technol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Eur Food Res Technol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1438-2385</style></isbn><abstract><style face="normal" font="default">Milk adulteration is a globally upcoming problem that concerns consumers, food industries and control authorities. Milk authenticity testing of dairy products is necessary, to protect consumers from fraudulent products, mislabeling and health risks and avoid unfair competition of food industries. Milk-based products produced by milk from specific animal origin are considered as healthier dairy products compared to others, leading to widespread acceptance of the consumers and food industries. This has made these animal-originated products extremely vulnerable to substitution with cheaper milk for economic profit. In addition, milk derived from specific animals (e.g., bovine) has been accused for allergenicity issues and other health problems, especially to sensitive human groups. Therefore, there is a great need for sensitive, accurate and quantitative analytical methods for milk adulteration detection in raw and processed milk-based products</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Greece -</style></notes><work-type><style face="normal" font="default">10.1007/s00217-017-3016-x</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s00217-017-3016-x</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Food Res Technol\20171130-KalogianniDespinaP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Food Res Technol\20171130-KalogianniDespinaP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171130, Kalogianni Despina P</style></custom2><misc3><style face="normal" font="default">10.1007/s00217-017-3016-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86873</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kong,F.</style></author><author><style face="normal" font="default"> Martin,D.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Rheumatology and Allergy, Xuanwu Hospital, Capital Medical University, Beijing, ChinaDepartment of Pediatrics and Communicable Diseases, The University of Michigan Medical School, Ann Arbor, MI, USA; Department of Human Genetics, The University of Michigan Medical School, Ann Arbor, MI, USA. Electronic address: donnamm@umich.edu</style></auth-address><titles><title><style face="normal" font="default">Atopic disorders in CHARGE syndrome: A retrospective study and literature review</style></title><secondary-title><style face="normal" font="default">Eur J Med Genet</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur J Med Genet</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">BACKGROUND: Atopic disorders have been reported in CHARGE syndrome, but the prevalence and underlying mechanisms are not known. METHODS: We performed a retrospective study of atopic disorders in 23 individuals with CHARGE syndrome, and reviewed other published reports of atopic disorders in CHARGE syndrome. We assayed for enrichment of atopic disorders in CHARGE syndrome based on gender and presence of a CHD7 pathogenic variant. RESULTS: In our cohort, 65% (15/23) of individuals with CHARGE syndrome were found to have a pathogenic CHD7 variant. Overall, 65% (15/23) of individuals with CHARGE had atopic disorders. Among the 23 individuals with CHARGE, 22% (5/23) had food allergy, 26% (6/23) exhibited drug allergy, 22% (5/23) had contact allergy, 9% (2/23) had allergic rhinitis, and 22% (5/23) had asthma. In our cohort, the proportion of males to females with CHARGE and atopic disorders was 11:4 (P &lt; 0.01), and there was no significant difference between atopic disorders in individuals with CHD7 pathogenic variants and those without CHD7 pathogenic variants (P > 0.05). CONCLUSION: In our cohort of 23 individuals with CHARGE syndrome, 15 (65%) exhibited atopic disorders, with a slight male predominance</style></abstract><notes><style face="normal" font="default">IS - 1878-0849 (Electronic)IS - 1769-7212 (Linking)LA - engPT - Journal ArticleCO - China -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.ejmg.2017.11.019</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29191495">PM:29191495</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur J Med Genet\20171127-KongF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur J Med Genet\20171127-KongF.pdf</url></text-urls><related-urls><url ppv-ref="no">suppl. non funzionante</url></related-urls></urls><custom2><style face="normal" font="default">20171127, Kong F</style></custom2><misc3><style face="normal" font="default">10.1016/j.ejmg.2017.11.019</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86874</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yu,L.</style></author><author><style face="normal" font="default"> Liu,Q.</style></author><author><style face="normal" font="default"> Canning,B.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Medicine, Tongji Hospital, Tongii University School of Medicine, Shanghai 200065, China</style></auth-address><titles><title><style face="normal" font="default">Evidence for autocrine and paracrine regulation of allergen-induced mast cell mediator release in the guinea pig airways</style></title><secondary-title><style face="normal" font="default">Eur J Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur J Pharmacol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">Mast cells play an essential role in immediate type hypersensitivity reactions and in chronic allergic diseases of the airways, including asthma. Mast cell mediator release can be modulated by locally released autacoids and circulating hormones, but surprisingly little is known about the autocrine effects of mediators released upon mast cell activation. We thus set out to characterize the autocrine and paracrine effects of mast cell mediators on mast cell activation in the guinea pig airways. By direct measures of histamine, cysteinyl-leukotriene and thromboxane release and with studies of allergen-evoked contractions of airway smooth muscle, we describe a complex interplay amongst these autacoids. Notably, we observed an autocrine effect of the cysteinyl-leukotrienes acting through cysLT1 receptors on mast cell leukotriene release. We confirmed the results of previous studies demonstrating a marked enhancement of mast cell mediator release following cyclooxygenase inhibition, but we have extended these results by showing that COX-2 derived eicosanoids inhibit cysteinyl-leukotriene release and yet are without effect on histamine release. Given the prominent role of COX-1 inhibition in aspirin-sensitive asthma, these data implicate preformed mediators stored in granules as the initial drivers of these adverse reactions. Finally, we describe the paracrine signaling cascade leading to thromboxane synthesis in the guinea pig airways following allergen challenge, which occurs indirectly, secondary to cysLT1 receptor activation on structural cells and/ or leukocytes within the airway wall, and a COX-2 dependent synthesis of the eicosanoid. The results highlight the importance of cell-cell and autocrine interactions in regulating allergic responses in the airways</style></abstract><notes><style face="normal" font="default">IS - 1879-0712 (Electronic)IS - 0014-2999 (Linking)LA - engPT - Journal ArticleCO - China -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.ejphar.2017.11.017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29157985">PM:29157985</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur J Pharmacol\20171120-YuL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur J Pharmacol\20171120-YuL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Yu L</style></custom2><misc3><style face="normal" font="default">10.1016/j.ejphar.2017.11.017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86875</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,J.R.</style></author><author><style face="normal" font="default"> Perumalsamy,H.</style></author><author><style face="normal" font="default"> Shin,H.M.</style></author><author><style face="normal" font="default"> Lee,S.G.</style></author><author><style face="normal" font="default"> Ahn,Y.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Experiment and Analysis Division, Animal and Plant Quarantine Agency, Honam Regional Office, Gunsan-si, Jeollabuk-do, 54096, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Toxicity of Juniperus oxycedrus oil constituents and related compounds and the efficacy of oil spray formulations to Dermatophagoides farinae (Acari: Pyroglyphidae)</style></title><secondary-title><style face="normal" font="default">Exp Appl Acarol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Exp Appl Acarol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">The American house dust mite (AHDM), Dermatophagoides farinae Hughes (Acari: Pyroglyphidae), is recognized as an important source of allergens in the domestic environment. This study was conducted to determine whether 19 constituents from essential oil of cade, Juniperus oxycedrus L. (Cupressaceae), eight structurally related compounds, and another 16 previously known cade oil constituents were toxic for adult AHDMs and to determine the route of acaricidal action of the test compounds, as well as to assess the control efficacy of four experimental spray formulations containing the oil (10-40 mg/L sprays). In a fabric-circle contact mortality bioassay, methyleugenol (LD50, 5.82 microg/cm(2)) and guaiacol (8.24 microg/cm(2)) were the most toxic compounds against the mites, and the toxicity of these compounds and benzyl benzoate did not significantly differ. High toxicity was also observed with eugenol, m-cresol, and nerolidol (LD50, 12.52-19.52 microg/cm(2)), and these compounds were significantly more toxic than N,N-diethyl-3-methylbenzamide (DEET) (LD50, 37.67 microg/cm(2)). Cade applied as 30 or 40 mg/L experimental sprays provided 96 and 100% mortality against the mites, respectively, whereas permethrin (cis:trans, 25:75) 2.5 g/L spray treatment resulted in 17% mortality. In vapor-phase mortality tests, the compounds described were consistently more toxic in closed versus open containers, indicating that toxicity was achieved mainly through the action of vapor. Reasonable mite control in indoor environments can be achieved by spray formulation containing the 40 mg/L cade oil as potential contact-action fumigants</style></abstract><notes><style face="normal" font="default">IS - 1572-9702 (Electronic)IS - 0168-8162 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1007/s10493-017-0201-3</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29181675">PM:29181675</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Exp Appl Acarol\20171127-KimJR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Exp Appl Acarol\20171127-KimJR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171127, Kim JR</style></custom2><misc3><style face="normal" font="default">10.1007/s10493-017-0201-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86876</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Urbanova,A.</style></author><author><style face="normal" font="default"> Medvedova,I.</style></author><author><style face="normal" font="default"> Kertys,M.</style></author><author><style face="normal" font="default"> Mikolka,P.</style></author><author><style face="normal" font="default"> Kosutova,P.</style></author><author><style face="normal" font="default"> Mokra,D.</style></author><author><style face="normal" font="default"> Mokry,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Pharmacology , Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava , Martin , Slovakia</style></auth-address><titles><title><style face="normal" font="default">Dose dependent effects of tadalafil and roflumilast on ovalbumin-induced airway hyperresponsiveness in guinea pigs</style></title><secondary-title><style face="normal" font="default">Exp Lung Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Exp Lung Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword></keywords><dates><year Day="8" Month="12" Year="2017">2017/12/8</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Chronic obstructive diseases of airways associated with cough and/or airway smooth muscle hyperresponsiveness are usually treated with bronchodilating and anti-inflammatory drugs. Recently, selective phosphodiesterase (PDE) 4 inhibitors have been introduced into the therapy of chronic obstructive pulmonary disease. Several studies have demonstrated their ability to influence the airway reactivity and eosinophilic inflammation by increasing the intracellular cAMP concentrations also in bronchial asthma. Furthermore, the expression of PDE5 in several immune cells suggests perspectives of PDE5 inhibitors in the therapy of inflammation, as well. PURPOSE: The aim of this study was to assess the dose-dependent effects of PDE4 and PDE5 inhibitors in allergic inflammation. Therefore, the effects of 7-days administration of PDE4 inhibitor roflumilast and PDE5 inhibitor tadalafil at two different doses in experimentally-induced allergic inflammation were evaluated. MATERIALS AND METHODS: In the study, male adult guinea pigs were used. Control group was non-sensitized. Other animals were sensitized with ovalbumin over two weeks and thereafter treated intraperitoneally for 7 days with roflumilast or tadalafil (daily dose 0.5 mg/kg or 1.0 mg/kg b.w.), or with vehicle. RESULTS: Both roflumilast and tadalafil reduced specific airway resistance after nebulization of histamine (marker of in vivo airway reactivity) at both doses used. The in vitro airway reactivity to cumulative doses of acetylcholine was significantly reduced for roflumilast at higher dose, predominantly in the lung tissue strips. Histamine-induced contractile responses were significantly influenced in both lung and tracheal tissue strips, predominantly at the higher doses. Tadalafil led to a decrease in contractile responses induced by both acetylcholine and histamine, with more significant effects in the lung tissue strips. These changes were associated with decreased numbers of circulating leukocytes and eosinophils and concentrations of interleukin (IL)-4, IL-5 and TNF-alpha in the lung homogenate. CONCLUSIONS: The selective PDE4 and PDE5 inhibitors alleviated allergic airway inflammation, with more significant effects at the higher doses</style></abstract><notes><style face="normal" font="default">IS - 1521-0499 (Electronic)IS - 0190-2148 (Linking)LA - engPT - Journal ArticleCO - Slovakia -</style></notes><work-type><style face="normal" font="default">10.1080/01902148.2017.1386735</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29220595">PM:29220595</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Exp Lung Res\20172408-UrbanovaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Exp Lung Res\20172408-UrbanovaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20172408, Urbanova A</style></custom2><misc3><style face="normal" font="default">10.1080/01902148.2017.1386735</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86877</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rodriguez,H.</style></author><author><style face="normal" font="default"> Gonzalez,A.F.</style></author><author><style face="normal" font="default"> Abollo,E.</style></author><author><style face="normal" font="default"> Pascual,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Re-evaluation of anchovies (Engraulis encrasicolus) as an important risk factor for sensitization to zoonotic nematodes in Spain</style></title><secondary-title><style face="normal" font="default">Fish Res</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Fish Res</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anchovy</style></keyword><keyword><style face="normal" font="default"> Anisakidosis</style></keyword><keyword><style face="normal" font="default"> Anisakis</style></keyword><keyword><style face="normal" font="default"> Hysterothylacium</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Zoonotic parasites</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0165-7836</style></isbn><abstract><style face="normal" font="default">In recent years, scientific evidence from clinical case studies has been accumulated to suggest that consumption of homemade raw anchovies (Engraulis encrasicolus) in vinegar (referred to locally as </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£boquerones en vinagre</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ) represented the main potential risk source for anisakiasis and IgE sensitization to Anisakis in Spain. Conversely, most epidemiological surveys for this fish species in fishing grounds along the Spanish coast and in Spanish markets showed parasite-free fish lots or parasite prevalence below 10%. In order to update the anchovy infection data and to re-evaluate the importance of this species as a potential source of risk exposure to zoonotic and allergy diseases, 956 anchovies collected by Spanish commercial fishing vessels operating in NE Atlantic fishing grounds were analyzed, using a high performance methodology. Results revealed an overall mean prevalence for zoonotic nematodes (genera Anisakis and Hysterothylacium combined) of 64.33% (14.75% in the flesh). Infection values reached 87% in one of the lots. Prevalence in anchovy muscle was 28.65%, which represents the highest value of parasitization of the flesh ever reported for European stocks of this species. An enhanced risk communication plan focused on control measures, such as removal of anchovy viscera by retailers, and educational campaigns stressing the importance of freezing anchovies that are intended for raw consumption, may clearly contribute to avoid this emergent biohazard in seafood</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.fishres.2017.11.013</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.fishres.2017.11.013</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Fish Res\20171126-RodriguezH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Fish Res\20171126-RodriguezH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171126, Rodriguez H</style></custom2><misc3><style face="normal" font="default">10.1016/j.fishres.2017.11.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86881</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,W.</style></author><author><style face="normal" font="default"> Tu,Z.</style></author><author><style face="normal" font="default"> Wang,H.</style></author><author><style face="normal" font="default"> Zhang,L.</style></author><author><style face="normal" font="default"> Kaltashov,I.A.</style></author><author><style face="normal" font="default"> Zhao,Y.</style></author><author><style face="normal" font="default"> Niu,C.</style></author><author><style face="normal" font="default"> Yao,H.</style></author><author><style face="normal" font="default"> Ye,W.</style></author></authors></contributors><auth-address><style face="normal" font="default">State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, Jiangxi, 330047, P. R. China.</style></auth-address><titles><title><style face="normal" font="default">The mechanism of reduced IgG/IgE-binding of beta-lactoglobulin by pulsed electric field pretreatment combined with glycation revealed by ECD/FTICR-MS</style></title><secondary-title><style face="normal" font="default">Food Funct</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Funct</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="8" Month="12" Year="2017">2017/12/8</year></dates><abstract><style face="normal" font="default">Bovine beta-lactoglobulin (beta-Lg) is a major allergen existing in milk and causes about 90% of IgE-mediated cow's milk allergies. Previous studies showed that pulsed electric field (PEF) treatment could partially unfold the protein, which may contribute to the improvement of protein glycation. In this study, the effect of PEF pretreatment combined with glycation on the IgG/IgE-binding ability and the structure of beta-Lg was investigated. The result showed that PEF pretreatment combined with glycation significantly reduced the IgG and IgE binding abilities, which was attributed to the changes of secondary and tertiary structure and the increase in glycation sites and degree of substitution per peptide (DSP) value determined by electron capture dissociation Fourier transform ion cyclotron resonance mass spectrometry (ECD/FTICR-MS). Unexpectedly, glycation sites (K47, K91 and K135) added by two mannose molecules were identified in glycated beta-Lg with PEF pretreatment. Moreover, the results indicated that PEF pretreatment at 25 kV cm(-1) for 60 mus promoted the reduction of IgG/IgE-binding capacity by increasing the glycation degree of beta-Lg, whereas single PEF treatment under the same conditions markedly enhanced the IgG/IgE-binding ability by partially unfolding the structure of beta-Lg. The results suggested that ECD/FTICR-MS could help us to understand the mechanism of reduction in the IgG/IgE-binding of beta-Lg by structural characterization at the molecular level. Therefore, PEF pretreatment combined with glycation may provide an alternative method for beta-Lg desensitization</style></abstract><notes><style face="normal" font="default">IS - 2042-650X (Electronic)IS - 2042-6496 (Linking)LA - engPT - Journal ArticleCO - China -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1039/c7fo01082f.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29220053">PM:29220053</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Funct\20171204-YangW.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Funct\20171204-YangW.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Yang W</style></custom2><misc3><style face="normal" font="default">10.1039/c7fo01082f.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86884</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Soares,S.</style></author><author><style face="normal" font="default"> Grazina,L.</style></author><author><style face="normal" font="default"> Mafra,I.</style></author><author><style face="normal" font="default"> Costa,J.</style></author><author><style face="normal" font="default"> Pinto,M.A.</style></author><author><style face="normal" font="default"> Duc,H.P.</style></author><author><style face="normal" font="default"> Oliveira,M.B.</style></author><author><style face="normal" font="default"> Amaral,J.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Novel diagnostic tools for Asian (Apis cerana) and European (Apis mellifera) honey authentication</style></title><secondary-title><style face="normal" font="default">Food Res Int</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Food Res Int</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Authenticity</style></keyword><keyword><style face="normal" font="default"> Honey</style></keyword><keyword><style face="normal" font="default"> Honeybee</style></keyword><keyword><style face="normal" font="default"> HRM analysis</style></keyword><keyword><style face="normal" font="default"> Mitochondrial DNA</style></keyword><keyword><style face="normal" font="default"> Species differentiation</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0963-9969</style></isbn><abstract><style face="normal" font="default">Honey can be produced by different species of honeybees, with two being of economic importance due to their use in apiculture, namely Apis mellifera (known as European honeybee) and Apis cerana (known as Asian honeybee). Due to the decline of the wild populations of the Asian honeybee, this honey generally attains much higher market value, being prone to adulteration. This work aims at proposing new tools, based on the use of molecular markers, for the entomological authentication of honey. To this end, new species-specific primers were designed targeting the tRNAleu-cox2 intergenic region and allowing the detection of A. cerana DNA by qualitative polymerase chain reaction (PCR). Additionally, a novel real-time PCR method with high resolution melting analysis was developed to target the 16S rRNA gene of both bee species, allowing their discrimination in different clusters. The proposed methodologies were further applied with success in the authentication of Asian and European honey samples by the identification of honeybee DNA, demonstrating the usefulness of these simple and cost-effective new approaches</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Portugal -CO - Vietnam -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodres.2017.11.081</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.foodres.2017.11.081</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Res Int\20171202-SoaresS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Res Int\20171202-SoaresS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Soares S</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodres.2017.11.081</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86893</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Virtanen,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">a University of Eastern Finland, Kuopio Campus, School of Medicine, Institute of Clinical Medicine , Department of Clinical Microbiology , Canthia-building, Room 4011, P.O.B. 1627, Yliopistonranta 1 C, FIN-70211 Kuopio , Finland</style></auth-address><titles><title><style face="normal" font="default">Immunotherapy for pet allergies</style></title><secondary-title><style face="normal" font="default">Hum Vaccin Immunother</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Hum Vaccin Immunother</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">Allergic diseases compose a serious challenge for modern societies. Their individual, medical and economical burden is large. As humans spend most of their time indoors, exposure to indoor allergens is a significant contributor to the development of allergic sensitization and respiratory allergies, such as allergic rhinoconjunctivitis and asthma. One important source of indoor allergens are pets, in particular cats and dogs. Allergens from these and other mammals spread effectively and they are encountered widely in public places. If patient education, allergen avoidance and pharmacotherapy do not suffice for controlling the symptoms of pet allergy, allergen immunotherapy can be a treatment option. Current information on allergen immunotherapy in pet allergy suggests that it can be effective in reducing allergic symptoms. However, the low number of high-quality randomized controlled trials of allergen immunotherapy in pet allergy warrants for further investigations</style></abstract><notes><style face="normal" font="default">IS - 2164-554X (Electronic)IS - 2164-5515 (Linking)LA - engPT - Journal ArticleCO - Finland -</style></notes><work-type><style face="normal" font="default">10.1080/21645515.2017.1409315</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29182437">PM:29182437</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Hum Vaccin Immunother\20171128-VirtanenT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Hum Vaccin Immunother\20171128-VirtanenT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171128, Virtanen T</style></custom2><misc3><style face="normal" font="default">10.1080/21645515.2017.1409315</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86894</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Scott-Taylor,T.H.</style></author><author><style face="normal" font="default"> Axinia,S.C.</style></author><author><style face="normal" font="default"> Amin,S.</style></author><author><style face="normal" font="default"> Pettengell,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Life Sciences, London Metropolitan University, 166-220 Holloway Road, London, N7 8DB</style></auth-address><titles><title><style face="normal" font="default">Immunoglobulin G; structure and functional implications of different subclass modifications in initiation and resolution of allergy</style></title><secondary-title><style face="normal" font="default">Immun Inflamm Dis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immun Inflamm Dis</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">IgE and not IgG is usually associated with allergy. IgE lodged on mast cells in skin or gut and basophils in the blood allows for the prolonged duration of allergy through the persistent expression of high affinity IgE receptors. However, many allergic reactions are not dependent on IgE and are generated in the absence of allergen specific and even total IgE. Instead, IgG plasma cells are involved in induction of, and for much of the pathogenesis of, allergic diseases. The pattern of IgG producing plasma cells in atopic children and the tendency for direct or further class switching to IgE are the principle factors responsible for long-lasting sensitization of mast cells in allergic children. Indirect class switching from IgG producing plasma cells has been shown to be the predominant pathway for production of IgE while a Th2 microenvironment, genetic predisposition, and the concentration and nature of allergens together act on IgG plasma cells in the atopic tendency to undergo further immunoglobulin gene recombination. The seminal involvement of IgG in allergy is further indicated by the principal role of IgG4 in the natural resolution of allergy and as the favourable immunological response to immunotherapy. This paper will look at allergy through the role of different antibodies than IgE and give current knowledge of the nature and role of IgG antibodies in the start, maintenance and resolution of allergy</style></abstract><notes><style face="normal" font="default">IS - 2050-4527 (Electronic)IS - 2050-4527 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1002/iid3.192</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29164823">PM:29164823</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immun Inflamm Dis\20171121-ScottTaylorTH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immun Inflamm Dis\20171121-ScottTaylorTH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Scott-Taylor TH</style></custom2><misc3><style face="normal" font="default">10.1002/iid3.192</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86895</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jiang,S.</style></author><author><style face="normal" font="default"> Da,Y.</style></author><author><style face="normal" font="default"> Han,S.</style></author><author><style face="normal" font="default"> He,Y.</style></author><author><style face="normal" font="default"> Che,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, No.17 Qinghua Donglu, Haidian District, Beijing, People's Republic of China</style></auth-address><titles><title><style face="normal" font="default">Notch ligand Delta-like1 enhances degranulation and cytokine production through a novel Notch/Dok-1/MAPKs pathway in vitro</style></title><secondary-title><style face="normal" font="default">Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">Food allergy includes sensitization phase and effect phase, and effect cells degranulate and secrete cytokines in the effect phase, causing allergic clinical symptoms. We have demonstrated that Notch signaling plays an important role in the sensitization phase, but its role in effect phases still remains unclear. In this study, we investigated the role of Notch signaling in degranulation and cytokine production of the effect phase response. A RBL-2H3 cell model was used and Notch signaling was induced by priming with Notch ligands. Our results showed after priming with Notch ligand, Delta-like1(Dll1)-Fc, beta-hexosaminidase release, and cytokines production, including TGF-beta, IL-1beta, IL-4, IL-6, and IL-13, were increased significantly, and the enhancement was abolished after DAPT treatment, a gamma-secretase inhibitor, indicating that Dll1 Notch signaling enhanced RBL-2H3 cell degranulation and cytokine production. Western blot analysis showed that Dll1 Notch signaling augmented high-affinity IgE receptors-mediated phosphorylation of MAPKs through suppressing the expression of downstream tyrosine kinases 1 (Dok-1). Besides, a passive systemic anaphylaxis mouse model was used to confirm the role of Notch signaling. And our data showed that allergic clinical features of mice were alleviated, and the level of degranulation was decreased significantly after inhibiting Notch signaling in vivo. Therefore, we demonstrated Notch ligand Dll1 enhanced RBL-2H3 cell degranulation and cytokine production through a novel Notch/Dok-1/MAPKs pathway, suggesting Notch signaling played a key role in the effect phase of food allergy</style></abstract><notes><style face="normal" font="default">IS - 1559-0755 (Electronic)IS - 0257-277X (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s12026-017-8977-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29181775">PM:29181775</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunol Res\20171128-JiangS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunol Res\20171128-JiangS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171128, Jiang S</style></custom2><misc3><style face="normal" font="default">10.1007/s12026-017-8977-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86896</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tanaka,M.</style></author><author><style face="normal" font="default"> Inoue,K.I.</style></author><author><style face="normal" font="default"> Shimada,A.</style></author><author><style face="normal" font="default"> Takano,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering , Kyoto University , Kyoto , Japan</style></auth-address><titles><title><style face="normal" font="default">Physiological effects of brominated flame retardants on NC/Nga mice</style></title><secondary-title><style face="normal" font="default">Immunopharmacol Immunotoxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunopharmacol Immunotoxicol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="8" Month="12" Year="2017">2017/12/8</year></dates><abstract><style face="normal" font="default">PURPOSE: Brominated flame retardants (BFRs) are used as an additive or reactive components in various materials. Regarding their health concerns, their immunotoxicity have not been clarified yet. MATERIALS AND METHODS: In the current study, we examined the effects of systemic exposure to two types of BFRs, DE71 and DE79, on pathophysiologic traits of murine atopic dermatitis (AD). Male NC/Nga mice were repeatedly injected intraperitoneally with DE71 and DE79 and/or mite allergen (Dermatophagoides pteronyssinus: Dp) into their right ears. Thereafter, clinical scores, macroscopic findings of inflammatory foci, and Ig values in serum were examined. RESULTS: Both DEs significantly aggravated clinical scores induced by mite allergen including skin dryness and edema. Total IgE titer was significantly greater in the Dp + DE79 group than in the Dp group. CONCLUSIONS: Taken together, exposure to BFRs can exacerbate AD-like skin lesions related to mite allergen in mice. The accentuating effects may be mediated, at least in part, through hyperproduction of IgE</style></abstract><notes><style face="normal" font="default">IS - 1532-2513 (Electronic)IS - 0892-3973 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1080/08923973.2017.1405440</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29219636">PM:29219636</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunopharmacol Immunotoxicol\20171208-TanakaM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunopharmacol Immunotoxicol\20171208-TanakaM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Tanaka M</style></custom2><misc3><style face="normal" font="default">10.1080/08923973.2017.1405440</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86899</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bonini,M.</style></author><author><style face="normal" font="default"> Sikoparija,B.</style></author><author><style face="normal" font="default"> Skjoth,C.A.</style></author><author><style face="normal" font="default"> Cislaghi,G.</style></author><author><style face="normal" font="default"> Colombo,P.</style></author><author><style face="normal" font="default"> Testoni,C.</style></author><author><style face="normal" font="default"> Smith,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Hygiene and Health Prevention, Local Health Authority ATS della Citta Metropolitana di Milano, Parabiago, MI, Italy</style></auth-address><titles><title><style face="normal" font="default">Ambrosia pollen source inventory for Italy: a multi-purpose tool to assess the impact of the ragweed leaf beetle (Ophraella communa LeSage) on populations of its host plant</style></title><secondary-title><style face="normal" font="default">Int J Biometeorol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Biometeorol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">Here, we produce Ambrosia pollen source inventories for Italy that focuses on the periods before and after the accidental introduction of the Ophraella communa beetle. The inventory uses the top-down approach that combines the annual Ambrosia pollen index from a number of monitoring stations in the source region as well as Ambrosia ecology, local knowledge of Ambrosia infestation and detailed land cover information. The final inventory is gridded to a 5 x 5-km resolution using a stereographic projection. The sites with the highest European Infection levels were recorded in the north of Italy at Busto Arsizio (VA3) (European Infection level 2003-2014 = 52.1) and Magenta (MI7) (European Infection level 2003-2014 = 51.3), whereas the sites with the lowest (i.e. around 0.0) were generally located to the south of the country. Analysis showed that the European Infection level in all of Italy was significantly lower in 2013-2014 compared to 2003-2012, and this decrease was even more pronounced at the sites in the area where Ophraella communa was distributed. Cross-validations show that the sensitivity to the inclusion of stations is typically below 1% (for two thirds of the stations) and that the station Magenta (MI7) had the largest impact compared to all other stations. This is the first time that pollen source inventories from different temporal periods have been compared in this way and has implications for simulating interannual variations in pollen emission as well as evaluating the management of anemophilous plants like Ambrosia artemisiifolia</style></abstract><notes><style face="normal" font="default">IS - 1432-1254 (Electronic)IS - 0020-7128 (Linking)LA - engPT - Journal ArticleCO - Italy -CO - Serbia -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1007/s00484-017-1469-z</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29159703">PM:29159703</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Biometeorol\20171121-BoniniM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Biometeorol\20171121-BoniniM.pdf</url></text-urls><related-urls><url ppv-ref="no">suppl. file zippato, con files per programmi specifici</url></related-urls></urls><custom2><style face="normal" font="default">20171121, Bonini M</style></custom2><misc3><style face="normal" font="default">10.1007/s00484-017-1469-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86900</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Buselic,I.</style></author><author><style face="normal" font="default"> Botic,A.</style></author><author><style face="normal" font="default"> Hrabar,J.</style></author><author><style face="normal" font="default"> Staglicic,N.</style></author><author><style face="normal" font="default"> Cipriani,P.</style></author><author><style face="normal" font="default"> Mattiucci,S.</style></author><author><style face="normal" font="default"> Mladineo,I.</style></author></authors></contributors><titles><title><style face="normal" font="default">Geographic and host size variations as indicators of Anisakis pegreffii infection in European pilchard (Sardina pilchardus) from the Mediterranean Sea: Food safety implications</style></title><secondary-title><style face="normal" font="default">Int J Food Microbiol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Int J Food Microbiol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adriatic Sea</style></keyword><keyword><style face="normal" font="default"> Anisakidae</style></keyword><keyword><style face="normal" font="default"> Anisakis</style></keyword><keyword><style face="normal" font="default"> European pilchards</style></keyword><keyword><style face="normal" font="default"> Hysterothylacium</style></keyword><keyword><style face="normal" font="default"> Hysterothylacium sp.</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Western Mediterranean Sea</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0168-1605</style></isbn><abstract><style face="normal" font="default">European pilchards are traditionally eaten marinated or salted in the Mediterranean countries often without thermal processing or gutting due to small size. Since ingestion of live third stage Anisakis larvae represents a causing agent in the onset of anisakiasis, the aim of our study was to assess prevalence and intensity of Anisakis infection in European pilchards originating from different Mediterranean regions in a three-year sampling period (2013</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô2015). A total of 1564 specimens of European pilchard collected from two geographically distinct sampling regions (western Mediterranean and Adriatic Sea) were examined using the UV-Press method, which utilises the fluorescence of frozen anisakids in flattened and subsequently frozen fillets and viscera. A subsample of 67 isolated larvae was identified as A. pegreffii by diagnostic allozyme markers and sequence analyses of the mtDNA cox2 locus. The overall prevalence in pilchards was 12.2% (range 0</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô44.9% for different sampling points) and mean intensity 1.8. More importantly, we have observed an overall larval prevalence of 1.5% in fillets. The highest prevalence (44.9%) was recorded in pilchards caught in western parts of the Mediterranean. As fish host size was a significant predictor of parasite abundance, it should be highlighted that these pilchards were also the largest (mean total length 173.2 mm); on average &amp;gt; 2 cm larger than the rest of the samples. Other isolated nematode species included Hysterothylacium sp. in viscera, showing almost a double of A. pegreffii prevalence, 20.1%. In summary, our study demonstrates that the presence of A. pegreffii in European pilchards from the Mediterranean Sea is highly influenced by both geographic and host size variation. This implies that, before future risk management measures are developed, these variables should be assessed in order to minimize public health concerns</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Croatia -CO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.ijfoodmicro.2017.11.021</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.ijfoodmicro.2017.11.021</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Food Microbiol\20171129-BuselicI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Food Microbiol\20171129-BuselicI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Buselic I</style></custom2><misc3><style face="normal" font="default">10.1016/j.ijfoodmicro.2017.11.021</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86901</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tsai,Y.M.</style></author><author><style face="normal" font="default"> Chiang,K.H.</style></author><author><style face="normal" font="default"> Hung,J.Y.</style></author><author><style face="normal" font="default"> Chang,W.A.</style></author><author><style face="normal" font="default"> Lin,H.P.</style></author><author><style face="normal" font="default"> Shieh,J.M.</style></author><author><style face="normal" font="default"> Chong,I.W.</style></author><author><style face="normal" font="default"> Hsu,Y.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan, R.O.C</style></auth-address><titles><title><style face="normal" font="default">Der f1 induces pyroptosis in human bronchial epithelia via the NLRP3 inflammasome</style></title><secondary-title><style face="normal" font="default">Int J Mol Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Mol Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Damage to the bronchial epithelium leads to persistent inflammation and airway remodelling in various respiratory diseases, such as asthma and chronic obstructive pulmonary disease. To date, the mechanisms underlying bronchial epithelial cell damage and death by common allergens remain largely unknown. The aim of the present study was to investigate Der f1, an allergen of Dermatophagoides farinae, which may result in the death of human bronchial epithelial cells (HBECs). Der f1 induces BECs to undergo the inflammatory cell death referred to as pyroptosis, induced by increasing lactate dehydrogenase release and propidium iodide penetration. Stimulation by Der f1 enhances interleukin (IL)1beta cleavage and release, which is associated with caspase1 activation. In addition, the NODlike receptor family pyrin domaincontaining 3 (NLRP3), is required for the activation of caspase1 through increasing the formation of the inflammasome complex. Consistent with these findings, pretreatment of HBECs with a caspase1 inhibitor, or silencing of NLRP3 by siRNA transfection, reduced Der f1mediated IL1beta and pyroptosis. Therefore, the common allergen Der f1 was not only found to induce allergy, but also led to pyroptosis and IL1beta secretion via the NLRP3caspase1 inflammasome in HBECs. This newly identified connection of the Der f1 allergen with BEC damage and inflammation may play an important role in the pathogenesis of asthma</style></abstract><notes><style face="normal" font="default">IS - 1791-244X (Electronic)IS - 1107-3756 (Linking)LA - engPT - Journal ArticleCO - Taiwan -</style></notes><work-type><style face="normal" font="default">10.3892/ijmm.2017.3310</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29207030">PM:29207030</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Mol Med\20171205-TsaiYM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Mol Med\20171205-TsaiYM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Tsai YM</style></custom2><misc3><style face="normal" font="default">10.3892/ijmm.2017.3310</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86902</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,N.</style></author><author><style face="normal" font="default"> Zhang,H.</style></author><author><style face="normal" font="default"> Cai,X.</style></author><author><style face="normal" font="default"> Shang,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Epigallocatechin-3-gallate inhibits inflammation and epithelialmesenchymal transition through the PI3K/AKT pathway via upregulation of PTEN in asthma</style></title><secondary-title><style face="normal" font="default">Int J Mol Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Mol Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">Asthma is a chronic disease associated with hyperresponsiveness, obstruction and remodeling of the airways. Epithelial-mesenchymal transition (EMT) has an important role in these alterations and may account for the accumulation of subepithelial mesenchymal cells, thus contributing to airway hyperresponsiveness and remodeling. Epigallo-catechin3gallate (EGCG), which is a type of polyphenol, is the most potent ingredient in green tea, and exhibits antibacterial, antiviral, antioxidative, anticancer and chemopreventive activities. Recently, numerous studies have investigated the protective effects of EGCG against asthma and other lung diseases. In the present study, the role of EGCG in ovalbumin (OVA)challenged asthmatic mice was determined. In addition, the inhibitory effects of EGCG against transforming growth factor (TGF)beta1induced EMT and migration of 16HBE cells, and the underlying mechanisms of the phosphatidylinositol 3kinase/protein kinase B (PI3K/Akt) signaling pathway, were investigated by immuno fl uorescence, Transwell, wound healing assay and western blot analysis, respectively. The results indicated that EGCG may suppress inflammation and inflammatory cell infiltration into the lungs of OVAchallenged asthmatic mice, and may also inhibit EMT via the PI3K/Akt signaling pathway through upregulating the expression of phosphatase and tensin homolog (PTEN) in vivo and in vitro. The present study also revealed the antimigratory effects of EGCG in TGFbeta1induced 16HBE cells, thus suggesting it may reduce airway remodeling. The present study provides a novel insight into understanding the protective effects of EGCG on airway remodeling in asthma, and indicates that EGCG may be useful as an adjuvant therapy for bronchial asthma</style></abstract><notes><style face="normal" font="default">IS - 1791-244X (Electronic)IS - 1107-3756 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/ijmm.2017.3292</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29207033">PM:29207033</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Mol Med\20171128-YangN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Mol Med\20171128-YangN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171128, Yang N</style></custom2><misc3><style face="normal" font="default">10.3892/ijmm.2017.3292</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86904</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Carpio-Escalona,L.V.</style></author><author><style face="normal" font="default"> Gonzalez-de-Olano,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Department, Hospital Universitario Ramon y Cajal, Madrid, Spain.</style></auth-address><titles><title><style face="normal" font="default">Use of the Internet by patients attending allergy clinics and its potential as a tool that better meets patients' needs</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/14/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.034</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29196086">PM:29196086</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171129-CarpioEscalonaLV.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171129-CarpioEscalonaLV.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Carpio-Escalona LV</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.034</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86905</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Salo,P.M.</style></author><author><style face="normal" font="default"> Wilkerson,J.</style></author><author><style face="normal" font="default"> Rose,K.M.</style></author><author><style face="normal" font="default"> Cohn,R.D.</style></author><author><style face="normal" font="default"> Calatroni,A.</style></author><author><style face="normal" font="default"> Mitchell,H.E.</style></author><author><style face="normal" font="default"> Sever,M.L.</style></author><author><style face="normal" font="default"> Gergen,P.J.</style></author><author><style face="normal" font="default"> Thorne,P.S.</style></author><author><style face="normal" font="default"> Zeldin,D.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NCSocial &amp; Scientific Systems, Durham, NC</style></auth-address><titles><title><style face="normal" font="default">Bedroom allergen exposures in US households</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">BACKGROUND: Bedroom allergen exposures contribute to allergic disease morbidity because people spend considerable time in bedrooms, where they come into close contact with allergen reservoirs. OBJECTIVE: We investigated participant and housing characteristics, including sociodemographic, regional, and climatic factors, associated with bedroom allergen exposures in a nationally representative sample of the US population. METHODS: Data were obtained from National Health and Nutrition Examination Survey 2005-2006. Information on participant and housing characteristics was collected by using questionnaires and environmental assessments. Concentrations of 8 indoor allergens (Alt a 1, Bla g 1, Can f 1, Fel d 1, Der f 1, Der p 1, Mus m 1, and Rat n 1) in dust vacuumed from nearly 7000 bedrooms were measured by using immunoassays. Exposure levels were classified as increased based on percentile (75th/90th) cutoffs. We estimated the burden of exposure to multiple allergens and used multivariable logistic regression to identify independent predictors for each allergen and household allergen burden. RESULTS: Almost all participants (>99%) had at least 1 and 74.2% had 3 to 6 allergens detected. More than two thirds of participants (72.9%) had at least 1 allergen and 18.2% had 3 or more allergens exceeding increased levels. Although exposure variability showed significant racial/ethnic and regional differences, high exposure burden to multiple allergens was most consistently associated with the presence of pets and pests, living in mobile homes/trailers and older and rental homes, and living in nonmetropolitan areas. CONCLUSIONS: Exposure to multiple allergens is common. Despite highly variable exposures, bedroom allergen burden is strongly associated with the presence of pets and pests</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.08.033</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29198587">PM:29198587</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171123-SaloPM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171123-SaloPM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, Salo PM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.08.033</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86906</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,P.H.</style></author><author><style face="normal" font="default"> Watts,T.J.</style></author><author><style face="normal" font="default"> Lui,M.S.</style></author><author><style face="normal" font="default"> Lau,C.S.</style></author><author><style face="normal" font="default"> Chung,H.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Rheumatology and Clinical Immunology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Pokfulam, Hong Kong</style></auth-address><titles><title><style face="normal" font="default">Recall Urticaria in Adalimumab Hypersensitivity</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/14/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">immunology</style></keyword></keywords><dates><year Day="22" Month="11" Year="2017">2017/11/22</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - Hong Kong -CO - United KIngdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.031</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29175008">PM:29175008</url></web-urls><pdf-urls><url ppv-ref="no">philipli@connect.hku.hk</url></pdf-urls><text-urls><url ppv-ref="no">researchgate</url></text-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171122, Li PH</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.031</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86907</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rachid,R.</style></author><author><style face="normal" font="default"> Keet,C.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Immunology, Boston Children's Hospital, Boston, Mass; Department of Pediatrics, Harvard Medical School, Boston, Mass.</style></auth-address><titles><title><style face="normal" font="default">Current Status and Unanswered Questions for Food Allergy Treatments</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/14/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="18" Month="11" Year="2017">2017/11/18</year></dates><abstract><style face="normal" font="default">Although there is no FDA approved therapy for food allergy, over the past decades, several routes of immunotherapy have been investigated for food allergy. Thus far, these therapies have shown variable levels of efficacy at desensitizing to foods, with oral immunotherapy (OIT) far more successful than sublingual immunotherapy (SLIT) or epicutaneous immunotherapy (EPIT). However, desensitization tends to be temporary, and safety remains a major concern with OIT. Moreover, although it seems logical that desensitization will result in fewer reactions, it is not clear whether OIT or other immunotherapies are associated with an overall lower or higher risk of reactions over the long term. Eosinophilic esophagitis is a known complication of OIT, and may also be a risk with SLIT and possibly EPIT, although it has not been reported in the relatively few patients treated thus far. Adjuvants such as omalizumab or probiotics may improve the safety and/or efficacy of immunotherapy for food allergy, but more research is needed. In the future, biomarkers may identify subsets of patients who are better candidates for specific treatments. As therapies become commercially available, patients and providers will need to consider whether the benefits justify the risks and burdens of these treatments</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.023</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29162426">PM:29162426</url></web-urls><pdf-urls><url ppv-ref="no">rima.rachid@childrens.harvard.edu</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171118, Rachid R</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.023</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86908</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Straesser,M.D.</style></author><author><style face="normal" font="default"> Oliver,E.</style></author><author><style face="normal" font="default"> Palacios,T.</style></author><author><style face="normal" font="default"> Kyin,T.</style></author><author><style face="normal" font="default"> Patrie,J.</style></author><author><style face="normal" font="default"> Borish,L.</style></author><author><style face="normal" font="default"> Saini,S.S.</style></author><author><style face="normal" font="default"> Lawrence,M.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Clinical Immunology, University of Virginia Health System, Charlottesville, Va</style></auth-address><titles><title><style face="normal" font="default">Serum IgE as an immunological marker to predict response to omalizumab treatment in symptomatic chronic urticaria</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/14/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.030</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29175369">PM:29175369</url></web-urls><pdf-urls><url ppv-ref="no">ml4nz@virginia.edu</url></pdf-urls><text-urls><url ppv-ref="no">researchgate</url></text-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171123, Straesser MD</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.030</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86909</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yamani,A.</style></author><author><style face="normal" font="default"> Wu,D.</style></author><author><style face="normal" font="default"> Waggoner,L.</style></author><author><style face="normal" font="default"> Noah,T.</style></author><author><style face="normal" font="default"> Koleske,A.J.</style></author><author><style face="normal" font="default"> Finkelman,F.</style></author><author><style face="normal" font="default"> Hogan,S.P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Immunology</style></auth-address><titles><title><style face="normal" font="default">Vascular endothelial specific IL-4Ralpha-ABL1 kinase signaling axis regulates severity of IgE-mediated anaphylactic reactions</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">BACKGROUND: Severe IgE-mediated, food-induced anaphylactic reactions are characterized by pulmonary venous vasodilatation and fluid extravasation, which is thought to lead to the life-threatening anaphylactic phenotype. The underlying immunological and cellular processes involved in driving fluid extravasation and the severe anaphylactic phenotype are not fully elucidated. OBJECTIVE: To define the interaction and requirement of IL-4 and vascular endothelial (VE) IL-4Ralpha chain signaling in histamine-ABL1-mediated VE dysfunction and fluid extravasation in the severity of IgE-mediated anaphylactic reactions in mice. METHODS: Mice deficient in VE IL-4Ralpha and models of passive and active oral antigen- and IgE-induced anaphylaxis were employed to define the requirements of VE IL-4Ralpha and ABL1 pathway in severe anaphylactic reactions. Human VE cell line (EA.hy926 cells) and pharmacologic (imatinib) and genetic approaches (shRNA knockdown of IL4RA and ABL1) were used to define the requirement of this pathway in VE barrier dysfunction. RESULTS: IL-4 exacerbation of histamine-induced hypovolemic shock in mice was dependent on VE expression of the IL-4Ralpha. IL-4 and histamine induced ABL1 activation in human VE cells and VE barrier dysfunction was ABL1 dependent. Development of severe IgE-mediated hypovolemia and shock required VE-restricted ABL1 expression. Treatment of mice with a history of food-induced anaphylaxis with the ABL kinase inhibitor imatinib protected the mice from developing severe IgE-mediated anaphylaxis. CONCLUSION: IL-4 amplifies IgE- and histamine-induced VE dysfunction, fluid extravasation, and severity of anaphylaxis via a VE IL-4Ralpha-ABL1-dependent mechanism. These studies implicate an important contribution by the VE compartment in the severity of anaphylaxis and identify a new</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.08.046</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29157947">PM:29157947</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-YamaniA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171117-YamaniA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Yamani A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.08.046</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86910</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wolf,M.</style></author><author><style face="normal" font="default"> Aglas,L.</style></author><author><style face="normal" font="default"> Twaroch,T.E.</style></author><author><style face="normal" font="default"> Steiner,M.</style></author><author><style face="normal" font="default"> Huber,S.</style></author><author><style face="normal" font="default"> Hauser,M.</style></author><author><style face="normal" font="default"> Parigiani,M.A.</style></author><author><style face="normal" font="default"> Hofer,H.</style></author><author><style face="normal" font="default"> Ebner,C.</style></author><author><style face="normal" font="default"> Bohle,B.</style></author><author><style face="normal" font="default"> Briza,P.</style></author><author><style face="normal" font="default"> Neubauer,A.</style></author><author><style face="normal" font="default"> Stolz,F.</style></author><author><style face="normal" font="default"> Wallner,M.</style></author><author><style face="normal" font="default"> Ferreira,F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Molecular Biology, University of Salzburg, Salzburg, Austria</style></auth-address><titles><title><style face="normal" font="default">Endolysosomal protease susceptibility of Amb a 1 as a determinant of allergenicity</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">In the absence of extrinsic adjuvants, purified Amb a 1 induced a strong Th2-polarized immune response in mice. This high allergenic activity seems to be linked to the allergen's susceptibility to endolysosomal proteolysis</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.027</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29157946">PM:29157946</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-WolfM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171120-WolfM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Wolf M</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.027</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86911</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sicherer,S.H.</style></author><author><style face="normal" font="default"> Sampson,H.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">The Elliot and Roslyn Jaffe Food Allergy Institute, Division of Allergy and Immunology, Kravis Children's Hospital, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York.</style></auth-address><titles><title><style face="normal" font="default">Food Allergy: A review and update on epidemiology, pathogenesis, diagnosis, prevention and management</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Diagnosis of food allergy</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">This review provides general information to serve as a primer for those embarking on understanding food allergy and also details advances and updates in epidemiology, pathogenesis, diagnosis and treatment that have occurred over the four years since our last comprehensive review. Although firm prevalence data are lacking, there is a strong impression that food allergy has increased, and rates as high as approximately 10% have been documented. Genetic, epigenetic and environmental risk factors are being increasingly elucidated, opening the potential for improved prevention and treatment strategies targeted to those at risk. Insights on pathophysiology are revealing a complex interplay of epithelial barrier, mucosal and systemic immune response, route of exposure and microbiome among other influences resulting in allergy or tolerance. The diagnosis of food allergy is largely reliant on the medical history, tests for sensitization, and oral food challenges, but emerging use of component resolved diagnostics are improving diagnostic accuracy. Additional novel diagnostics such as basophil activation tests, determination of epitope binding, DNA methylation signatures and bioinformatics approaches will further change the landscape. A number of prevention strategies are under investigation, but early introduction of peanut has been advised as a public health measure based on existing data. Management remains largely based on allergen avoidance, but a panoply of promising treatment strategies are in phase 2 and 3 studies, giving immense hope that better treatment will be imminently and widely available, while numerous additional promising treatments are in the preclinical and clinical pipeline</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29157945">PM:29157945</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171121-SichererSH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171121-SichererSH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Sicherer SH</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86912</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">du Toit,G.</style></author><author><style face="normal" font="default"> Sampson,H.</style></author><author><style face="normal" font="default"> Plaut,M.</style></author><author><style face="normal" font="default"> Burks,W.</style></author><author><style face="normal" font="default"> Akdis,C.</style></author><author><style face="normal" font="default"> Lack,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Paediatric Allergy, Division of Asthma, Allergy and Lung Biology, King's College London and Guy's and St. Thomas' NHS Foundation Trust, London</style></auth-address><titles><title><style face="normal" font="default">Food Allergy: Update on Prevention and Tolerance</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">Of the many possible hypotheses which explain the recent rise in childhood food allergy, the dual allergen exposure hypothesis has been the most extensively investigated. This chapter serves as a review and update on the prevention of food allergy, and focuses on recently published Randomized Controlled Trials (RCTs) exploring the efficacy of oral tolerance induction in infancy for the prevention of food allergy. As a result of these RCTs, National Institutes of Health (NIH) recommendations now actively encourage the early introduction of peanut for the prevention of peanut allergy and other countries/settings recommend the inclusion of potential common food allergens including peanut and egg in complementary feeding regimens commencing at approximately 6 months of age, but not before 4 months.(1-3) Further studies which explore the efficacy of oral tolerance induction to other common food allergens, and which focus on optimal timing, duration and adherence are required</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29191680">PM:29191680</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171127-DuToitG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171127-DuToitG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171127, Du Toit G</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86913</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">McWilliam,V.L.</style></author><author><style face="normal" font="default"> Koplin,J.J.</style></author><author><style face="normal" font="default"> Field,M.J.</style></author><author><style face="normal" font="default"> Sasaki,M.</style></author><author><style face="normal" font="default"> Dharmage,S.C.</style></author><author><style face="normal" font="default"> Tang,M.L.K.</style></author><author><style face="normal" font="default"> Sawyer,S.M.</style></author><author><style face="normal" font="default"> Peters,R.L.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Murdoch Children's Research Institute, Royal Children's Hospital Melbourne, Melbourne, Australia</style></auth-address><titles><title><style face="normal" font="default">Self-reported adverse food reactions and anaphylaxis in the SchoolNuts study: A population-based study of adolescents</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Adolescents are at the highest risk of death from anaphylaxis, yet few population-based studies have described the frequencies and risk factors for allergic reactions caused by accidental allergen ingestion in this group. METHODS: We describe the prevalence, frequency, and associated risk factors for recent adverse food reactions in 10- to 14-year-olds in Melbourne, Australia, recruited from a stratified, random, population-based sample of schools (SchoolNuts, n = 9663; 48% response rate). Self-reported food allergy and adverse reaction details, including anaphylaxis, were identified by using a student questionnaire over the past year. RESULTS: Of 547 students with possible IgE-mediated food allergy, 243 (44.4%; 95% CI, 40.3% to 48.7%) reported a reaction to a food. Fifty-three (9.7%; 95% CI, 7.2% to 12.2%) students reported 93 anaphylaxis episodes. Peanut and tree nuts were the most common food triggers. Among students with current IgE-mediated food allergy, those with resolved or current asthma (adjusted odds ratio [aOR], 1.9 [95% CI, 1.1-1.3] and 1.7 [95% CI, 1.1-2.6]) and those with more than 2 food allergies (aOR, 1.9 [95% CI, 1.1-3.1]) were at greatest risk of any adverse food reaction, and those with nut allergy were most at risk of severe reactions (aOR, 2.9 [95% CI, 1.1-4.4]). Resolved or current asthma was not associated with increased risk of severe reactions (aOR, 0.8 [95% CI, 0.3-2.2] and 1.6 [95% CI, 0.7-3.7]). CONCLUSIONS: Adolescents with food allergy are frequently exposed to food allergens. Those with asthma and more than 2 food allergies were at the greatest risk for adverse food reactions. Those with nut allergies were most at risk of severe reactions</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.012</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29174346">PM:29174346</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171123-McWilliamVL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171123-McWilliamVL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, McWilliam VL</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.012</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86914</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Leung,A.S.</style></author><author><style face="normal" font="default"> Wong,G.W.</style></author><author><style face="normal" font="default"> Tang,M.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Paediatrics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong Special Administrative Region, China</style></auth-address><titles><title><style face="normal" font="default">Food Allergy in the developing world</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="22" Month="11" Year="2017">2017/11/22</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - EditorialCO - China -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29174528">PM:29174528</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171122-LeungAS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171122-LeungAS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171122, Leung AS</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86915</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yeung,J.</style></author><author><style face="normal" font="default"> Robert,M.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Nestle Nutrition R&amp;D Centers, Inc., Nestle Development Center Fremont, Fremont, MI 49413Nestec, Nestle Research Center, CH--1000 Lausaane 26, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Challenges and Path Forward on Mandatory Allergen Labeling and Voluntary Precautionary Allergen Labeling for a Global Company</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">For food manufacturers, the label on a food package is a tool meant to alert consumers to the presence of specific allergens, allowing consumers to make informed decisions and not unnecessarily limit their food choices. Mandatory allergen labeling is used when the allergen is an intentionally added ingredient, whereas voluntary allergen labeling is used when the presence of the allergen is unintentional and may be in the finished product as a result of cross-contact. In a globalized economy, ensuring food safety is a growing challenge for manufacturers. When ingredients and technologies are sourced worldwide from multiple business partners, complexity rises, which can increase the chance for errors, leading to potential harm. Threshold science, Voluntary Incidental Trace Allergen Labelling (VITAL) reference doses, fit-for-purpose analytical technology, and common sense enable us to optimize allergen management for the benefit of allergic consumers. This is a good strategy because all stakeholders share the common goal of making foods safe and wholesome for all. Herein, we recommend that (1) senior management make science-based thresholds a priority for both regulatory authorities and the food industry; (2) VITAL 2.0 be adopted as a risk assessment and risk management tool for precautionary allergen labeling (PAL); (3) a standardized message for PAL, i.e., "may contain x," be used to make it easily understandable to allergic consumers so they can make informed food choices; and (4) validated fit-for-purpose allergen methods be used to meet analytical needs. This is an opportunity for us to speak with one voice and demonstrate that food safety is not a competitive issue, but a shared responsibility. This approach could significantly improve allergic consumers' lives</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0391</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202907">PM:29202907</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-YeungJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-YeungJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Yeung J</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0391</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86916</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Walker,M.J.</style></author><author><style face="normal" font="default"> Gowland,M.H.</style></author><author><style face="normal" font="default"> Points,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of the Government Chemist, Queen's Rd, Teddington, Middlesex TW11 0LY, United KingdomAllergy Action, 23 Charmouth Rd, St. Albans AL1 4RS, United KingdomJohn Points Consulting Ltd, 28 Priory Road, Newbury RG14 7QN, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Managing Food Allergens in the U.K. Retail Supply Chain</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">The U.K. food and grocery market is highly significant financially and dominated by 10 retailers within a regulated and extremely economically competitive environment. We summarize the approach of U.K. retailers to allergen risk assessment (RA) and risk management (RM) within the U.K. legal framework and explore public visibility of retailers' allergen policies. RA and RM of allergens appear effective in curtailing retail-triggered severe food allergy reactions. However, allergen recalls remain high, precautionary allergen labeling (PAL) remains an area of confusion, and there is no consistent Web-based provision of information for consumers who have allergies. Resolution of PAL awaits an agreed-on threshold framework, but a key challenge is to engage with patients and gain their trust rather than thrust education at them. It would be helpful for retailers to publish their allergen RA and RM policies. A target should be agreed on between government and retailers for a reduction in the proliferation of PAL wording variants by a given date within the next 3 years. A further hurdle is potentially flawed allergen analysis-development of reference methods and reference materials are acknowledged needs. Laboratories should report allergen results in an informative manner, communicating uncertainty and caveats. Ideally a laboratory representative would be included on any incident control team. Efforts must continue to standardize preparedness for protecting and defending food and drink from deliberate attack</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0385</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202906">PM:29202906</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-WalkerMJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-WalkerMJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Walker MJ</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0385</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86917</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Do,A.B.</style></author><author><style face="normal" font="default"> Khuda,S.E.</style></author><author><style face="normal" font="default"> Sharma,G.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition, 8301 Muirkirk Rd, Laurel, MD 20708</style></auth-address><titles><title><style face="normal" font="default">Undeclared Food Allergens and Gluten in Commercial Food Products Analyzed by ELISA</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Undeclared allergen(s) in commercial food products are responsible for many food recalls, as reported by regulatory agencies in various countries, including the United States. Correct allergen labeling practices are essential for the safety of food-allergic consumers. However, this practice may be hindered by the introduction of allergens all along the food supply chain, including unintentionally through cross-contact. To understand the pervasiveness of undeclared allergen(s) in commercial food products, the objective of this review is to summarize the prevalence of undeclared milk, egg, hazelnut, peanut, soy, and gluten as detected by ELISA from previously published surveys. The prevalence of undeclared allergen(s) in products with or without an advisory statement was also summarized and compared. As compiled by this review, there are some food categories that may be at higher risk for containing undeclared allergen(s). However, the data on prevalence and amount of allergen present may vary widely within any particular allergen or food category. Factors, such as food survey product selection, geography, awareness of allergen/gluten issues, and/or the choice of ELISA method, may be responsible for such differences</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0384</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202905">PM:29202905</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-DoAB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-DoAB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Do AB</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0384</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86918</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Boo,C.C.</style></author><author><style face="normal" font="default"> Parker,C.H.</style></author><author><style face="normal" font="default"> Jackson,L.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition, 5001 Campus Dr., College Park, MD 20740U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition, 6502 South Archer Rd, Bedford Park, IL 60501</style></auth-address><titles><title><style face="normal" font="default">A Targeted LC-MS/MS Method for the Simultaneous Detection and Quantitation of Egg, Milk, and Peanut Allergens in Sugar Cookies</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Food allergy is a growing public health concern, with many individuals reporting allergies to multiple food sources. Compliance with food labeling regulations and prevention of inadvertent cross-contact in manufacturing requires the use of reliable methods for the detection and quantitation of allergens in processed foods. In this work, a novel liquid chromatography-tandem mass spectrometry multiple-reaction monitoring method for multiallergen detection and quantitation of egg, milk, and peanut was developed and evaluated in an allergen-incurred baked sugar cookie matrix. A systematic evaluation of method parameters, including sample extraction, concentration, and digestion, were optimized for candidate allergen peptide markers. The optimized method enabled the reliable detection and quantitation of egg, milk, and peanut allergens in sugar cookies, with allergen concentrations as low as 5 ppm allergen-incurred ingredient</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0400</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202910">PM:29202910</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-BooCC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-BooCC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Boo CC</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0400</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86919</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lacorn,M.</style></author><author><style face="normal" font="default"> Lindeke,S.</style></author><author><style face="normal" font="default"> Siebeneicher,S.</style></author><author><style face="normal" font="default"> Weiss,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">R-Biopharm AG, An der neuen Bergstrasse 17, 64297 Darmstadt, Germany</style></auth-address><titles><title><style face="normal" font="default">Commercial ELISA Measurement of Allergens and Gluten: What We Can Learn from Case Studies</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">During the last decade, results from ELISA test kits have often been criticized as being flawed. Therefore, itmay appear counterintuitive that ELISAs are used for most food allergen and gluten analytical needs. One reason, in addition to the nonavailability of comparable alternative methods, is the fact that the methods used underwent a long validation and learning period in the market. This publication presents several case studies on interference, cross-reactivity issues, calibrators, fragmented allergens and gluten, matrix influences, and misunderstood intended-use statements. Afterward, the relevant validation parameter LOD, LOQ, selectivity, and precision are discussed. Finally, a comprehensive list of practical recommendations for ELISA test kit users is presented</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0399</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202909">PM:29202909</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-LacornM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-LacornM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Lacorn M</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0399</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86920</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shoji,M.</style></author><author><style face="normal" font="default"> Adachi,R.</style></author><author><style face="normal" font="default"> Akiyama,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Morinaga Institute of Biological Science, Inc., Sachiura 2-1-16, Kanazawa-ku, Yokohama, Kanagawa, JapanNational Institutes of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo, JapanNational Institutes of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo, Japan</style></auth-address><titles><title><style face="normal" font="default">Japanese Food Allergen Labeling Regulation: An Update</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">The Japanese food allergen labeling regulation was designed to match real Japanese food allergy circumstancesand also to be enforced effectively; thus, (1) regulated food allergens were selected by prevalence and seriousness according to food allergy surveys in Japan; (2) the detection criterion for ELISA monitoring, 10 mug food allergen protein/g (or mL) food, was set up as the threshold value to regulate commercial prepackaged foods; and (3) official food allergen analytical methods, which can determine the threshold value accurately, were developed. These three points are distinctive from other countries. Furthermore, as an on-going project, the regulation has been amended according to food allergy circumstances and requirements of society. This paper presents recent changes regarding the Japanese food allergen labeling regulation. To date, the Japanese food allergen labeling regulation has been enforced for more than 15 years and seems to be working effectively. Now would be an opportune time to review the regulation for its next level of development</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0389</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202908">PM:29202908</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-ShojiM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-ShojiM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Ahoji M</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0389</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86921</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Diaz-Amigo,C.</style></author><author><style face="normal" font="default"> Popping,B.</style></author></authors></contributors><auth-address><style face="normal" font="default">FOCOS GbR-Food Consulting Strategically Zum Kalterhaus 6b, 63755 Alzenau, Germany</style></auth-address><titles><title><style face="normal" font="default">A Global Reflection on Food Allergen Regulations, Management, and Analysis</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0380</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202904">PM:29202904</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-DiazAmigoC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-DiazAmigoC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Diaz-Amigo C</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0380</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86922</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lopez,M.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">National Institute of Industrial Technology, Agrifoods Center, Buenos Aires, Argentina</style></auth-address><titles><title><style face="normal" font="default">Food Allergen Labeling: A Latin American Approach</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Food allergy is a public health concern almost all over the world. Although most of the countries that regulate the declaration of allergens in prepackaged foods include the list recommended by the Codex Alimentarius, some countries have added other allergens to this list due to prevalence data and regional incidence, whereas others have incorporated exceptions for some products derived from allergenic foods. Within this context, the situation in Latin America regarding these regulations is diverse. Data about prevalence of food hypersensitivity are very limited in the region. The countries that have established regulations are Brazil, Colombia, Costa Rica, Guatemala, Honduras, El Salvador, Nicaragua, Chile, Mexico, and Venezuela. Argentina has approved a regulation for the labeling of food allergens in November 2016. It only needs to be published in the Official Bulletin to go into effect. All countries follow the Codex list that includes latex and excludes sulfites, except Brazil. On the other hand, Argentina is the only country that includes exceptions. As for the methodologies for the detection of allergens in foods, this issue is a serious problem for both the food industry and control laboratories. Available methodologies are based mainly on commercial ELISA kits; currently, there are no Latin American companies that produce them, so ELISA kits are expensive and their acquisition is complicated. There is an initiative in Argentina to address all these gaps in the region through the Platform of Food Allergens (PFA), a nonprofit organization that integrates health professionals, patients, representatives of the food industry, government, and scientists. The different actions carried out by the PFA have made it possible to contact different scientific groups from other Latin American countries in order to expand this initiative and thereby promote and strengthen both public and private capacities in the region</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Argentina -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0382</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202900">PM:29202900</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-LopezMC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-LopezMC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Lopez MC</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0382</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86923</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Groves,K.</style></author><author><style face="normal" font="default"> Cryar,A.</style></author><author><style face="normal" font="default"> Walker,M.</style></author><author><style face="normal" font="default"> Quaglia,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">LGC Limited, Queen's Rd, Teddington, Middlesex TW11 0LY, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Assessment of Recovery of Milk Protein Allergens from Processed Food for Mass Spectrometry Quantification</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Flour</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Assessing the recovery of food allergens from solid processed matrixes is one of the most difficult steps thatneeds to be overcome to enable the accurate quantification of protein allergens by immunoassay and MS. A feasibility study is described herein applying International System of Units (SI)-traceably quantified milk protein solutions to assess recovery by an improved extraction method. Untargeted MS analysis suggests that this novel extraction method can be further developed to provide high recoveries for a broad range of food allergens. A solution of alpha-casein was traceably quantified to the SI for the content of alpha-S1 casein. Cookie dough was prepared by spiking a known amount of the SI-traceable quantified solution into a mixture of flour, sugar, and soya spread, followed by baking. A novel method for the extraction of protein food allergens from solid matrixes based on proteolytic digestion was developed, and its performance was compared with the performance of methods reported in the literature</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0214</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202899">PM:29202899</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-GrovesK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-GrovesK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Groves K</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0214</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86924</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Koizumi,D.</style></author><author><style face="normal" font="default"> Shirota,K.</style></author><author><style face="normal" font="default"> Oda,H.</style></author><author><style face="normal" font="default"> Adachi,R.</style></author><author><style face="normal" font="default"> Sakai,S.</style></author><author><style face="normal" font="default"> Akiyama,H.</style></author><author><style face="normal" font="default"> Nishimaki-Mogami,T.</style></author><author><style face="normal" font="default"> Teshima,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Central Research Institute, Maruha Nichiro Corp., 16-2 Wadai, Tsukuba, Ibaraki 300-4295, JapanNational Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan</style></auth-address><titles><title><style face="normal" font="default">Development and Evaluation of an Enzyme-Linked Immunosorbent Assay Using a Nonpoisonous Extraction System for the Determination of Crustacean Protein in Processed Foods</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="30" Month="11" Year="2017">2017/11/30</year></dates><abstract><style face="normal" font="default">Crustacean proteins are food allergens that cause severe allergic reactions in patients with food allergies; therefore, the identification of crustaceans such as shrimp, crab, and lobster as ingredients in processed food products is mandatory in Japan. We previously developed and validated an ELISA method coupled with an extraction process using the surfactant sodium dodecyl sulfate and the reductant 2-mercaptoethanol (2-ME) to quantify crustacean protein. However, 2-ME was designated as poisonous in Japan in 2008. Therefore, in this study, we developed and evaluated an ELISA method for detecting and quantifying crustacean protein that uses sodium sulfite (Na(2)SO(3)) in place of 2-ME for extraction. The proposed ELISA method showed high sensitivity, with an LOQ of 0.66 &amp;#956;g protein/g food sample. Furthermore, the proposed method showed high specificity for the Decapoda order within the subphylum Crustacea, with recoveries ranging from 83.8 to 100.8% for model processed foods, as well as high reproducibility (intra- and interassay CVs of &amp;#8804;8.2%) and high correlation with our previously validated ELISA method for processed foods (correlation coefficient of 0.996). The proposed ELISA method does not require the use of poisonous reagents, provides acceptable accuracy, and is useful for the routine monitoring of food products</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0324</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29187265">PM:29187265</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171130, Koizumi D</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0324</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86925</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Koeberl,M.</style></author><author><style face="normal" font="default"> Clarke,D.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author><author><style face="normal" font="default"> Fleming,F.</style></author><author><style face="normal" font="default"> Katzer,L.</style></author><author><style face="normal" font="default"> Lee,N.A.</style></author><author><style face="normal" font="default"> Lopata,A.L.</style></author><author><style face="normal" font="default"> Said,M.</style></author><author><style face="normal" font="default"> Scheelings,P.</style></author><author><style face="normal" font="default"> Shepherd,N.</style></author><author><style face="normal" font="default"> Sherlock,R.</style></author><author><style face="normal" font="default"> Roberts,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Industry, Science and Innovation, National Measurement Institute of Australia, Melbourne, VIC, AustraliaLr:14636200</style></auth-address><titles><title><style face="normal" font="default">Food Allergen Management in Australia</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Food allergies are increasing globally, including numbers of allergens, the sensitization rate, and the prevalence rate. To protect food-allergic individuals in the community, food allergies need to be appropriately managed. This paper describes current Australian food allergen management practices. In Australia, the prevalence of food allergies, the anaphylaxis rate, and the fatal anaphylaxis rate are among the highest in the world. Interagency and stakeholder collaboration is facilitated and enhanced as Australia moves through past, current, and ongoing food allergen challenges. As a result, Australia has been a global leader in regulating the labeling of common allergens in packaged foods and their disclosure in foods not required to bear a label. Moreover, the food industry in Australia and New Zealand has developed a unique food allergen risk management tool, the Voluntary Incidental Trace Allergen Labelling program, which is managed by the Allergen Bureau. This paper summarizes insights and information provided by the major stakeholders involved to protect food-allergic consumers from any allergic reaction. Stakeholders include government; consumer protection, regulation, and enforcement agencies; the food industry; and food allergen testing and food allergen/allergy research bodies in Australia. The ongoing goal of all stakeholders in food allergen management in Australia is to promote best practice food allergen management procedures and provide a wide choice of foods, while enabling allergic consumers to manage their food allergies and reduce the risk of an allergic reaction</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Australia -CO - New Zealand -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0386</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202903">PM:29202903</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-KoeberlM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-KoeberlM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Koeberl M</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0386</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86926</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Waiblinger,H.U.</style></author><author><style face="normal" font="default"> Schulze,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Chemisches und Veterinaruntersuchungsamt Freiburg, Bissierstrasse 5, 79114 Freiburg, GermanyBayerisches Landesamt fur Gesundheit und Lebensmittelsicherheit, Eggenreuther Weg 43, 91058 Erlangen, Germany</style></auth-address><titles><title><style face="normal" font="default">Action Levels for Food Allergens: An Approach for Official Food Control in Germany</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Official food control laboratories in Germany have established internal action values for the assessment of analytical results of food allergens especially obtained from samples without declaration of the specified allergen. A pragmatic approach was chosen considering the current situation for European food information legislation. Accordingly, when a positive result is obtained for an unlabeled allergen, it is not necessarily an irregularity if it can be demonstrated that the result was caused by cross-contamination. Action values take into account current analytical experiences as well as published allergologic reference doses. They are considered as internal de minimis thresholds by food control authorities that are used to support laboratories in the decision-making process and when a written expert opinion is requested by an enforcement authority. If only minor traces are detected at concentrations below the action values, further investigation of the issue and inspections at the location of manufacture can be abandoned. The present report includes a collection of results from official food control laboratories in Germany that have been evaluated in line with the aforementioned system of action levels</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0383</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202902">PM:29202902</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-WaiblingerHU.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-WaiblingerHU.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Waiblinger HU</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0383</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86927</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Popping,B.</style></author><author><style face="normal" font="default"> Diaz-Amigo,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">FOCOS GbR, Food Consulting... Strategically, Zum Kalterhaus 6b, 63755 Alzenau, Germany</style></auth-address><titles><title><style face="normal" font="default">European Regulations for Labeling Requirements for Food Allergens and Substances Causing Intolerances: History and Future</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Food allergens and intolerances have been diagnosed by doctors for decades, but have received heightened attention in the last two decades because diagnosis and awareness have increased. Consequently, regulators in many jurisdictions have addressed this topic by introducing labeling requirements for substances causing allergies and intolerance reactions in affected individuals. Mandatory labeling of food allergens allows persons suffering from these to make informed choices. However, regulations in some geographic areas have resulted in significant problems for manufacturers as well as consumers. This has been mainly due to frequent changes and amendments, and it has been difficult for all stakeholders to follow and understand the status quo of legislation. The present paper describes the development of European directives and regulations for the labeling of food allergens and intolerances to substances like gluten over the past decades and provides an outlook of what can reasonably be expected to change in the coming years. It also identifies existing gaps, like a lack of threshold levels for adventitious contamination and consequently a proliferation of precautionary allergen labeling, which neither benefits the consumer nor the food industry in its current form</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0381</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202901">PM:29202901</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-PoppingB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-PoppingB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Popping B</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0381</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86928</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Downs,M.L.</style></author><author><style face="normal" font="default"> Johnson,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Nebraska-Lincoln, Department of Food Science and Technology, Food Allergy Research and Resource Program, 1901 North 21st St, Lincoln, NE 68588-6205</style></auth-address><titles><title><style face="normal" font="default">Target Selection Strategies for LC-MS/MS Food Allergen Methods</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">The detection and quantitation of allergens as contaminants in foods using MS is challenging largely due to the requirement to detect proteins in complex, mixed, and often processed matrixes. Such methods necessarily rely on the use of proteotypic peptides as indicators of the presence and amount of allergenic foods. These peptides should represent the allergenic food in question in such a way that their use is both sensitive (no false-negatives) and specific (no false-positives). Choosing such peptides to represent food allergens is beset with issues, including, but not limited to, separated ingredients (e.g., casein and whey), extraction difficulties (particularly from thermally processed foods), and incomplete sequence information, as well as the more common issues associated with protein quantitation in biological samples. Here, we review the workflows that have been used to select peptide targets for food allergen detection. We describe the use and limitations of both in silico-based analyses and experimental methods relying on high-resolution MS. The variation in the way in which target selection is performed highlights a lack of standardization, even around the principles describing what the detection method should achieve. A lack of focus on the food matrixes to which the method will be applied is also apparent during the peptide target selection process. It is hoped that highlighting some of these issues will assist in the generation of MS-based allergen detection methods that will encourage uptake and use by the analytical community at large</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0404</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202920">PM:29202920</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-DownsML.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-DownsML.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Downs ML</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0404</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86929</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Popping,B.</style></author><author><style face="normal" font="default"> Allred,L.</style></author><author><style face="normal" font="default"> Bourdichon,F.</style></author><author><style face="normal" font="default"> Brunner,K.</style></author><author><style face="normal" font="default"> Diaz-Amigo,C.</style></author><author><style face="normal" font="default"> Galan-Malo,P.</style></author><author><style face="normal" font="default"> Lacorn,M.</style></author><author><style face="normal" font="default"> North,J.</style></author><author><style face="normal" font="default"> Parisi,S.</style></author><author><style face="normal" font="default"> Rogers,A.</style></author><author><style face="normal" font="default"> Sealy-Voyksner,J.</style></author><author><style face="normal" font="default"> Thompson,T.</style></author><author><style face="normal" font="default"> Yeung,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">FOCOS-Food Consulting Strategically, Zum Kalterhaus 6b, 63755 Alzenau, Germany</style></auth-address><titles><title><style face="normal" font="default">Stakeholders' Guidance Document for Consumer Analytical Devices with a Focus on Gluten and Food Allergens</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Until recently, analytical tests for food were performed primarily in laboratories, but technical developmentsnow enable consumers to use devices to test their food at home or when dining out. Current consumer devices for food can determine nutritional values, freshness, and, most recently, the presence of food allergens and substances that cause food intolerances. The demand for such products is driven by an increase in the incidence of food allergies, as well as consumer desire for more information about what is in their food. The number and complexity of food matrixes creates an important need for properly validated testing devices with comprehensive user instructions (definitions of technical terms can be found in ISO 5725-1:1994 and the International Vocabulary of Metrology). This is especially important with food allergen determinations that can have life-threatening consequences. Stakeholders-including food regulators, food producers, and food testing kit and equipment manufacturers, as well as representatives from consumer advocacy groups-have worked to outline voluntary guidelines for consumer food allergen- and gluten-testing devices. These guidelines cover areas such as kit validation, user sampling instructions, kit performance, and interpretation of results. The recommendations are based on (1) current known technologies, (2) analytical expertise, and (3) standardized AOAC INTERNATIONAL allergen community guidance and best practices on the analysis of food allergens and gluten. The present guidance document is the first in a series of papers intended to provide general guidelines applicable to consumer devices for all food analytes. Future publications will give specific guidance and validation protocols for devices designed to detect individual allergens and gluten, as statistical analysis and review of any validation data, preferably from an independent third party, are necessary to establish a device's fitness-for-purpose. Following the recommendations of these guidance documents will help ensure that consumers are equipped with sufficient information to make an informed decision based on an analytical result from a consumer device. However, the present guidance document emphasizes that consumer devices should not be used in isolation to make a determination as to whether a food is safe to eat. As advances are made in science and technology, these recommendations will be reevaluated and revised as appropriate</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - France -CO - Austria -CO - Germany -CO - Spain -CO - Italy -CO - United Kingdom -CO - United States -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0425</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202919">PM:29202919</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171206-PoppingB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171206-PoppingB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171206, Popping B</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0425</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86930</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Walker,M.J.</style></author><author><style face="normal" font="default"> Burns,M.</style></author><author><style face="normal" font="default"> Quaglia,M.</style></author><author><style face="normal" font="default"> Nixon,G.</style></author><author><style face="normal" font="default"> Hopley,C.J.</style></author><author><style face="normal" font="default"> Gray,K.M.</style></author><author><style face="normal" font="default"> Moore,V.</style></author><author><style face="normal" font="default"> Singh,M.</style></author><author><style face="normal" font="default"> Cowen,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of the Government Chemist, Queens Rd, Teddington TW11 0LY, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Almond or Mahaleb? Orthogonal Allergen Analysis During a Live Incident Investigation by ELISA, Molecular Biology, and Protein Mass Spectrometry</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">It is now well known that an incident investigated in the United Kingdom in 2015 of cumin alleged to be contaminated with almond, a risk for people with almond allergy, was caused by the Prunus species, Prunus mahaleb. In the United Kingdom, the Government Chemist offers a route of technical appeal from official findings in the food control system. Findings of almond in two official samples, cumin and paprika, which had prompted action to exclude the consignments from the food chain, were so referred. Herein are described the approaches deployed to resolve the analytical issues during the investigation of the incidents. The cross-reactivity of ELISA to Prunus species was confirmed, and although this is useful in screening for the genus, orthogonal techniques are required to identify the species and confirm its presence. Two novel PCR assays were developed: one specific for P. mahaleb and the other a screening method capable of identifying common Prunus DNA. Peptides unique to almond and mahaleb were identified, permitting LC-tandem MS and criteria were developed for peptide identification to forensic standards. This work enables a staged approach to be taken to any future incident thought to involve Prunus species and provides a template for the investigation of similar incidents</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0405</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202918">PM:29202918</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171206-WalkerMJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171206-WalkerMJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Walker MJ</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0405</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86931</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Spotz,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Grocery Manufacturers Association, Food Safety and Quality Assurance, 1350 I Street, NW, Suite 300, Washington DC 2005</style></auth-address><titles><title><style face="normal" font="default">Allergens: An Enhanced Focus</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Food Allergy Awareness Week was created with the purpose of placing a spotlight on the seriousness of food allergies. Recognized in the United States in mid-May every year, Food Allergy Awareness Week serves as a reminder of the over 15 million Americans who suffer from food allergies. The importance of allergies and allergen labeling can be seen when looking at U.S. Food and Drug Administration recall data: of the 764 recalls in 2016, 305 (representing more than 40%) were due to undeclared allergens. However, recalls for undeclared allergens are a complex issue with numerous factors. The implementation of prevention-based systems with the necessary management components and further error-proofing the systems, along with allergen awareness embedded throughout a company's food safety culture, can likely help reduce the number of recalls for undeclared allergens. As a resource to manufacturers, the Grocery Manufacturers Association and the Food Allergy Research and Resource Program have developed several resources to assist with developing robust allergen management programs. By reducing the number of recalls for undeclared allergens, the food industry will likely increase and maintain consumer confidence and trust of the food-allergic community. This enhanced consumer confidence and trust could eventually open the door for further collaboration with the food-allergic community and, potentially, advance allergen-related policies</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0435</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202923">PM:29202923</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-SpotzK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-SpotzK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Spotz K</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0435</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86932</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">New,L.S.</style></author><author><style face="normal" font="default"> Schreiber,A.</style></author><author><style face="normal" font="default"> Stahl-Zeng,J.</style></author><author><style face="normal" font="default"> Liu,H.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">SCIEX, 10 Biopolis Rd, No. 03-06, Chromos, Singapore 138670, SingaporeSCIEX, Landwehrstrasse 54, 64293 Darmstadt, GermanySCIEX, 1201 Radio Rd, Redwood City, CA 94065</style></auth-address><titles><title><style face="normal" font="default">Simultaneous Analysis of Multiple Allergens in Food Products by LC-MS/MS</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">There is currently no cure for food allergies, and sufferers can only rely on the correct labeling of foods toavoid allergens. Hence, it is important that analytical methods are sensitive and accurate enough to screen for the presence of multiple allergens in food products. In this study, we developed an LC-tandem MS method that is able to simultaneously screen or quantify the signature tryptic peptides of multiple allergen commodities. This method is capable of screening and identifying egg white, skim milk, peanut, soy, and tree nuts (almond, Brazil nut, cashew, hazelnut, pecan, pine nut, pistachio, and walnut) at a detection limit of 10 ppm in incurred bread and cookies. It was further tested for the quantitative analysis of whole-egg, whole-milk, peanut butter, and hazelnut commodities, which are incurred or spiked into selected food matrixes as defined in AOAC INTERNATIONAL Standard Method Performance Requirement (SMPR((R))) 2016.002. The method demonstrated excellent sensitivity with a Method quantitative limit of 3 ppm for whole egg and 10 ppm for the remaining three allergen commodities. It also demonstrated good recovery (60119%) and repeatability (RSDr &lt;20%), with an analytical range of 10-1000 ppm for each allergen commodity and was able to meet the minimum performance requirements of the SMPR</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Singapore -CO - Germany -CO - United States -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0403</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202922">PM:29202922</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-NewLS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-NewLS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, New LS</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0403</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86933</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ladenburger,E.M.</style></author><author><style face="normal" font="default"> Dehmer,M.</style></author><author><style face="normal" font="default"> Grunberg,R.</style></author><author><style face="normal" font="default"> Waiblinger,H.U.</style></author><author><style face="normal" font="default"> Stoll,D.</style></author><author><style face="normal" font="default"> Bergemann,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Applied Sciences Albstadt-Sigmaringen, Faculty of Life Sciences, Department of Biomedical Sciences, Anton-Gunther-Strasse 51, 72488 Sigmaringen, GermanyChemisches und Veterinaruntersuchungsamt Freiburg, Bissierstrasse 5, 79114 Freiburg, GermanyUniversity of Applied Sciences Albstadt-Sigmaringen, Faculty of Life Sciences, Department of Biomedical Sciences, Anton-Gunther-Strasse 51, 72488 Sigmaringen, Germany</style></auth-address><titles><title><style face="normal" font="default">Highly Sensitive Matrix-Independent Quantification of Major Food Allergens Peanut and Soy by Competitive Real-Time PCR Targeting Mitochondrial DNA</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Mitochondrial DNA</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">The development of two competitive real-time PCR assays for the quantitative detection of trace amounts of twomajor food allergens, peanut and soybean, is reported. In order to achieve very low detection levels for both allergens, we established PCR primers and probes targeting mitochondrial DNA sequences. We were able to demonstrate that this approach led to an increase in detection sensitivity in the range of at least 1 order of magnitude compared with published assays targeting nuclear DNA. Furthermore, we generated corresponding competitor molecules, which were used as internal standards to compete with matrix effects that are evident during DNA extraction and PCR amplification in heterogeneous analytical matrixes like food. According to the recently described competitive quantitative PCR method published by Holzhauser et al. (2014), we performed threshold calibration against milk powder spiked with 10 ppm peanut and soy. Matrix-independent quantitative determination of peanut and soy could be demonstrated for three different calibrated food matrix standards in a range between 1 and 100 ppm. The data presented indicate that both assay concepts are powerful analytical tools for the quantitative detection of trace amounts of peanut and soy in commercial food products</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0406</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202921">PM:29202921</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-LadenburgerEM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-LadenburgerEM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Ladenburger EM</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0406</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86934</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Crevel,R.R.W.</style></author><author><style face="normal" font="default"> Ronsmans,S.</style></author><author><style face="normal" font="default"> Marsaux,C.F.M.</style></author><author><style face="normal" font="default"> Banati,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Unilever, Safety and Environmental Assurance Centre, Bedford, United KingdomCoca-Cola Services, Brussels, BelgiumInternational Life Sciences Institute (ILSI) Europe, Brussels, Belgium</style></auth-address><titles><title><style face="normal" font="default">ILSI Europe's Food Allergy Task Force: From Defining the Hazard to Assessing the Risk from Food Allergens</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">The International Life Sciences Institute (ILSI) Europe Food Allergy Task Force was founded in response to early public concerns about the growing impact of food allergies almost coincidentally with the publication of the 1995 Food and Agriculture Organization-World Health Organization Technical Consultation on Food Allergies. In line with ILSI principles aimed to foster collaboration between stakeholders to promote consensus on science-based approaches to food safety and nutrition, the task force has played a central role since then in the development of risk assessment for food allergens. This ranged from consideration of the criteria to be applied to identifying allergens of public health concern through methodologies to determine the relationship between dose and the proportion of allergic individuals reacting, as well as the nature of the observed responses. The task force also promoted the application of novel, probabilistic risk assessment methods to better delineate the impact of benchmarks, such as reference doses, and actively participated in major European food allergy projects, such as EUROPREVALL, the European Union (EU)-funded project "The prevalence, cost and basis of food allergy across Europe;" and iFAAM, "Integrated approaches to food allergen and allergy risk management," also an EU-funded project. Over the years, the task force's work has evolved as answers to initial questions raised further issues: Its current work program includes a review of analytical methods and how different ones can best be deployed given their strengths and limitations. Another activity, which has just commenced, aims to develop a framework for stakeholders to achieve consensus on acceptable risk</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Belgium -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0397</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202913">PM:29202913</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-CrevelRR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-CrevelRR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Crevel RR</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0397</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86935</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Daly,M.</style></author><author><style face="normal" font="default"> Ansari,P.</style></author><author><style face="normal" font="default"> Haubl,G.</style></author><author><style face="normal" font="default"> Rogers,A.</style></author><author><style face="normal" font="default"> Brunner,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Romer Laboratories UK Ltd, The Heath Business and Technical Park, Runcorn, Cheshire, United KingdomRomer Laboratories Division Holding GmbH, Technopark 1, 3430 Tulln, AustriaRomer Laboratories UK Ltd, The Heath Business and Technical Park, Runcorn, Cheshire, United KingdomRomer Laboratories Division Holding GmbH, Technopark 1, 3430 Tulln, Austria</style></auth-address><titles><title><style face="normal" font="default">Assessing Almond and Peanut Allergens Using Commercially Available Immunoanalytical Kits and LC-MS/MS: A Case Study</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">With an ever-increasing allergic population and an emerging market for allergen-free foods, accurate detectionof allergens in foods has never been more important. Although ELISA-based methods are the most widely used for detection of allergens in food, there is a need for the development of orthogonal approaches. A commercial ELISA detected a relatively high concentration of peanut and almond in an allergen-free product. However, another commercial ELISA declared a low peanut concentration and was negative for almond. Further testing using a commercial almond lateral-flow device confirmed the results from the second ELISA kit and demonstrated that the positive detection of almond was due to cross-reactivity. An MS method was used for final confirmation that the reported results were negative for both almond and peanut</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0398</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202912">PM:29202912</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-DalyM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-DalyM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Daly M</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0398</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86936</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Taylor,S.B.</style></author><author><style face="normal" font="default"> Christensen,G.</style></author><author><style face="normal" font="default"> Grinter,K.</style></author><author><style face="normal" font="default"> Sherlock,R.</style></author><author><style face="normal" font="default"> Warren,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergen Bureau, Hobart, TAS, Australia</style></auth-address><titles><title><style face="normal" font="default">The Allergen Bureau VITAL Program</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">This paper sets out the role of the Allergen Bureau and the Voluntary Incidental Trace Allergen Labelling (VITAL) Program from its origin in 2007 to its current iteration, VITAL 2. Herewith are outlined the scientific principles that support the program; the program's application in the food chain; and the benefits of the program's use to the food industry, clinicians, and the allergic consumer. VITAL was developed by the Australian and New Zealand food industry in consultation with multiple stakeholders, including consumer organizations, industry bodies, regulators, and retailers, to provide a standardized, science-based risk assessment process for the investigation of the potential presence of food allergens due to cross-contact and to determine whether, for cases in which the allergen is unable to be removed or controlled consistently, precautionary statements are required. The aim of the program is to provide a consistent process, a standardized approach, and a relevant cross-contact statement to allow the allergic consumer to make an informed decision regarding consumption of food</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0392</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202911">PM:29202911</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-TaylorSB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-TaylorSB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Taylor SB</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0392</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86937</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Slotwinski,E.</style></author><author><style face="normal" font="default"> Almy,D.</style></author><author><style face="normal" font="default"> Viator,R.</style></author><author><style face="normal" font="default"> Abouzied,M.</style></author><author><style face="normal" font="default"> Klein,F.</style></author><author><style face="normal" font="default"> Rice,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Neogen Corp., 620 Lesher Pl., Lansing, MI 48912</style></auth-address><titles><title><style face="normal" font="default">Development and Validation of a Quantitative ELISA for the Detection of Almond Residues in Foods</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Neogen Corp. has developed Veratox for Almond Allergen for use in the quantitative analysis and screening of almond protein residues in food products, such as cookies, crackers, chocolate bars, cereals, beverages, and clean-in-place rinses. Quantitation with Veratox for Almond Allergen ranges from 2.5 to 25 ppm and, with dilution, it can be extended for highly positive samples. This paper describes the findings of internal testing and validation studies designed to establish product claims for the assay of Veratox for Almond Allergen</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0401</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202917">PM:29202917</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-SlotwinskiE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-SlotwinskiE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Slotwinski E</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0401</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86938</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Brockmeyer,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">University Stuttgart, Institute of Biochemistry and Technical Biochemistry, Department of Food Chemistry, Allmandring 5b, 70563 Stuttgart, Germany</style></auth-address><titles><title><style face="normal" font="default">Novel Approaches for the MS-Based Detection of Food Allergens: High Resolution, MS(3), and Beyond</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">The prevalence of allergic reactions to food is believed to be increasing in industrialized countries worldwide. One of the major tasks in risk management is, therefore, the analytical surveillance of allergen contamination in food and targeted proteomics using MS, which is of hugely growing interest due to its specificity and sensitivity and the possibility to analyze multiple allergens in parallel. Though approximately 200 different foods have been described as having the potential to elicit allergic reactions, current regional labeling requirements are focused on the 5-14 priority allergens that elicit the vast majority of severe reactions or that pose a risk as hidden allergens in food production. MS-based detection methods have been published for the majority of priority allergens, and this review provides an overview of the different methodological approaches, namely multiple-reaction monitoring-, high-resolution MS-, and triple-stage MS-based methods. In addition, requirements for the identification and validation of specific marker peptides and the influence of thermal processing and structural heterogeneity of allergens are discussed</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0402</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202915">PM:29202915</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-BrockmeyerJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-BrockmeyerJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Brockmeyer J</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0402</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86939</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nitride,C.</style></author><author><style face="normal" font="default"> Lee,V.</style></author><author><style face="normal" font="default"> Baricevic-Jones,I.</style></author><author><style face="normal" font="default"> Adel-Patient,K.</style></author><author><style face="normal" font="default"> Baumgartner,S.</style></author><author><style face="normal" font="default"> Mills,E.N.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Lr:14636232Lr:14636233Lr:14636234Lr:14636235</style></auth-address><titles><title><style face="normal" font="default">Integrating Allergen Analysis Within a Risk Assessment Framework: Approaches to Development of Targeted Mass Spectrometry Methods for Allergen Detection and Quantification in the iFAAM Project</style></title><secondary-title><style face="normal" font="default">J AOAC Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J AOAC Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Allergen analysis is central to implementing and monitoring food allergen risk assessment and management processes by the food industry, but current methods for the determination of allergens in foods give highly variable results. The European Union-funded "Integrated Approaches to Food Allergen and Allergy Risk Management" (iFAAM) project has been working to address gaps in knowledge regarding food allergen management and analysis, including the development of novel MS and immuno-based allergen determination methods. Common allergenic food ingredients (peanut, hazelnut, walnut, cow's milk [Bos domesticus], and hen's egg [Gallus domesticus]) and common food matrixes (chocolate dessert and cookie) have been used for both clinical studies and analytical method development to ensure that the new methods are clinically relevant. Allergen molecules have been used as analytical targets and allergenic ingredients incurred into matrixes at levels close to reference doses that may trigger the use of precautionary allergen labeling. An interlaboratory method comparison has been undertaken for the determination of peanut in chocolate dessert using MS and immuno-based methods. The iFAAM approach has highlighted the need for methods to report test results in allergenic protein. This will allow food business operators to use them in risk assessments that are founded on clinical study data in which protein has been used as a measure of allergenic potency</style></abstract><notes><style face="normal" font="default">IS - 1060-3271 (Print)IS - 1060-3271 (Linking)LA - engPT - Journal ArticleCO - United KIngdom -CO - France -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.5740/jaoacint.17-0393</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29202914">PM:29202914</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J AOAC Int\20171205-NitrideC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J AOAC Int\20171205-NitrideC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Nitride C</style></custom2><misc3><style face="normal" font="default">10.5740/jaoacint.17-0393</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86943</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,C.F.</style></author><author><style face="normal" font="default"> Yang,C.C.</style></author><author><style face="normal" font="default"> Wang,I.J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Association between allergic diseases, allergic sensitization and attention-deficit/hyperactivity disorder in children: A large-scale, population-based study</style></title><secondary-title><style face="normal" font="default">J Chin Med Assoc</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Chin Med Assoc</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">ADHD</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Atopic disorders</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Cockroaches</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1726-4901</style></isbn><abstract><style face="normal" font="default">Background Increasing prevalence of allergic diseases has been matched by parallel trends in attention-deficit/hyperactivity disorder (ADHD). However, previous studies concerning the association between ADHD and allergic diseases have been inconsistent. Moreover, it is not clear whether this association is modified by allergic sensitization status. Therefore, we evaluated the association between allergic diseases, allergic sensitization, and ADHD in children. Methods We conducted a large-scale cross-sectional, population-based survey to investigate the relationship between allergic diseases, allergic sensitization, and ADHD. Children aged between 3 and 6 years were selected from kindergartens, and received skin prick tests (SPTs) for mite, cockroach, dog, milk, egg, and crab allergens. Information about allergic diseases, environmental exposures, and physician-diagnosed ADHD were collected. Multiple logistic regressions were performed to estimate the association between allergic diseases and ADHD, with adjustments made for potential confounders. Result A total of 2772 children were found to be eligible for analysis; of these 411 (14.8%) had atopic dermatitis (AD), 954 (34.4%) had allergic rhinitis (AR), 451 (16.3%) had asthma, and 28 (1.01%) had ADHD. Children who had AD and asthma with allergic sensitization were found to be at increased risk for ADHD, with adjusted ORs (95% CI) of 4.50 (1.28</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô15.86) and 3.65 (1.07</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô12.49). Children who had AR, allergic conjunctivitis, or food allergies were also related to ADHD, though failed to reach statistical significance. Conclusion Our results suggest that AD and asthma with allergic sensitization are associated with ADHD in children. As allergic sensitization is an increased factor of developing allergic diseases, early control of environmental and allergens exposure could help to modify the burden of ADHD</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Taiwan -</style></notes><work-type><style face="normal" font="default">10.1016/j.jcma.2017.07.016</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29239851">PM:29239851</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Chin Med Assoc\20171124-YangCF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Chin Med Assoc\20171124-YangCF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Yang CF</style></custom2><misc3><style face="normal" font="default">10.1016/j.jcma.2017.07.016</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86947</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ohsaki,A.</style></author><author><style face="normal" font="default"> Venturelli,N.</style></author><author><style face="normal" font="default"> Buccigrosso,T.M.</style></author><author><style face="normal" font="default"> Osganian,S.K.</style></author><author><style face="normal" font="default"> Lee,J.</style></author><author><style face="normal" font="default"> Blumberg,R.S.</style></author><author><style face="normal" font="default"> Oyoshi,M.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Immunology, Boston Children's Hospital, Boston, MA</style></auth-address><titles><title><style face="normal" font="default">Maternal IgG immune complexes induce food allergen-specific tolerance in offspring</style></title><secondary-title><style face="normal" font="default">J Exp Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Exp Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">The role of maternal immune responses in tolerance induction is poorly understood. To study whether maternal allergen sensitization affects offspring susceptibility to food allergy, we epicutaneously sensitized female mice with ovalbumin (OVA) followed by epicutaneous sensitization and oral challenge of their offspring with OVA. Maternal OVA sensitization prevented food anaphylaxis, OVA-specific IgE production, and intestinal mast cell expansion in offspring. This protection was mediated by neonatal crystallizable fragment receptor (FcRn)-dependent transfer of maternal IgG and OVA immune complexes (IgG-IC) via breast milk and induction of allergen-specific regulatory T (T reg) cells in offspring. Breastfeeding by OVA-sensitized mothers or maternal supplementation with IgG-IC was sufficient to induce neonatal tolerance. FcRn-dependent antigen presentation by CD11c(+) dendritic cells (DCs) in offspring was required for oral tolerance. Human breast milk containing OVA-IgG-IC induced tolerance in humanized FcRn mice. Collectively, we demonstrate that interactions of maternal IgG-IC and offspring FcRn are critical for induction of T reg cell responses and control of food-specific tolerance in neonates</style></abstract><notes><style face="normal" font="default">IS - 1540-9538 (Electronic)IS - 0022-1007 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1084/jem.20171163</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29158374">PM:29158374</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Exp Med\20171120-OhsakiA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Exp Med\20171120-OhsakiA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Ohsaki A</style></custom2><misc3><style face="normal" font="default">10.1084/jem.20171163</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86948</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xi,J.</style></author><author><style face="normal" font="default"> He,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">High hydrostatic pressure (HHP) effects on antigenicity and structural properties of soybean +¦-conglycinin</style></title><secondary-title><style face="normal" font="default">J Food Sci Technol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Food Sci Technol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0975-8402</style></isbn><abstract><style face="normal" font="default">In this study, the effect of high hydrostatic pressure (HHP) on antigenicity, free sulfhydryl group (SH) content, hydrophobicity (Ho), fluorescence intensity and circular dichroism data of soybean ß-conglycinin was studied. The antigenicity of soybean ß-conglycinin was decreased significantly at pressures 200-400 MPa. The antigenicity inhibition rate of ß-conglycinin declined from 92.72 to 55.15%, after being treated at 400 MPa for 15 min. Results indicated that free sulphydryl (SH) groups and surface Ho of ß-conglycinin were significantly increased at pressures 200-400 MPa and 5-15 min, whereas these properties decreased at the treatments above 400 MPa and 15 min. The maximum fluorescence intensity was noticed at 400 MPa and 15 min. The circular dichroism data analysis revealed that the amount of ß-turns and unordered structure significantly increased, while the content of a-helix1 and ß-strand1 noticeably decreased. These results provide evidence that HHP-induced the structural modification of ß-conglycinin and could alter the antigenicity of ß-conglycinin.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s13197-017-2972-2</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s13197-017-2972-2</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Food Sci Technol\20171125-XiJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Food Sci Technol\20171125-XiJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171125, Xi J</style></custom2><misc3><style face="normal" font="default">10.1007/s13197-017-2972-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86950</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kiyotani,K.</style></author><author><style face="normal" font="default"> Mai,T.H.</style></author><author><style face="normal" font="default"> Yamaguchi,R.</style></author><author><style face="normal" font="default"> Yew,P.Y.</style></author><author><style face="normal" font="default"> Kulis,M.</style></author><author><style face="normal" font="default"> Orgel,K.</style></author><author><style face="normal" font="default"> Imoto,S.</style></author><author><style face="normal" font="default"> Miyano,S.</style></author><author><style face="normal" font="default"> Burks,A.W.</style></author><author><style face="normal" font="default"> Nakamura,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, The University of Chicago, Chicago, IL, 60637, USA</style></auth-address><titles><title><style face="normal" font="default">Characterization of the B-cell receptor repertoires in peanut allergic subjects undergoing oral immunotherapy</style></title><secondary-title><style face="normal" font="default">J Hum Genet</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Hum Genet</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Quantitative real-time PCR</style></keyword></keywords><dates><year Day="30" Month="11" Year="2017">2017/11/30</year></dates><abstract><style face="normal" font="default">B-cell receptors (BCRs) play a critical role in adaptive immunity as they generate highly diverse immunoglobulin repertoires to recognize a wide variety of antigens. To better understand immune responses, it is critically important to establish a quantitative and rapid method to analyze BCR repertoire comprehensively. Here, we developed "Bcrip", a novel approach to characterize BCR repertoire by sequencing millions of BCR cDNA using next-generation sequencer. Using this method and quantitative real-time PCR, we analyzed expression levels and repertoires of BCRs in a total of 17 peanut allergic subjects' peripheral blood samples before and after receiving oral immunotherapy (OIT) or placebo. By our methods, we successfully identified all of variable (V), joining (J), and constant (C) regions, in an average of 79.1% of total reads and 99.6% of these VJC-mapped reads contained the C region corresponding to the isotypes that we aimed to analyze. In the 17 peanut allergic subjects' peripheral blood samples, we observed an oligoclonal enrichment of certain immunoglobulin heavy chain alpha (IGHA) and IGH gamma (IGHG) clones (P = 0.034 and P = 0.027, respectively) in peanut allergic subjects after OIT. This newly developed BCR sequencing and analysis method can be applied to investigate B-cell repertoires in various research areas, including food allergies as well as autoimmune and infectious diseases</style></abstract><notes><style face="normal" font="default">IS - 1435-232X (Electronic)IS - 1434-5161 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Japan -</style></notes><work-type><style face="normal" font="default">10.1038/s10038-017-0364-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29192240">PM:29192240</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK_MOESM3_ESM.xlsxC:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK_MOESM4_ESM.xlsxC:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK_MOESM5_ESM.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK_MOESM3_ESM.xlsxF:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK_MOESM4_ESM.xlsxF:\A&amp;H HMW Papers\J Hum Genet\20171130-KiyotaniK_MOESM5_ESM.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20171130, Kiyotani K</style></custom2><misc3><style face="normal" font="default">10.1038/s10038-017-0364-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86952</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Herreros,B.</style></author><author><style face="normal" font="default"> Mendez,Y.</style></author><author><style face="normal" font="default"> Feo-Brito,F.</style></author><author><style face="normal" font="default"> Urra,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunology, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain</style></auth-address><titles><title><style face="normal" font="default">Usefulness of basophil activation test for the diagnosis of IgE mediated hypersensitivity to tetanus toxoid vaccine</style></title><secondary-title><style face="normal" font="default">J Immunol Methods</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol Methods</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">A great number of vaccinated patients develop specific anti-tetanus toxoid IgE, but usually do not undergo any adverse effect. Most of the allergic reactions to tetanus toxoid vaccine usually present with unspecific symptoms of local inflammation. In the presence of severe reactions, and in a special way if the vaccine is provided together with other drugs, it is difficult to establish which is the harmful drug responsible for IgE-mediated adverse reaction. A patient with an anaphylactic reaction after the administration of Toxoid Tetanic (TT) along with several drugs is described. All skin test were negative. The basophils activation test (BAT) in a clear way, identified TT as the allergen that triggered anaphylaxis. The results achieved demonstrates the usefulness of BAT to clarify patients with hypersensibility to tetanus toxoide when the clinic is severe and the vaccine has been administered together with other drugs</style></abstract><notes><style face="normal" font="default">IS - 1872-7905 (Electronic)IS - 0022-1759 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.jim.2017.11.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29162425">PM:29162425</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol Methods\20171121-HerrerosB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol Methods\20171121-HerrerosB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Herreros B</style></custom2><misc3><style face="normal" font="default">10.1016/j.jim.2017.11.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86954</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,D.I.</style></author><author><style face="normal" font="default"> Kang,S.A.</style></author><author><style face="normal" font="default"> Md,A.</style></author><author><style face="normal" font="default"> Jeong,U.C.</style></author><author><style face="normal" font="default"> Jin,F.</style></author><author><style face="normal" font="default"> Kang,S.J.</style></author><author><style face="normal" font="default"> Lee,J.Y.</style></author><author><style face="normal" font="default"> Yu,H.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">1 Department of Parasitology and Tropical Medicine, School of Medicine, Pusan National University , Yangsan-si, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Sea Cucumber Lipid-Soluble Extra Fraction Prevents Ovalbumin-Induced Allergic Airway Inflammation</style></title><secondary-title><style face="normal" font="default">J Med Food</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Med Food</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">In a previous study, our research group demonstrated that sea cucumber (Apostichopus japonicus) extracts ameliorated allergic airway inflammation through CD4(+)CD25(+)Foxp3(+) T (regulatory T; Treg) cell activation and recruitment to the lung. In this study, we aimed to determine which components of sea cucumber contribute to the amelioration of airway inflammation. We used n-hexane fractionation to separate sea cucumber into three phases (n-hexane, alcohol, and solid) and evaluated the ability of each phase to elevate Il10 expression in splenocytes and ameliorate symptoms in mice with ovalbumin (OVA)/alum-induced asthma. Splenocytes treated with the n-hexane phase showed a significant increase in Il10 expression. In the n-hexane phase, 47 fatty acids were identified. Individual fatty acids that comprised at least 5% of the total fatty acids were 16:0, 16:1n-7, 18:0, 18:1n-7, 20:4n-6, and 20:5n-3 (eicosapentaenoic acid). After administering the n-hexane phase to mice with OVA/alum-induced asthma, their asthma symptoms were ameliorated. Several immunomodulatory effects were observed in the n-hexane phase-pretreated group, compared with a vehicle control group. First, eosinophil infiltration and goblet cell hyperplasia were significantly reduced around the airways. Second, the concentrations of Th2-related cytokines (IL-4, IL-5, and IL-13) and Th17-related cytokines (IL-17) were significantly decreased in the spleen and bronchoalveolar lavage fluid (BALF). Finally, the concentrations of TGF-beta and IL-10, which are associated with Treg cells, were significantly increased in the BALF and splenocyte culture medium. In conclusion, a fatty acid-rich fraction (n-hexane phase) of sea cucumber extract ameliorated allergic airway inflammation in a mouse model</style></abstract><notes><style face="normal" font="default">IS - 1557-7600 (Electronic)IS - 1096-620X (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1089/jmf.2017.3994</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29161525">PM:29161525</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Med Food\20171121-LeeDI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Med Food\20171121-LeeDI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Lee DI</style></custom2><misc3><style face="normal" font="default">10.1089/jmf.2017.3994</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86955</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ulambayar,B.</style></author><author><style face="normal" font="default"> Chen,Y.H.</style></author><author><style face="normal" font="default"> Ban,G.Y.</style></author><author><style face="normal" font="default"> Lee,J.H.</style></author><author><style face="normal" font="default"> Jung,C.G.</style></author><author><style face="normal" font="default"> Yang,E.M.</style></author><author><style face="normal" font="default"> Park,H.S.</style></author><author><style face="normal" font="default"> Ye,Y.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea</style></auth-address><titles><title><style face="normal" font="default">Detection of circulating IgG autoantibody to FcepsilonRIalpha in sera from chronic spontaneous urticaria patients</style></title><secondary-title><style face="normal" font="default">J Microbiol Immunol Infect</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Microbiol Immunol Infect</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">BACKGROUNDS: Chronic spontaneous urticaria (CSU) is a common skin disorder characterized by itchy wheals of at least 6 weeks in duration, wherein the autoimmune mechanism is involved to activate IgE receptors (FcepsilonRIalpha) on mast cells. We aimed to assess levels of IgG autoantibody against FcepsilonRIalpha in sera from CSU patients using dot-blot immunoassay. METHODS: We performed a hospital-based cross-sectional study of 125 CSU patients (64 ASST-positive, 61 ASST-negative) and 64 age-and sex-matched healthy controls. The cut-off value of IgG FcepsilonRIalpha autoantibody was determined as the mean intensity plus two standard deviations of values in controls. Positivity for IgG autoantibody to FcepsilonRIalpha was analyzed according to clinical parameters of disease duration, urticaria activity score (UAS), ASST, response to antihistamine treatment, complement levels, and the presence of other autoantibodies. Nonparametric tests were applied for statistical analyses. RESULTS: IgG positivity to FcepsilonRIalpha was noted in 24.8% of CSU patients and was significantly more frequent in ASST-positive patients than in ASST-negative patients (32.8% vs 16.4%, P = 0.040). Only 3.1% of healthy controls had this autoantibody. Complement 3 levels were significantly lower in anti-FcepsilonRIalpha antibody-positive patients than antibody-negative patients (109.8 +/- 19.9 vs 123.1 +/- 30.9, P = 0.035). No significant associations were found between IgG positivity to FcepsilonRIalpha and UAS, serum total IgE levels, atopic status, clinical responses to antihistamines, or the presence of anti-thyroid and anti-nuclear antibodies. CONCLUSION: These findings suggest that circulating IgG autoantibody to FcepsilonRIalpha in a subset of patients may be involved in the autoimmune mechanism of CSU. Further studies are needed to clarify its clinical significance</style></abstract><notes><style face="normal" font="default">IS - 1995-9133 (Electronic)IS - 1684-1182 (Linking)LA - engPT - Journal ArticleCO - South Korea -CO - Taiwan -</style></notes><work-type><style face="normal" font="default">10.1016/j.jmii.2017.10.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29169972">PM:29169972</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Microbiol Immunol Infect\20171114-UlambayarB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Microbiol Immunol Infect\20171114-UlambayarB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Ulambayar B</style></custom2><misc3><style face="normal" font="default">10.1016/j.jmii.2017.10.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86957</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Savilahti,E.M.</style></author><author><style face="normal" font="default"> Ilonen,J.</style></author><author><style face="normal" font="default"> Kukkonen,A.K.</style></author><author><style face="normal" font="default"> Savilahti,E.</style></author><author><style face="normal" font="default"> Kuitunen,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">the Children's Hospital, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland</style></auth-address><titles><title><style face="normal" font="default">Celiac Disease by The Age of 13 Years is Not Associated With Probiotics Administration in Infancy</style></title><secondary-title><style face="normal" font="default">J Pediatr Gastroenterol Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pediatr Gastroenterol Nutr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword></keywords><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">Probiotics are theoretically promising in primary prevention of celiac disease (CD), but research evidence on the topic is scarce. We used the data and material of a clinical double-blind randomized placebo-controlled trial on primary allergy prevention (n = 1223) to investigate in an exploratory study whether administration of a mix of pro- and prebiotics during late pregnancy and first 6 months of life was associated with prevalence of CD during 13-year follow-up. Children who fulfilled diagnostic criteria for CD (n = 11) and subjects with a serum sample available for analyzing CD-antibodies (n = 867) were included. CD or elevated tissue transglutaminase IgA antibodies were not associated with probiotics or placebo. Nor were there any associations with the mode of delivery, the duration of exclusive or total breastfeeding or respiratory infections during the first 2 years of life. Allergic diseases or sensitization by the age of 2 or 5 years were not clearly associated with the development of CD</style></abstract><notes><style face="normal" font="default">IS - 1536-4801 (Electronic)IS - 0277-2116 (Linking)LA - engPT - Journal ArticleCO - Finland -</style></notes><work-type><style face="normal" font="default">10.1097/MPG.0000000000001846</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29210921">PM:29210921</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pediatr Gastroenterol Nutr\20171209-SavilahtiEM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pediatr Gastroenterol Nutr\20171209-SavilahtiEM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171209, Savilahti EM</style></custom2><misc3><style face="normal" font="default">10.1097/MPG.0000000000001846</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86959</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mukai,K.</style></author><author><style face="normal" font="default"> Kuda,Y.</style></author><author><style face="normal" font="default"> Shibamoto,T.</style></author><author><style face="normal" font="default"> Tanida,M.</style></author><author><style face="normal" font="default"> Kurata,Y.</style></author><author><style face="normal" font="default"> Yokoyama,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Nephrology, Kanazawa Medical University, Ishikawa, 920-0293, Japan</style></auth-address><titles><title><style face="normal" font="default">Renal response to anaphylaxis in anesthetized rats and isolated perfused rat kidneys: roles of nitric oxide</style></title><secondary-title><style face="normal" font="default">J Physiol Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Physiol Sci</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">We determined the renal responses to anaphylaxis and the effects of a nitric oxide synthesis inhibitor, L-NAME, in anesthetized rats and isolated perfused rat kidneys. After the ovalbumin antigen injection, the sensitized rats showed transient and substantial decreases in mean blood pressure and renal blood flow and an increase in renal vascular resistance. Creatinine clearance, a measure of renal function, decreased to 53% baseline at 2 h after antigen. L-NAME pretreatment significantly enhanced the antigen-induced renal vasoconstriction and renal dysfunction. Moreover, plasma creatinine levels significantly increased only in the L-NAME pretreated rats. Separately, in isolated perfused kidneys, we observed the antigen-induced renal vasoconstriction and its augmentation by L-NAME. In conclusion, the renal vascular response to the antigen is vasoconstriction, which is enhanced by L-NAME in both isolated perfused rat kidneys and anesthetized rats; it is accompanied by renal dysfunction, which is also augmented by L-NAME</style></abstract><notes><style face="normal" font="default">IS - 1880-6562 (Electronic)IS - 1880-6546 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1007/s12576-017-0583-3</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29209891">PM:29209891</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Physiol Sci\20171205-MukaiK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Physiol Sci\20171205-MukaiK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Mukai K</style></custom2><misc3><style face="normal" font="default">10.1007/s12576-017-0583-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86962</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cirillo,I.</style></author><author><style face="normal" font="default"> Gallo,F.</style></author><author><style face="normal" font="default"> Ciprandi,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Respiratory Medicine and Allergy, Italian Navy, La Spezia, ItalyBiostatistics Dept, Universita degli Studi di Genova Scuola di Scienze Mediche e Farmaceutiche, Genova, Liguria, ItalyInternal Medicine, Ospedale Policlinico San Martino, Genova, Italy</style></auth-address><titles><title><style face="normal" font="default">Could routine spirometry suggest sensitisation in the military medicine setting?</style></title><secondary-title><style face="normal" font="default">J R Army Med Corps</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J R Army Med Corps</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Providing evidence of sensitisation is the formal requirement for allergy diagnosis. The aim of this study was to evaluate whether spirometry may be able to predict sensitisation in a representative cohort of Italian Navy military personnel. METHODS: 2043 (1875 men, 168 women, mean age 28.35+/-11.6 years) Italian Navy military personnel were enrolled into this study. Spirometry and skin prick testing were performed to predict sensitisation. RESULTS: Sensitisation, assessed by skin prick test, was documented in 658 (32.2%) subjects. Impaired forced expiratory flow at the 25% and 75% of the pulmonary volume (FEF25-75) as demonstrated on spirometry was detected in 82 subjects, of whom 69 were sensitised (P&lt;0.0001). Impaired FEF25-75 was significantly associated with sensitisation (OR 7.43; 95% CI 4.04 to 14.66; P&lt;0.0001). DISCUSSION: The findings of this study suggest that impaired FEF25-75 may predict sensitisation in this cohort of Italian Navy personnel. This outcome is relevant in the military medical setting, as it could allow early identification of subjects with subclinical asthma</style></abstract><notes><style face="normal" font="default">IS - 0035-8665 (Print)IS - 0035-8665 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1136/jramc-2017-000841</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29176005">PM:29176005</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto - 1 anno</url></related-urls></urls><custom2><style face="normal" font="default">20171124, Cirillo I</style></custom2><misc3><style face="normal" font="default">10.1136/jramc-2017-000841</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86963</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Stanciuc,N.</style></author><author><style face="normal" font="default"> Cretu,A.A.</style></author><author><style face="normal" font="default"> Banu,I.</style></author><author><style face="normal" font="default"> Aprodu,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dunarea de Jos University of Galati, Faculty of Food Science and Engineering, Domneasca Street 111, 800201, Galati, Romania</style></auth-address><titles><title><style face="normal" font="default">Advances on the impact of thermal processing on structure and antigenicity of chicken ovomucoid</style></title><secondary-title><style face="normal" font="default">J Sci Food Agric</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Sci Food Agric</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Conformation</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Ovomucoid (OVM) is the dominant allergen found in egg white. The heat induced changes on chicken OVM structure and antigenic properties were assessed at acidic, neutral and alkaline pH values. RESULTS: The fluorescence spectroscopy measurements indicated changes in the conformation of OVM caused by both pH and thermal treatment. The OVM molecule exhibited higher exposure of hydrophobic residues at 7.0, as indicated by the synchronous spectra, intrinsic fluorescence and quenching experiments. When heating the protein at pH 9.5, the molecular structure appeared more compact. The antigenic properties of OVM, estimated through the enzyme-linked immunosorbent assay, appeared not to be sensitive to heat at pH 7.0 and 4.5. Single molecule level investigations indicated that the secondary and tertiary structure of OVM was affected by the thermal treatment. CONCLUSIONS: Experimental results indicated over 90% reduction of the antigenicity at pH 9.5 and temperature of 100 degrees C. Significant changes of the linear epitopes exposure and location of the conformational epitopes were highlighted after performing heating molecular dynamics simulations of OVM from 25 degrees C to 100 degrees C</style></abstract><notes><style face="normal" font="default">IS - 1097-0010 (Electronic)IS - 0022-5142 (Linking)LA - engPT - Journal ArticleCO - Romania -</style></notes><work-type><style face="normal" font="default">10.1002/jsfa.8813</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29210457">PM:29210457</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Sci Food Agric\20171206-StanciucN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Sci Food Agric\20171206-StanciucN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171206, Stanciuc N</style></custom2><misc3><style face="normal" font="default">10.1002/jsfa.8813</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86964</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Graziano,S.</style></author><author><style face="normal" font="default"> Gulli,M.</style></author><author><style face="normal" font="default"> Marmiroli,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, Parco Area delle Scienze 11/A, 43124, Parma, ItalyDepartment of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, Parco Area delle Scienze 11/A, 43124, Parma, ItalyInterdepartmental Center SITEIA.PARMA, University of Parma, Parco Area delle Scienze 181/A, 43124, Parma, ItalyDepartment of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, Parco Area delle Scienze 11/A, 43124, Parma, ItalyInterdepartmental Center SITEIA.PARMA, University of Parma, Parco Area delle Scienze 181/A, 43124, Parma, Italy</style></auth-address><titles><title><style face="normal" font="default">Detection of allergen coding sequences of kiwi, peach, and apple in processed food by qPCR</style></title><secondary-title><style face="normal" font="default">J Sci Food Agric</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Sci Food Agric</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Quantitative real-time PCR</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Food traceability becomes lifesaving for persons suffering severe allergy or intolerance, and therefore need a complete avoidance of the immune-trigger food. This paper describes how to fingerprint the presence of some allergenic species (kiwi, peach, and apple) in foods by quantitative Real-Time PCR (qPCR). RESULTS: Five DNA extraction procedures were tested on fruits and foods. The results were statistically evaluated, and discussed. Analysis by qPCR with SYBR Green was developed to detect traces of these allergenic species in foods. Plasmids containing the target sequences of kiwi, peach and apple were employed as Internal Reference Standard. Analysis of spiked food samples showed a Limit of Detection of 25 mg kg(-1) for kiwi, 20 mg kg(-1) for peach and 50 mg kg(-1) for apple. CONCLUSION: The qPCR method here developed, combined with the use of Internal Plasmid Reference Standard, represent a specific system for the quick detection of allergenic species in complex food matrices, with a Limit of Detection comparable with those reported using more time-consuming methods</style></abstract><notes><style face="normal" font="default">IS - 1097-0010 (Electronic)IS - 0022-5142 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1002/jsfa.8814</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29210450">PM:29210450</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Sci Food Agric\20171206-GrazianiS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Sci Food Agric\20171206-GrazianiS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20161206, Graziano S</style></custom2><misc3><style face="normal" font="default">10.1002/jsfa.8814</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86965</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Miyashita,K.</style></author><author><style face="normal" font="default"> Ohori,J.</style></author><author><style face="normal" font="default"> Nagano,H.</style></author><author><style face="normal" font="default"> Fukuyama,S.</style></author><author><style face="normal" font="default"> Kurono,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology-Head and Neck Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan</style></auth-address><titles><title><style face="normal" font="default">Intranasal immunization with phosphorylcholine suppresses allergic rhinitis in mice</style></title><secondary-title><style face="normal" font="default">Laryngoscope</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Laryngoscope</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">OBJECTIVES/HYPOTHESIS: Intranasal immunization with phosphorylcholine (PC) is known to reduce immunoglobulin (Ig)E production. However, its effects on the occurrence of allergic rhinitis (AR) are unknown. This study was performed to evaluate the effects of PC-keyhole limpet hemocyanin (PC-KLH) and to examine the effects on the occurrence of AR in a murine model of AR. STUDY DESIGN: In vivo study using an animal model. METHODS: Forty-five female BALB/c mice were divided into three groups; those pretreated with intranasal administration of PC-KLH followed by intraperitoneal sensitization and nasal challenge with ovalbumin (OVA) (group A), those untreated with PC-KLH followed by sensitization and nasal challenge with OVA (group B), and those untreated with PC-KLH or OVA as controls (group C). Nasal symptoms, allergic inflammation in the nasal mucosa, OVA specific IgE production, and cytokine profile were compared among those three groups. Dendritic cells (DCs) were isolated from splenic cells and PC-KLH-stimulated interleukin (IL)-12p40 production was measured. RESULTS: The mice pretreated with PC-KLH showed lower allergic nasal symptoms and inflammation compared to untreated mice. The levels of total IgE and OVA-specific IgE in serum, and IL-4 production by nasal and splenic CD4(+) T cells were significantly reduced by PC-KLH pretreatment. Furthermore, IL-12p40 production by DCs was induced by PC-KLH in a dose-dependent manner. CONCLUSIONS: Intranasal administration of PC-KLH suppressed allergic inflammation in nasal mucosa and antigen-specific IgE production by downregulating Th2-type immune response. Intranasal immunization with PC might be useful to prevent AR and upper airway bacterial infection. LEVEL OF EVIDENCE: NA Laryngoscope, 2017</style></abstract><notes><style face="normal" font="default">IS - 1531-4995 (Electronic)IS - 0023-852X (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1002/lary.27030</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29193138">PM:29193138</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Laryngoscope\20171129-MiyashitaK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Laryngoscope\20171129-MiyashitaK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Miyashita K</style></custom2><misc3><style face="normal" font="default">10.1002/lary.27030</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86967</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hannya,N.</style></author><author><style face="normal" font="default"> Ogita-Nakanishi,H.</style></author><author><style face="normal" font="default"> Kato,R.</style></author><author><style face="normal" font="default"> Ijiri,Y.</style></author><author><style face="normal" font="default"> Hayashi,T.</style></author><author><style face="normal" font="default"> Tanaka,K.</style></author><author><style face="normal" font="default"> Kawata,R.</style></author><author><style face="normal" font="default"> Takenaka,H.</style></author><author><style face="normal" font="default"> Kubota,T.</style></author><author><style face="normal" font="default"> Yoshida,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Departments of Physiology, Osaka Medical College, Takatsuki 569-8686, Japan</style></auth-address><titles><title><style face="normal" font="default">The 1(st) step essential for allergen-specific IgE antibody production upon the 2(nd) step: Induction of non-specific IgE(+) small B cells containing secondly-sensitized allergen-specific ones in mice firstly-sensitized with an allergen</style></title><secondary-title><style face="normal" font="default">Microbiol Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Microbiol Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">There was a significant amount of non-specific, but not of allergen (e.g., papain, mite feces, and 4 kinds of pollen)-specific, IgE antibodies (Abs) in the serum of normal mice. An intranasal (i.n.) injection of each allergen without adjuvant into mice caused an increase in total IgE Ab titers with a similar time course in the serum; but the stage in the initiation of allergy varied from allergen to allergen. Submandibular lymph node cells from normal mice contained papain-, but not mite feces- or pollen-specific IgE(+) cells; and an i.n. injection of papain induced papain-specific IgE Abs in the serum. In contrast, 1 (i.n.) or 2 [i.n. and subcutaneous (s.c.)] injections of mite feces induced neither mite feces-specific IgE(+) cells in the lymph nodes nor mite feces-specific IgE Abs in the serum. An i.n. sensitization with cedar pollen induced cedar pollen-specific IgE(+) small B cells in the lymph nodes on day 10, when non-specific IgE Ab titers reached a peak in the serum, implying the induction of related allergen-specific IgE(+) small cells as well. In fact, a 2(nd) (s.c.) injection of ragweed (or cedar) pollen into mice sensitized i.n. once with cedar (or ragweed) pollen, but not with mite feces, induced a large amount of ragweed (or cedar) pollen-specific IgE Abs in the serum. These results revealed that when non-specific IgE(+) small B cells in the lymph nodes from mice firstly-sensitized with an allergen contained secondly-sensitized allergen-specific ones, the mice produced IgE Abs specific for the secondly-injected allergen</style></abstract><notes><style face="normal" font="default">IS - 1348-0421 (Electronic)IS - 0385-5600 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/1348-0421.12558</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29193290">PM:29193290</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Microbiol Immunol\20171129-HannyaN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Microbiol Immunol\20171129-HannyaN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Hannya N</style></custom2><misc3><style face="normal" font="default">10.1111/1348-0421.12558</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86970</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hwang,Y.H.</style></author><author><style face="normal" font="default"> Hong,S.G.</style></author><author><style face="normal" font="default"> Mun,S.K.</style></author><author><style face="normal" font="default"> Kim,S.J.</style></author><author><style face="normal" font="default"> Lee,S.J.</style></author><author><style face="normal" font="default"> Kim,J.J.</style></author><author><style face="normal" font="default"> Kang,K.Y.</style></author><author><style face="normal" font="default"> Yee,S.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">College of Pharmacy, Sunchon National University, 255 Jungangno, Suncheon 540-950, Korea.</style></auth-address><titles><title><style face="normal" font="default">The Protective Effects of Astaxanthin on the OVA-Induced Asthma Mice Model</style></title><secondary-title><style face="normal" font="default">Molecules</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Molecules</style></abbr-1></periodical><pages end="" start="">-</pages><volume><style face="normal" font="default">22</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Respiratory System</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">Although astaxanthin has a variety of biological activities such as anti-oxidant effects, inhibitory effects on skin deterioration and anti-inflammatory effects, its effect on asthma has not been studied. In this paper, the inhibitory effect of astaxanthin on airway inflammation in a mouse model of ovalbumin (OVA)-induced asthma was investigated. We evaluated the number of total cells, Th1/2 mediated inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and airway hyperresponsiveness as well as histological structure. The level of total IgE, IgG1, IgG2a, OVA-specific IgG1, and OVA-specific IgG2a were also examined. The oral administration of 50 mg/mL astaxanthin inhibited the respiratory system resistance, elastance, newtonian resistance, tissue damping, and tissue elastance. Also, astaxanthin suppressed the total cell number, IL-4, and IL-5, and increased the IFN-gamma in the BALF. In the sera, total IgE, IgG1, and OVA-specific IgG1 were reduced by astaxanthin exposure and IgG2a and OVA-specific IgG2a were enhanced via oral administration of astaxanthin. Infiltration of inflammatory cells in the lung, production of mucus, lung fibrosis, and expression of caspase-1 or caspase-3 were suppressed in OVA-induced asthmatic animal treated with astaxanthin. These results suggest that astaxanthin may have therapeutic potential for treating asthma via inhibiting Th2-mediated cytokine and enhancing Th1-mediated cytokine</style></abstract><notes><style face="normal" font="default">IS - 1420-3049 (Electronic)IS - 1420-3049 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.3390/molecules22112019</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29160801">PM:29160801</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Molecules\20171121-HwangY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Molecules\20171121-HwangY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Hwang YH</style></custom2><misc3><style face="normal" font="default">10.3390/molecules22112019</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86976</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">El-Zaemey,S.</style></author><author><style face="normal" font="default"> Carey,R.N.</style></author><author><style face="normal" font="default"> Darcey,E.</style></author><author><style face="normal" font="default"> Reid,A.</style></author><author><style face="normal" font="default"> Glass,D.C.</style></author><author><style face="normal" font="default"> Benke,G.P.</style></author><author><style face="normal" font="default"> Driscoll,T.R.</style></author><author><style face="normal" font="default"> Peters,S.</style></author><author><style face="normal" font="default"> Si,S.</style></author><author><style face="normal" font="default"> Abramson,M.J.</style></author><author><style face="normal" font="default"> Fritschi,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Public Health, Curtin University, Perth, Western Australia, Australia</style></auth-address><titles><title><style face="normal" font="default">Prevalence of occupational exposure to asthmagens derived from animals, fish and/or shellfish among Australian workers</style></title><secondary-title><style face="normal" font="default">Occup Environ Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Occup Environ Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Cooking</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">OBJECTIVE: Several animal, fish and/or shellfish derived substances encountered in the workplace can initiate or exacerbate asthma. The aims of this study were: to produce a population-based estimate of the current prevalence of occupational exposure to animal, fish and/or shellfish derived asthmagens, to identify the main circumstances of exposures and to identify occupations with the highest proportions of exposed respondents. METHODS: We used data from the Australian Work Exposure Study-Asthma, a national telephone survey that investigated the current prevalence of occupational exposure to asthmagens among Australian workers. A web-based tool was used to collect job task information and assign exposure to asthmagens, including animal, fish and/or shellfish derived asthmagens. Prevalence ratios to determine risk factors for exposure were estimated using modified Poisson regression. RESULTS: Of the 4878 respondents, 12.4% were exposed to asthmagens derived from animals, fish and/or shellfish. Exposure to these asthmagens was significantly higher in workers residing in regional and remote areas, compared with major cities. The main circumstance of exposure to animal derived asthmagens was through cleaning up rat/mice infestations, while the main circumstance of exposure to fish and/or shellfish derived asthmagens was through preparing and cooking salmon. Occupational groups with the highest proportion of exposure to animal or fish and/or shellfish derived asthmagens were farmers/animal workers and food workers, respectively. CONCLUSIONS: This is the first study investigating occupational exposure to animal, fish and/or shellfish derived asthmagens in a nationwide working population. The results of this study can be used to inform the direction of occupational interventions and policies to reduce work-related asthma</style></abstract><notes><style face="normal" font="default">IS - 1470-7926 (Electronic)IS - 1351-0711 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1136/oemed-2017-104459</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29175990">PM:29175990</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Occup Environ Med\20171124-ElZaemeyS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Occup Environ Med\20171124-ElZaemeyS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, El-Zaemey S</style></custom2><misc3><style face="normal" font="default">10.1136/oemed-2017-104459</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86978</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nkurunungi,G.</style></author><author><style face="normal" font="default"> Kabagenyi,J.</style></author><author><style face="normal" font="default"> Nampijja,M.</style></author><author><style face="normal" font="default"> Sanya,R.E.</style></author><author><style face="normal" font="default"> Walusimbi,B.</style></author><author><style face="normal" font="default"> Nassuuna,J.</style></author><author><style face="normal" font="default"> Webb,E.L.</style></author><author><style face="normal" font="default"> Elliott,A.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunomodulation and Vaccines Programme, MRC/UVRI Uganda Research Unit, Entebbe, Uganda</style></auth-address><titles><title><style face="normal" font="default">Schistosoma mansoni-specific immune responses and allergy in Uganda</style></title><secondary-title><style face="normal" font="default">Parasite Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Parasite Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">Low allergy-related disease (ARD) prevalence in low-income countries may be partly attributed to helminth infections. In the Schistosoma mansoni (Sm)-endemic Lake Victoria islands (Uganda), we recently observed positive helminth-allergy associations, despite low ARD prevalence. To understand how Sm-induced cytokine and antibody profiles might influence allergic response profiles in this population, we assessed Schistosoma worm (SWA)- and egg antigen (SEA)-specific Th1 (IFN-gamma), Th2 (IL-5, IL-13) and regulatory (IL-10) cytokine profiles (n=407), and total (n=471), SWA-, SEA- and allergen (house dust mite [HDM] and cockroach)-specific (as)IgE and IgG4 profiles (n=2117) by ELISA. Wheeze was inversely associated with SWA-specific IFN-gamma (p&lt;0.001) and IL-10 (p=0.058), and SEA-specific IL-5 (p=0.004). Conversely, having a detectable asIgE response was positively associated with SWA-specific IL-5 (p=0.006) and IL-10 (p&lt;0.001). Total, SWA-, SEA- and allergen-specific IgE and IgG4 responses were higher among Sm Kato-Katz positive (SmKK+) and skin prick test (SPT)+ individuals compared to SmKK- and SPT- individuals. However, total and asIgG4/IgE ratios were lower among SPT+ and wheezing individuals. We conclude that, in this population, helminth-induced antibody and cytokine responses may underlie individual positive helminth-atopy associations, while the overall IgG4-IgE balance may contribute to the low overall prevalence of clinical allergies in such settings. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-3024 (Electronic)IS - 0141-9838 (Linking)LA - engPT - Journal ArticleCO - Uganda -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/pim.12506</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29171863">PM:29171863</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Parasite Immunol\20171124-NkurunungiG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Parasite Immunol\20171124-NkurunungiG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Nkurunungi G</style></custom2><misc3><style face="normal" font="default">10.1111/pim.12506</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86979</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mourglia-Ettlin,G.</style></author><author><style face="normal" font="default"> Miles,S.</style></author><author><style face="normal" font="default"> Hernandez,A.</style></author><author><style face="normal" font="default"> Dematteis,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Area Inmunologia, DEPBIO/Area Inmunologia, DEPBIO/Area Inmunologia, DEPBIO/Area Inmunologia, DEPBIO/</style></auth-address><titles><title><style face="normal" font="default">Ageing impairs parasite-specific antibody responses in cystic echinococcosis</style></title><secondary-title><style face="normal" font="default">Parasite Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Parasite Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Middle Aged</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">Humoral immunity wanes during healthy ageing, increasing susceptibility to infections in the elderly. In this sense, information about parasite infections and human immunosenescence is scarce. Cystic echinococcosis (CE) is an infectious disease caused by the larval stage of the cestode parasite Echinococcus granulosus, whose prevalence in humans shows an increase with host age. Susceptibility to human CE has been associated with humoral immunity to some extent; and therefore, we have here analyzed the influence of host age on the serological profile of young, middle-aged, and aged patients. Our results highlighted the detrimental influence of ageing on the intensity and quality of the anti-parasite antibody response. Remarkable differences in serological profiles between young and aged individuals were observed. In this sense, through Principal Components Analysis we identified aged patients as those exhibiting overall less intense antibody responses, mainly in isotypes/subclasses supposed to exert efficient anti-parasite activities (e.g. IgE and IgG1). Thus, these humoral defects could at least partially explain the reported increase in CE prevalence among older individuals, since a weaker immune response in the elderly might facilitate the establishment and maintenance of the parasite infection. Finally, a possible association between age-dependent susceptibility to CE and host immunosenescence is discussed. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-3024 (Electronic)IS - 0141-9838 (Linking)LA - engPT - Journal ArticleCO - Uruguay -</style></notes><work-type><style face="normal" font="default">10.1111/pim.12505</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29161459">PM:29161459</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Parasite Immunol\20171121-MourgliaEttlinG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Parasite Immunol\20171121-MourgliaEttlinG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Mourglia-Ettlin G</style></custom2><misc3><style face="normal" font="default">10.1111/pim.12505</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86981</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Miceli Sopo,S.</style></author><author><style face="normal" font="default"> Monaco,S.</style></author><author><style face="normal" font="default"> Bersani,G.</style></author><author><style face="normal" font="default"> Romano,A.</style></author><author><style face="normal" font="default"> Fantacci,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit, Department of Pediatrics, Agostino Gemelli Hospital, Sacred Heart Catholic University, Rome, Italy</style></auth-address><titles><title><style face="normal" font="default">Proposal for management of the infant with suspected food protein-induced allergic proctocolitis</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword></keywords><dates><year Day="2" Month="12" Year="2017">2017/12/2</year></dates><abstract><style face="normal" font="default">A 13-month-old girl was referred to our allergologic ambulatory because of she presented haematochezia mixed with mucus in the stool when she was two months old; an endoscopy showed eosinophilic infiltrates in the rectal mucosa with lymphoid nodular hyperplasia. At the age of three months, a food protein-induced allergic proctocolitis (FPIAP) diagnosis was established. Her mother started a cow's milk (CM) free diet and then, due to the persistence of haematochezia after a month from the beginning of the elimination diet, also an egg- and beef-free diet. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - LetterCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12844</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29197125">PM:29197125</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171202-MiceliSOpoS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171202-MiceliSOpoS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Miceli Sopo S</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12844</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86982</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Schocker,F.</style></author><author><style face="normal" font="default"> Recke,A.</style></author><author><style face="normal" font="default"> Kull,S.</style></author><author><style face="normal" font="default"> Worm,M.</style></author><author><style face="normal" font="default"> Jappe,U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Clinical and Molecular Allergology, Priority Research Area Asthma and Allergy, Research Center Borstel, Germany; Airway Research Center North (ARCN), MemberGerman Center for Lung ResearchDepartment of Dermatology, University of Lubeck, Lubeck, GermanyDivision of Clinical and Molecular Allergology, Priority Research Area Asthma and Allergy, Research Center Borstel, Germany; Airway Research Center North (ARCN), MemberGerman Center for Lung ResearchDepartment of Dermatology and Allergology, Allergy-Center-Charite, Charite - Universitatsmedizin Berlin, Berlin, GermanyDivision of Clinical and Molecular Allergology, Priority Research Area Asthma and Allergy, Research Center Borstel, Germany; Airway Research Center North (ARCN), MemberGerman Center for Lung ResearchInterdisciplinary Allergy Outpatient Clinic, Department of Pneumology, University of Lubeck, Lubeck</style></auth-address><titles><title><style face="normal" font="default">Persistent cow's milk anaphylaxis from early childhood monitored by IgE and BAT to cow's and human milk under therapy</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="2" Month="12" Year="2017">2017/12/2</year></dates><abstract><style face="normal" font="default">Cow's milk allergy affects approximately 2 to 3% of children under 3 years. Allergic reactions often occur at an early onset within the first months of age [1]. In 80 to 85% of the described cases a natural tolerance develops until the age of 5 years. However, a proportion of 1% of adults remain cow's milk allergic, often associated with severe reactions [2]. Some breast-fed babies with cow's milk allergy still show symptoms despite a strict cow's milk-free diet of the nursing mother, and they react until the mother discontinues breast feeding. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - LetterCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12843</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29197130">PM:29197130</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171202-SchockerF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171202-SchockerF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Schocker F</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12843</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86983</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tsilochristou,O.</style></author><author><style face="normal" font="default"> Maggina,P.</style></author><author><style face="normal" font="default"> Zolkipli,Z.</style></author><author><style face="normal" font="default"> Sanchez,G.S.</style></author><author><style face="normal" font="default"> Uysal,P.</style></author><author><style face="normal" font="default"> Alvaro Lozano,M.</style></author><author><style face="normal" font="default"> Atanaskovic-Markovic,M.</style></author><author><style face="normal" font="default"> Baghdasaryan,A.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author><author><style face="normal" font="default"> DuToit,G.</style></author><author><style face="normal" font="default"> van Wijk,R.G.</style></author><author><style face="normal" font="default"> Host,A.</style></author><author><style face="normal" font="default"> O'Hourihane,J.</style></author><author><style face="normal" font="default"> Ingemann,L.</style></author><author><style face="normal" font="default"> Kivisto,J.E.</style></author><author><style face="normal" font="default"> Lopes Dos Santos,J.M.</style></author><author><style face="normal" font="default"> Melen,E.</style></author><author><style face="normal" font="default"> Antonella,M.</style></author><author><style face="normal" font="default"> Nieto,A.</style></author><author><style face="normal" font="default"> Pajno,G.</style></author><author><style face="normal" font="default"> Rose,K.</style></author><author><style face="normal" font="default"> Rethy,L.A.</style></author><author><style face="normal" font="default"> Sackesen,C.</style></author><author><style face="normal" font="default"> Schmid Grendelmeier,P.</style></author><author><style face="normal" font="default"> Valovirta,E.</style></author><author><style face="normal" font="default"> Wickman,M.</style></author><author><style face="normal" font="default"> EIgenmann,P.A.</style></author><author><style face="normal" font="default"> Wahn,U.</style></author><author><style face="normal" font="default"> van der Poel,L.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Asthma, Allergy and Lung Biology, King's College London, London, UK</style></auth-address><titles><title><style face="normal" font="default">Current state and future of Paediatric Allergology in Europe: A road map</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">The history of pediatric allergology (PA) in Europe is relatively youthful, dating back to 1984, when a small group of pediatricians founded the European Working Group on Pediatric Allergy and Immunology - later giving rise to ESPACI (European Society on Pediatric Allergology and Clinical Immunology). In 1990, the first dedicated journal, Pediatric Allergy and Immunology (PAI), was founded. There are striking differences across Europe, and even within European countries, in relation to the training pathways for doctors seeing children with allergic disease(s). In a sponsored collaboration with the European Academy of Allergy and Clinical Immunology (EAACI) Pediatric Section, the EAACI-Clemens von Piquet Foundation (CvP) organised in 2016 a workshop on the future of PA with a deliberate focus on education, research and networking/advocacy. The delegates representing many countries across Europe, have endorsed the concept that optimal care of children with allergic diseases is delivered by pediatricians who have received dedicated training in allergy, or allergists who have received dedicated training in pediatrics. In order to meet the needs of children and families with allergic disease(s), the pediatric allergist is highly encouraged to develop several networks. Our challenge is to reinforce a clear strategic approach to scientific excellence to across our member base, to ensure and enhance the relevance of European pediatric research in allergy. With research opportunities in basic, translational, clinical, and epidemiological trials, more trainees and trained specialists are needed and an exciting time to be a pediatric allergologist. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Greece -CO - Spain -CO - Turkey -CO - Serbia -CO - Armenia -CO - Germany -CO - Netherlands -CO - Ireland -CO - Finland -CO - Sweden -CO - Italy -CO - Switzerland -CO - Hungary -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12833</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29168232">PM:29168232</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171123-TsilochristouO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171123-TsilochristouO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, Tsilochristou O</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12833</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86984</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Anvari,S.</style></author><author><style face="normal" font="default"> Tran,D.</style></author><author><style face="normal" font="default"> Nguyen,A.</style></author><author><style face="normal" font="default"> Devaraj,S.</style></author><author><style face="normal" font="default"> Davis,C.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Baylor College of Medicine, Section of Pediatric Immunology, Allergy and Rheumatology Houston, TX, USA</style></auth-address><titles><title><style face="normal" font="default">Peanut Oral Immunotherapy Dose Variations Do Not Result in Allergic Reactions</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">Peanut allergy is the leading cause of death related to food-anaphylaxis in the United States and a growing public health concern with the prevalence of peanut allergies tripling in the last 10 years, currently affecting 2% of the population (1,2). It occurs early in life and only 20% of children may outgrow their allergy causing a significant decline in quality of life (3,4). Peanut oral immunotherapy (POIT) has been demonstrated to be effective for peanut desensitization. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - LetterCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12837</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29168272">PM:29168272</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171123-AnvariS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171123-AnvariS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, Anvari S</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12837</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86985</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jackson Cullison,S.R.</style></author><author><style face="normal" font="default"> Siegfried,E.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, University of Pittsburgh Medical Center, Pittsburgh, PA, USADepartment of Pediatric Dermatology, School of Medicine, Saint Louis University, St. Louis, MO, USA</style></auth-address><titles><title><style face="normal" font="default">Paradoxic eczema in infants after heart transplantation</style></title><secondary-title><style face="normal" font="default">Pediatr Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword></keywords><dates><year Day="1" Month="12" Year="2017">2017/12/1</year></dates><abstract><style face="normal" font="default">New-onset psoriasis in patients receiving tumor necrosis factor inhibitors is well recognized in children and adults. We describe three children who underwent cardiac transplantation and developed an analogous form of paradoxic eczema occurring 2-48 months after starting systemic tacrolimus, a drug widely used topically to treat eczema. Anecdotal reports and our experience suggest that tacrolimus taper with alternative systemic antirejection immunosuppressant may lead to skin clearance. Pending additional insight, treatment should include optimizing skin barrier function, minimizing microbial and allergic triggers, and coordinating care to choose the best-tolerated systemic immunosuppressant regimen at the lowest effective dose</style></abstract><notes><style face="normal" font="default">IS - 1525-1470 (Electronic)IS - 0736-8046 (Linking)LA - engPT - Case ReportsCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/pde.13342</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29194735">PM:29194735</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Dermatol\20171201-JacksonCullisonSR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Dermatol\20171201-JacksonCullisonSR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Jackson Cullison SR</style></custom2><misc3><style face="normal" font="default">10.1111/pde.13342</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86986</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Candy,D.C.A.</style></author><author><style face="normal" font="default"> Van Ampting,M.T.J.</style></author><author><style face="normal" font="default"> Nijhuis,M.M.O.</style></author><author><style face="normal" font="default"> Wopereis,H.</style></author><author><style face="normal" font="default"> Butt,A.M.</style></author><author><style face="normal" font="default"> Peroni,D.G.</style></author><author><style face="normal" font="default"> Vandenplas,Y.</style></author><author><style face="normal" font="default"> Fox,A.T.</style></author><author><style face="normal" font="default"> Shah,N.</style></author><author><style face="normal" font="default"> West,C.E.</style></author><author><style face="normal" font="default"> Garssen,J.</style></author><author><style face="normal" font="default"> Harthoorn,L.F.</style></author><author><style face="normal" font="default"> Knol,J.</style></author><author><style face="normal" font="default"> Michaelis,L.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Royal Alexandra Children's Hospital, Brighton, UK</style></auth-address><titles><title><style face="normal" font="default">A synbiotic-containing amino acid-based formula improves gut microbiota in non-IgE-mediated allergic infants</style></title><secondary-title><style face="normal" font="default">Pediatr Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Res</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">BACKGROUND: Prebiotics and probiotics (synbiotics) can modify gut microbiota and have potential in allergy management when combined with amino acid-based formula (AAF) for infants with cow's milk allergy (CMA). METHODS: This multicenter, double-blind, randomized controlled trial investigated the effects of an AAF including synbiotic blend on percentages of bifidobacteria and Eubacterium rectale/Clostridium coccoides group (ER/CC) in feces from infants with suspected non-IgE-mediated CMA. Feces from age matched healthy breastfed infants were used as reference (HBR) for primary outcomes. CMA subjects were randomized and received test or control formula for 8 weeks. Test formula was a hypoallergenic, nutritionally complete AAF including a prebiotic blend of fructo-oligosaccharides and the probiotic strain Bifidobacterium breve M-16V. Control formula was AAF without synbiotics. RESULTS: Thirty-five (test) and 36 (control) subjects were randomized; HBR included 51 infants. At week 8, median percentage of bifidobacteria was higher in test group vs control group (35.4 vs. 9.7%, respectively P&lt;0.001), whereas ER/CC was lower (9.5 vs. 24.2%, respectively; P&lt;0.001). HBR levels of bifidobacteria and ER/CC were 55 and 6.5%, respectively. CONCLUSION: AAF including specific synbiotics, which results in levels of bifidobacteria and ER/CC approximating levels in HBR group, improves the fecal microbiota of infants with suspected non-IgE-mediated CMA.Pediatric Research accepted article preview online, 20 November 2017. doi:10.1038/pr.2017.270</style></abstract><notes><style face="normal" font="default">IS - 1530-0447 (Electronic)IS - 0031-3998 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Netherlands -CO - Italy -CO - Belgium -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1038/pr.2017.270</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29155807">PM:29155807</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Res\20171206-CandyDC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Res\20171206-CandyDC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171206, Candy DC</style></custom2><misc3><style face="normal" font="default">10.1038/pr.2017.270</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86987</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Narumoto,S.</style></author><author><style face="normal" font="default"> Sakamoto,S.</style></author><author><style face="normal" font="default"> Uchida,H.</style></author><author><style face="normal" font="default"> Sasaki,K.</style></author><author><style face="normal" font="default"> Shigeta,T.</style></author><author><style face="normal" font="default"> Fukuda,A.</style></author><author><style face="normal" font="default"> Nosaka,S.</style></author><author><style face="normal" font="default"> Irie,R.</style></author><author><style face="normal" font="default"> Yoshioka,T.</style></author><author><style face="normal" font="default"> Kasahara,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Organ Transplantation Center, National Center for Child Health and Development, Setagaya, Tokyo, Japan</style></auth-address><titles><title><style face="normal" font="default">Necrotizing enterocolitis in the setting of milk allergy after pediatric living donor liver transplantation</style></title><secondary-title><style face="normal" font="default">Pediatr Transplant</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Transplant</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunosuppressive Agents</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">NEC is an idiopathic intestinal mucosal injury that may progress to transmural bowel necrosis without mesenteric ischemia. NEC usually affects 7- to 10-day-old neonates following enteral feeding. A 10-month-old girl with no history of laparotomy underwent LDLT for acute liver failure. After starting enteral feeding on postoperative day 5, she developed abdominal distention. Diffuse PVG and PI were detected by radiologic modalities. Exploratory laparotomy revealed patchy necrosis of the intestine without perforation. The microscopic findings of a resected specimen revealed transmural coagulative necrosis with multiple small thromboses compatible with neonatal NEC features, and eosinophil infiltration was also observed. Subsequently, after the resumption of enteral feeding with cow's milk, she developed severe diarrhea, the symptoms of which were eliminated after the administration of cow's milk was stopped. These clinical and pathological findings support the speculation that NEC might have been induced by a CMA. Food allergies, which can be induced by immunosuppressive agents, should be considered as a potential cause of NEC in the setting of pediatric liver transplantation</style></abstract><notes><style face="normal" font="default">IS - 1399-3046 (Electronic)IS - 1397-3142 (Linking)LA - engPT - Case ReportsCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/petr.13096</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29218832">PM:29218832</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Transplant\20171207-NarumotoS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Transplant\20171207-NarumotoS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Narumoto S</style></custom2><misc3><style face="normal" font="default">10.1111/petr.13096</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86988</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Morgado-Carrasco,D.</style></author><author><style face="normal" font="default"> Fusta-Novell,X.</style></author><author><style face="normal" font="default"> Podlipnik,S.</style></author><author><style face="normal" font="default"> Combalia,A.</style></author><author><style face="normal" font="default"> Aguilera,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Hospital Clinic de Barcelona, Universitat de Barcelona, Barcelona, Spain</style></auth-address><titles><title><style face="normal" font="default">Clinical and photobiological response in eight patients with solar urticaria under treatment with omalizumab, and review of the literature</style></title><secondary-title><style face="normal" font="default">Photodermatol Photoimmunol Photomed</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Photodermatol Photoimmunol Photomed</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="24" Month="11" Year="2017">2017/11/24</year></dates><abstract><style face="normal" font="default">BACKGROUND: Solar urticaria (SU) is a rare photodermatosis. Treatment is challenging and outcomes are often disappointing. Omalizumab is an anti-IgE, currently approved for treatment of chronic spontaneous urticaria. We sought to evaluate therapy with omalizumab in refractory SU and describe predictive factors for response. MATERIALS/METHODS: Patients with refractory SU under treatment with omalizumab were included in this study. Clinical outcome was evaluated using the Urticaria Activity score 7 (UAS7), Dermatology Life Quality Index (DLQI) and Pruritus Visual Analogue scale (VAS). Complete clinical response (CCR) was defined as having an UAS7=0, DLQI&lt;6 and VAS=0. Phototesting was performed and compared to baseline. We performed a PUBMED search to identify reported cases of SU in adults treated with omalizumab, analyzing their characteristics in order to predict response to omalizumab RESULTS: Eight patients were included. Median age was 45.5 years (range, 23-64). Light spectrum most commonly implicated was UV-A. Clinical outcomes: 89% (7/8) achieved CCR with omalizumab. Phototesting was normal in 42.8% (3/7) of them. In our review we identified 38 patients (including the current case series), 68.4% showed favourable outcomes with omalizumab. Median time since onset of SU was lower in responders. CONCLUSIONS: Omalizumab can be an effective treatment in refractory SU</style></abstract><notes><style face="normal" font="default">IS - 1600-0781 (Electronic)IS - 0905-4383 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1111/phpp.12370</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29171925">PM:29171925</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Photodermatol Photoimmunol Photomed\20171124-MorgadoCarrascoD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Photodermatol Photoimmunol Photomed\20171124-MorgadoCarrascoD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Morgado-Carrasco D</style></custom2><misc3><style face="normal" font="default">10.1111/phpp.12370</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86989</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ishibashi,M.</style></author><author><style face="normal" font="default"> Nabe,T.</style></author><author><style face="normal" font="default"> Nitta,Y.</style></author><author><style face="normal" font="default"> Tsuruta,H.</style></author><author><style face="normal" font="default"> Iduhara,M.</style></author><author><style face="normal" font="default"> Uno,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Plant Resource Science, Graduate School of Agricultural Science, Kobe University, Rokko, Kobe, Hyogo, 657-8501, Japan</style></auth-address><titles><title><style face="normal" font="default">Analysis of major paralogs encoding the Fra a 1 allergen based on their organ-specificity in Fragaria x ananassa</style></title><secondary-title><style face="normal" font="default">Plant Cell Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Plant Cell Rep</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="25" Month="11" Year="2017">2017/11/25</year></dates><abstract><style face="normal" font="default">KEY MESSAGE: Fra a 1 protein in strawberry causes oral allergic syndrome. Over 39 Fra a 1 paralogs have been identified in strawberry genome. Fra a 1.01 is major accumulating protein in edible organs. Strawberry fruits contain allergenic proteins that cause oral allergic syndrome. The hypothesized major allergen is Fra a 1, an ortholog of the birch pollen allergen protein Bet v 1. We organized Fra a 1 genes and analyzed their localizations at the transcriptional and translational levels. In total, 15 new Fra a 1 proteins were identified from the genomic database, increasing the total number of Fra a 1 to 30 proteins encoded by 39 genes. Fra a 1.02 was mostly expressed in receptacles, and Fra a 1.01 in achenes, when analyzed by RNA sequencing. Immunoblotting showed that the Fra a 1.01 protein was broadly accumulated in strawberry organs, while the Fra a 1.02 protein was mostly expressed in receptacles. Recombinant Fra a 1.01 strongly reacted with human IgE. The mRNA and protein expression levels of Fra a 1 did not correlate, indicating the importance of protein levels when evaluating the abundance of allergens in strawberry. Based on the localizations, accumulation levels and reactivity to human IgE, we determined that Fra a 1.01 was the most important allergen, followed by Fra a 1.02, and then other Fra a 1 proteins. The information obtained here will be useful for selecting the target Fra a 1 paralogs when breeding hypoallergenic strawberry</style></abstract><notes><style face="normal" font="default">IS - 1432-203X (Electronic)IS - 0721-7714 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1007/s00299-017-2237-6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29177844">PM:29177844</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM_MOESM1_ESM.xlsxC:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM_MOESM2_ESM.xlsxC:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM_MOESM3_ESM.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM_MOESM1_ESM.xlsxF:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM_MOESM2_ESM.xlsxF:\A&amp;H HMW Papers\Plant Cell Rep\20171125-IshibashiM_MOESM3_ESM.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20171125, Ishibashi M</style></custom2><misc3><style face="normal" font="default">10.1007/s00299-017-2237-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86997</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nasiri-Kalmarzi,R.</style></author><author><style face="normal" font="default"> Abdi,M.</style></author><author><style face="normal" font="default"> Hosseini,J.</style></author><author><style face="normal" font="default"> Babaei,E.</style></author><author><style face="normal" font="default"> Mokarizadeh,A.</style></author><author><style face="normal" font="default"> Vahabzadeh,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">Cellular and Molecular Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran</style></auth-address><titles><title><style face="normal" font="default">Evaluation of 1,25-dihydroxyvitamin D3 Pathway in Patients with Chronic Urticaria</style></title><secondary-title><style face="normal" font="default">QJM</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">QJM</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">BACKGROUND: Previous studies showed the role of vitamin D (Vit D) on the progression of chronic urticaria. To the best of our knowledge, there are no other results regarding the contribution of single nucleotide polymorphisms (SNPs) in the vitamin D receptor (VDR) and vitamin D binding protein (VDBP) genes in Chronic Urticaria (CU). AIM: In the present study, we investigated the Vit pathway and the association between VDR and VDBP gene polymorphisms and CU risk in Iranian population. METHODS: All participating individuals in the present study were evaluated for serum Vit D and VDBP concentration VDR rs1544410 and rs2228570 and VDBP rs7041using a polymerase chain reactionrestriction fragment length polymorphism (PCR-RFLP) analysis. The associations of studied analytes and 3 SNPs with clinical and laboratory outcomes were investigated in CU patients. RESULTS: Patients with CU showed lower Vit D compared to controls (19.26 +/- 1.26 vs. 31.72 +/- 7.14 ng/ml, p value=0.006). There was a significant correlation between vitamin D levels and urticaria activity score. Serum VDBP was significantly higher in CU patients than controls (1317.3 +/- 183.71 vs. 395.77 +/- 12.96 microg/mL, p value &lt; 0.0001) and had a positive correlation to progression of CU. The A allele of this polymorphism might be a potential risk factor for progression of CU (OR = 4.3434, 95%CI = (1.7331 to 10.8852), Z statistic= 3.133, p value=0.0017). CONCLUSION: In Summary, this study demonstrated that change in Vit D pathway in the level of gene or protein may be a risk factor for progression of CU</style></abstract><notes><style face="normal" font="default">IS - 1460-2393 (Electronic)IS - 1460-2393 (Linking)LA - engPT - Journal ArticleCO - Iran -</style></notes><work-type><style face="normal" font="default">10.1093/qjmed/hcx223</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29165650">PM:29165650</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\QJM\20171120-NasiriKalmarziR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\QJM\20171120-NasiriKalmarziR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Nasiri-Kalmarzi R</style></custom2><misc3><style face="normal" font="default">10.1093/qjmed/hcx223</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87002</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hamidou,T.</style></author><author><style face="normal" font="default"> Maizoumbou,D.A.</style></author><author><style face="normal" font="default"> Laouali,S.</style></author><author><style face="normal" font="default"> Jacquier,J.P.</style></author><author><style face="normal" font="default"> Dumur,J.P.</style></author><author><style face="normal" font="default"> Issaka,H.</style></author><author><style face="normal" font="default"> Yacouba,S.</style></author><author><style face="normal" font="default"> Abba,A.</style></author><author><style face="normal" font="default"> Gagara,A.</style></author><author><style face="normal" font="default"> Assao,M.</style></author><author><style face="normal" font="default"> Moulaye,A.</style></author><author><style face="normal" font="default"> Tapsoba,P.</style></author><author><style face="normal" font="default"> Chabert,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Co-sensitisation between edible crickets (Ornithacris turbida cavroisi) and other arthropods in the town of Niamey (Niger): A prospective study of 99 cases</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Cockroaches</style></keyword><keyword><style face="normal" font="default"> Cosensibilisation</style></keyword><keyword><style face="normal" font="default"> Entomophagy</style></keyword><keyword><style face="normal" font="default"> Locusts</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Shrimps</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - FRECO - Niger -CO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.09.006</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.09.006</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\20171116-HamidouT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\20171116-HamidouT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171116, Hamidou T</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.09.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87004</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Senechal,H.</style></author><author><style face="normal" font="default"> Charpin,D.</style></author><author><style face="normal" font="default"> Couderc,R.</style></author><author><style face="normal" font="default"> Poncet,P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Gibberellin-regulated proteins and the enigma of the "missing link"</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> BP14</style></keyword><keyword><style face="normal" font="default"> Cypress pollen</style></keyword><keyword><style face="normal" font="default"> Gibberellin regulated proteins</style></keyword><keyword><style face="normal" font="default"> Peach</style></keyword><keyword><style face="normal" font="default"> Pollen/food associated syndrome</style></keyword><keyword><style face="normal" font="default"> Pru p 7</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - FRECO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.09.007</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.09.007</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\20171121-SenechalH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\20171121-SenechalH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Senechal H</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.09.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87005</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Frealle,E.</style></author><author><style face="normal" font="default"> Bex,V.</style></author><author><style face="normal" font="default"> Reboux,G.</style></author><author><style face="normal" font="default"> Roussel,S.</style></author><author><style face="normal" font="default"> Bretagne,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Universite Lille, CNRS, Inserm, CHU de Lille, institut Pasteur de Lille, U1</style></auth-address><titles><title><style face="normal" font="default">Classical and molecular methods for identification and quantification of domestic moulds</style></title><secondary-title><style face="normal" font="default">Rev Mal Respir</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Mal Respir</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Quantitative real-time PCR</style></keyword></keywords><dates><year Day="15" Month="11" Year="2017">2017/11/15</year></dates><abstract><style face="normal" font="default">INTRODUCTION: To study the impact of the constant and inevitable inhalation of moulds, it is necessary to sample, identify and count the spores. BACKGROUND: Environmental sampling methods can be separated into three categories: surface sampling is easy to perform but non quantitative, air sampling is easy to calibrate but provides time limited information, and dust sampling which is more representative of long term exposure to moulds. The sampling strategy depends on the objectives (evaluation of the risk of exposure for individuals; quantification of the household contamination; evaluation of the efficacy of remediation). The mould colonies obtained in culture are identified using microscopy, Maldi-TOF, and/or DNA sequencing. VIEWPOINTS: Electrostatic dust collectors are an alternative to older methods for identifying and quantifying household mould spores. They are easy to use and relatively cheap. Colony counting should be progressively replaced by quantitative real-time PCR, which is already validated, while waiting for more standardised high throughput sequencing methods for assessment of mould contamination without technical bias. CONCLUSION: Despite some technical recommendations for obtaining reliable and comparable results, the huge diversity of environmental moulds, the variable quantity of spores inhaled and the association with other allergens (mites, plants) make the evaluation of their impact on human health difficult. Hence there is a need for reliable and generally applicable quantitative methods</style></abstract><notes><style face="normal" font="default">IS - 1776-2588 (Electronic)IS - 0761-8425 (Linking)LA - frePT - English AbstractPT - Journal ArticlePT - ReviewCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.rmr.2017.01.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29153274">PM:29153274</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Mal Respir\20171204-FrealleE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Mal Respir\20171204-FrealleE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Frealle E</style></custom2><misc3><style face="normal" font="default">10.1016/j.rmr.2017.01.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87006</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Drouet,M.</style></author><author><style face="normal" font="default"> Moreau,A.S.</style></author><author><style face="normal" font="default"> Hoppe,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Unite d'allergologie generale, departement de pneumologie, oncologie thoracique et allergologie, CHU d'Angers, 49000 Anger, France.</style></auth-address><titles><title><style face="normal" font="default">Eight-year-old children with numerous food allergy inducer by passive exposition to cannabis</style></title><secondary-title><style face="normal" font="default">Rev Pneumol Clin</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Pneumol Clin</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/14/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">We present a clinical case of a 8 old children with numerous food allergy inducer pas passive exposition to cannabis</style></abstract><notes><style face="normal" font="default">IS - 0761-8417 (Print)IS - 0761-8417 (Linking)LA - frePT - English AbstractPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.pneumo.2017.09.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29169678">PM:29169678</url></web-urls><pdf-urls><url ppv-ref="no">madrouet@chu-angers.fr</url></pdf-urls></urls><custom2><style face="normal" font="default">20171205, Drouet M</style></custom2><misc3><style face="normal" font="default">10.1016/j.pneumo.2017.09.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87007</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gomes dos Reis Pimentel,R.A.</style></author><author><style face="normal" font="default"> Oliveira,G.</style></author><author><style face="normal" font="default"> Ferreira Chaves Loureiro e Lemos,C.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Accelerated subcutaneous immunotherapy in pediatric population </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô Systematic review</style></title><secondary-title><style face="normal" font="default">Rev Port Pneumol (2006)</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Port Pneumol (2006)</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2173-5115</style></isbn><abstract><style face="normal" font="default">Background Accelerated subcutaneous immunotherapy (SCIT) schedules represent an alternative to conventional SCIT, providing immunotherapy benefits in a shorter period of time. The objectives of this systematic review were to assess clinical and immunological efficacy as well as safety of accelerated SCIT build-up schedules for the treatment of respiratory allergy in pediatric patients. Methods Studies were located by searching PubMed, using </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£immunotherapy</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ and </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£desensitization</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ as keywords. The selection of studies, published from January 1st, 2006, to December 31th, 2015, was performed in two stages: screening of titles and abstracts, and assessment of the full papers identified as relevant, considering the inclusion criteria. Data were extracted in a standardized way and synthesized qualitatively to assess efficacy and safety of accelerated schedules in respiratory allergy. Results Eleven trials were included: two evaluated rush SCIT and nine assessed cluster SCIT. This review demonstrated that rush and cluster schedules are clinically and immunological efficacious, with faster effect than conventional schedules. No relevant difference with respect to clinical outcomes was noticed between subgroups (pediatric, adult and mixed populations). Regarding safety, most local adverse reactions were mild and there were neither life-threatening systemic reactions nor fatal events. No relevant differences in the incidence and severity of either local or systemic reactions between the accelerated schedule group and control group were registered. Conclusions Accelerated SCIT build-up schedules are effective in the treatment of respiratory allergy in pediatric patients, representing a safe alternative to the conventional schedules with the advantage of achieving clinical effectiveness sooner</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Portugal -</style></notes><work-type><style face="normal" font="default">10.1016/j.rppnen.2017.07.009</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.rppnen.2017.07.009</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Port Pneumol (2006)\20171201-GomesdosReisPimentelRA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Port Pneumol (2006)\20171201-GomesdosReisPimentelRA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Gomes dos Reis Pimentel RA</style></custom2><misc3><style face="normal" font="default">10.1016/j.rppnen.2017.07.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87014</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Franchini,M.</style></author><author><style face="normal" font="default"> Mannucci,P.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Transfusion Medicine and Hematology, Carlo Poma Hospital, Mantova, ItalyAngelo Bianchi Bonomi Hemophilia and Thrombosis Center, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico and University of Milan, Italy</style></auth-address><titles><title><style face="normal" font="default">Alloantibodies in von Willebrand Disease</style></title><secondary-title><style face="normal" font="default">Semin Thromb Hemost</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Semin Thromb Hemost</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/24/2017" status="on-request"/><keywords/><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">von Willebrand disease (VWD), the most commonly known inherited bleeding disorder, is caused by a partial (type 1) or total (type 3) deficiency or dysfunction (type 2) of von Willebrand factor (VWF). Its management encompasses the prevention or treatment of bleeding by raising endogenous VWF levels using a synthetic agent, such as desmopressin, or providing exogenous VWF concentrates. The development of inhibitory alloantibodies against VWF is a rare but often severe complication encountered during the treatment of type 3 VWD, which is associated with a lack of hemostatic response to infused VWF concentrates and more rarely with allergic, even anaphylactic, reactions. This narrative review will focus on the characteristics of such alloantibodies and their management, which can be very challenging for physicians operating at hemophilia treatment centers</style></abstract><notes><style face="normal" font="default">IS - 1098-9064 (Electronic)IS - 0094-6176 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1055/s-0037-1607440</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29165738">PM:29165738</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171117, Franchini M</style></custom2><misc3><style face="normal" font="default">10.1055/s-0037-1607440</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87022</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Alebiosu,O.S.</style></author><author><style face="normal" font="default"> Adekanmbi,O.H.</style></author><author><style face="normal" font="default"> Nodza,G.I.</style></author><author><style face="normal" font="default"> Ogundipe,O.T.</style></author></authors></contributors><titles><title><style face="normal" font="default">Aeropalynological study of two selected locations in North-Central Nigeria</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Humans</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">Pollen and spores have been found as major biological sources of morbidity among individuals sensitive to respiratory disorders. The aim of the present study was to analyse the deposition rate of atmospheric pollen and fern spores at selected sites in Benue and Plateau states of the North-Central Nigeria between July 2015 and June 2016. This was accomplished by: (1) determining the pollen and fern spore content of each monitoring station; (2) establishing the relationship between total pollen count and meteorological parameters; and (3) comparing the recovered airborne pollen spectra with identified plants in the surrounding vegetation types of the sampling sites. The collection of atmospheric pollen was done using a modified Tauber sampler and plants in the surrounding environment of the sampling sites were enumerated. The residual solution was collected monthly and acetolysed, after which slide preparation and microscopy of the treated residue were done. Meteorological data were obtained from the Nigerian Meteorological Agency, Lagos. The results obtained reveal seasonal distribution patterns of various airborne pollen grains in the study locations. The most abundant pollen types recovered in Plateau State were produced by Syzygium guineense, Tridax procumbens, Alchornea sp., Terminalia sp., Poaceae and Amaranthaceae. Pollen types of Casuarina equisetifolia, Syzygium guineense, Tridax procumbens, Poaceae and Cyperaceae were preponderant in Benue State. Pteris sp., Nephrolepis sp. and a trilete fern spore were also represented in this study. The recovered airborne pollen spectra correspond favourably with some identified plants in the study locations. There was no significant correlation between monthly total pollen count and mean monthly values of meteorological parameters in Benue State. Air temperature and wind speed correlated significantly with monthly total pollen count in Plateau State. It is suggested that the allergenic effect of these abundant pollen types on humans should be further examined</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Nigeria -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-017-9506-2</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-017-9506-2</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20171118-AlebiosuOS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20171118-AlebiosuOS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Alebiosu OS</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-017-9506-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87023</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Magyar,D.</style></author><author><style face="normal" font="default"> Kallai,Z.</style></author><author><style face="normal" font="default"> Sipiczki,M.</style></author><author><style face="normal" font="default"> Dobolyi,C.</style></author><author><style face="normal" font="default"> Sebok,F.</style></author><author><style face="normal" font="default"> Beregszaszi,T.</style></author><author><style face="normal" font="default"> Bihari,Z.</style></author><author><style face="normal" font="default"> Kredics,L.</style></author><author><style face="normal" font="default"> Oros,G.</style></author></authors></contributors><titles><title><style face="normal" font="default">Survey of viable airborne fungi in wine cellars of Tokaj, Hungary</style></title><secondary-title><style face="normal" font="default">Aerobiologia</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aerobiologia</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-3025</style></isbn><abstract><style face="normal" font="default">The composition of fungal biota and air quality of five traditional subterranean wine cellars and one store building of a modern wine production facility were examined in the Tokaj wine region (northeastern Hungary). Air samples were collected with SAS IAQ sampler onto PDA, MEA and RBA. Strains representing morphotypes were isolated from colonies formed on agar plates from either air or surface samples. The internal transcribed spacer (ITS) region of the rRNA gene cluster was amplified with primers ITS1 and ITS4. Altogether 90 morphotypes were isolated, 48 and 12 strains (43 species) from the air and surfaces, respectively. The number of spore-forming species generated high diversity of indoor fungi and differences between the cellars</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖ fungal compositions; however, their dominant species were proved to be the same. Among the isolated strains Penicillium spp. were the most frequent. The walls of cellars were covered by colonies of Zasmidium (Cladosporium) cellare often referred to as a noble mold. Even so, this mold has been found only at a small concentration in the air samples (10</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô30-áCFU/m3). The walls of the modern store were free of molds. Diversity of fungi of the examined wine cellars was influenced by environmental conditions to a certain degree, such as elevation (height above sea level), age, reconstruction time of cellars, indoor ethanol concentration and the number of chimneys. The location of cellars poorly influenced the concentration of fungi of the air inside cellars, contrary to outdoors where the air of the municipal area contained more CFUs than that of rural spaces</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Hungary -</style></notes><work-type><style face="normal" font="default">10.1007/s10453-017-9505-3</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10453-017-9505-3</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Aerobiologia\20171118-MagyarD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Aerobiologia\20171118-MagyarD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Magyar D</style></custom2><misc3><style face="normal" font="default">10.1007/s10453-017-9505-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87024</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Natsume,O.</style></author><author><style face="normal" font="default"> Ohya,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pediatrics, Hamamatsu University School of Medicine, Shizuoka, Japan; Division of Allergy, Department of Medical Subspecialties, National Center for Child Health and Development, Tokyo, JapanDivision of Allergy, Department of Medical Subspecialties, National Center for Child Health and Development, Tokyo, Japan. Electronic address: ohya-y@ncchd.go.jp</style></auth-address><titles><title><style face="normal" font="default">Recent advancement to prevent the development of allergy and allergic diseases and therapeutic strategy in the perspective of barrier dysfunction</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">Therapeutic strategy in late 20th century to prevent allergic diseases was derived from a conceptual framework of allergens elimination which was as same as that of coping with them after their onset. Manifold trials were implemented; however, most of them failed to verify the effectiveness of their preventive measures. Recent advancement of epidemiological studies and cutaneous biology revealed epidermal barrier dysfunction plays a major role of allergen sensitization and development of atopic dermatitis which ignites the inception of allergy march. For this decade, therapeutic strategy to prevent the development of food allergy has been confronted with a paradigm shift from avoidance and delayed introduction of allergenic foods based on the theoretical concept to early introduction of them based on the clinical and epidemiological evidences. Especially, prevention of peanut allergy and egg allergy has been established with the highest evidence verified by randomized controlled trials, although application in clinical practice should be done with attention. This paradigm shift concerning food allergy was also due to the discovery of cutaneous sensitization risk of food allergens for an infant with eczema revealed by prospective studies. Here we have recognized the increased importance of prevention of eczema/atopic dermatitis in infancy. Two randomized controlled trials using emollients showed successful results in prevention of atopic dermatitis in infancy; however, longer term safety and prognosis including allergy march should be pursued. To establish more fundamental strategy for prevention of the development of allergy, further studies clarifying the mechanisms of interaction between barrier dysfunction and microbial milieu are needed with macroscope to understand the relationship between allergic diseases and a diversity of environmental influences</style></abstract><notes><style face="normal" font="default">IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.11.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29233462">PM:29233462</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171119-NatsumeO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171119-NatsumeO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171119, Natsume O</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.11.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87025</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fujisawa,T.</style></author><author><style face="normal" font="default"> Shimoda,T.</style></author><author><style face="normal" font="default"> Masuyama,K.</style></author><author><style face="normal" font="default"> Okubo,K.</style></author><author><style face="normal" font="default"> Honda,K.</style></author><author><style face="normal" font="default"> Okano,M.</style></author><author><style face="normal" font="default"> Katsunuma,T.</style></author><author><style face="normal" font="default"> Urisu,A.</style></author><author><style face="normal" font="default"> Kondo,Y.</style></author><author><style face="normal" font="default"> Odajima,H.</style></author><author><style face="normal" font="default"> Kurihara,K.</style></author><author><style face="normal" font="default"> Nagata,M.</style></author><author><style face="normal" font="default"> Taniguchi,M.</style></author><author><style face="normal" font="default"> Taniuchi,S.</style></author><author><style face="normal" font="default"> Doi,S.</style></author><author><style face="normal" font="default"> Matsumoto,T.</style></author><author><style face="normal" font="default"> Hashimoto,S.</style></author><author><style face="normal" font="default"> Tanaka,A.</style></author><author><style face="normal" font="default"> Natsui,K.</style></author><author><style face="normal" font="default"> Abe,N.</style></author><author><style face="normal" font="default"> Ozaki,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Center, Mie National Hospital, Mie, Japan.</style></auth-address><titles><title><style face="normal" font="default">Long-term safety of subcutaneous immunotherapy with TO-204 in Japanese patients with house dust mite-induced allergic rhinitis and allergic bronchial asthma: Multicenter, open label clinical trial</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">BACKGROUND: To evaluate the long-term safety of subcutaneous immunotherapy with TO-204, a standardized house dust mite (HDM) allergen extracts, we conducted a multicenter, open label clinical trial. METHODS: Japanese patients aged 5-65 years were eligible for the study, if they had HDM-induced allergic rhinitis (AR), allergic bronchial asthma (BA), or both. TO-204 was administered in a dose titration scheme, and the maintenance dose was determined according to the predefined criteria. The treatment period was 52 weeks, and patients who were willing to continue the treatment received TO-204 beyond 52 weeks. This clinical trial is registered at the Japan Pharmaceutical Information Center (Japic CTI-121900). RESULTS: Between July 2012 and May 2015, 44 patients (28 with AR and 16 with allergic BA) were enrolled into the study. All patients were included in the analysis. The duration of treatment ranged from 23 to 142 weeks and the median maintenance dose was 200 Japanese allergy units (JAU). Adverse events occurred in 22 patients (50%). The most common adverse event was local reactions related to the injection sites. Four patients experienced anaphylactic reactions when they were treated with the dose of 500 JAU. Two patients experienced anaphylactic shock with the doses of 1000 JAU at onset. These 6 patients could continue the study with dose reduction. CONCLUSIONS: Safety profile of TO-204 was acceptable in Japanese patients with HDM-induced AR or allergic BA. Higher doses should be administered carefully, because the risk of anaphylaxis increased at doses of 500 or 1000 JAU</style></abstract><notes><style face="normal" font="default">IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.11.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29233461">PM:29233461</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171119-FujisawaT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171119-FujisawaT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171119, Fujisawa T</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.11.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87026</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Makita,E.</style></author><author><style face="normal" font="default"> Yanagida,N.</style></author><author><style face="normal" font="default"> Sato,S.</style></author><author><style face="normal" font="default"> Asaumi,T.</style></author><author><style face="normal" font="default"> Ebisawa,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Sagamihara National Hospital, Kanagawa, Japan</style></auth-address><titles><title><style face="normal" font="default">Increased ratio of pollock roe-specific IgE to salmon roe-specific IgE levels is associated with a positive reaction to cooked pollock roe oral food challenge</style></title><secondary-title><style face="normal" font="default">Allergol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Int</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Anaphylaxis and immediate-type fish roe allergies have been reported worldwide, and, in Japan, fish roe is the sixth most common food allergen. No oral food challenges (OFCs) have used pollock roe (PR), which is reported to have high cross-reactivity with salmon roe (SR). Therefore, we administered an OFC using cooked PR to evaluate PR- and SR-specific immunoglobulin E (IgE) levels and allergic reactions in patients with PR sensitivity. METHODS: This retrospective study evaluating patient characteristics and responses to OFCs was conducted with 10-20 g of cooked PR, between April 2006 and November 2016. RESULTS: We assessed 51 patients (median age: 6.8 years). All had PR sensitization, 6 (12%) with a history of immediate reactions to PR, and 18 (35%) of immediate reactions to SR. Median PR-specific and SR-specific IgE values were 3.4 kUA/L and 9.9 kUA/L, respectively. Seven patients (14%) had a positive OFC. There was no anaphylaxis. Induced symptoms were mild and included localized urticaria, throat pruritus, intermittent cough, and mild abdominal pain. We treated one patient with mild abdominal pain with oral antihistamines. There were no significant differences in history of immediate reaction to PR and PR-specific IgE titers between OFC-positive and OFC-negative patients, although significant differences were found for PR-specific IgE titers adjusted for SR-specific IgE (p = 0.025) and PR-specific IgE/SR-specific IgE ratio (p = 0.009). CONCLUSIONS: Increased PR-specific IgE/SR-specific IgE ratio or PR-specific IgE levels adjusted for SR-specific IgE levels were risk factors for OFC positivity</style></abstract><notes><style face="normal" font="default">IS - 1440-1592 (Electronic)IS - 1323-8930 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.alit.2017.11.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29242143">PM:29242143</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Int\20171119-MakitaE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Int\20171119-MakitaE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171119, Makita E</style></custom2><misc3><style face="normal" font="default">10.1016/j.alit.2017.11.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87027</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fu,W.</style></author><author><style face="normal" font="default"> Gao,Z.</style></author><author><style face="normal" font="default"> Gao,L.</style></author><author><style face="normal" font="default"> Jin,J.</style></author><author><style face="normal" font="default"> Liu,M.</style></author><author><style face="normal" font="default"> Sun,Y.</style></author><author><style face="normal" font="default"> Wu,S.</style></author><author><style face="normal" font="default"> Wu,L.</style></author><author><style face="normal" font="default"> Ma,H.</style></author><author><style face="normal" font="default"> Dong,Y.</style></author><author><style face="normal" font="default"> Wang,X.</style></author><author><style face="normal" font="default"> Gao,B.</style></author><author><style face="normal" font="default"> Wang,H.</style></author><author><style face="normal" font="default"> Akkerdaas,J.H.</style></author><author><style face="normal" font="default"> Versteeg,S.A.</style></author><author><style face="normal" font="default"> van Ree,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Research Center, Zhejiang University, Hangzhou, 310058, China</style></auth-address><titles><title><style face="normal" font="default">Identification of a 62 kDa major allergen from Artemisia pollen as a putative galactose oxidase</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="8" Month="12" Year="2017">2017/12/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: Around 20 years ago, a 60-70 kDa protein was reported as a major allergen of mugwort (Artemisia vulgaris) pollen. This study was to identify and characterize its molecular properties. METHODS: Sera from 113 Chinese and 20 Dutch Artemisia allergic/sensitized subjects (and pools thereof) were used to identify the 60-70 kDa allergen. Pollen extracts of seven Artemisia species were compared by immunoblotting. Transcriptomics and proteomics (mass spectrometry) of A. annua pollen were used to identify the putative 60-70 kDa Artemisia allergen. Both the natural purified and recombinant allergens were evaluated for IgE reactivity by ImmunoCAP. Fourteen Chinese Artemisia allergic patients were tested intradermally with purified natural allergen. RESULTS: Immunoblots revealed two major bands at 12 and 25 kDa, and a weak band at 70 kDa for all seven Artemisia species. Using a combined transcriptomic and proteomic approach, the high molecular mass allergen in A. annua pollen was shown to be a 62 kDa putative galactose oxidase, with a putative N-glycosylation site. More than 94% of Artemisia pollen allergic patients had IgE response to this allergen. Although recognition of a non-glycosylated recombinant version was only confirmed in a minority (16%) and at much lower IgE levels, this discrepancy cannot be explained simply by reactivity to the carbohydrate moiety on the natural allergen. Intradermal testing with the natural allergen was positive in five out of nine sensitized patients. CONCLUSIONS: The previously reported 60-70 kDa allergen of Artemisia pollen is most likely a 62 kD putative galactose oxidase here designated Art an 7. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - Journal ArticleCO - China -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1111/all.13375</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29220102">PM:29220102</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\20171119-FuW.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy\20171119-FuW.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171119, Fu W</style></custom2><misc3><style face="normal" font="default">10.1111/all.13375</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87032</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bian,Y.</style></author><author><style face="normal" font="default"> Liu,C.</style></author><author><style face="normal" font="default"> She,T.</style></author><author><style face="normal" font="default"> Wang,M.</style></author><author><style face="normal" font="default"> Yan,J.</style></author><author><style face="normal" font="default"> Wei,D.</style></author><author><style face="normal" font="default"> Li,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Development of a light-initiated chemiluminescent assay for the quantitation of sIgE against egg white allergens based on component-resolved diagnosis</style></title><secondary-title><style face="normal" font="default">Anal Bioanal Chem</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Anal Bioanal Chem</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Diagnosis of food allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1618-2650</style></isbn><abstract><style face="normal" font="default">The determination of specific IgE (sIgE) level is of great importance in IgE-mediated food allergies. Our aim was to develop a homogeneous immunoassay</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çölight-initiated chemiluminescent assay (LICA)</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çöfor measuring allergen sIgE of a single component in egg white, thus evaluating the LICA-sIgE assay as a useful tool in the diagnosis of food allergy. The LICA-sIgE assay was performed by incubating serum sample with anti-human IgE antibody coated with chemiluminescer beads, streptavidin-coated sensitizer beads, and biotinylated antigens, which consist of four components in egg white. Serum samples from egg allergic patients (n</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë=</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë70) and healthy volunteers (n</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë=</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë30) were collected. For calibration, purified human IgE was used as the calibrator. Working conditions of this homogeneous immunoassay were optimized, analytical performance was determined, and correlation of the results between LICA and ImmunoCAP was evaluated. The assays were performed in 8-well plates with a sample volume diluted to 1:10 of 25-á++l. Intra-assay precision (% coefficient of variation) ranged from 1.83 to 4.13%, and inter-assay precision ranged from 2.70 to 8.70%. It exhibited excellent sensitivity, which could distinguish between positive samples and negative samples even at a large dilution level. The sIgE-LICA and ImmunoCAP correlated well in patients allergic to single component (r 2</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë=</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çë0.929). Also, the components ovomucoid and ovalbumin were best at predicting ImmunoCAP results, with the same area under the ROC curve (AUC) of 0.81, and a specificity of 90.0 and 93.3%, respectively. Our data show effective performance characteristics of LICA to detect sIgE in human serum based on component-resolved diagnostic tests (CRD). The homogeneous sIgE-LICA assay has the following key advantages: requires no washing, simplicity and rapidity, reproducibility, high-throughput, good performance in a liquid phase assay, and good suitability for sIgE diagnosis in food allergy based on CRD</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s00216-017-0791-y</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247381">PM:29247381</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Anal Bioanal Chem\20171119-BianY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Anal Bioanal Chem\20171119-BianY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171119, Bian Y</style></custom2><misc3><style face="normal" font="default">10.1007/s00216-017-0791-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87033</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhou,H.</style></author><author><style face="normal" font="default"> Li,X.I.</style></author><author><style face="normal" font="default"> Kim,J.H.</style></author><author><style face="normal" font="default"> Salam,M.T.</style></author><author><style face="normal" font="default"> Kim,H.B.</style></author><author><style face="normal" font="default"> McConnell,R.S.</style></author><author><style face="normal" font="default"> Habre,R.</style></author><author><style face="normal" font="default"> Bastain,T.</style></author><author><style face="normal" font="default"> Farzan,S.F.</style></author><author><style face="normal" font="default"> Johnston,J.</style></author><author><style face="normal" font="default"> Gilliland,F.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Preventive Medicine, University of Southern California Keck School of Medicine, Los Angeles, California</style></auth-address><titles><title><style face="normal" font="default">Effect of inhaled allergens and air pollutants on childhood rhinitis development</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -CO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.036</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29217086">PM:29217086</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-ZhouH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-ZhouH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Zhou H</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.036</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87034</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hamadani,S.</style></author><author><style face="normal" font="default"> Wang,B.</style></author><author><style face="normal" font="default"> Gupta,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Basic and Clinical Immunology, University of California, Irvine, Irvine, California</style></auth-address><titles><title><style face="normal" font="default">IgG4-related disease presenting as hoarseness and postcricoid ulcer</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">immunology</style></keyword></keywords><dates><year Day="4" Month="12" Year="2017">2017/12/4</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.035</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29217085">PM:29217085</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-HamadaniS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-HamadaniS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Hamadani S</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.035</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87035</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Peterson,C.C.</style></author><author><style face="normal" font="default"> Harrison,L.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Psychology, Eastern Michigan University, Ypsilanti, Michigan.</style></auth-address><titles><title><style face="normal" font="default">Development of a brief assessment of activity limitations in children with food allergy</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="1" Month="12" Year="2017">2017/12/1</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.032</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29203234">PM:29203234</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-PetersonCC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-PetersonCC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Peterson CC</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.032</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87036</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Woolnough,K.</style></author><author><style face="normal" font="default"> Craner,M.</style></author><author><style face="normal" font="default"> Pashley,C.H.</style></author><author><style face="normal" font="default"> Wardlaw,A.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Infection, Immunity and Inflammation, Leicester Institute for Lung Health, University of Leicester, Glenfield Hospital, Leicester, UK</style></auth-address><titles><title><style face="normal" font="default">rAsp f 3 and rAsp f 4 are associated with bronchiectasis in allergic fungal airways disease</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.026</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29223501">PM:29223501</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-WoolnoughK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20171217-WoolnoughK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Woolnough K</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.026</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87052</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Saidova,A.</style></author><author><style face="normal" font="default"> Hershkop,A.M.</style></author><author><style face="normal" font="default"> Ponce,M.</style></author><author><style face="normal" font="default"> Eiwegger,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Allergen-Specific T Cells in IgE-Mediated Food Allergy</style></title><secondary-title><style face="normal" font="default">Arch Immunol Ther Exp (Warsz)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arch Immunol Ther Exp (Warsz)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="18" Month="12" Year="2017">2017/12/18</year></dates><abstract><style face="normal" font="default">Food allergy is the major reason for severe anaphylaxis in childhood and adolescence. Currently, effective and safe treatments for food allergy are unavailable. Allergen-specific CD4(+) T cells have a pivotal role in causing and maintaining the allergic response to food allergens. The purpose of this review is to provide an overview on the role of allergen-specific T cells in food allergy during allergic sensitization, natural tolerance development and allergen immunotherapy. Allergen-specific T cells in the context of food allergy are predominantly of a Th2 type with slightly different surface marker expression patterns in different food allergies. During the process of reverting food allergy to a status of tolerance or sustained unresponsiveness there is a loss of this Th2 committed compartment with an asymptotic approximation to a regulatory and Th0/Th1 dominated compartment seen in non-allergic individuals. This process is accompanied by a significant reduction of absolute frequencies of allergen-specific T cells. Particularly, regulatory T cells may provide significant help to achieve sustained control of the effector cell populations via suppression of effector cell function and possibly induction of blocking antibodies</style></abstract><notes><style face="normal" font="default">IS - 1661-4917 (Electronic)IS - 0004-069X (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Austria -CO - Uzbekistan -CO - Canada -</style></notes><work-type><style face="normal" font="default">10.1007/s00005-017-0501-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29256092">PM:29256092</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Arch Immunol Ther Exp (Warsz)\20171213-SaidovaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Arch Immunol Ther Exp (Warsz)\20171213-SaidovaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Saidova A</style></custom2><misc3><style face="normal" font="default">10.1007/s00005-017-0501-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87053</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ajmi,H.</style></author><author><style face="normal" font="default"> Jemmali,N.</style></author><author><style face="normal" font="default"> Mabrouk,S.</style></author><author><style face="normal" font="default"> Hassayoun,S.</style></author><author><style face="normal" font="default"> Ben-Ali,M.</style></author><author><style face="normal" font="default"> Barbouche,M.R.</style></author><author><style face="normal" font="default"> Mokni,M.</style></author><author><style face="normal" font="default"> Abroug,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of pediatrics, Sahloul University Hospital, 4054, Sousse Tunisia.</style></auth-address><titles><title><style face="normal" font="default">Staphylococcal scalded skin syndrome: An uncommon symptomatology revealing an immune deficiency</style></title><secondary-title><style face="normal" font="default">Arch Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arch Pediatr</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Hyper-IgE syndrome</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">Primary immune deficiencies associated with hyper-IgE syndrome are rare diseases with clinical features dominated by recurring cutaneous and visceral bacterial infections, particularly infections due to Staphylococcus species. Most of these infections are associated with milder inflammation compared to normal. We report a primary immune deficiency associated with a hyper-IgE syndrome revealed by a staphylococcal scalded skin syndrome in a 5-year-old girl. The patient presented with a severe staphylococcal infection with extensive skin lesions and disseminated intravascular coagulation. She received intravenous fluids to compensate for fluid losses and anti-staphylococcal antibiotics. Coagulopathy was also corrected. However, the progression was rapidly fatal</style></abstract><notes><style face="normal" font="default">IS - 1769-664X (Electronic)IS - 0929-693X (Linking)LA - engPT - Journal ArticleCO - Tunisia -</style></notes><work-type><style face="normal" font="default">10.1016/j.arcped.2017.11.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29248323">PM:29248323</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Arch Pediatr\20171212-AjmiH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Arch Pediatr\20171212-AjmiH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171212, Ajmi H</style></custom2><misc3><style face="normal" font="default">10.1016/j.arcped.2017.11.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87058</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hasegawa,A.</style></author><author><style face="normal" font="default"> Watanabe,M.</style></author><author><style face="normal" font="default"> Osada,H.</style></author><author><style face="normal" font="default"> Ogawa,M.</style></author><author><style face="normal" font="default"> Ohno,H.</style></author><author><style face="normal" font="default"> Yanuma,N.</style></author><author><style face="normal" font="default"> Sasaki,K.</style></author><author><style face="normal" font="default"> Shimoda,M.</style></author><author><style face="normal" font="default"> Shirai,J.</style></author><author><style face="normal" font="default"> Ohmori,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Cooperative Department of Veterinary Medicine, Faculty of Agriculture, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu, Tokyo 183-8509, Japan</style></auth-address><titles><title><style face="normal" font="default">Influence of glucocorticoids on time-of-day-dependent variations in IgE-, histamine-, and platelet-activating factor-mediated systemic anaphylaxis in different mouse strains</style></title><secondary-title><style face="normal" font="default">Biochem Biophys Res Commun</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biochem Biophys Res Commun</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="18" Month="12" Year="2017">2017/12/18</year></dates><abstract><style face="normal" font="default">A time-of-day-dependent variation in IgE-mediated passive systemic anaphylaxis was previously reported in ICR mice. In the present study, we investigated time-of-day-dependent variations in IgE-, histamine-, and platelet-activating factor (PAF)-mediated systemic anaphylaxis in C57BL/6, BALB/c, and NC/Nga mice at 9:00h and 21:00h, and evaluated the potential influence of glucocorticoids (GCs) on these variations. We found significant time-of-day-dependent variations in IgE-mediated systemic anaphylaxis in C57BL/6 mice, and in histamine- and PAF-mediated systemic anaphylaxis in BALB/c mice. Significant daily variations in IgE-, histamine-, and PAF-mediated systemic anaphylaxis were not observed in NC/Nga mice. Pretreatment with dexamethasone and adrenalectomy abolished the daily variations in IgE-mediated systemic anaphylaxis in C57BL/6 mice and in PAF-mediated systemic anaphylaxis in BALB/c mice, suggesting that GCs from adrenal glands were pivotal in regulating these variations. In contrast, pretreatment with dexamethasone and adrenalectomy did not abolish the daily variation in histamine-mediated systemic anaphylaxis in BALB/c mice, suggesting that mechanisms independent of GCs and adrenal glands are important for the variation. The present study demonstrated that time-of-day-dependent variations in systemic anaphylaxis differed among inbred mouse strains and with anaphylaxis-inducing substances. Thus, mouse strains, time of experiment, and anaphylaxis-inducing substances used must be considered to obtain appropriate experimental results</style></abstract><notes><style face="normal" font="default">IS - 1090-2104 (Electronic)IS - 0006-291X (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.bbrc.2017.12.099</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29269296">PM:29269296</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biochem Biophys Res Commun\20171215-HasegawaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biochem Biophys Res Commun\20171215-HasegawaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Hasegawa A</style></custom2><misc3><style face="normal" font="default">10.1016/j.bbrc.2017.12.099</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87059</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lommen,S.T.E.</style></author><author><style face="normal" font="default"> Hallmann,C.A.</style></author><author><style face="normal" font="default"> Jongejans,E.</style></author><author><style face="normal" font="default"> Chauvel,B.</style></author><author><style face="normal" font="default"> Leitsch-Vitalos,M.</style></author><author><style face="normal" font="default"> Aleksanyan,A.</style></author><author><style face="normal" font="default"> Toth,P.</style></author><author><style face="normal" font="default"> Preda,C.</style></author><author><style face="normal" font="default"> Scepanovic,M.</style></author><author><style face="normal" font="default"> Onen,H.</style></author><author><style face="normal" font="default"> Tokarska-Guzik,B.</style></author><author><style face="normal" font="default"> Anastasiu,P.</style></author><author><style face="normal" font="default"> Dorner,Z.</style></author><author><style face="normal" font="default"> Fenesi,A.</style></author><author><style face="normal" font="default"> Karrer,G.</style></author><author><style face="normal" font="default"> Nagy,K.</style></author><author><style face="normal" font="default"> Pinke,G.</style></author><author><style face="normal" font="default"> Tiborcz,V.</style></author><author><style face="normal" font="default"> Zagyvai,G.</style></author><author><style face="normal" font="default"> Zalai,M.</style></author><author><style face="normal" font="default"> Kazinczi,G.</style></author><author><style face="normal" font="default"> Leskovsek,R.</style></author><author><style face="normal" font="default"> Stesevic,D.</style></author><author><style face="normal" font="default"> Fried,G.</style></author><author><style face="normal" font="default"> Kalatozishvili,L.</style></author><author><style face="normal" font="default"> Lemke,A.</style></author><author><style face="normal" font="default"> Muller-Scharer,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Explaining variability in the production of seed and allergenic pollen by invasive Ambrosia artemisiifolia across Europe</style></title><secondary-title><style face="normal" font="default">Biol Invasions</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biol Invasions</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1573-1464</style></isbn><abstract><style face="normal" font="default">To better manage invasive populations, it is vital to understand the environmental drivers underlying spatial variation in demographic performance of invasive individuals and populations. The invasive common ragweed, Ambrosia artemisiifolia, has severe adverse effects on agriculture and human health, due to its vast production of seeds and allergenic pollen. Here, we identify the scale and nature of environmental factors driving individual performance of A. artemisiifolia, and assess their relative importance. We studied 39 populations across the European continent, covering different climatic and habitat conditions. We found that plant size is the most important determinant in variation of per-capita seed and pollen production. Using plant volume as a measure of individual performance, we found that the local environment (i.e. the site) is far more influential for plant volume (explaining 25% of all spatial variation) than geographic position (regional level; 8%) or the neighbouring vegetation (at the plot level; 4%). An overall model including environmental factors at all scales performed better (27%), including the weather (bigger plants in warm and wet conditions), soil type (smaller plants on soils with more sand), and highlighting the negative effects of altitude, neighbouring vegetation and bare soil. Pollen and seed densities varied more than 200-fold between sites, with highest estimates in Croatia, Romania and Hungary. Pollen densities were highest on arable fields, while highest seed densities were found along infrastructure, both significantly higher than on ruderal sites. We discuss implications of these findings for the spatial scale of management interventions against A. artemisiifolia</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Switzerland -CO - Netherlands -CO - France -CO - Austria -CO - Armenia -CO - Slovakia -CO - Romania -CO - Croatia -CO - Turkey -CO - Poland -CO - Hungary -CO - Slovenia -CO - Montenegro -CO - Georgia -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s10530-017-1640-9</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s10530-017-1640-9</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biol Invasions\20171216-LommenST.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biol Invasions\20171216-LommenST.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171216, Lommen ST</style></custom2><misc3><style face="normal" font="default">10.1007/s10530-017-1640-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87060</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Price,L.</style></author><author><style face="normal" font="default"> Glynn,P.</style></author><author><style face="normal" font="default"> Zarkar,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">The Cancer Centre, Queen Elizabeth Hospital Birmingham, Birmingham, UK</style></auth-address><titles><title><style face="normal" font="default">Interstitial lung disease secondary to Cetuximab in bladder cancer: an Oncologist's perspective</style></title><secondary-title><style face="normal" font="default">BMJ Case Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMJ Case Rep</style></abbr-1></periodical><pages end="" start="">-</pages><volume><style face="normal" font="default">2017</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword></keywords><dates><year Day="20" Month="12" Year="2017">2017/12/20</year></dates><abstract><style face="normal" font="default">A wide variety of cytotoxic medications cause interstitial lung disease (ILD). For the first time, we describe ILD in an 82-year-old woman with muscle invasive bladder cancer 10 days after receiving cetuximab as part of a novel trial. She had no significant medical history or drug allergies, had good exercise tolerance and a 5 pack-year smoking history. She received neoadjuvant chemotherapy (gemcitabine, cisplatin) with a good response on MRI. She was eligible for a phase 2 trial of cetuximab with chemotherapy and radiotherapy for muscle invasive bladder cancer (TUXEDO), in which the trial arm used cetuximab plus standard chemoradiotherapy to the bladder (64 grey in 32 fractions plus mitomycinandfluorouracil). Ten days after her third infusion of cetuximab, she was presented with type 1 respiratory failure. Thoracic CT scan demonstrated new widespread ground glass change in the lungs. She received high-dose steroids (prednisolone 1 mg/kg), broad spectrum antibacterial cover and non-invasive ventilation. She survived to be discharged with residual respiratory failure</style></abstract><notes><style face="normal" font="default">IS - 1757-790X (Electronic)IS - 1757-790X (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1136/bcr-2017-220181</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29269357">PM:29269357</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMJ Case Rep\20171205-PriceL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMJ Case Rep\20171205-PriceL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Price L</style></custom2><misc3><style face="normal" font="default">10.1136/bcr-2017-220181</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87061</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kuskonmaz,B.</style></author><author><style face="normal" font="default"> Ayvaz,D.</style></author><author><style face="normal" font="default"> Tezcan,I.</style></author><author><style face="normal" font="default"> Yuce,A.</style></author><author><style face="normal" font="default"> Sanal,O.</style></author><author><style face="normal" font="default"> Cetinkaya,D.U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Faculty of Medicine, Department of Pediatrics, Division of Bone Marrow Transplantation Unit, Hacettepe University, Sihhiye, 06100, Ankara, Turkey.</style></auth-address><titles><title><style face="normal" font="default">Successful hematopoietic stem cell transplantation after myeloablative conditioning in three patients with dedicator of cytokinesis 8 deficiency (DOCK8) related Hyper IgE syndrome</style></title><secondary-title><style face="normal" font="default">Bone Marrow Transplant</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Bone Marrow Transplant</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">IgE</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="21" Month="12" Year="2017">2017/12/21</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1476-5365 (Electronic)IS - 0268-3369 (Linking)LA - engPT - LetterCO - Turkey -</style></notes><work-type><style face="normal" font="default">10.1038/s41409-017-0040-1</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29269803">PM:29269803</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Bone Marrow Transplant\20171204-KuskonmazB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Bone Marrow Transplant\20171204-KuskonmazB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Kuskonmaz B</style></custom2><misc3><style face="normal" font="default">10.1038/s41409-017-0040-1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87062</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kruse,B.</style></author><author><style face="normal" font="default"> Simon,L.V.</style></author></authors></contributors><titles><title><style face="normal" font="default">Bites, Fire Ant</style></title><secondary-title><style face="normal" font="default">Books</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Books</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> New Zealand</style></keyword></keywords><dates><year Day="0" Month="6" Year="2017">2017/6</year></dates><abstract><style face="normal" font="default">Fire ants tend to be an aggressive insect that will sting causing very painful reactions. There are two types of fire ants which belong to the Solenopsis species. The first is a red, imported fire ant, Solenopsis invicta and the second is the black imported fire ant, Solenopsis richteri. They were introduced into the United States at Mobile, Alabama about 40 years ago. Red fire ants are predominately seen in 14 states: Alabama, Arkansas, California, Florida, Georgia, Louisiana, Mississippi, New Mexico, North Carolina, Oklahoma, South Carolina, Tennessee, Texas, and Virginia. Worldwide locations include the Caribbean islands, Puerto Rico, the Bahamas, the British and United States Virgin Islands, Antigua, and Trinidad, Australia, New Zealand, Taiwan, and China. The black fire ant is seen only in northern Alabama, northern Mississippi, and southern Tennessee. Over the next decade, the fire and Solenopsis invicta is expected to spread to California and towards the Pacific coast nearing the Canadian border. Fire ants do not need to be provoked to attack, and their venom is capable of causing a painful local reaction and, in some instances, result in life-threatening anaphylaxis</style></abstract><notes><style face="normal" font="default">DA - 20171222LA - engPT - ReviewPT - Book ChapterCO - United States</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29261949">PM:29261949</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Books\Bites_Fire_Ant.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Books\Bites_Fire_Ant.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Kruse B</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87063</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">de Wit,J.</style></author><author><style face="normal" font="default"> Totte,J.E.E.</style></author><author><style face="normal" font="default"> van Buchem,F.J.M.</style></author><author><style face="normal" font="default"> Pasmans,S.G.M.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Erasmus University Medical Centre, Rotterdam, the Netherlands</style></auth-address><titles><title><style face="normal" font="default">The prevalence of antibody responses against Staphylococcus aureus antigens in patients with atopic dermatitis: a systematic review and meta-analysis</style></title><secondary-title><style face="normal" font="default">Br J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">Staphylococcus (S.) aureus plays a role in the pathogenesis of atopic dermatitis (AD), possibly via the expression of various virulence antigens. An altered antibody response towards these antigens might contribute to inflammation. We aimed to provide an overview of the varying prevalences and odds of antibody responses against S. aureus antigens in AD patients. Data were systematically obtained from Embase, Medline, Web of Science, Scopus, Cochrane, PubMed and Google Scholar (up to February 12(th) 2016). We selected all original observational and experimental studies assessing anti-staphylococcal antibodies in serum of AD patients. Prevalences and odds ratios (ORs) of immunoglobulin (Ig) E, IgG, IgM, IgA against S. aureus in AD patients versus healthy controls were pooled using the random-effects model. We calculated I(2) statistics to assess heterogeneity and rated study quality using the Newcastle-Ottawa Scale. Twenty-six articles (2369 patients) were included of which 10 controlled studies. Study quality was fair to poor. AD patients had higher prevalences of IgE against staphylococcal enterotoxin (SE) A (OR 8.37, 95% CI 2.93-23.92) and SEB (OR 9.34, 95% CI 3.54-24.93) compared to controls. Prevalences of anti-staphylococcal IgE were 33% for SEA, 35% for SEB and 16% for toxic shock syndrome toxin (TSST)-1. However, study heterogeneity and imprecision should be taken into consideration when interpreting the results. Data on IgG, IgM and IgA as well as other antigens are limited. In conclusion, AD patients more often show an IgE antibody response directed against S. aureus superantigens compared to healthy controls supporting a role for S. aureus in the AD pathogenesis. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2133 (Electronic)IS - 0007-0963 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1111/bjd.16251</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247497">PM:29247497</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Dermatol\20171221-deWitJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Dermatol\20171221-deWitJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171721, de Wit J</style></custom2><misc3><style face="normal" font="default">10.1111/bjd.16251</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87064</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shen,M.</style></author><author><style face="normal" font="default"> Joshi,A.</style></author><author><style face="normal" font="default"> Vannam,R.</style></author><author><style face="normal" font="default"> Dixit,C.</style></author><author><style face="normal" font="default"> Hamilton,R.</style></author><author><style face="normal" font="default"> Kumar,C.V.</style></author><author><style face="normal" font="default"> Rusling,J.F.</style></author><author><style face="normal" font="default"> Peczuh,M.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Connecticut, Dept. of Chemistry, 55 North Eagleville Road U-3060, 06269, Storrs, UNITED STATES</style></auth-address><titles><title><style face="normal" font="default">Epitope Resolved Detection of Peanut Specific IgE Antibodies by SPR Imaging</style></title><secondary-title><style face="normal" font="default">Chembiochem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Chembiochem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Arachis</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword></keywords><dates><year Day="12" Month="12" Year="2017">2017/12/12</year></dates><abstract><style face="normal" font="default">Peanut allergy can be life-threatening and is mediated by allergen-specific immunoglobulin E (IgE) antibodies. Investigation of IgE antibody binding to allergenic epitopes identifies specific interactions underlying the allergic response. Here we report a surface plasmon resonance imaging (SPRi) immunoassay for differentiating IgE antibodies by epitope resolved detection. IgE antibodies are first captured by magnetic beads bearing IgE epsilon-chain specific antibodies and then introduced to an SPRi array immobilized with epitopes from the major peanut allergen glycoprotein Arachis hypogaea h2 (Ara h2). Differential epitope responses are achieved by establishing a binding environment that minimizes cross-reactivity while maximizes analytical sensitivity. IgE antibody binding to each Ara h2 epitope was distinguished and quantified from 10 muL patient serum samples in a 45 min assay. Excellent correlation of Ara h2-specific IgE values was found between ImmunoCAP assays and the new SPRi method</style></abstract><notes><style face="normal" font="default">IS - 1439-7633 (Electronic)IS - 1439-4227 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/cbic.201700513</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29232483">PM:29232483</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Chembiochem\20171202-ShenM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Chembiochem\20171202-ShenM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Shen M</style></custom2><misc3><style face="normal" font="default">10.1002/cbic.201700513</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87065</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ramu,S.</style></author><author><style face="normal" font="default"> Menzel,M.</style></author><author><style face="normal" font="default"> Bjermer,L.</style></author><author><style face="normal" font="default"> Andersson,C.</style></author><author><style face="normal" font="default"> Akbarshahi,H.</style></author><author><style face="normal" font="default"> Uller,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Experimental Medical Science, Lund University, Lund, Sweden</style></auth-address><titles><title><style face="normal" font="default">Allergens produce serine proteases-dependent distinct release of metabolite DAMPs in human bronchial epithelial cells</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Alternaria</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: The respiratory epithelium is a major site for disease interaction with inhaled allergens. Additional to IgE-dependent effects, allergens contain proteases that may stimulate human bronchial epithelial cells (HBECs) through protease-activated receptors, causing the release of mediators important in driving Th2 mediated immune responses. OBJECTIVE: We aimed to investigate if different allergens induce metabolite DAMPs such as ATP and uric acid (UA) release in HBECs. METHODS: HBECs (BEAS-2B cell line) was exposed to different allergen extracts; house dust mite (HDM), Alternaria alternata, Artemisia vulgaris and Betula pendula and UA, ATP, IL-8 and IL-33 release were measured. Allergen extracts were heat-inactivated or pre-incubated with serine (AEBSF) or cysteine (E64) protease inhibitor to study involvement of protease activity in ATP, UA and IL-8 release. HDM-induced release of UA was studied in a mouse model of allergic inflammation. RESULTS: All allergens caused dose-dependent rapid release of ATP and IL-8, but only HDM induced UA release from HBECs. HDM also caused release of UA in vivo in our mouse model of allergic inflammation. ATP release by all four allergen extracts was significantly reduced by heat-inactivation and by serine protease inhibitors. Similarly, the HDM induced UA release was also abrogated by heat-inactivation of HDM extract and dependent on serine proteases. Furthermore, allergen-induced IL-8 mRNA expression was inhibited by serine protease inhibitors. CONCLUSIONS AND CLINICAL RELEVANCE: ATP was released by all four allergens in HBECs supporting the role of ATP involvement in asthma pathology. However, HDM stands out by its capacity to cause UA release, which is of interest in view of the proposed role of UA in early initiation of allergic asthma. Although serine proteases may be involved in the activity of all the studied allergens, further work is warranted to explain differences between HDM and the other three allergens regarding effects on UA release. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13071</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29210131">PM:29210131</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-RamuS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-RamuS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Ramu S</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13071</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87066</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Burton,O.T.</style></author><author><style face="normal" font="default"> Tamayo,J.M.</style></author><author><style face="normal" font="default"> Stranks,A.J.</style></author><author><style face="normal" font="default"> Miller,S.</style></author><author><style face="normal" font="default"> Koleoglou,K.J.</style></author><author><style face="normal" font="default"> Weinberg,E.O.</style></author><author><style face="normal" font="default"> Oettgen,H.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, MA, USA</style></auth-address><titles><title><style face="normal" font="default">IgE promotes type 2 innate lymphoid cells in murine food allergy</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">BACKGROUND: Mast cells serve an important sentinel function at mucosal barriers and have been implicated as key early inducers of Type 2 immune responses in food allergy. The generation of Th2 and IgE following food allergen ingestion is inhibited in the absence of mast cells. Group 2 innate lymphoid cells are also thought to play an important early role in nascent allergic responses. OBJECTIVE: To test whether IgE-mediated mast cell activation promotes intestinal ILC2 responses following ingestion of food allergens and whether ILC2 amplify food allergy. METHODS: Two different mouse models of food allergy, one using intraperitoneally ovalbumin (OVA) primed BALB/c animals and the other using enterally peanut-sensitized inherently atopic IL4raF709 mice, were applied to test the contributions of IgE antibodies and mast cells to ILC2 responses. The effect of ILC2 on mast cell activation and on anaphylaxis was tested. RESULTS: ILC2 responses were significantly impaired in both models of food allergy in Igh7(-/-) mice harboring a targeted deletion of the gene encoding IgE. A similar reduction in food allergen-induced ILC2 was observed in mast cell deficient Il4raF709 Kit(W-sh) mice and this was partially corrected by reconstituting these animals using cultured bone marrow mast cells. Mast cells activated ILC2 for IL-13 production in an IL-4Ralpha-dependent manner. Activated ILC2 amplified systemic anaphylaxis by increasing target tissue sensitivity to mast cell mediators. CONCLUSIONS &amp; CLINICAL RELEVANCE: These findings support an important role for IgE-activated mast cells in driving intestinal ILC2 expansion in food allergy and reveal that ILC2, in turn, can enhance responsiveness to the mediators of anaphylaxis produced by mast cells. Strategies designed to inhibit IgE signaling or mast cell activation are likely to inhibit both Type 2 immunity and immediate hypersensitivity in food allergy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13075</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247574">PM:29247574</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-BurtonOT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-BurtonOT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Burton OT</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13075</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87067</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chan,A.</style></author><author><style face="normal" font="default"> Terry,W.</style></author><author><style face="normal" font="default"> Zhang,H.</style></author><author><style face="normal" font="default"> Karmaus,W.</style></author><author><style face="normal" font="default"> Ewart,S.</style></author><author><style face="normal" font="default"> Holloway,J.W.</style></author><author><style face="normal" font="default"> Roberts,G.</style></author><author><style face="normal" font="default"> Kurukulaaratchy,R.</style></author><author><style face="normal" font="default"> Arshad,S.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory and Critical Care Medicine, Singapore General Hospital, Singapore</style></auth-address><titles><title><style face="normal" font="default">Filaggrin Mutations Increase Allergic Airway Disease in Childhood and Adolescence Through Interactions with Eczema and Aeroallergen Sensitization</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="19" Month="12" Year="2017">2017/12/19</year></dates><abstract><style face="normal" font="default">BACKGROUND: Filaggrin loss-of-function (FLG-LOF) mutations are an established genetic cause of eczema. These mutations have subsequently been reported to increase the risk of aeroallergen sensitization and allergic airway disease. However, it is unclear whether FLG variants require both eczema and aeroallergen sensitization to influence airway disease development long-term outcomes. OBJECTIVE: To examine the effects of FLG-LOF mutations on allergic airway disease outcomes, with eczema and aeroallergen sensitization as intermediate variables, using the Isle of Wight birth cohort. METHODS: Study participants were evaluated at ages 1, 2, 4, 10 and 18 years to ascertain the development of allergic diseases (eczema, asthma and allergic rhinitis) and aeroallergen sensitization (determined by skin prick tests). FLG-LOF mutations were genotyped in 1150 subjects. To understand the complex associations between FLG mutations, intermediate variables (eczema and aeroallergen sensitization) and airway disease, path analysis was performed. RESULTS: There were significant total effects of FLG-LOF mutations on both asthma and allergic rhinitis at all ages as well as on aeroallergen sensitization up till 10 years old. In the filaggrin-asthma analysis, a direct effect of FLG-LOF mutations was observed on early childhood eczema (age 1 and 2 years) (relative risk (RR) 2.01, 95% CI: 1.74 - 2.31, p &lt; 0.001), and all significant indirect pathways on asthma outcomes passed through eczema at these ages. In contrast, for the filaggrin-rhinitis model, FLG-LOF mutations exerted significant direct effects on early eczema as well as rhinitis at 10 years (RR 1.99; 95% CI: 1.72 - 2.29, p = 0.002). CONCLUSION: FLG-LOF mutations are a significant risk factor for later childhood asthma and rhinitis. However, the pathway to asthma is only through early childhood eczema while a direct effect was observed for childhood rhinitis. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - Singapore -CO - United States -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13077</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29266469">PM:29266469</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-Chan A.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-Chan A.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Chan A</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13077</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87068</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Begen,F.M.</style></author><author><style face="normal" font="default"> Barnett,J.</style></author><author><style face="normal" font="default"> Payne,R.</style></author><author><style face="normal" font="default"> Gowland,H.M.</style></author><author><style face="normal" font="default"> DunnGalvin,A.</style></author><author><style face="normal" font="default"> Lucas,J.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Psychology, University of Bath, Bath, UK</style></auth-address><titles><title><style face="normal" font="default">Eating out with a food allergy in the UK: Change in the eating out practices of consumers with food allergy following introduction of allergen information legislation</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="8" Month="12" Year="2017">2017/12/8</year></dates><abstract><style face="normal" font="default">BACKGROUND: Strict allergen avoidance is important in day-to-day management of food allergy and avoidance when eating outside the home can present particular difficulties. EU legislation (EU FIC) introduced in December 2014 aimed to improve food allergen information provision for customers by requiring retailers of non-prepacked foods to provide information related to the content of one or more of 14 specified food allergens within their foods. OBJECTIVES: To investigate the impact of EU FIC on the behaviours, experiences and attitudes of consumers with food allergy when eating out. METHODS: As part of longitudinal research, participants with food allergy from across the UK took part in either A) pre and post legislation in-depth interviews, or B) pre and post legislation surveys. In-depth interviews were carried out with 28 participants pre and post legislation, and analysed using the framework approach. Self-report surveys were completed by 129 participants pre and post legislation, and responses were subject to quantitative analyses. RESULTS: Improvements in allergen information provision and raised awareness of food allergy in eating out venues was reported following introduction of EU FIC. Whilst participants favoured written allergen information, they expressed greater confidence in communicating with eating out staff and in trusting the allergen information that they provided. Improvements were judged to be gradual, sporadic or inconsistent in implementation. CONCLUSION &amp; CLINICAL RELEVANCE: For many participants, the 'ideal' eating out experience was one in which a range of information resources were available, and where written allergen information was complemented by proactive and accommodating staff within an allergy-aware environment. Whilst the onus is on legislators and food providers to ensure that adequate allergen information is provided, clinicians play an important role in encouraging patients with food allergy to pursue their legal right to make allergen enquiries in order to avoid accidental allergen ingestion when eating out. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - Ireland -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13072</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29220107">PM:29220107</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-BegenFM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\20171221-BegenFM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Begen FM</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13072</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87069</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,K.C.</style></author><author><style face="normal" font="default"> Le Cras,T.D.</style></author><author><style face="normal" font="default"> Larcombe,A.N.</style></author><author><style face="normal" font="default"> Zosky,G.R.</style></author><author><style face="normal" font="default"> Elliot,J.G.</style></author><author><style face="normal" font="default"> James,A.L.</style></author><author><style face="normal" font="default"> Noble,P.B.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Human Sciences, University of Western Australia, 35 Stirling Highway, Crawley, 6009, Australia Australia</style></auth-address><titles><title><style face="normal" font="default">Independent and combined effects of airway remodelling and allergy on airway responsiveness</style></title><secondary-title><style face="normal" font="default">Clin Sci (Lond)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Sci (Lond)</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="21" Month="12" Year="2017">2017/12/21</year></dates><abstract><style face="normal" font="default">Airway remodelling and allergic inflammation are key features of airway hyperresponsiveness in asthma, however their interrelationships are unclear. This study investigated the separate and combined effects of increased airway smooth muscle (ASM) layer thickness and allergy on airway hyperresponsiveness. We integrated a protocol of ovalbumin (OVA)-induced allergy into a non-inflammatory mouse model of ASM remodelling induced by conditional and airway-specific expression of TGF-alpha in Egr-1 deficient transgenic mice, which produced thickening of the ASM layer following ingestion of doxycycline. Mice were sensitised to OVA and assigned to one of four treatment groups: Allergy - normal chow diet and OVA challenge; Remodelling - doxycycline in chow and saline challenge; Allergy and Remodelling - doxycycline in chow and OVA challenge; and Control - normal chow diet and saline challenge. Airway responsiveness to methacholine and histology were assessed. Compared with the Control group, airway responsiveness to methacholine was increased in the Allergy group, independently of changes in wall structure, whereas airway responsiveness in the Remodelling group was increased independent of exposure to aeroallergen. The combined effects of allergy and remodelling on airway responsiveness were greater than either alone. There was a positive relationship between the thickness of the ASM layer with airway responsiveness, which was upward shifted in the presence of allergy. These findings support allergy and airway remodelling as independent causes of variable and excessive airway narrowing</style></abstract><notes><style face="normal" font="default">IS - 1470-8736 (Electronic)IS - 0143-5221 (Linking)LA - engPT - Journal ArticleCO - Australia -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1042/CS20171386</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29269381">PM:29269381</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Sci (Lond)\20171201-WangKC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Sci (Lond)\20171201-WangKC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Wang KC</style></custom2><misc3><style face="normal" font="default">10.1042/CS20171386</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87091</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mortuaire,G.</style></author><author><style face="normal" font="default"> Gengler,I.</style></author><author><style face="normal" font="default"> Balden,M.</style></author><author><style face="normal" font="default"> Capron,M.</style></author><author><style face="normal" font="default"> Lefevre,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Service d'ORL et de chirurgie cervico-faciale, hopital Huriez, CHRU, 59000 Lille, France; Inserm U995, Lille Inflammation Research International Center, universite de Lille, 59000 Lille, France.</style></auth-address><titles><title><style face="normal" font="default">Impact of allergy on phenotypic and endotypic profiles of nasal polyposis</style></title><secondary-title><style face="normal" font="default">Eur Ann Otorhinolaryngol Head Neck Dis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Otorhinolaryngol Head Neck Dis</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="8" Month="12" Year="2017">2017/12/8</year></dates><abstract><style face="normal" font="default">OBJECTIVES: To assess the impact of allergy on clinical presentations (phenotypes) and inflammatory patterns (endotypes) of chronic rhinosinusitis with nasal polyps (CRSwNP). METHODS: A single-center prospective study was conducted over an 18-month period. Fifty-seven patients with refractory CRSwNP were included. The diagnosis of allergy was based on concordant skin prick tests and symptoms. Phenotypes were determined on symptom severity score, polyp size classification and Lund-Mackay CT staging. Inflammatory endotypes were determined on biomarker analysis (IgE, IgA, IL-5, IL-9, ECP, EDN) in blood and nasal secretions. Eosinophil counts were obtained in blood, nasal secretions and polyps. RESULTS: Phenotype and endotype profiles were comparable in patients with (n=15) or without (n=42) allergy. Only asthma with high total IgE blood concentration showed association with allergy. CONCLUSIONS: The present results suggest that allergy is not directly involved in the clinical expression and specific inflammatory pathways of CRSwNP. New therapies target inflammation signaling pathways, and identifying accurate blood and tissue biomarkers will be the line of research most likely to improve treatment of CRSwNP</style></abstract><notes><style face="normal" font="default">IS - 1879-730X (Electronic)IS - 1879-7296 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.anorl.2017.11.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29229196">PM:29229196</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Otorhinolaryngol Head Neck Dis\20171205-MortuaireG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Otorhinolaryngol Head Neck Dis\20171205-MortuaireG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Mortuaire G</style></custom2><misc3><style face="normal" font="default">10.1016/j.anorl.2017.11.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87092</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Martorano,L.M.</style></author><author><style face="normal" font="default"> Grayson,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy &amp; Immunology, Department of Pediatrics. The Ohio State University Wexner Medical Center &amp; Nationwide Children's Hospital, Columbus, OH, United States</style></auth-address><titles><title><style face="normal" font="default">Respiratory viral infections and atopic development: From possible mechanisms to advances in treatment</style></title><secondary-title><style face="normal" font="default">Eur J Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur J Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="15" Month="12" Year="2017">2017/12/15</year></dates><abstract><style face="normal" font="default">Atopic sensitization and allergic diseases are increasing in modernized countries. These diseases affect millions of individuals, but the mechanisms behind their development are not fully understood. One hypothesis relates to early life respiratory viral infections driving the development of atopic disease including asthma. This review presents the current state of the field, focusing on epidemiologic data supporting a role for early life respiratory viruses in the development of specific IgE, both against aeroallergens and the respiratory virus. Our own work using the Sendai mouse model is then summarized to provide a potential mechanistic explanation for how a respiratory viral infection could drive development of atopic sensitization and disease. We then discuss the components of this mechanistic pathway that have and have not been validated in humans. Finally, we discuss areas ripe for research, as well as potential and current therapeutics that might disrupt the link between respiratory viral infections in early life and atopic sensitization/disease. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1521-4141 (Electronic)IS - 0014-2980 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/eji.201747052</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29244204">PM:29244204</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur J Immunol\20171215-MartoranoLM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur J Immunol\20171215-MartoranoLM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Martorano LM</style></custom2><misc3><style face="normal" font="default">10.1002/eji.201747052</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87093</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,S.H.</style></author><author><style face="normal" font="default"> Saba,E.</style></author><author><style face="normal" font="default"> Kim,B.K.</style></author><author><style face="normal" font="default"> Yang,W.K.</style></author><author><style face="normal" font="default"> Park,Y.C.</style></author><author><style face="normal" font="default"> Shin,H.J.</style></author><author><style face="normal" font="default"> Han,C.K.</style></author><author><style face="normal" font="default"> Lee,Y.C.</style></author><author><style face="normal" font="default"> Rhee,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Traditional Medicine and Bioscience, Daejeon University, Daejeon 34520, Republic of Korea.</style></auth-address><titles><title><style face="normal" font="default">Luteolin attenuates airway inflammation by inducing the transition of CD4(+)CD25(-) to CD4(+)CD25(+) regulatory T cells</style></title><secondary-title><style face="normal" font="default">Eur J Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur J Pharmacol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Autoimmunity</style></keyword><keyword><style face="normal" font="default"> Cyclosporine</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">Regulatory T cells (Th2) play an important role in autoimmunity and have been shown to exert anti-inflammatory effects in allergic asthma. Mouse model of airway inflammation was used to examine the suppressive activity of luteolin-induced CD4(+)CD25(+) regulatory T cells (Tregs) in vivo. In this study, BALB/c mice were sensitized with ovalbumin antigen (OVA) by aerosol challenge. Then, various biological processes were examined, including airway eosinophilia; mucus hypersecretion; elevation of OVA-specific IgE, expression of Th2 cytokines and chemokine levels; expression of eotaxin 2 and CCR3; and airway hyper responsiveness (AHR). Luteolin significantly inhibited OVA-induced increase in immune cell and eosinophil counts as well as IL-4, IL-5, IL-13, and eotaxin levels in bronchoalveolar lavage fluid (BAL Fluid). Luteolin and cyclosporine A (CsA) which was a positive control also substantially reduced OVA-specific IgE levels, eotaxin 2 levels, and CCR3 expression in BAL Fluid. In contrast, luteolin significantly increased IL-10 and IFN-gamma protein levels, as well as IL-10 and TGF-beta1 mRNA expression in the lung. In vitro studies showed that the number of luteolin-induced CD4(+)CD25(+) Treg (iTreg) cells was higher, with elevated levels of TGF-beta1 and foxp3 mRNA expression in lungs tissue. Transfer of iTreg cells into OVA-sensitized mice reduced AHR, eosinophil recruitment, eotaxin, IgE, and Th2 cytokine expressions, and increased IFN-gamma production in BAL Fluid after allergen challenge. Furthermore, adoptive transfer of iTreg cells prevented disease in a CD25-depleted mouse asthma model. Luteolin via induction of foxp3 and CD4(+)CD25(+) Treg cells may represent a new strategy in the development of therapies for managing asthma</style></abstract><notes><style face="normal" font="default">IS - 1879-0712 (Electronic)IS - 0014-2999 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1016/j.ejphar.2017.12.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29225189">PM:29225189</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur J Pharmacol\20171210-KimSH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur J Pharmacol\20171210-KimSH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Kim SH</style></custom2><misc3><style face="normal" font="default">10.1016/j.ejphar.2017.12.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87097</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Remington,B.</style></author><author><style face="normal" font="default"> Broekman,H.C.H.</style></author><author><style face="normal" font="default"> Blom,W.M.</style></author><author><style face="normal" font="default"> Capt,A.</style></author><author><style face="normal" font="default"> Crevel,R.W.R.</style></author><author><style face="normal" font="default"> Dimitrov,I.</style></author><author><style face="normal" font="default"> Faeste,C.K.</style></author><author><style face="normal" font="default"> Fernandez-Canton,R.</style></author><author><style face="normal" font="default"> Giavi,S.</style></author><author><style face="normal" font="default"> Houben,G.F.</style></author><author><style face="normal" font="default"> Glenn,K.C.</style></author><author><style face="normal" font="default"> Madsen,C.B.</style></author><author><style face="normal" font="default"> Kruizinga,A.K.</style></author><author><style face="normal" font="default"> Constable,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">TNO, Zeist, The Netherlands.</style></auth-address><titles><title><style face="normal" font="default">Approaches to assess IgE mediated allergy risks (sensitization and cross-reactivity) from new or modified dietary proteins</style></title><secondary-title><style face="normal" font="default">Food Chem Toxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem Toxicol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Dietary Proteins</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">The development and introduction of new dietary protein sources has the potential to improve food supply sustainability. Understanding the potential allergenicity of these new or modified proteins is crucial to ensure protection of public health. Exposure to new proteins may result in de novo sensitization, with or without clinical allergy, or clinical reactions through cross-reactivity. In this paper we review the potential of current methodologies (in silico, in vitro degradation, in vitro IgE binding, animal models and clinical studies) to address these outcomes for risk assessment purposes for new proteins, and especially to identify and characterise the risk of sensitization for IgE mediated allergy from oral exposure. Existing tools and tests are capable of assessing potential crossreactivity. However, there are few possibilities to assess the hazard due to de novo sensitization. The only methods available are in vivo models, but many limitations exist to use them for assessing risk. We conclude that there is a need to understand which criteria adequately define allergenicity for risk assessment purposes, and from these criteria develop a more suitable battery of tests to distinguish between proteins of high and low allergenicity, which can then be applied to assess new proteins with unknown risks</style></abstract><notes><style face="normal" font="default">IS - 1873-6351 (Electronic)IS - 0278-6915 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Netherlands -CO - France -CO - United Kingdom -CO - Bulgaria -CO - Norway -CO - Belgium -CO - Greece -CO - United states -CO - Denmark -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1016/j.fct.2017.12.025</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29258956">PM:29258956</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem Toxicol\20171212-RemingtonB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem Toxicol\20171212-RemingtonB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171212, Remington B</style></custom2><misc3><style face="normal" font="default">10.1016/j.fct.2017.12.025</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87101</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Klimek,L.</style></author><author><style face="normal" font="default"> Werfel,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Zentrum fur Rhinologie und Allergologie, An den Quellen 10, 65183, Wiesbaden, Deutschland.</style></auth-address><titles><title><style face="normal" font="default">[Important information regarding the guideline for (allergen-)specific immunotherapy (SIT)]</style></title><secondary-title><style face="normal" font="default">Hautarzt</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Hautarzt</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Immunotherapy</style></keyword></keywords><dates><year Day="14" Month="12" Year="2017">2017/12/14</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1432-1173 (Electronic)IS - 0017-8470 (Linking)LA - gerPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s00105-017-4093-2</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29242961">PM:29242961</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Hautarzt\20171201-KlimekL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Hautarzt\20171201-KlimekL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Klimek L</style></custom2><misc3><style face="normal" font="default">10.1007/s00105-017-4093-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87102</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jappe,U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Forschungsgruppe Klinische und Molekulare Allergologie, Forschungszentrum Borstel, Mitglied im Deutschen Zentrum fur Lungenforschung (DZL), Parkallee 35, 23845, Borstel, Deutschland.</style></auth-address><titles><title><style face="normal" font="default">[Allergen nomenclature]</style></title><secondary-title><style face="normal" font="default">Hautarzt</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Hautarzt</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="19" Month="12" Year="2017">2017/12/19</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1432-1173 (Electronic)IS - 0017-8470 (Linking)LA - gerPT - LetterCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s00105-017-4103-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29260247">PM:29260247</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Hautarzt\20171201-JappeU.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Hautarzt\20171201-JappeU.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Jappe U</style></custom2><misc3><style face="normal" font="default">10.1007/s00105-017-4103-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87103</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chirumbolo,S.</style></author><author><style face="normal" font="default"> Bjorklund,G.</style></author><author><style face="normal" font="default"> Sboarina,A.</style></author><author><style face="normal" font="default"> Vella,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Neurological and Movement Sciences , University of Verona , Verona , Italyd Unit of Immunology-Azienda Ospedaliera Universitaria Integrata (AOUI) , Verona , Italy</style></auth-address><titles><title><style face="normal" font="default">The role of basophils as innate immune regulatory cells in allergy and immunotherapy</style></title><secondary-title><style face="normal" font="default">Hum Vaccin Immunother</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Hum Vaccin Immunother</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="19" Month="12" Year="2017">2017/12/19</year></dates><abstract><style face="normal" font="default">Basophils are circulating cells that are associated quite exclusively with allergy response and hypersensitivity reactions but their role in the immune network might be much more intriguing and complex than previously expected. The feasibility of testing their biology in vitro for allergy research and diagnosis, due fundamentally to their quite easy availability in the peripheral blood, made them the major source for assessing allergy in the laboratory assay, when yet many further cells such as mast cells and eosinophils are much more involved as effector cells in allergy than circulating basophils. Interestingly, basophil numbers change rarely in peripheral blood during an atopic response, while we might yet observe an increase in eosinophils and modification in the biology of mast cells in the tissue during an hypersensitivity response. Furthermore, the fact that basophils are very scanty in numbers suggests that they should mainly serve as regulatory cells in immunity, rather than effector leukocytes, as still believed by the majority of physicians. In this review we will try to describe and elucidate the possible role of these cells, known as "innate IL4-producing cells" in the immune regulation of allergy and their function in allergen immunotherapy</style></abstract><notes><style face="normal" font="default">IS - 2164-554X (Electronic)IS - 2164-5515 (Linking)LA - engPT - Journal ArticleCO - Italy -CO - Norway -</style></notes><work-type><style face="normal" font="default">10.1080/21645515.2017.1417711</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29257936">PM:29257936</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Hum Vaccin Immunother\20171201-ChirumboloS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Hum Vaccin Immunother\20171201-ChirumboloS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Chirumbolo S</style></custom2><misc3><style face="normal" font="default">10.1080/21645515.2017.1417711</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87104</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Morales,M.</style></author><author><style face="normal" font="default"> Gallego,M.T.</style></author><author><style face="normal" font="default"> Iraola,V.</style></author><author><style face="normal" font="default"> Moya,R.</style></author><author><style face="normal" font="default"> Santana,S.</style></author><author><style face="normal" font="default"> Carnes,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Research &amp; Development Department, Laboratorios LETI, Tres Cantos, Spain</style></auth-address><titles><title><style face="normal" font="default">Preclinical safety and immunological efficacy of Alternaria alternata polymerized extracts</style></title><secondary-title><style face="normal" font="default">Immun Inflamm Dis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immun Inflamm Dis</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Alternaria</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="19" Month="12" Year="2017">2017/12/19</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Alternaria alternata is a widespread fungi whose allergy is a risk factor for asthma development. The use of a polymerized allergen extract (allergoid) may be safer than native extract based treatments while maintaining efficacy. The objective of this study was to characterize biochemically and immunochemically a new Alternaria alternata allergoid. METHODS: Characterization of native and allergoid extracts was performed by determination of protein content, protein and allergenic profile, biological potency, identification of Alternaria allergens, and Alt a 1 quantification. Safety was evaluated in toxicological assays (Ames test, limit test, and fish embryo acute toxicity test in zebrafish, and maximum tolerated dose and Dose-range finding study in rats). Efficacy was evaluated as the capacity to induce IgG antibodies that block IgE-binding to the allergen and cytokine induction (IFN-gamma, IL-4, IL-6, IL-10, and TNF-alpha) in PBMC from atopic donors. RESULTS: Protein and antigenic profiles showed significant modification of the depigmented allergoid with respect to the native extract, inducing a lower IgE binding capacity. Alt a 1, Alt a 3, Alt a 6, and Alt a 8 allergen sequences were identified in the polymer. No toxicological nor genotoxicity effects were observed. The polymer induced IgG antibodies that blocked human IgE binding epitopes, and it induced higher IL-10 levels and similar levels of the other cytokines than native extract in PBMC. CONCLUSIONS: This new A. alternata allergoid could be an effective immunotherapy treatment leading to cytokine stimulation and inducing synthesis of IgG antibodies able to block IgE binding to the allergen. In addition, no toxicological effect was observed, and it may be safer than native extract due to its lower IgE binding capacity and cytokine induction that suggest tolerance induction via T cell shift to Treg (IL-10)</style></abstract><notes><style face="normal" font="default">IS - 2050-4527 (Electronic)IS - 2050-4527 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1002/iid3.212</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29265735">PM:29265735</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immun Inflamm Dis\20171201-MoralesM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immun Inflamm Dis\20171201-MoralesM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Morales M</style></custom2><misc3><style face="normal" font="default">10.1002/iid3.212</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87105</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chang,H.C.</style></author><author><style face="normal" font="default"> Huang,P.H.</style></author><author><style face="normal" font="default"> Syu,F.S.</style></author><author><style face="normal" font="default"> Hsieh,C.H.</style></author><author><style face="normal" font="default"> Chang,S.L.</style></author><author><style face="normal" font="default"> Lu,J.</style></author><author><style face="normal" font="default"> Chen,H.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Graduate Institute of Life Science, National Defense Medical Center, Taipei, Taiwan</style></auth-address><titles><title><style face="normal" font="default">Critical involvement of atypical chemokine receptor CXCR7 in allergic airway inflammation</style></title><secondary-title><style face="normal" font="default">Immunology</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunology</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="18" Month="12" Year="2017">2017/12/18</year></dates><abstract><style face="normal" font="default">Trafficking and recruitment of immune cells to the site of inflammation with spatial and temporal synchronization is crucial for the development of allergic airway inflammation. Particularly, chemokines are known to be key players in these processes. Previous studies revealed that the CXCL12/CXCR4 axis plays an important role in regulating allergic airway inflammation. However, the role of CXCR7, a recently discovered second receptor for CXCL12, in regulating airway inflammation has not been explored. Initially, CXCR7 was considered as a decoy receptor; however, numerous subsequent studies revealed that engagement of CXCR7 triggered its own signaling or modulated CXCR4-mediated signaling. In the present study, we detected the expression of CXCR7 in airway epithelial cells. Use of a lentiviral-delivery system to knock down the expression of CXCR7 in the lung of sensitized mice abrogated the cardinal features of asthma, indicating that CXCR7 plays a role in regulating allergic airway inflammation. The activation of MAPK and AKT signaling in response to CXCL12 in mouse epithelial cell line, MLE-12, was reduced when CXCR7 expression was knocked down. However, either knockdown or overexpression of CXCR7 in MLE-12 did not affect CXCL12-mediated calcium influx, indicating that CXCR7 does not modulate CXCR4-mediated signaling, and that it functions as a signaling receptor rather than a decoy receptor. Finally, we found that the expression of chemokine CCL2 is regulated by CXCR7/CXCL12-mediated signaling through beta-arrestin in airway epithelial cells. Thus, regulating the expression of CCL2 in airway epithelial cells may be one mechanism by which CXCR7 participates in regulating allergic airway inflammation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1365-2567 (Electronic)IS - 0019-2805 (Linking)LA - engPT - Journal ArticleCO - Taiwan -</style></notes><work-type><style face="normal" font="default">10.1111/imm.12881</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29250768">PM:29250768</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunology\20171201-ChangHC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunology\20171201-ChangHC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Chang HC</style></custom2><misc3><style face="normal" font="default">10.1111/imm.12881</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87111</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kaffenberger,T.M.</style></author><author><style face="normal" font="default"> Dedhia,R.C.</style></author><author><style face="normal" font="default"> Schwarzbach,H.L.</style></author><author><style face="normal" font="default"> Mady,L.J.</style></author><author><style face="normal" font="default"> Lee,S.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, PADepartment of Otolaryngology, Emory University School of Medicine, Atlanta, GAUniversity of Pittsburgh School of Medicine, Pittsburgh, PADepartment of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, PADepartment of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, PA</style></auth-address><titles><title><style face="normal" font="default">Comparative effectiveness of allergy testing method in driving immunotherapy outcomes</style></title><secondary-title><style face="normal" font="default">Int Forum Allergy Rhinol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Forum Allergy Rhinol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="20" Month="12" Year="2017">2017/12/20</year></dates><abstract><style face="normal" font="default">BACKGROUND: Skin-prick testing (SPT), in vitro testing (IVT), and intradermal-dilutional testing (IDT) are methods to detect patient sensitivities to specific allergens and direct immunotherapy dosing. We used objective and subjective measures of improvement to compare outcomes based on test method. METHODS: Patients underwent 1 of 3 protocols: SPT, screening SPT followed by IDT, or IVT. We used institution billing data to do a cost analysis of these tests. The time to maintenance (TTM) therapy was analyzed and patients were stratified into high and low reactors. The Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) was used to quantify symptoms pre-maintenance and post-maintenance. RESULTS: Of 177 patients (SPT, n = 40; IVT, n = 91; IDT, n = 46), 115 (SPT, n = 35; IVT, n = 39; IDT, n = 41) were high reactors. Out of 90 patients (SPT, n = 17; IVT, n = 37; IDT, n = 36) reaching maintenance, 58 were high reactors (SPT, n = 15; IVT, n = 12; IDT, n = 31). Overall, SPT, IVT, and IDT median TTM were 542, 329, and 578.5 days, respectively. IDT TTM was shorter compared to IVT overall and in high reactors (hazard ratio [HR] = 1.91, p = 0.02; HR = 2.12, p = 0.03), but was not significant compared to SPT high reactors (p = 0.33). The IDT cost was $62.66, translating to an incremental cost-effectiveness ratio of $0.23 per day of shortened TTM. Median RQLQ change for the SPT, IVT, and IDT groups was 6.5, 1, and 1.5, respectively, but was not significant (p = 0.60). CONCLUSION: IDT reached maintenance immunotherapy quicker than IVT but there was no difference compared to SPT. TTM did not correlate with improvements in patient symptoms between testing methods. This study represents a novel comparison of outcomes based on initial allergy testing method</style></abstract><notes><style face="normal" font="default">IS - 2042-6984 (Electronic)IS - 2042-6976 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/alr.22061</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29266815">PM:29266815</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171208-KaffenbergerTM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171208-KaffenbergerTM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, KaffenbergerTM</style></custom2><misc3><style face="normal" font="default">10.1002/alr.22061</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87112</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mady,L.J.</style></author><author><style face="normal" font="default"> Schwarzbach,H.L.</style></author><author><style face="normal" font="default"> Moore,J.A.</style></author><author><style face="normal" font="default"> Boudreau,R.M.</style></author><author><style face="normal" font="default"> Kaffenberger,T.M.</style></author><author><style face="normal" font="default"> Willson,T.J.</style></author><author><style face="normal" font="default"> Lee,S.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PAUniversity of Pittsburgh School of Medicine, Pittsburgh, PADepartment of Otolaryngology, University of Pittsburgh, Pittsburgh, PADepartment of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PADepartment of Otolaryngology, University of Pittsburgh, Pittsburgh, PADepartment of Otolaryngology, San Antonio Military Medical Center, Uniformed Services University of the Health Sciences, San Antonio, TXDepartment of Otolaryngology, University of Pittsburgh, Pittsburgh, PA</style></auth-address><titles><title><style face="normal" font="default">The association of air pollutants and allergic and nonallergic rhinitis in chronic rhinosinusitis</style></title><secondary-title><style face="normal" font="default">Int Forum Allergy Rhinol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Forum Allergy Rhinol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: There has been little investigation regarding air quality and rhinitis in the pathophysiology of upper airway disease. In this study, we assessed the impact of inhalant pollutants (particulate matter 2.5 [PM2.5 ] and black carbon [BC]) on allergic rhinitis and chronic rhinosinusitis (CRS) disease severity. METHODS: CRS patients with nasal polyps (CRSwNP) and without polyps (CRSsNP) were identified. Spatial modeling from pollutant monitoring sites was used to estimate exposures for patients meeting the inclusion criteria (total, n = 125; CRSsNP, n = 67; CRSsNP, n = 58). Skin-prick, intradermal dilutional, and in-vitro testing methods were utilized to determine aeroallergen sensitization. Disease severity indicators were measured by modified Lund-Mackay score (LMS), the 22-item Sino-Nasal Outcome Test (SNOT-22), systemic steroid therapy, and number of functional endoscopic sinus surgeries (FESS). RESULTS: Thirty-six percent (n = 45) of patients who described rhinitis symptoms demonstrated no reactivity to aeroallergen testing. Sixty-four percent (n = 80) tested positive for at least 1 allergen, with no differences found between CRSsNP and CRSwNP (62.1% vs 67.2%). There were significant differences in air pollutants between patients testing negative and positive for allergies (nonallergic vs allergic: PM2.5 , 11.32 vs 11.07 mug/m(3) , p = 0.030; BC, 0.81 vs 0.76 absorbance, p =0.044). Nonallergic CRSwNP demonstrated higher PM2.5 compared with allergic counterparts (11.48 vs 11.09 mug/m(3) , p = 0.032). A similar pattern was observed with BC (0.82 vs 0.75 absorbance, p = 0.017). In CRSsNP, BC correlated significantly with SNOT-22 (r = 0.55, p = 0.042). CONCLUSION: Our results suggest that small inhalant pollutants may contribute to nonallergic symptomatology in patients with and without nasal polyps. Regardless of allergy status, BC may play a role in CRS symptom severity</style></abstract><notes><style face="normal" font="default">IS - 2042-6984 (Electronic)IS - 2042-6976 (Linking)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">10.1002/alr.22060</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29227043">PM:29227043</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171208-MadyLJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Forum Allergy Rhinol\20171208-MadyLJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Mady LJ</style></custom2><misc3><style face="normal" font="default">10.1002/alr.22060</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87113</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ohno,T.</style></author><author><style face="normal" font="default"> Zhang,C.</style></author><author><style face="normal" font="default"> Kondo,Y.</style></author><author><style face="normal" font="default"> Kang,S.</style></author><author><style face="normal" font="default"> Furusawa,E.</style></author><author><style face="normal" font="default"> Tsuchiya,K.</style></author><author><style face="normal" font="default"> Miyazaki,Y.</style></author><author><style face="normal" font="default"> Azuma,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan</style></auth-address><titles><title><style face="normal" font="default">The immune checkpoint molecule VISTA regulates allergen-specific Th2-mediated immune responses</style></title><secondary-title><style face="normal" font="default">Int Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="15" Month="12" Year="2017">2017/12/15</year></dates><abstract><style face="normal" font="default">V-domain Ig suppressor of T cell activation (VISTA) is a novel immune checkpoint receptor and ligand that regulates T cell activation. We investigated the functional involvement of VISTA in Th2 cell-mediated immune responses using an ovalbumin (OVA)-induced allergic asthma model. Treatment with an anti-VISTA monoclonal antibody (mAb) during allergen sensitization increased the production of antibodies, including total IgE, OVA-specific IgG1 and IgG2a, and allergen-specific interleukin (IL)-5 and IL-13; it also increased the expression of IL-13 by splenic CD4 + T cells. However, treatment with the anti-VISTA mAb during sensitization did not accelerate asthmatic responses, including airway hyper-responsiveness (AHR) or the number of eosinophils in bronchoalveolar lavage (BAL) fluid. In contrast, treatment with the anti-VISTA mAb during allergen challenge significantly augmented AHR and BAL fluid eosinophilia. This treatment also increased the production of IL-5 and IL-13 in BAL fluid and the expression of IL-13 by CD4 + T cells in draining lymph nodes. These results suggest that VISTA is involved in the regulation of Th2 cell generation and Th2 cell-mediated antibody production, and regulates asthmatic responses, especially in the effector phase</style></abstract><notes><style face="normal" font="default">IS - 1460-2377 (Electronic)IS - 0953-8178 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1093/intimm/dxx070</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29267882">PM:29267882</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Immunol\20171208-OhnoT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Immunol\20171208-OhnoT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Ohno T</style></custom2><misc3><style face="normal" font="default">10.1093/intimm/dxx070</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87116</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rowicka,G.</style></author><author><style face="normal" font="default"> Strucinska,M.</style></author><author><style face="normal" font="default"> Riahi,A.</style></author><author><style face="normal" font="default"> Weker,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Diet and Nutritional Status of Children with Cow's Milk Protein Allergy, Treated with a Milk-Free Diet</style></title><secondary-title><style face="normal" font="default">Int J Allergy Medic</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Int J Allergy Medic</style></full-title></periodical><pages end="" start="">-</pages><volume><style face="normal" font="default">3</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Children with Cow's Milk Protein Allergy (CMPA), treated with a milk-free diet, may be at risk of deficiency of nutrients important for appropriate development. The aim of the study was to evaluate the diets and the nutritional status of children with CMPA.The study included 48 children, aged 4-6 years, with CMPA treated with a milk-free diet. The principles of the milk-free diet were defined and the compliance with the diet by children was monitored by a physician and a dietician. The control group consisted of 30 healthy controls, aged 4-6 years, on a traditional diet containing milk and milk products. The energy and nutritional value of the diets was determined on the basis of 3-day dietary records. Children's nutritional status was evaluated based on the normalised Body Mass Index (BMI z-score) and selected biochemical indices. The energy value of the diets of children with CMPA was higher compared to recommendations and significantly higher than the energy value of the diets of healthy controls. The intake of protein in both groups exceeded approximately three times the daily requirement. Children with CMPA consumed significantly more long-chainpoly-unsaturated fatty acids, carbohydrates, iron, iodine, copper and vitamins D, E, B1, B6 and PP. Vitamin D deficiency was found in the diets of children from both groups. Calcium deficiency was recorded in the diets of 93.8% of children withCMPA and 90% of the controls. The evaluated biochemical indices in both groups did not different significantly and, except for the concentration of 25(OH) vitamin D in blood serum of children with allergy, were within the reference range. Milk-free diets in children with CMPA were adequate for most nutrients, but the children are at risk of vitamin D insufficiency despite the higher vitamin D content of their diets compared to the group of healthy children. The better balancing of the diets of children with allergy was probably due to continuous medical and nutritional care provided by paediatricians and dieticians.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.23937/2572-3308/1510025</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.23937/2572-3308/1510025</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Allergy Medic\20171220-RowickaG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Allergy Medic\20171220-RowickaG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Rowicka G</style></custom2><misc3><style face="normal" font="default">10.23937/2572-3308/1510025</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87117</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Qin,X.</style></author><author><style face="normal" font="default"> Li,Y.</style></author><author><style face="normal" font="default"> Sun,X.</style></author><author><style face="normal" font="default"> Meng,L.</style></author><author><style face="normal" font="default"> Wang,X.</style></author></authors></contributors><auth-address><style face="normal" font="default">Peking University, Beijing, China</style></auth-address><titles><title><style face="normal" font="default">Transport pathway and source area for Artemisia pollen in Beijing, China</style></title><secondary-title><style face="normal" font="default">Int J Biometeorol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Biometeorol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">Artemisia pollen is an important allergen responsible for allergic rhinitis in Beijing, China. To explore the transport pathways and source areas of Artemisia pollen, we used Burkard 7-day traps to monitor daily pollen concentrations in 2016 in an urban and suburban locality. Backward trajectories of 24- and 96-h and their cluster analysis were performed to identify transport pathways of Artemisia pollen using the HYSPLIT model on 0.5 degrees x 0.5 degrees GADS meteorological data. The potential source contribution function (PSCF) and concentration weighted trajectory (CWT) were calculated to further identify the major potential source areas at local, regional, and long-range scales. Our results showed significant differences in Artemisia pollen concentration between urban and suburban areas, attributed to differences in plant distribution and altitude of the sampling locality. Such differences arisen from both pollen emission and air mass movements, hence pollen dispersal. At local or regional scales, source area of northwestern parts of Beijing City, Hebei Province and northern and northwestern parts of Inner Mongolia influenced the major transport pathways of Artemisia pollen. Transport pathway at a long-range scale and its corresponding source area extended to northwestern parts of Mongolia. The regional-scale transport affected by wind and altitude is more profound for Artemisia pollen at the suburban than at the urban station</style></abstract><notes><style face="normal" font="default">IS - 1432-1254 (Electronic)IS - 0020-7128 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s00484-017-1467-1</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29236152">PM:29236152</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Biometeorol\20171208-QinX.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Biometeorol\20171208-QinX.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Qin X</style></custom2><misc3><style face="normal" font="default">10.1007/s00484-017-1467-1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87118</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cho,J.M.</style></author><author><style face="normal" font="default"> Davis,D.M.R.</style></author><author><style face="normal" font="default"> Wetter,D.A.</style></author><author><style face="normal" font="default"> Bartley,A.C.</style></author><author><style face="normal" font="default"> Brewer,J.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA</style></auth-address><titles><title><style face="normal" font="default">Association between atopic dermatitis and squamous cell carcinoma: a case-control study</style></title><secondary-title><style face="normal" font="default">Int J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int J Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Cyclosporine</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="15" Month="12" Year="2017">2017/12/15</year></dates><abstract><style face="normal" font="default">BACKGROUND: Conflicting data have been published on whether an association exists between atopic dermatitis (AD) and nonmelanoma skin cancer. This study aimed to determine whether individuals with AD had an increased risk of squamous cell carcinoma (SCC) development. METHODS: We conducted a retrospective, case-control study of patients residing in Olmsted County, Minnesota. Cases were selected from patients seen at Mayo Clinic (Rochester, Minnesota) who had an initial SCC diagnosis (either invasive SCC or SCC in situ) from January 1, 1996, through December 23, 2010. Age- and sex-matched controls were selected from patients seen at Mayo Clinic with no history of SCC before the case event date. RESULTS: Three hundred ninety-nine individuals with a documented history of SCC were identified and matched with 780 controls who did not have a history of SCC. After adjusting for race, smoking history, ionizing radiation exposure, corticosteroid and cyclosporine use, and non-SCC skin cancers, the odds ratio for SCC development between patients with history of AD versus patients without history of AD was 1.75 (95% CI, 1.05-2.93). CONCLUSIONS: Our findings support an increased risk of SCC development in the setting of AD</style></abstract><notes><style face="normal" font="default">IS - 1365-4632 (Electronic)IS - 0011-9059 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/ijd.13857</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29243817">PM:29243817</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Dermatol\20171208-ChoJM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Dermatol\20171208-ChoJM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Cho JM</style></custom2><misc3><style face="normal" font="default">10.1111/ijd.13857</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87121</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Song,B.</style></author><author><style face="normal" font="default"> Oehrle,N.W.</style></author><author><style face="normal" font="default"> Liu,S.</style></author><author><style face="normal" font="default"> Krishnan,H.B.</style></author></authors></contributors><titles><title><style face="normal" font="default">Development and characterization of a soybean experimental line lacking the alpha' subunit of beta-conglycinin and G1, G2, and G4 glycinin</style></title><secondary-title><style face="normal" font="default">J Agric Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Agric Food Chem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Amino Acids</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">A soybean experimental line (BSH-3) devoid of a subset of seed storage proteins was developed by crossing a mutant donor line 'HS99B' with a Chinese cultivar 'Dongnong47' (DN47). One dimensional and high-resolution 2-D gel electrophoresis revealed the absence of G1 (A1aB2), G2 (A2B1a), and G4 (A5A4B3) glycinin and the alpha' subunit of beta-conglycinin in BSH-3 seeds. Despite the lack of these abundant seed proteins, BSH-3 seeds still accumulated 38% protein. BSH-3 seeds also accumulated high levels of free amino acids as compared to DN47 seeds, particularly arginine, and the amount of several essential amino acids were significantly elevated in BSH-3 seeds. Elevated accumulation of alpha and beta-subunit of beta-conglycinin, G5 glycinin, Kunitz trypsin inhibitor, and Bowman-Birk protease inhibitor indicates seed proteome rebalancing in BSH-3 seeds. Immunoblot analysis using sera from soybean allergic patients demonstrated the complete lack of a major allergen (alpha' subunit of beta-conglycinin) in BSH-3 seeds. However, elevated levels of other allergens were found in BSH-3 seeds due to proteome rebalancing. Transmission electron microscopy observation of mature seeds of BSH-3 revealed striking differences in the appearance of the protein storage vacuoles when compared to DN47</style></abstract><notes><style face="normal" font="default">IS - 1520-5118 (Electronic)IS - 0021-8561 (Linking)LA - engPT - Journal ArticleCO - United States -CO - China -</style></notes><work-type><style face="normal" font="default">10.1021/acs.jafc.7b05011</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29227096">PM:29227096</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Agric Food Chem\20171215-SongB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Agric Food Chem\20171215-SongB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Song B</style></custom2><misc3><style face="normal" font="default">10.1021/acs.jafc.7b05011</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87122</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nowak-Wegrzyn,A.</style></author><author><style face="normal" font="default"> Lawson,K.</style></author><author><style face="normal" font="default"> Masilamani,M.</style></author><author><style face="normal" font="default"> Kattan,J.</style></author><author><style face="normal" font="default"> Bahnson,H.T.</style></author><author><style face="normal" font="default"> Sampson,H.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Allergy &amp; Immunology, Jaffe Food Allergy Institute, Icahn School of Medicine at Mount Sinai, New York, NY</style></auth-address><titles><title><style face="normal" font="default">Increased Tolerance to Less Extensively Heat-Denatured (Baked) Milk Products in Milk-Allergic Children</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Most milk-allergic children tolerate baked milk. OBJECTIVE: To investigate the effect of more frequent versus less frequent introduction of higher doses of more allergenic (less heat-denatured) forms of milk (MAFM) on progression to tolerance. METHODS: Milk-allergic children were challenged with increasing doses of MAFM; baked foods were incorporated into the diet; challenges were repeated at 6- or 12-month intervals over 36 months. RESULTS: A total of 136 children (70% males) were enrolled in the active group (median age, 7 years). At baseline, 41 (30%) reacted to muffin, 31 (23%) to pizza, 11 (8%) to rice pudding, 43 (32%) to non-baked milk; and 10 (7%) tolerated non-baked milk. Children who tolerated baked milk but reacted to non-baked liquid milk were randomized to MAFM challenges every 6 months (n = 41) or 12 months (n = 44). At month 36, 61% children in the 6-month and 73% in the 12-month escalation groups tolerated MAFM. Overall, 41 (48%) children who ingested baked-milk diet became tolerant to non-baked milk; no difference was seen between 6- and 12- month escalations. Among children who reacted to muffin at baseline and continued avoidance, 20% developed tolerance to baked milk and 0% tolerated non-baked milk. None of the 34 children who qualified for inclusion but chose not to take part in the active study became tolerant to any form of milk by history. CONCLUSIONS: Majority of children tolerated baked milk at baseline. Baked-milk diets were associated with progressive immunomodulation. Most children who incorporated baked milk into their diet progressed to tolerating MAFM, but there was no advantage to more frequent attempts to escalate to MAFM, per intention-to-treat analysis</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.021</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29226808">PM:29226808</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171120-NowakWegrzynA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\20171120-NowakWegrzynA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Nowak-Wegrzyn A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.021</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87123</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vercelli,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Cellular and Molecular Medicine, Arizona Center for the Biology of Complex Diseases, and Asthma and Airway Disease Research Center, University of Arizona.</style></auth-address><titles><title><style face="normal" font="default">Are We What Our Mothers Made Us? Lessons from Epigenetics</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="20" Month="12" Year="2017">2017/12/20</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.12.973</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29274413">PM:29274413</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171213-VercelliD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171213-VercelliD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Vercelli D</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.12.973</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87124</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sun,S.A.</style></author><author><style face="normal" font="default"> Ma,X.</style></author><author><style face="normal" font="default"> Li,G.</style></author><author><style face="normal" font="default"> Ing,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Anesthesiology, Columbia University College of Physicians and Surgeons, New York, NY</style></auth-address><titles><title><style face="normal" font="default">Epidemiologic Patterns of In-Hospital Anaphylaxis in Pediatric Surgical Patients</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword></keywords><dates><year Day="20" Month="12" Year="2017">2017/12/20</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.030</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29274411">PM:29274411</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171213-SunSA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171213-SunSA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Sun SA</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.030</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87125</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mishra,A.</style></author><author><style face="normal" font="default"> Yao,X.</style></author><author><style face="normal" font="default"> Saxena,A.</style></author><author><style face="normal" font="default"> Gordon,E.M.</style></author><author><style face="normal" font="default"> Kaler,M.</style></author><author><style face="normal" font="default"> Cuento,R.A.</style></author><author><style face="normal" font="default"> Barochia,A.V.</style></author><author><style face="normal" font="default"> Dagur,P.K.</style></author><author><style face="normal" font="default"> McCoy,J.P.</style></author><author><style face="normal" font="default"> Keeran,K.J.</style></author><author><style face="normal" font="default"> Jeffries,K.R.</style></author><author><style face="normal" font="default"> Qu,X.</style></author><author><style face="normal" font="default"> Yu,Z.X.</style></author><author><style face="normal" font="default"> Levine,S.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory of Asthma and Lung Inflammation, Division of Intramural Research, NHLBI, NIH</style></auth-address><titles><title><style face="normal" font="default">LRP-1 Attenuates House Dust Mite-induced Eosinophilic Airway Inflammation by Suppressing Dendritic Cell-mediated Adaptive Immune Responses</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="20" Month="12" Year="2017">2017/12/20</year></dates><abstract><style face="normal" font="default">BACKGROUND: The LDL-receptor related protein 1 (LRP-1) is a scavenger receptor that regulates adaptive immunity and inflammation. LRP-1 is not known to modulate the pathogenesis of allergic asthma. OBJECTIVE: To assess whether LRP-1 expression by dendritic cells (DCs) modulates adaptive immune responses in house dust mite (HDM)-induced airways disease. METHODS: LRP-1 expression on peripheral blood DCs was quantified by flow cytometry. The role of LRP-1 in modulating HDM-induced airways disease was assessed in mice with a deletion of LRP-1 in CD11c(+) cells (Lrp1(fl/fl); CD11c-Cre) and by the adoptive transfer of HDM-pulsed CD11b(+) DCs from Lrp1(fl/fl); CD11c-Cre mice to wild-type mice. RESULTS: Human peripheral blood myeloid DC subsets from eosinophilic asthmatics have lower LRP-1 expression than cells from healthy, non-asthmatic subjects. Similarly, LRP-1 expression by CD11b(+) lung DCs was significantly reduced in HDM-challenged wild-type mice. HDM-challenged LRP-1(fl/fl); CD11c-Cre mice have a phenotype of increased eosinophilic airway inflammation, allergic sensitization, Th2 cytokine production, and mucous cell metaplasia. The adoptive transfer of HDM-pulsed LRP-1-deficient CD11b(+) DCs into wild-type mice generated a similar phenotype of enhanced eosinophilic inflammation and allergic sensitization. Furthermore, CD11b(+) DCs in the lungs of Lrp1(fl/fl); CD11c-Cre mice have an increased ability to take up HDM antigen, whereas bone marrow-derived DCs display enhanced antigen presentation capabilities. CONCLUSION: This identifies a novel role for LRP-1 as a negative regulator of DC-mediated adaptive immune responses in HDM-induced eosinophilic airway inflammation. Furthermore, the reduced LRP-1 expression by circulating myeloid DCs from eosinophilic asthmatics suggests a possible role for LRP-1 in modulating type 2-high asthma</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.044</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29274414">PM:29274414</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171213-MishraA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171213-MishraA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Mishra A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.044</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87126</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Blom,L.H.</style></author><author><style face="normal" font="default"> Juel-Berg,N.</style></author><author><style face="normal" font="default"> Larsen,L.F.</style></author><author><style face="normal" font="default"> Hansen,K.S.</style></author><author><style face="normal" font="default"> Poulsen,L.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Clinic, Department of Dermatology and Allergy, Copenhagen University Hospital Herlev-Gentofte, Denmark.</style></auth-address><titles><title><style face="normal" font="default">Circulating allergen-specific Th2 lymphocytes: CCR4(+) rather than CLA(+) is the predominant phenotype in peanut allergic subjects</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">The skin and airway homing chemokine CCR4, but not CLA, emerged as the primary discriminating homing factor, of Th2 lymphocytes, suggesting that peanut sensitization occurs both via the skin and airways</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.037</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29225086">PM:29225086</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-BlomLH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-BlomLH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Blom LH</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.037</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87127</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Thurmann,L.</style></author><author><style face="normal" font="default"> Grutzmann,K.</style></author><author><style face="normal" font="default"> Klos,M.</style></author><author><style face="normal" font="default"> Bieg,M.</style></author><author><style face="normal" font="default"> Winter,M.</style></author><author><style face="normal" font="default"> Polte,T.</style></author><author><style face="normal" font="default"> Bauer,T.</style></author><author><style face="normal" font="default"> Schick,M.</style></author><author><style face="normal" font="default"> Bewerunge-Hudler,M.</style></author><author><style face="normal" font="default"> Roeder,S.</style></author><author><style face="normal" font="default"> Bauer,M.</style></author><author><style face="normal" font="default"> Wissenbach,D.K.</style></author><author><style face="normal" font="default"> Sack,U.</style></author><author><style face="normal" font="default"> Weichenhan,D.</style></author><author><style face="normal" font="default"> Mucke,O.</style></author><author><style face="normal" font="default"> Plass,C.</style></author><author><style face="normal" font="default"> Borte,M.</style></author><author><style face="normal" font="default"> von Bergen,M.</style></author><author><style face="normal" font="default"> Lehmann,I.</style></author><author><style face="normal" font="default"> Eils,R.</style></author><author><style face="normal" font="default"> Trump,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Environmental Immunology, Helmholtz Centre for Environmental Research Leipzig - UFZ, Permoserstrasse 15, Leipzig, 04318, Germany</style></auth-address><titles><title><style face="normal" font="default">Early-onset childhood atopic dermatitis is related to NLRP2 repression</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="9" Month="12" Year="2017">2017/12/9</year></dates><abstract><style face="normal" font="default">Early-onset atopic dermatitis (AD) related repression of the immune regulatory NLRP2 is driven by promoter hypermethylation starting already at time of birth providing an early opportunity to modulate innate immunity to potentially mitigate AD development</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29233739">PM:29233739</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-ThurmannL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-ThurmannL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Thurmann L</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87128</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">McNamara,K.B.</style></author><author><style face="normal" font="default"> Schroer,B.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Low Rates of Tree Nut Allergy in Peanut-Allergic Patients</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.11.014</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.11.014</url></web-urls><pdf-urls><url ppv-ref="no">mcnamak@ccf.org</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171221, McNamara KB</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.11.014</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87129</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nugraha,R.</style></author><author><style face="normal" font="default"> Kamath,S.D.</style></author><author><style face="normal" font="default"> Johnston,E.</style></author><author><style face="normal" font="default"> Zenger,K.R.</style></author><author><style face="normal" font="default"> Rolland,J.M.</style></author><author><style face="normal" font="default"> O'Hehir,R.E.</style></author><author><style face="normal" font="default"> Lopata,A.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre for Biodiscovery and Molecular Development of Therapeutics, James Cook University, Townsville, Australia</style></auth-address><titles><title><style face="normal" font="default">Rapid and comprehensive discovery of unreported shellfish allergens using large-scale transcriptomic and proteomic resources</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.028</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29258834">PM:29258834</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-NugrahaR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-NugrahaR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Nugraha R</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.028</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87130</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tsai,C.T.</style></author><author><style face="normal" font="default"> Mukai,K.</style></author><author><style face="normal" font="default"> Robinson,P.V.</style></author><author><style face="normal" font="default"> Gray,M.A.</style></author><author><style face="normal" font="default"> Waschmann,M.B.</style></author><author><style face="normal" font="default"> Lyu,S.C.</style></author><author><style face="normal" font="default"> Tsai,M.</style></author><author><style face="normal" font="default"> Chinthrajah,R.S.</style></author><author><style face="normal" font="default"> Nadeau,K.C.</style></author><author><style face="normal" font="default"> Bertozzi,C.R.</style></author><author><style face="normal" font="default"> Galli,S.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Chemistry, Stanford University School of Humanities and Sciences, Stanford, CA 94305, USA</style></auth-address><titles><title><style face="normal" font="default">Isotype-Specific Agglutination-PCR (ISAP): a sensitive and multiplex method for measuring allergen-specific IgE</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">chemistry</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="14" Month="12" Year="2017">2017/12/14</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.021</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29248495">PM:29248495</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-TsaiCT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-TsaiCT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Tsai CT</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.021</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87132</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Peters,R.L.</style></author><author><style face="normal" font="default"> Koplin,J.J.</style></author><author><style face="normal" font="default"> Allen,K.J.</style></author><author><style face="normal" font="default"> Lowe,A.J.</style></author><author><style face="normal" font="default"> Lodge,C.J.</style></author><author><style face="normal" font="default"> Tang,M.L.K.</style></author><author><style face="normal" font="default"> Wake,M.</style></author><author><style face="normal" font="default"> Ponsonby,A.L.</style></author><author><style face="normal" font="default"> Erbas,B.</style></author><author><style face="normal" font="default"> Abramson,M.J.</style></author><author><style face="normal" font="default"> Hill,D.</style></author><author><style face="normal" font="default"> Gurrin,L.C.</style></author><author><style face="normal" font="default"> Dharmage,S.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Murdoch Children's Research Institute, Parkville, Melbourne, Victoria, Australia; Department of Paediatrics, University of Melbourne, Parkville, Melbourne, Victoria, Australia</style></auth-address><titles><title><style face="normal" font="default">The Prevalence of Food Sensitization Appears Not to Have Changed between 2 Melbourne Cohorts of High-Risk Infants Recruited 15 Years Apart</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: Although food allergy has probably risen over recent decades, recent reports suggest that the prevalence of food sensitization in the general population has not changed. However, this has not been analyzed in infants at high risk of food allergy. OBJECTIVE: The objective of this study was to compare the prevalence of food sensitization in high-risk infants from 2 cohorts recruited 15 years apart in the same region. METHODS: This study includes 620 high-risk infants with a family history of allergy (Melbourne Atopy Cohort Study [MACS]) born 1990-1994, and a subgroup of high-risk infants from the population-based HealthNuts study (n = 3,661/5,276), born 2006-2010. Both studies undertook skin prick tests (SPT) to peanut, egg, and milk at age 12 months. A logistic regression model generated adjusted prevalences to account for differences in sampling frame. SPT >/= 95% positive predictive values (PPVs) for food allergy were used as proxies for food allergy. RESULTS: The adjusted prevalence of sensitization in MACS was similar to the observed prevalence of sensitization in the high-risk subgroup of HealthNuts: 7.9% (95% confidence interval 6.8-8.9) and 7.9% (7.0-8.8) respectively for peanut, 15.0% (13.4-16.6) and 14.5% (13.4-15.7) respectively for egg, and 2.4% (1.6-3.1) and 2.6% (2.0-3.4) respectively for cow's milk. The prevalence of SPT >/= 95% PPVs was similar between the 2 studies. CONCLUSIONS: The prevalence of food sensitization among high-risk infants has remained stable in Australia since the 1990s, despite the reported increase in food-related anaphylaxis in the same period. This discrepancy could be due to increased food allergy in the low-risk population, increased conversion of food sensitization to allergy, or increased number of high-risk infants. Alternatively, increased awareness or severity of reactions may have led to an apparent increase in food allergy</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.11.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29248387">PM:29248387</url></web-urls><pdf-urls><url ppv-ref="no">s.dharmage@unimelb.edu.au</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171120, Peters RL</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.11.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87133</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,J.</style></author><author><style face="normal" font="default"> Bingemann,T.</style></author><author><style face="normal" font="default"> Russell,A.F.</style></author><author><style face="normal" font="default"> Young,M.C.</style></author><author><style face="normal" font="default"> Sicherer,S.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Division of Allergy and Immunology, Icahn School of Medicine at Mount Sinai, New York, NY. Electronic address: julie.wang@mssm.eduAllergy and Clinical Immunology, Rochester Regional Health and the University of Rochester School of Medicine and Dentistry, Rochester, NYFood Allergy and Anaphylaxis Michigan Association, Ann Arbor, MichDivision of Allergy and Immunology, Boston Children's Hospital, Boston, MassDepartment of Pediatrics, Division of Allergy and Immunology, Icahn School of Medicine at Mount Sinai, New York, NY</style></auth-address><titles><title><style face="normal" font="default">The Allergist's Role in Anaphylaxis and Food Allergy Management in the School and Childcare Setting</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Childcare</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">Anaphylaxis and food allergy management in childcare facilities and schools are growing challenges. An increasing number of children experience severe allergic reactions on school grounds as evidenced by reports of epinephrine use. Data also suggest that the prevalence of food allergy may be increasing, with a large percentage of school-aged children at risk for anaphylaxis. Moreover, anaphylaxis may occur for the first time in a previously undiagnosed child at school or childcare setting, suggesting that general preparedness is essential. Management includes strategies for minimizing the risk of reactions and allergen exposures as well as readiness to recognize and treat allergic reactions of any severity. The primary objective of this report is to offer health care providers an overview of relevant evidence, resources, and expert opinion to assist with developing interprofessional collaborative counsel on school food allergy management and anaphylaxis preparedness with families, schools, and childcare settings. We present the current evidence base, suggest resources, and highlight areas of current controversy that warrant further study</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.11.022</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29258790">PM:29258790</url></web-urls><pdf-urls><url ppv-ref="no">julie.wang@mssm.edu</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171120, Wang J</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.11.022</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87134</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dolence,J.J.</style></author><author><style face="normal" font="default"> Kobayashi,T.</style></author><author><style face="normal" font="default"> Iijima,K.</style></author><author><style face="normal" font="default"> Krempski,J.</style></author><author><style face="normal" font="default"> Drake,L.Y.</style></author><author><style face="normal" font="default"> Dent,A.L.</style></author><author><style face="normal" font="default"> Kita,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine and Immunology, Mayo Clinic Rochester, Rochester, MN, 55905</style></auth-address><titles><title><style face="normal" font="default">Airway exposure initiates peanut allergy by involving the IL-1 pathway and T follicular helper cells in mice</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Flour</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">BACKGROUND: Little is currently known regarding the immunological mechanism(s) that initiate peanut allergy. Notably, peanut proteins have been detected in house dust, and their levels correlate with peanut allergy prevalence. OBJECTIVE: This study aimed to develop a new mouse model for peanut allergy and to investigate the immunological mechanisms involved in peanut allergen sensitization. METHODS: To mimic environmental exposure, naive mice were exposed to peanut flour by inhalation for up to 4 weeks. We then analyzed serum levels of IgE antibody and challenged mice with peanut proteins. Immunological mechanisms involved in sensitization were analyzed using cytokine reporter mice, an adoptive cell transfer model, and gene knockout mice. RESULTS: When exposed to peanut flour by inhalation, both BALB/c and C57BL/6 mice developed peanut allergy, as demonstrated by the presence of peanut-specific IgE antibodies and manifestation of acute anaphylaxis upon challenge. A large number of follicular helper T (Tfh) cells were also detected in draining lymph nodes of allergic mice. These cells produced IL-4 and IL-21, and more robustly promoted peanut-specific IgE production than Th2 cells. Genetic depletion of Tfh cells decreased IgE antibody levels and protected mice from anaphylaxis, without affecting Th2 cells. Furthermore, peanut flour exposure increased lung levels of IL-1alpha and IL-1beta, and mice deficient in the receptor for these cytokines showed a significant decrease in Tfh cells compared to wild-type mice. CONCLUSION: Tfh cells play a key role in peanut allergy, and the IL-1 pathway is involved in the Tfh response to peanut allergen exposure</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.020</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247716">PM:29247716</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-DolenceJJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-DolenceJJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Dolence JJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.020</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87135</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Oliveria,J.P.</style></author><author><style face="normal" font="default"> El-Gammal,A.I.</style></author><author><style face="normal" font="default"> Yee,M.</style></author><author><style face="normal" font="default"> Obminski,C.D.</style></author><author><style face="normal" font="default"> Scime,T.X.</style></author><author><style face="normal" font="default"> Watson,R.M.</style></author><author><style face="normal" font="default"> Howie,K.</style></author><author><style face="normal" font="default"> O'Byrne,P.M.</style></author><author><style face="normal" font="default"> Sehmi,R.</style></author><author><style face="normal" font="default"> Gauvreau,G.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, Division of Respirology, McMaster University, Hamilton, Ontario</style></auth-address><titles><title><style face="normal" font="default">Changes in regulatory B cell levels in bone marrow, blood and sputum of asthmatics following inhaled allergen challenge</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">CAPSULE SUMMARY: Following allergen exposure in the airways of subjects with allergic asthma, Bregs appear to efflux from the bone marrow and accumulate in the lungs with a possible role in dampening local inflammatory responses</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.013</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29221714">PM:29221714</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-OliveriaJP.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-OliveriaJP.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Oliveria JP</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87136</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bonura,A.</style></author><author><style face="normal" font="default"> Di Blasi,D.</style></author><author><style face="normal" font="default"> Barletta,B.</style></author><author><style face="normal" font="default"> Butteroni,C.</style></author><author><style face="normal" font="default"> Corinti,S.</style></author><author><style face="normal" font="default"> Gervasi,F.</style></author><author><style face="normal" font="default"> MelisMario,R.</style></author><author><style face="normal" font="default"> Uasuf,C.</style></author><author><style face="normal" font="default"> Fabio,C.</style></author><author><style face="normal" font="default"> Di Felice,G.</style></author><author><style face="normal" font="default"> Colombo,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Istituto di Biomedicina ed Immunologia Molecolare "Alberto Monroy" del Consiglio Nazionale delle Ricerche, Palermo, ITALY</style></auth-address><titles><title><style face="normal" font="default">Modulating allergic response by engineering the major Parietaria allergens</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">An engineered recombinant hybrid composed of the two major Parietaria allergens (PjEDcys) with reduced allergenicity, retained immunogenicity but immunomodulatory activity for Allergen Immunotherapy of Parietaria allergic patients</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.036</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29221712">PM:29221712</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-BonuraA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-BonuraA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Bonura A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.036</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87137</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Barzaghi,F.</style></author><author><style face="normal" font="default"> Amaya Hernandez,L.C.</style></author><author><style face="normal" font="default"> Neven,B.</style></author><author><style face="normal" font="default"> Ricci,S.</style></author><author><style face="normal" font="default"> Kucuk,Z.Y.</style></author><author><style face="normal" font="default"> Bleesing,J.</style></author><author><style face="normal" font="default"> Nademi,Z.</style></author><author><style face="normal" font="default"> Slatter,M.A.</style></author><author><style face="normal" font="default"> Ulloa,E.R.</style></author><author><style face="normal" font="default"> Shcherbina,A.</style></author><author><style face="normal" font="default"> Roppelt,A.</style></author><author><style face="normal" font="default"> Worth,A.</style></author><author><style face="normal" font="default"> Silva,J.</style></author><author><style face="normal" font="default"> Aiuti,A.</style></author><author><style face="normal" font="default"> Murguia-Favela,L.</style></author><author><style face="normal" font="default"> Speckmann,C.</style></author><author><style face="normal" font="default"> Carneiro-Sampaio,M.</style></author><author><style face="normal" font="default"> Fernandes,J.F.</style></author><author><style face="normal" font="default"> Baris,S.</style></author><author><style face="normal" font="default"> Ozen,A.</style></author><author><style face="normal" font="default"> Karakoc-Aydiner,E.</style></author><author><style face="normal" font="default"> Kiykim,A.</style></author><author><style face="normal" font="default"> Schulz,A.</style></author><author><style face="normal" font="default"> Steinmann,S.</style></author><author><style face="normal" font="default"> Notarangelo,L.D.</style></author><author><style face="normal" font="default"> Gambineri,E.</style></author><author><style face="normal" font="default"> Lionetti,P.</style></author><author><style face="normal" font="default"> Shearer,W.T.</style></author><author><style face="normal" font="default"> Forbes,L.</style></author><author><style face="normal" font="default"> Martinez,C.</style></author><author><style face="normal" font="default"> Moshous,D.</style></author><author><style face="normal" font="default"> Blanche,S.</style></author><author><style face="normal" font="default"> Fisher,A.</style></author><author><style face="normal" font="default"> Ruemmele,F.M.</style></author><author><style face="normal" font="default"> Tissandier,C.</style></author><author><style face="normal" font="default"> Ouachee-Chardin,M.</style></author><author><style face="normal" font="default"> Rieux-Laucat,F.</style></author><author><style face="normal" font="default"> Cavazzana,M.</style></author><author><style face="normal" font="default"> Qasim,W.</style></author><author><style face="normal" font="default"> Lucarelli,B.</style></author><author><style face="normal" font="default"> Albert,M.H.</style></author><author><style face="normal" font="default"> Kobayashi,I.</style></author><author><style face="normal" font="default"> Alonso,L.</style></author><author><style face="normal" font="default"> Diaz De Heredia,C.</style></author><author><style face="normal" font="default"> Kanegane,H.</style></author><author><style face="normal" font="default"> Lawitschka,A.</style></author><author><style face="normal" font="default"> Seo,J.J.</style></author><author><style face="normal" font="default"> Gonzalez-Vicent,M.</style></author><author><style face="normal" font="default"> Diaz,M.A.</style></author><author><style face="normal" font="default"> Goyal,R.K.</style></author><author><style face="normal" font="default"> Sauer,M.G.</style></author><author><style face="normal" font="default"> Yesilipek,A.</style></author><author><style face="normal" font="default"> Kim,M.</style></author><author><style face="normal" font="default"> Yilmaz-Demirdag,Y.</style></author><author><style face="normal" font="default"> Bhatia,M.</style></author><author><style face="normal" font="default"> Khlevner,J.</style></author><author><style face="normal" font="default"> Richmond Padilla,E.J.</style></author><author><style face="normal" font="default"> Martino,S.</style></author><author><style face="normal" font="default"> Montin,D.</style></author><author><style face="normal" font="default"> Neth,O.</style></author><author><style face="normal" font="default"> Molinos-Quintana,A.</style></author><author><style face="normal" font="default"> Valverde-Fernandez,J.</style></author><author><style face="normal" font="default"> Broides,A.</style></author><author><style face="normal" font="default"> Pinsk,V.</style></author><author><style face="normal" font="default"> Ballauf,A.</style></author><author><style face="normal" font="default"> Haerynck,F.</style></author><author><style face="normal" font="default"> Bordon,V.</style></author><author><style face="normal" font="default"> Dhooge,C.</style></author><author><style face="normal" font="default"> Garcia-Lloret,M.L.</style></author><author><style face="normal" font="default"> Bredius,R.G.</style></author><author><style face="normal" font="default"> Kalwak,K.</style></author><author><style face="normal" font="default"> Haddad,E.</style></author><author><style face="normal" font="default"> Seidel,M.G.</style></author><author><style face="normal" font="default"> Duckers,G.</style></author><author><style face="normal" font="default"> Pai,S.Y.</style></author><author><style face="normal" font="default"> Dvorak,C.C.</style></author><author><style face="normal" font="default"> Ehl,S.</style></author><author><style face="normal" font="default"> Locatelli,F.</style></author><author><style face="normal" font="default"> Goldman,F.</style></author><author><style face="normal" font="default"> Gennery,A.R.</style></author><author><style face="normal" font="default"> Cowan,M.J.</style></author><author><style face="normal" font="default"> Roncarolo,M.G.</style></author><author><style face="normal" font="default"> Bacchetta,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), Pediatric Immunohematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy</style></auth-address><titles><title><style face="normal" font="default">Long-term follow up of IPEX syndrome patients after different therapeutic strategies: an international multicenter retrospective study</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">complications</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Immunedysregulation Polyendocrinopathy Enteropathy X-linked (IPEX) syndrome is a monogenic autoimmune disease caused by FOXP3 mutations. Because it is a rare disease, the natural history and response to treatments, including allogeneic hematopoietic stem cell transplantation (HSCT) and immunosuppression (IS), have not been thoroughly examined. OBJECTIVE: To evaluate disease onset, progression and long-term outcome of the two main treatments in long-term IPEX survivors. METHODS: Clinical histories of 96 patients with a genetically proven IPEX syndrome were collected from 38 institutions worldwide and retrospectively analyzed. To investigate possible factors suitable to predict the outcome, an organ involvement (OI) scoring system was developed. RESULTS: We confirm neonatal onset with enteropathy, type 1 diabetes (T1D), and eczema. In addition, we found less common manifestations in delayed onset patients or during disease evolution. There is no correlation between the site of mutation and the disease course or outcome, and the same genotype can present with variable phenotypes. HSCT patients (n=58) had a median follow-up of 2.7 years (range: 1 week - 15 years). Patients receiving chronic IS (n=34) had a median follow-up of 4 years (range: 2 months - 25 years). The overall survival (OS) after HSCT was 73.2% (95% confidence interval [CI], 59.4 to 83.0) and after IS was 65.1% (95 % CI, 62.8 to 95.8). The pre-treatment OI score was the only significant predictor of OS after transplant (p=0.035) but not under IS. CONCLUSIONS: Patients receiving chronic IS were hampered by disease recurrence or complications, impacting long-term disease-free survival. When performed in patients with a low OI score, HSCT resulted in disease resolution with better quality of life, independent of age, donor source or conditioning regimen</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Italy -CO - United States -CO - France -CO - United Kingdom -CO - Russia -CO - Canada -CO - Germany -CO - Brazil -CO - Turkey -CO - Japan -CO - Austria -CO - South Korea -CO - Spain -CO - Costa Rica -CO - Israel -CO - Poland -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.041</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29241729">PM:29241729</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-BarzaghiF.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-BarzaghiF.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Barzaghi F</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.041</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87138</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Renz,H.</style></author><author><style face="normal" font="default"> Adkins,B.D.</style></author><author><style face="normal" font="default"> Bartfeld,S.</style></author><author><style face="normal" font="default"> Blumberg,R.S.</style></author><author><style face="normal" font="default"> Farber,D.L.</style></author><author><style face="normal" font="default"> Garssen,J.</style></author><author><style face="normal" font="default"> Ghazal,P.</style></author><author><style face="normal" font="default"> Hackam,D.J.</style></author><author><style face="normal" font="default"> Marsland,B.J.</style></author><author><style face="normal" font="default"> McCoy,K.D.</style></author><author><style face="normal" font="default"> Penders,J.</style></author><author><style face="normal" font="default"> Prinz,I.</style></author><author><style face="normal" font="default"> Verhasselt,V.</style></author><author><style face="normal" font="default"> von Mutius,E.</style></author><author><style face="normal" font="default"> Weiser,J.N.</style></author><author><style face="normal" font="default"> Wesemann,D.R.</style></author><author><style face="normal" font="default"> Hornef,M.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Marburg, Germany.</style></auth-address><titles><title><style face="normal" font="default">The neonatal window of opportunity - early priming for life</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">The concept of the neonatal window of opportunity assigns the early postnatal period a critical role for life-long host-microbial and immune homeostasis. It is supported by epidemiological evidence that links postnatal environmental exposure with disease susceptibility and mechanisms in the neonate host that facilitate the postnatal transposition, establish a stable microbiome and promote immune maturation. During the conference on "The neonatal window of opportunity - early priming for life", postnatal microbiome and immune maturation, epidemiological evidence and fundamental mechanisms were discussed to identify new targets for future preventive and interventional measures</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - EditorialCO - Germany -CO - United States -CO - Germany -CO - United Kingdom -CO - Switzerland -CO - Canada -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.019</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247715">PM:29247715</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-RenzH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-RenzH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Renz H</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.019</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87139</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Karasuyama,H.</style></author><author><style face="normal" font="default"> Miyake,K.</style></author><author><style face="normal" font="default"> Yoshikawa,S.</style></author><author><style face="normal" font="default"> Yamanishi,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immune Regulation, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU).</style></auth-address><titles><title><style face="normal" font="default">Multifaceted roles of basophils in health and disease</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">Until recently, basophils had often been neglected in immunological studies because of their minority status among immune cells, or confused with tissue-resident mast cells due to some phenotypic similarities between them in spite of different anatomical localization. It is now appreciated that basophils and mast cells are distinct cell lineages, and that basophils play important and non-redundant roles distinct from those played by mast cells. On the one hand, basophils contribute beneficially to protective immunity, particularly against parasitic infections. On the other hand, basophils are involved in the development of various disorders, including allergy and autoimmune disease. Basophils interact with other immune cells and non-hematopoietic cells through cell to cell contact or basophil-derived factors such as cytokines and proteases, contributing to the regulation of immune and allergic responses. In this review article, we highlight recent advances in our understanding of basophil pathophysiology in humans and animal models by consolidating research findings reported during the past five years. Further studies on basophils and their products will help identify suitable targets for novel therapeutics in allergy and effective vaccines against parasitic infection</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - EditorialCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.042</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247714">PM:29247714</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-KarasuyamaH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-KarasuyamaH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Karasuyama H</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.042</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87140</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Salabert-Le Guen,N.</style></author><author><style face="normal" font="default"> Hemont,C.</style></author><author><style face="normal" font="default"> Delbove,A.</style></author><author><style face="normal" font="default"> Poli,C.</style></author><author><style face="normal" font="default"> Braudeau,C.</style></author><author><style face="normal" font="default"> Fantou,A.</style></author><author><style face="normal" font="default"> Amouriaux,K.</style></author><author><style face="normal" font="default"> Beriou,G.</style></author><author><style face="normal" font="default"> Martin,J.C.</style></author><author><style face="normal" font="default"> Colas,L.</style></author><author><style face="normal" font="default"> Soumelis,V.</style></author><author><style face="normal" font="default"> Josien,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">CHU Nantes, Laboratoire d'Immunologie, CIMNA, Nantes, France</style></auth-address><titles><title><style face="normal" font="default">Thymic stromal lymphopoietin does not activate human basophils</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="12" Year="2017">2017/12/2</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.11.012</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29208546">PM:29208546</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-SalbertLeGuenN.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-SalbertLeGuenN.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, SalabertLeGuenN</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.11.012</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87141</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Magnusson,J.</style></author><author><style face="normal" font="default"> Ekstrom,S.</style></author><author><style face="normal" font="default"> Kull,I.</style></author><author><style face="normal" font="default"> Hakansson,N.</style></author><author><style face="normal" font="default"> Nilsson,S.</style></author><author><style face="normal" font="default"> Wickman,M.</style></author><author><style face="normal" font="default"> Melen,E.</style></author><author><style face="normal" font="default"> Riserus,U.</style></author><author><style face="normal" font="default"> Bergstrom,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden</style></auth-address><titles><title><style face="normal" font="default">Polyunsaturated fatty acids in plasma at 8 years and subsequent allergic disease</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">BACKGROUND: Polyunsaturated fatty acids (PUFAs) are hypothesized to modulate the risk of allergic disease. However, evidence from previous studies is inconclusive, and limited longitudinal data exist using circulating biomarkers of PUFA intake and metabolism. OBJECTIVE: We aimed to investigate associations between n-3 and n-6 PUFAs at age 8 years and asthma, rhinitis, and aeroallergen sensitization at age 16 years. METHODS: Proportions of n-3 PUFAs (very long-chain n-3 [VLC n-3; sum of eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid] and alpha-linolenic acid) and n-6 PUFAs (linoleic acid and arachidonic acid [AA]) in blood samples at age 8 years were measured for 940 children from the prospective Swedish birth cohort BAMSE (Children, Allergy, Milieu, Stockholm, Epidemiology). Allergic disease phenotypes were defined by using questionnaires and IgE measures at the ages of 8 and 16 years. Logistic regression was used to examine potential associations. RESULTS: A higher proportion of total VLC n-3 PUFAs in plasma at age 8 years was associated with a reduced risk of prevalent asthma, rhinitis, and aeroallergen sensitization at age 16 years and with incidence of asthma between 8 and 16 years (adjusted odds ratio, 0.67; 95% CI, 0.47-0.94). AA was associated with a reduced risk of asthma, aeroallergen sensitization, and allergic rhinitis. The findings were most evident for allergic phenotypes of asthma and rhinitis. Additionally, AA was associated with an increased probability of asthma and rhinitis remission between 8 and 16 years of age. CONCLUSION: Higher proportions of certain VLC n-3 and very long-chain n-6 PUFAs in plasma phospholipids at age 8 years were associated with a reduced risk of allergic disease at age 16 years</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.023</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29221817">PM:29221817</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-MagnussonJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-MagnussonJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Magnusson J</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.023</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87142</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Schuyler,A.J.</style></author><author><style face="normal" font="default"> Tripathi,A.</style></author><author><style face="normal" font="default"> Workman,L.J.</style></author><author><style face="normal" font="default"> Wilson,J.M.</style></author><author><style face="normal" font="default"> Erwin,E.A.</style></author><author><style face="normal" font="default"> Lawrence,M.G.</style></author><author><style face="normal" font="default"> McGowan,E.C.</style></author><author><style face="normal" font="default"> Hamilton,R.G.</style></author><author><style face="normal" font="default"> Platts-Mills,T.A.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy &amp; Clinical Immunology, University of Virginia, Charlottesville, Va</style></auth-address><titles><title><style face="normal" font="default">Underestimation of specific IgE measurements using extract-based assays on undiluted sera revealed through dilution</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.10.037</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29226806">PM:29226806</url></web-urls><pdf-urls><url ppv-ref="no">tap2z@virginia.edu</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171220, Schuyler AJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.10.037</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87143</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kaur,A.</style></author><author><style face="normal" font="default"> Skoner,D.</style></author><author><style face="normal" font="default"> Ibrahim,J.</style></author><author><style face="normal" font="default"> Li,Q.</style></author><author><style face="normal" font="default"> Lockey,R.F.</style></author><author><style face="normal" font="default"> Blaiss,M.</style></author><author><style face="normal" font="default"> Bufe,A.</style></author><author><style face="normal" font="default"> Andersen,J.S.</style></author><author><style face="normal" font="default"> Canonica,G.W.</style></author><author><style face="normal" font="default"> Nolte,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Merck &amp; Co., Inc., Kenilworth, NJ</style></auth-address><titles><title><style face="normal" font="default">Effect of Grass Sublingual Tablet Immunotherapy is Similar in Children and Adults: A Bayesian Approach To Design Pediatric Sublingual Immunotherapy Trials</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">BACKGROUND: Large sample sizes are needed for sublingual immunotherapy (SLIT) trials due to inherent data variability secondary to inconsistent allergen exposure. Obtaining large sample sizes for pediatric SLIT trials is challenging, but a Bayesian approach using prior adult data can reduce the necessary sample size. OBJECTIVE: To describe how a Bayesian framework utilizing prior information from adult trials can be used to improve pediatric SLIT clinical development. METHODS: Data were compiled using a frequentist approach (conventional clinical trial approach independent of prior data) from trials conducted during the clinical development of timothy grass SLIT-tablet. RESULTS: The treatment effect of timothy grass SLIT-tablet was considered similar between pediatric (N=795) and adult (N=2299) data pools, with relative total combined symptom plus medication score improvement (95% CI) vs placebo of 21% (11.0, 30.4) and 20% (14.6, 24.4), respectively. Phleum pratense-specific IgG4 and IgE blocking factor increased from baseline in both children and adults treated with timothy grass SLIT-tablet. Given the reasonable assumption in similarity of treatment response between adults and children, a Bayesian approach is described to demonstrate rigorous efficacy criterion for pediatric trials incorporating information from prior adult trials, and thereby reduce the sample size. CONCLUSIONS: Data support the similarity of efficacy and immunologic changes between children and adults treated with SLIT for allergic rhinoconjunctivitis. Therefore, it is appropriate to utilize data from adult trials to design feasible trials in children, which may reduce unsafe off-label use by promoting more quickly proper labeling of approved products</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Denmark -CO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.051</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29221713">PM:29221713</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-KaurA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-KaurA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Kaur A</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.051</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87144</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gunsoy,N.B.</style></author><author><style face="normal" font="default"> Cockle,S.M.</style></author><author><style face="normal" font="default"> Yancey,S.W.</style></author><author><style face="normal" font="default"> Keene,O.N.</style></author><author><style face="normal" font="default"> Bradford,E.S.</style></author><author><style face="normal" font="default"> Albers,F.C.</style></author><author><style face="normal" font="default"> Pavord,I.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical Statistics, GlaxoSmithKline, Stockley Park, Uxbridge, Middlesex, United Kingdom.</style></auth-address><titles><title><style face="normal" font="default">Evaluation of Potential Continuation Rules for Mepolizumab Treatment of Severe Eosinophilic Asthma</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">BACKGROUND: Mepolizumab significantly reduces exacerbations in patients with severe eosinophilic asthma. The early identification of patients likely to receive long-term benefit from treatment could ensure effective resource allocation. OBJECTIVE: To assess potential continuation rules for mepolizumab in addition to initiation criteria defined as 2 or more exacerbations in the previous year and blood eosinophil counts of 150 cells/muL or more at initiation or 300 cells/muL or more in the previous year. METHODS: This post hoc analysis included data from 2 randomized, double-blind, placebo-controlled studies (NCT01000506 and NCT01691521) of mepolizumab in patients with severe eosinophilic asthma (N = 1,192). Rules based on blood eosinophils, physician-rated response to treatment, FEV1, Asthma Control Questionnaire (ACQ-5) score, and exacerbation reduction were assessed at week 16. To assess these rules, 2 key metrics accounting for the effects observed in the placebo arm were developed. RESULTS: Patients not meeting continuation rules based on physician-rated response, FEV1, and the ACQ-5 score still derived long-term benefit from mepolizumab. Nearly all patients failing to reduce blood eosinophils had counts of 150 cells/muL or less at baseline. For exacerbations, assessment after 16 weeks was potentially premature for predicting future exacerbations. CONCLUSION: There was no evidence of a reliable physician-rated response, ACQ-5 score, or lung function-based continuation rule. The added value of changes in blood eosinophils at week 16 over baseline was marginal. Initiation criteria for mepolizumab treatment provide the best method for assessing patient benefit from mepolizumab treatment, and treatment continuation should be reviewed on the basis of a predefined reduction in long-term exacerbation frequency and/or oral corticosteroid dose</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United Kingdom -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.11.026</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29258789">PM:29258789</url></web-urls><pdf-urls><url ppv-ref="no">necdet.b.gunsoy@gsk.com</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171220, Gunsoy NB</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.11.026</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87145</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Schmetzer,O.</style></author><author><style face="normal" font="default"> Lakin,E.</style></author><author><style face="normal" font="default"> Topal,F.A.</style></author><author><style face="normal" font="default"> Preusse,P.</style></author><author><style face="normal" font="default"> Freier,D.</style></author><author><style face="normal" font="default"> Church,M.K.</style></author><author><style face="normal" font="default"> Maurer,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dept. of Dermatology and Allergy, Charite - Universitatsmedizin Berlin, Germany.</style></auth-address><titles><title><style face="normal" font="default">IL-24 is a common and specific autoantigen of IgE in chronic spontaneous urticaria</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="2" Month="12" Year="2017">2017/12/2</year></dates><abstract><style face="normal" font="default">BACKGROUND: The efficacy of omalizumab (anti-IgE) and elevated IgE levels in chronic spontaneous urticaria (CSU) suggest autoallergic mechanisms. OBJECTIVE: To identify autoallergic targets of IgE in CSU patients. METHODS: Sera of CSU patients together with idiopathic anaphylaxis patients and healthy controls (seven of each) were screened for IgE-autoantibodies using an array of >9,000 proteins. Sera of 1062 CSU patients and 482 healthy controls were used in an IgE-anti-Interleukin-24 (IL-24) specific ELISA to investigate the association of IgE-anti-IL-24 and CSU. RESULTS: By array analyses, over 200 IgE-autoantigens were found in CSU patients that were not in controls. Of the 31 IgE-autoantigens detected in >70% of patients, eight were soluble or membrane bound and expressed in skin. Of these, only IgE-autoantibodies to IL-24 were found in all CSU patients. In vitro studies showed IL-24 to release histamine from human mast cells sensitized with purified IgE of CSU patients but not controls. By ELISA analyses, the mean +/- SD levels of IgE-anti-IL-24 were 0.52 +/- 0.24 IU/ml in CSU and 0.27 +/- 0.08 IU/ml in controls with 80% of CSU patients but only 20% of controls having levels >0.33 IU/ml (P&lt; 0.0001). IgE-anti-IL-24 showed acceptable predictive properties for CSU, with a likelihood ratio of 3.9. Clinically, IgE-anti-IL-24 levels showed an association with disease activity as assessed by the urticaria activity score and with reduced basophil counts. CONCLUSION: Our findings show that CSU patients frequently exhibit IgE-autoantibodies against many autoantigens and that IL-24 is a common, specific, and functional autoantigen of IgE-antibodies in CSU</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.035</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29208545">PM:29208545</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-SchmetzerO.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\20171217-SchmetzerO.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Schmetzer O</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.035</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87146</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bonadonna,P.</style></author><author><style face="normal" font="default"> Zanotti,R.</style></author><author><style face="normal" font="default"> Pagani,M.</style></author><author><style face="normal" font="default"> Bonifacio,M.</style></author><author><style face="normal" font="default"> Scaffidi,L.</style></author><author><style face="normal" font="default"> Olivieri,E.</style></author><author><style face="normal" font="default"> Franchini,M.</style></author><author><style face="normal" font="default"> Reccardini,F.</style></author><author><style face="normal" font="default"> Costantino,M.T.</style></author><author><style face="normal" font="default"> Roncallo,C.</style></author><author><style face="normal" font="default"> Mauro,M.</style></author><author><style face="normal" font="default"> Boni,E.</style></author><author><style face="normal" font="default"> Rizzini,F.L.</style></author><author><style face="normal" font="default"> Bilo,M.B.</style></author><author><style face="normal" font="default"> Marcarelli,A.R.</style></author><author><style face="normal" font="default"> Passalacqua,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit, Azienda Ospedaliera Universitaria Integrata of Verona, Verona, Italy; Multidisciplinary Mastocytosis Outpatient Clinic, Azienda Ospedaliera Universitaria Integrata of Verona, Verona, Italy</style></auth-address><titles><title><style face="normal" font="default">Anaphylactic Reactions After Discontinuation of Hymenoptera Venom Immunotherapy: A Clonal Mast Cell Disorder Should Be Suspected</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> Mastocytosis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">BACKGROUND: Up to 75% of patients with severe anaphylactic reactions after Hymenoptera sting are at risk of further severe reactions if re-stung. Venom immunotherapy (VIT) is highly effective in protecting individuals with ascertained Hymenoptera venom allergy (HVA) and previous severe reactions. After a 3- to 5-year VIT course, most patients remain protected after VIT discontinuation. Otherwise, a lifelong treatment should be considered in high-risk patients (eg, in mastocytosis). Several case reports evidenced that patients with mastocytosis and HVA, although protected during VIT, can re-experience severe and sometimes fatal reactions after VIT discontinuation. OBJECTIVE: To evaluate whether patients who lost protection after VIT discontinuation may suffer from clonal mast cell disorders. METHODS: The survey describes the characteristics of patients who received a full course of VIT for previous severe reactions and who experienced another severe reaction at re-sting after VIT discontinuation. Those with a Red Espanola de Mastocitosis score of 2 or more or a serum basal tryptase level of more than 25 ng/mL underwent a hematological workup (bone marrow biopsy, KIT mutation, expression of aberrant CD25) and/or skin biopsy. RESULTS: Nineteen patients (mean age, 56.3 years; 89.5% males) were evaluated. All of them had received at least 4 years of VIT and were protected. After VIT discontinuation they were re-stung and developed, in all but 1 case, severe anaphylactic reactions (12 with loss of consciousness, in the absence of urticaria/angioedema). Eighteen patients (94.7%) had a clonal mast cell disorder, 8 of them with normal tryptase. CONCLUSIONS: Looking at this selected population, we suggest that mastocytosis should be considered in patients developing severe reactions at re-sting after VIT discontinuation and, as a speculation, patients with mastocytosis and HVA should be VIT-treated lifelong</style></abstract><notes><style face="normal" font="default">IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.11.025</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29258788">PM:29258788</url></web-urls><pdf-urls><url ppv-ref="no">passalacqua@unige.it</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171120, Bonadonna P</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.11.025</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87147</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hashizume,H.</style></author><author><style face="normal" font="default"> Fujiyama,T.</style></author><author><style face="normal" font="default"> Umayahara,T.</style></author><author><style face="normal" font="default"> Kageyama,R.</style></author><author><style face="normal" font="default"> Walls,A.F.</style></author><author><style face="normal" font="default"> Satoh,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Shimada Municipal Hospital, Shimada, Japan.</style></auth-address><titles><title><style face="normal" font="default">Repeated Amblyomma testudinarium tick bites are associated with elevated anti-galactose-alpha-1,3- galactose carbohydrate IgE antibody levels: A retrospective cohort study in a single institute</style></title><secondary-title><style face="normal" font="default">J Am Acad Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Acad Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="19" Month="12" Year="2017">2017/12/19</year></dates><abstract><style face="normal" font="default">BACKGROUND: Alpha gal syndrome is a hypersensitivity reaction to red meat mediated by specific IgE antibody to galactose-alpha-1,3-galactose carbohydrate (alpha gal). Amblyomma tick bites are associated with this condition although the pathophysiology is not understood. OBJECTIVE: To clarify the mechanism of development of alpha gal syndrome after tick bites. METHODS: We compared alpha gal antibodies between patients with and without a history of tick bites and examined the histology of tick bite lesions between patients with and without detectable anti-alpha-gal IgE antibody. RESULTS: Patients who had >/= 2 tick bites had higher levels of anti-alpha-gal IgE antibody compared with those with 1 tick bite or healthy individuals. On histological investigation, greater numbers of infiltrating basophils and eosinophils, but not mast cells, were observed in the lesions of patients with >/= 2 tick bites compared with those with 1 tick bite. Type 2 cytokine-producing T cell infiltration was also predominantly observed in such patients. LIMITATION: The study was conducted at a single institution in Japan. CONCLUSIONS: In Amblyomma tick bites, basophils, eosinophils and type 2 cytokine-producing T cells infiltrate the skin, and anti-alpha gal IgE antibodies are produced, which provides a potential mechanistic connection to red meat hypersensitivity</style></abstract><notes><style face="normal" font="default">IS - 1097-6787 (Electronic)IS - 0190-9622 (Linking)LA - engPT - Journal ArticleCO - Japan -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaad.2017.12.028</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29273488">PM:29273488</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Acad Dermatol\20171215-HashizumeH.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Acad Dermatol\20171215-HashizumeH.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Hashizume H</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaad.2017.12.028</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87148</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Faina,V.</style></author><author><style face="normal" font="default"> Paolino,G.</style></author><author><style face="normal" font="default"> Bavastrelli,M.</style></author><author><style face="normal" font="default"> Calvieri,S.</style></author><author><style face="normal" font="default"> Grieco,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dermatologic Clinic, "Sapienza" University of Rome, Viale del Policlinico 15,00161 Rome, Italy</style></auth-address><titles><title><style face="normal" font="default">Classification of cutaneous manifestations in patients with non-celiac gluten sensitivity (NCGS) and wheat allergy (WA)</style></title><secondary-title><style face="normal" font="default">J Am Acad Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Acad Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1097-6787 (Electronic)IS - 0190-9622 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaad.2017.12.013</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29246823">PM:29246823</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Acad Dermatol\20171215-FainaV.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Acad Dermatol\20171215-FainaV.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Faina V</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaad.2017.12.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87149</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vigo,M.</style></author><author><style face="normal" font="default"> Hassan,L.</style></author><author><style face="normal" font="default"> Vance,W.</style></author><author><style face="normal" font="default"> Jay,C.</style></author><author><style face="normal" font="default"> Brass,A.</style></author><author><style face="normal" font="default"> Cruickshank,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Computer Science, University of Manchester, Manchester, UK</style></auth-address><titles><title><style face="normal" font="default">Britain Breathing: using the experience sampling method to collect the seasonal allergy symptoms of a country</style></title><secondary-title><style face="normal" font="default">J Am Med Inform Assoc</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Med Inform Assoc</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="12" Month="12" Year="2017">2017/12/12</year></dates><abstract><style face="normal" font="default">Objective: Allergies are increasing, but the reasons for this are unclear. Although environmental factors are thought to be important, there is a lack of data on how they contribute to symptom development. To understand this relationship better, we need accurate data about both symptoms and environmental factors. Our objective here is to ascertain whether experience sampling is a reliable approach for collecting allergy symptom data in the general population, allowing us to map symptoms and understand etiology. Materials and Methods: We conducted a 32-week cross-sectional study where individuals reported their seasonal allergy symptoms and severity via a mobile application. Symptom geographical location and timestamp were also collected automatically. Results: The experience sampling method reliably infers the incidence of seasonal allergies as indicated by the strong correlation (r = 0.93, P &lt; .003) between the reported lack of wellness and the number of antihistamines prescribed by Global Positioning System. Discussion and Conclusion: The project has resulted in the first dataset to map allergy symptoms over time and place and reveals periods of peak hay fever symptoms in the UK</style></abstract><notes><style face="normal" font="default">IS - 1527-974X (Electronic)IS - 1067-5027 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1093/jamia/ocx148</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29240930">PM:29240930</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Med Inform Assoc\20171215-VigoM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Med Inform Assoc\20171215-VigoM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Vigo M</style></custom2><misc3><style face="normal" font="default">10.1093/jamia/ocx148</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87150</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Goss,F.R.</style></author><author><style face="normal" font="default"> Lai,K.H.</style></author><author><style face="normal" font="default"> Topaz,M.</style></author><author><style face="normal" font="default"> Acker,W.W.</style></author><author><style face="normal" font="default"> Kowalski,L.</style></author><author><style face="normal" font="default"> Plasek,J.M.</style></author><author><style face="normal" font="default"> Blumenthal,K.G.</style></author><author><style face="normal" font="default"> Seger,D.L.</style></author><author><style face="normal" font="default"> Slight,S.P.</style></author><author><style face="normal" font="default"> Wah,F.K.</style></author><author><style face="normal" font="default"> Chang,F.Y.</style></author><author><style face="normal" font="default"> Bates,D.W.</style></author><author><style face="normal" font="default"> Zhou,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Emergency Medicine, University of Colorado, Aurora, CO, USADepartment of Biomedical Informatics, University of Utah School of Medicine, Salt Lake City, UT, USADivision of General Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USADivision of Pharmacy, School of Medicine, Pharmacy and Health, Durham University, Durham, UKDivision of General Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USADivision of General Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USADepartment of Biomedical Informatics, University of Utah School of Medicine, Salt Lake City, UT, USADivision of General Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USADivision of Rheumatology, Allergy and Immunology, and Medical Practice Evaluation Center, Department of Medicine, Massachusetts General Hospital, Boston, MA, USAHarvard Medical School, Boston, MA, USAClinical and Quality Analysis, Partners HealthCare System, Boston, MA, USADivision of General Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USADivision of Pharmacy, School of Medicine, Pharmacy and Health, Durham University, Durham, UKNewcastle upon Tyne Hospitals NHS Foundation Trust, UKNational Library of Medicine, Bethesda, MD, USAClinical and Quality Analysis, Partners HealthCare System, Boston, MA, USADepartment of Biomedical Informatics, University of Utah School of Medicine, Salt Lake City, UT, USADivision of Pharmacy, School of Medicine, Pharmacy and Health, Durham University, Durham, UKHarvard Medical School, Boston, MA, USADivision of General Medicine and Primary Care, Brigham and Women's Hospital, Boston, MA, USAHarvard Medical School, Boston, MA, USAClinical Informatics, Partners eCare, Partners HealthCare System, Boston, MA, USA</style></auth-address><titles><title><style face="normal" font="default">A value set for documenting adverse reactions in electronic health records</style></title><secondary-title><style face="normal" font="default">J Am Med Inform Assoc</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Am Med Inform Assoc</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Emergency medicine</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="14" Month="12" Year="2017">2017/12/14</year></dates><abstract><style face="normal" font="default">Objective: To develop a comprehensive value set for documenting and encoding adverse reactions in the allergy module of an electronic health record. Materials and Methods: We analyzed 2 471 004 adverse reactions stored in Partners Healthcare's Enterprise-wide Allergy Repository (PEAR) of 2.7 million patients. Using the Medical Text Extraction, Reasoning, and Mapping System, we processed both structured and free-text reaction entries and mapped them to Systematized Nomenclature of Medicine - Clinical Terms. We calculated the frequencies of reaction concepts, including rare, severe, and hypersensitivity reactions. We compared PEAR concepts to a Federal Health Information Modeling and Standards value set and University of Nebraska Medical Center data, and then created an integrated value set. Results: We identified 787 reaction concepts in PEAR. Frequently reported reactions included: rash (14.0%), hives (8.2%), gastrointestinal irritation (5.5%), itching (3.2%), and anaphylaxis (2.5%). We identified an additional 320 concepts from Federal Health Information Modeling and Standards and the University of Nebraska Medical Center to resolve gaps due to missing and partial matches when comparing these external resources to PEAR. This yielded 1106 concepts in our final integrated value set. The presence of rare, severe, and hypersensitivity reactions was limited in both external datasets. Hypersensitivity reactions represented roughly 20% of the reactions within our data. Discussion: We developed a value set for encoding adverse reactions using a large dataset from one health system, enriched by reactions from 2 large external resources. This integrated value set includes clinically important severe and hypersensitivity reactions. Conclusion: This work contributes a value set, harmonized with existing data, to improve the consistency and accuracy of reaction documentation in electronic health records, providing the necessary building blocks for more intelligent clinical decision support for allergies and adverse reactions</style></abstract><notes><style face="normal" font="default">IS - 1527-974X (Electronic)IS - 1067-5027 (Linking)LA - engPT - Journal ArticleCO - United states -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1093/jamia/ocx139</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29253169">PM:29253169</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Am Med Inform Assoc\20171215-GossFR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Am Med Inform Assoc\20171215-GossFR.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Goss FR</style></custom2><misc3><style face="normal" font="default">10.1093/jamia/ocx139</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87151</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mazur,A.</style></author><author><style face="normal" font="default"> Szylling,A.</style></author><author><style face="normal" font="default"> Bielecka,T.</style></author><author><style face="normal" font="default"> Strzelak,A.</style></author><author><style face="normal" font="default"> Kulus,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Department of Pediatric Pulmonology and Allergy , Medical University of Warsaw , Warsaw , Poland</style></auth-address><titles><title><style face="normal" font="default">Is the "farm effect" hypothesis still current? Atopy and allergic diseases in rural and urban children in Poland</style></title><secondary-title><style face="normal" font="default">J Asthma</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Asthma</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">OBJECTIVE: The prevalence of allergic diseases has reached epidemic proportions in the Western world. Although farm-living has been associated with a lower prevalence of asthma and atopy, a marked increase in atopy among rural populations after accession to the European Union has been recently reported in Poland. Here, we aimed to investigate the effect of living environment on the prevalence of atopy and allergic diseases in Polish children. METHODS: 400 schoolchildren aged 10-14 years from the capital city (223) and from traditional rural part of the country (177) were recruited from June to November 2011. Data on allergic diseases and symptoms were collected by means of questionnaire and physical examination. Atopy was assessed based on skin prick tests (SPTs) reactivity to inhalant allergens in 350 children. RESULTS: A high discrepancy between the prevalence of allergic symptoms (46.7%) and doctor-diagnosed allergic diseases (25%) was demonstrated (p &lt; 0.0001). Urban children had a higher overall prevalence of allergic diseases and atopy than children living in rural areas, 29.3% versus 17.1% (p = 0.007) and 33.5% versus 20% (p = 0.0045), respectively. However, no significant differences in the rates of particular allergic diseases were noted (p > 0.05). There was higher SPT positivity to trees, grass, corn, weeds, animal dander, and molds in urban children (p &lt; 0.05). CONCLUSIONS: Our data support the protective effect of farm-living on the prevalence of atopy and overall allergic diseases, albeit not on particular allergic diseases, in children in Poland. The underlying mechanisms are not identified, but current socioeconomic changes may be responsible</style></abstract><notes><style face="normal" font="default">IS - 1532-4303 (Electronic)IS - 0277-0903 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1080/02770903.2017.1400046</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29211564">PM:29211564</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Asthma\20171215-MazurA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Asthma\20171215-MazurA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Mazur A</style></custom2><misc3><style face="normal" font="default">10.1080/02770903.2017.1400046</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87152</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bulut,I.</style></author><author><style face="normal" font="default"> Ozseker,Z.F.</style></author><author><style face="normal" font="default"> Coskun,A.</style></author><author><style face="normal" font="default"> Serteser,M.</style></author><author><style face="normal" font="default"> Unsal,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Health Science University, Sureyyapasa Chest Disease and Chest Surgery Research and Training Hospital , Department of Immunology and Allergy Disease , Istanbul , Turkey</style></auth-address><titles><title><style face="normal" font="default">Pregnancy-associated plasma protein-A (PAPP-A) levels in patients with severe allergic asthma are reduced by omalizumab</style></title><secondary-title><style face="normal" font="default">J Asthma</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Asthma</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="6" Month="12" Year="2017">2017/12/6</year></dates><abstract><style face="normal" font="default">BACKGROUND: Remodeling is a crucial feature of severe asthma and may be associated with activation of the allergic cascade by immunoglobulin E (IgE). Omalizumab, an anti-IgE monoclonal antibody, effectively targets the severe allergic asthma phenotype. Pregnancy-associated plasma protein-A (PAPP-A) is an insulin-like growth factor binding protein-4 (IGFBP-4) protease, increasing local insulin-like growth factor (IGF)-1 concentrations, which in turn initiating a cascade involved in the regulation of cell growth, differentiation, and proliferation in various tissues. In the present study, we evaluated the effects of omalizumab on serum PAPP-A, IGFBP-4, and IGF-1 levels in subjects with severe allergic asthma. METHODS: We studied 36 asthmatic subjects and 36 healthy controls. An ultrasensitive enzyme-linked immunosorbent assay (ELISA) kit was used to measure serum PAPP-A levels, and routine commercial ELISA kits were employed to assess serum levels of IGF-1, IGFBP-4 in control subjects and asthmatic subjects before therapy (baseline) and after six months of omalizumab therapy in patients with severe asthma. RESULTS: Compared to control subjects, serum PAPP-A and IGFB-4 levels were significantly higher in asthmatic subjects (both p values &lt; 0.001). However, the serum IGF-I levels of asthmatic subjects were similar to those of control subjects (p > 0.05). In asthma subjects, 6-month omalizumab treatment significantly decreased the serum PAPP-A (p &lt; 0.001), IGF-I (p = 0.031), and IGFB4 (p = 0.025) levels. CONCLUSION: PAPP-A level may be a useful biomarker for predicting airway remodeling in patients with severe asthma receiving omalizumab, and may also reflect the response to treatment</style></abstract><notes><style face="normal" font="default">IS - 1532-4303 (Electronic)IS - 0277-0903 (Linking)LA - engPT - Journal ArticleCO - Turkey -</style></notes><work-type><style face="normal" font="default">10.1080/02770903.2017.1396471</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29211611">PM:29211611</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Asthma\20171215-BulutI.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Asthma\20171215-BulutI.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171216, Bulut I</style></custom2><misc3><style face="normal" font="default">10.1080/02770903.2017.1396471</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87153</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dar,S.A.</style></author><author><style face="normal" font="default"> Rai,G.</style></author><author><style face="normal" font="default"> Ansari,M.A.</style></author><author><style face="normal" font="default"> Akhter,N.</style></author><author><style face="normal" font="default"> Gupta,N.</style></author><author><style face="normal" font="default"> Sharma,S.</style></author><author><style face="normal" font="default"> Haque,S.</style></author><author><style face="normal" font="default"> Ramachandran,V.G.</style></author><author><style face="normal" font="default"> Wahid,M.</style></author><author><style face="normal" font="default"> Shivprakash,M.R.</style></author><author><style face="normal" font="default"> Chakrabarti,A.</style></author><author><style face="normal" font="default"> Das,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Microbiology, University College of Medical Sciences (University of Delhi) &amp; Guru Teg Bahadur Hospital, Delhi, India</style></auth-address><titles><title><style face="normal" font="default">FcepsilonR1alpha gene polymorphism shows association with high IgE and anti-FcepsilonR1alpha in Chronic Rhinosinusitis with Nasal Polyposis</style></title><secondary-title><style face="normal" font="default">J Cell Biochem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Cell Biochem</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="15" Month="12" Year="2017">2017/12/15</year></dates><abstract><style face="normal" font="default">Despite large number of investigations, the etiology of chronic rhinosinusitis (CRS) remains unclear. Several factors are likely involved in its onset. The genetic susceptibility of IgE-responsiveness likely caused by polymorphism(s) in high affinity receptor for IgE (FcepsilonR1alpha) gene can help in understanding the pathophysiology of CRS with nasal polyposis (CRSwNP). A population-based case-control association analysis was conducted to assess the risk of CRSwNP conferred by single nucleotide polymorphisms (SNPs) in FcepsilonR1alpha gene in a North Indian cohort. Two promoter and three exonic regions of FcepsilonR1alpha gene were amplified and sequenced to investigate five SNPs - rs2427827, rs2251746, rs2298804, rs2298805, and rs2269718. BLAST analysis and subsequent multiple alignments, with known sequences available in the NCBI database, were performed. Total serum IgE and FcepsilonR1alpha antibody levels were estimated. Patient IgE level of 461.22 +/- 436.43 in comparison to 83.62 +/- 58.043 IU/mL in controls (p &lt; 0.0001), and FcepsilonR1alpha antibody level of 292.38 +/- 115.27 in comparison to 160.56 +/- 105.9 in controls (p &lt; 0.0001), depicts their highly significant associations with CRSwNP disease. However, no SNP showed evidence of association with CRSwNP; although relatively higher Odds ratios were observed with rs2427827, rs2251746 and rs2298804. Patient stratification revealed a significant association (p &lt; 0.05) of rs2427827 SNP with high IgE level CRSwNP patients. Nonetheless, we found no SNP associated with low serum IgE level patients. SNP (rs2427827) in the FcepsilonR1alpha gene region and high IgE levels may confer susceptibility to CRSwNP in north Indian population. However, further studies including larger sample size, gene-gene and gene-environment interactions are required for its elucidation. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1097-4644 (Electronic)IS - 0730-2312 (Linking)LA - engPT - Journal ArticleCO - India -CO - Saudi Arabia -</style></notes><work-type><style face="normal" font="default">10.1002/jcb.26619</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29243845">PM:29243845</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Cell Biochem\20171217-DarSA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Cell Biochem\20171217-DarSA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Dar SA</style></custom2><misc3><style face="normal" font="default">10.1002/jcb.26619</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87154</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tsujita,Y.</style></author><author><style face="normal" font="default"> Imai,K.</style></author><author><style face="normal" font="default"> Honma,K.</style></author><author><style face="normal" font="default"> Kamae,C.</style></author><author><style face="normal" font="default"> Horiuchi,T.</style></author><author><style face="normal" font="default"> Nonoyama,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-0042, Japan.</style></auth-address><titles><title><style face="normal" font="default">A Severe Anaphylactic Reaction Associated with IgM-Class Anti-Human IgG Antibodies in a Hyper-IgM Syndrome Type 2 Patient</style></title><secondary-title><style face="normal" font="default">J Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Clin Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="19" Month="12" Year="2017">2017/12/19</year></dates><abstract><style face="normal" font="default">PURPOSE: A 42-year-old man with hyper-IgM syndrome type 2 caused by activation-induced cytidine deaminase (AID) deficiency developed a severe anaphylactic reaction to intravenous immunoglobulin. The purpose of this study was to clarify the cause of the anaphylactic reaction of the patient. METHODS: We measured IgM-class anti-human IgG and anti-human IgA antibodies in his serum by sandwich enzyme-linked immunosorbent assay (ELISA). RESULTS: The sandwich ELISA assay revealed that serum from the patient, but not the controls, reacted to three different IgG products and purified human IgA. This indicated that the patient had IgM-class anti-human IgG and IgA antibodies in his serum, which associated with the anaphylactic reactions after the administration of IgG products. The anti-IgG antibody was likely to be the main cause of the reactions because an IgA-depleted IgG product also induced a severe reaction in this case and showed high absorbance in the ELISA system, similar to other IgG products containing more IgA. CONCLUSIONS: This is the first report of IgM-class anti-human IgG associated with an anaphylactic reaction to an IgG infusion. The anaphylactic reactions were very severe in this case, probably because IgM-class antibodies are potent activators of the complement pathway</style></abstract><notes><style face="normal" font="default">IS - 1573-2592 (Electronic)IS - 0271-9142 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1007/s10875-017-0466-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29255996">PM:29255996</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Clin Immunol\20171217-TsujitaY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Clin Immunol\20171217-TsujitaY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Tsujita Y</style></custom2><misc3><style face="normal" font="default">10.1007/s10875-017-0466-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87155</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ono-Ohmachi,A.</style></author><author><style face="normal" font="default"> Nakajima-Adachi,H.</style></author><author><style face="normal" font="default"> Morita,Y.</style></author><author><style face="normal" font="default"> Kato,K.</style></author><author><style face="normal" font="default"> Hachimura,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Milk Science Research Institute, Megmilk Snow Brand Co. Ltd., 1-1-2 Minamidai, Kawagoe, Saitama 350-1165, Japan</style></auth-address><titles><title><style face="normal" font="default">Milk basic protein supplementation exerts an anti-inflammatory effect in a food-allergic enteropathy model mouse</style></title><secondary-title><style face="normal" font="default">J Dairy Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Dairy Sci</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> autoimmune diseases</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="20" Month="12" Year="2017">2017/12/20</year></dates><abstract><style face="normal" font="default">To examine novel functions of milk basic protein (MBP) in T-cell-related inflammatory diseases, such as autoimmune diseases and allergies, we evaluated the effects of MBP on the causative responses of ovalbumin (OVA)-specific T cells in a food-allergic enteropathy model, OVA23-3 mice, which express an OVA-specific T-cell receptor gene. The OVA-specific CD4(+) T cells of the mesenteric lymph nodes (MLN) from OVA23-3 mice were cultured with CD11c(+) dendritic cells of MLN from BALB/cA mice in the absence or presence of MBP following stimulation with OVA; then the levels of CD69 expression and the levels of cytokine production by CD4(+) T cells were measured to evaluate activation. The effects of MBP supplementation of OVA 23-3 mice were assessed by feeding a diet containing OVA (OVA diet) with or without MBP for 28 d. Intestinal inflammation, together with activation and cytokine production of CD4(+) T cells by MLN, as well as femoral bone mineral density, were measured. In in vitro culture, MBP inhibited excess activation and IL-4 production by CD4(+) T cells. The supplementation of MBP to the OVA diet attenuated OVA-specific IgE production in OVA-diet-fed OVA23-3 mice and slightly resolved developing enteropathy caused by excess IL-4 production by CD4(+) T cells. Feeding OVA diet to OVA23-3 mice exhibited bone loss accompanied with enteropathy, whereas MBP supplementation prevented bone loss and increased osteoprotegerin, an osteoclastogenesis inhibitory factor, in the mice. The inhibition of T-cell-activation in both MLN and bone marrow by MBP supplementation may help prevent increased IgE levels caused by excessive IL-4 production and bone loss accompanied by enteropathy. Our findings show that MBP may help attenuate both T-cell-related inflammation and bone loss</style></abstract><notes><style face="normal" font="default">IS - 1525-3198 (Electronic)IS - 0022-0302 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.3168/jds.2017-13253</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29274967">PM:29274967</url></web-urls><pdf-urls><url ppv-ref="no">aryu@mail.ecc.u-tokyo.ac.jp</url></pdf-urls></urls><custom2><style face="normal" font="default">20171203, Ono-Ohmachi A</style></custom2><misc3><style face="normal" font="default">10.3168/jds.2017-13253</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87157</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Izadpanah,M.</style></author><author><style face="normal" font="default"> Mohebali,N.</style></author><author><style face="normal" font="default"> Elyasi gorji,Z.</style></author><author><style face="normal" font="default"> Farzaneh,P.</style></author><author><style face="normal" font="default"> Vakhshiteh,F.</style></author><author><style face="normal" font="default"> Shahzadeh Fazeli,S.A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Simple and fast multiplex PCR method for detection of species origin in meat products</style></title><secondary-title><style face="normal" font="default">J Food Sci Technol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Food Sci Technol</style></full-title></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0975-8402</style></isbn><abstract><style face="normal" font="default">Identification of animal species is one of the major concerns in food regulatory control and quality assurance system. Different approaches have been used for species identification in animal origin of feedstuff. This study aimed to develop a multiplex PCR approach to detect the origin of meat and meat products. Specific primers were designed based on the conserved region of mitochondrial Cytochrome C Oxidase subunit I (COX1) gene. This method could successfully distinguish the origin of the pig, camel, sheep, donkey, goat, cow, and chicken in one single reaction. Since PCR products derived from each species represent unique molecular weight, the amplified products could be identified by electrophoresis and analyzed based on their size. Due to the synchronized amplification of segments within a single PCR reaction, multiplex PCR is considered to be a simple, fast, and inexpensive technique that can be applied for identification of meat products in food industries. Nowadays, this technique has been considered as a practical method to identify the species origin, which could further applied for animal feedstuffs identification</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Iran -</style></notes><work-type><style face="normal" font="default">10.1007/s13197-017-2980-2</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s13197-017-2980-2</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Food Sci Technol\20171215-IzadpanahM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Food Sci Technol\20171215-IzadpanahM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Izadpanah M</style></custom2><misc3><style face="normal" font="default">10.1007/s13197-017-2980-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87158</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lin,L.</style></author><author><style face="normal" font="default"> Hwang,B.J.</style></author><author><style face="normal" font="default"> Culton,D.A.</style></author><author><style face="normal" font="default"> Li,N.</style></author><author><style face="normal" font="default"> Burette,S.</style></author><author><style face="normal" font="default"> Koller,B.H.</style></author><author><style face="normal" font="default"> Messingham,K.A.</style></author><author><style face="normal" font="default"> Fairley,J.A.</style></author><author><style face="normal" font="default"> Lee,J.J.</style></author><author><style face="normal" font="default"> Hall,R.P.</style></author><author><style face="normal" font="default"> An,L.</style></author><author><style face="normal" font="default"> Diaz,L.A.</style></author><author><style face="normal" font="default"> Liu,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA</style></auth-address><titles><title><style face="normal" font="default">Eosinophils mediate tissue injury in autoimmune skin disease bullous pemphigoid</style></title><secondary-title><style face="normal" font="default">J Invest Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Invest Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> autoimmune diseases</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword></keywords><dates><year Day="12" Month="12" Year="2017">2017/12/12</year></dates><abstract><style face="normal" font="default">Eosinophils are typically associated with unique inflammatory settings, including allergic inflammation and helminth infections. However, new information suggests that eosinophils contribute more broadly to inflammatory responses and participate in local immune regulation and the tissue remodeling/repair events linked with a variety of diseases. Eosinophilic infiltration has long been a histologic hallmark of bullous pemphigoid (BP), a subepidermal autoimmune blistering disease characterized by autoantibodies directed against basement membrane protein BP180. However, the exact role of eosinophils in disease pathogenesis remains largely unknown. We show here that eosinophils are necessary for IgE autoantibody mediated BP blister formation in a humanized IgE receptor mouse model of BP. Disease severity is IgE dose dependent and correlates with the degree of eosinophil infiltration in the skin. Furthermore, IgE autoantibodies fail to induce BP in eosinophil-deficient mice, confirming that eosinophils are required for IgE mediated tissue injury. Thus, eosinophils provide the cellular link between IgE autoantibodies and skin blistering in this murine model of BP. These findings suggest a role for eosinophils in autoimmune disease and have important implications for the treatment of BP as well as other antibody mediated inflammatory and autoimmune diseases</style></abstract><notes><style face="normal" font="default">IS - 1523-1747 (Electronic)IS - 0022-202X (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jid.2017.11.031</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29246800">PM:29246800</url></web-urls><pdf-urls><url ppv-ref="no">zhi_liu@med.unc.edu</url></pdf-urls><related-urls><url ppv-ref="no">presto - 1 anno ISS</url></related-urls></urls><custom2><style face="normal" font="default">20171210, Lin L</style></custom2><misc3><style face="normal" font="default">10.1016/j.jid.2017.11.031</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87168</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bruggenjurgen,B.</style></author><author><style face="normal" font="default"> Reinhold,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Institute for Health Economics, Steinbeis-Hochschule Berlin (SHB) , Gurtelstrasse 29 , Berlin , Germanyb Institute for Social Medicine, Epidemiology and Health Economics, Charite - Universitatsmedizin Berlin , Germany</style></auth-address><titles><title><style face="normal" font="default">Cost-effectiveness of grass pollen subcutaneous immunotherapy (SCIT) compared to sublingual immunotherapy (SLIT) and symptomatic treatment in Austria, Spain and Switzerland</style></title><secondary-title><style face="normal" font="default">J Med Econ</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Med Econ</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="22" Month="12" Year="2017">2017/12/22</year></dates><abstract><style face="normal" font="default">BACKGROUND: While specific immunotherapy (SIT) has been proven to be cost effective for the treatment of allergic rhinitis compared to symptomatic treatment, there is a lack of European studies in which sublingual (SLIT) and subcutaneous (SCIT) immunotherapy were compared. The present analysis is focused on the cost-effectiveness of SCIT compared to SLIT and symptomatic treatment of grass pollen allergy in Austria, Spain and Switzerland. It will address specific properties of the underlying healthcare systems. METHODS: The investigation is based on a previously published health economic model calculation. This was designed as a Markov model with predefined health stages and a duration of 9 years covering specific preparations for SCIT (Allergovit) and SLIT (Oralair). The effectiveness was assessed as symptom-score based quality-adjusted life years (QALYs). Additionally, total cost has been determined as well as the cost-effectiveness of SCIT. The robustness of model results was proved in further sensitivity analyses. RESULTS: With regard to the effectiveness of both SCIT and SLIT, preparations were dominant compared to pharmacological symptomatic therapy. Both strategies were associated with additional cost, but combined with the results on effectiveness, both have to be regarded as cost-effective. A direct comparison of the SCIT (Allergovit) and SLIT (Oralair) showed lower total costs of SCIT versus SLIT for Austria, Spain and Switzerland (1,368 euroversus 2,012 euro, 2,229 euroversus 2,547 euroand 1,901 euroversus 2,220 euro) and superior effectiveness (SCIT, 8.02 QALYs; SLIT, 7.98 QALYs; and symptomatic therapy, 7.90 QALYs). CONCLUSION: In patients with allergic rhinitis, SIT offers cost-effective treatment options compared to symptomatic treatment. When comparing SCIT (Allergovit) and SLIT (Oralair), SCIT was dominant in terms of QALYs as well as costs, in particular due to a slightly higher patient compliance and lower drug costs</style></abstract><notes><style face="normal" font="default">IS - 1941-837X (Electronic)IS - 1369-6998 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1080/13696998.2017.1419959</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29271271">PM:29271271</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Med Econ\20171221-BruggenjurgenB.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Med Econ\20171221-BruggenjurgenB.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Bruggenjurgen B</style></custom2><misc3><style face="normal" font="default">10.1080/13696998.2017.1419959</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87169</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gill,N.K.</style></author><author><style face="normal" font="default"> Dhaliwal,A.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Zoology and Environmental Sciences, Punjabi University, India</style></auth-address><titles><title><style face="normal" font="default">Seasonal Variation of Allergenic Acarofauna From the Homes of Allergic Rhinitis and Asthmatic Patients</style></title><secondary-title><style face="normal" font="default">J Med Entomol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Med Entomol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="13" Month="12" Year="2017">2017/12/13</year></dates><abstract><style face="normal" font="default">House dust mites (HDMs) play positive role in causing various kinds of allergenic manifestations such as allergic rhinitis (AR), asthma, dermatitis, and urticaria. HDMs are prevalent in temperate regions but various studies have shown the prevalence of HDMs in tropical and subtropical countries. The present study was conducted from March 2015 to February 2016. During the study period, a total of 500 dust samples were collected from 125 homes of 125 patients suffering from AR and asthma. From these 500 dust samples, 466 samples were found to be positive for mites. The year was divided into three climatic classes, i.e., CCL I (March, April, May, June), CCL II (July, August, September, October), and CCL III (November, December, January, February) A total of 7,710 mites were collected, from which 2,902 (37.63%) mites were found in samples collected during summer season, i.e., CCL-I, 3,728 (48.35%) mites were found in samples collected during rainy season, i.e., CCL-II and only 1,080 (14.01%) mites were found in samples collected during winter season, i.e., CCL-III. Total 7,710 mite specimens were isolated with 7,404, i.e., 96.03% were only from the hypoorder Astigmata, 240, i.e., 3.11% from suborder Prostigmata, 46, i.e., 0.60% from order Mesostigmata, and 20, i.e., 0.26% from suborder Oribatida. The present study indicates that Dermatophagoides pteronyssinus (Trouessart 1897) (Astigmata) was most abundant and frequently found allergenic mite species followed by D. farinae (Hughes 1961), D. microceras (Griffiths and Cunnington 1971), Acarus siro (Linnaeus 1758), Tyrophagus putrescentiae (Schrank 1781), Lepidoglyphus destructor (Schrank 1781), Euroglyphus maynei (Cooreman 1950), Cheyletus, Mesostigmatic, and Oribatida mites</style></abstract><notes><style face="normal" font="default">IS - 1938-2928 (Electronic)IS - 0022-2585 (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.1093/jme/tjx206</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29244180">PM:29244180</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Med Entomol\20171221-GillNK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Med Entomol\20171221-GillNK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Gill NK</style></custom2><misc3><style face="normal" font="default">10.1093/jme/tjx206</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87170</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Harada,E.</style></author><author><style face="normal" font="default"> D'Alessandro-Gabazza,C.N.</style></author><author><style face="normal" font="default"> Toda,M.</style></author><author><style face="normal" font="default"> Morizono,T.</style></author><author><style face="normal" font="default"> Totoki,T.</style></author><author><style face="normal" font="default"> Yasuma,T.</style></author><author><style face="normal" font="default"> Nishihama,K.</style></author><author><style face="normal" font="default"> Kobayashi,T.</style></author><author><style face="normal" font="default"> Sumiya,T.</style></author><author><style face="normal" font="default"> Kawagishi,H.</style></author><author><style face="normal" font="default"> Gabazza,E.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">1 Department of Immunology, Graduate School of Medicine Mie, Mie University , Tsu, Japan</style></auth-address><titles><title><style face="normal" font="default">The Medicinal Mushroom, Grifola gargal, Ameliorates Allergic Bronchial Asthma</style></title><secondary-title><style face="normal" font="default">J Med Food</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Med Food</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="20" Month="12" Year="2017">2017/12/20</year></dates><abstract><style face="normal" font="default">Grifola gargal Singer, a medicinal mushroom, has been found to be effective for the prevention and treatment of various chronic inflammatory diseases. However, the effects of G. gargal on allergic diseases are unknown. The present study investigated the effect of G. gargal extract on allergic bronchial asthma. Asthma was induced in mice by ovalbumin sensitization and inhalation. The grade of asthma was compared between mice fed with chow containing G. gargal extract and mice given standard chow. The human mast cell and eosinophilic cell lines were used for in vitro studies. G. gargal extract significantly reduced airway hyperresponsiveness, lung eosinophilic infiltration, lung interleukin (IL)-13 expression, and plasma IgE level and significantly increased IL-10 plasma levels compared to untreated control mice. Spleen regulatory T cells were significantly increased in mice treated with the G. gargal extract compared with untreated control mice. G. gargal extract significantly suppressed expression of cytokines in mast cells and eosinophils compared with control cells. Overall, these observations show that G. gargal extract augments the lung population of regulatory T cells and ameliorates allergic inflammation and airway hyperresponsiveness in mice with allergic bronchial asthma, suggesting the potential therapeutic benefit of G. gargal extract in allergic diseases</style></abstract><notes><style face="normal" font="default">IS - 1557-7600 (Electronic)IS - 1096-620X (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1089/jmf.2017.4016</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29261008">PM:29261008</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Med Food\20171221-HaradaE.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Med Food\20171221-HaradaE.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Harada E</style></custom2><misc3><style face="normal" font="default">10.1089/jmf.2017.4016</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87171</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Moran,G.</style></author><author><style face="normal" font="default"> Uberti,B.</style></author><author><style face="normal" font="default"> Ortloff,A.</style></author><author><style face="normal" font="default"> Folch,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of pharmacology, faculty of veterinary science, universidad Austral de Chile, Valdivia, Chile.</style></auth-address><titles><title><style face="normal" font="default">Aspergillus fumigatus-sensitive IgE is associated with bronchial hypersensitivity in a murine model of neutrophilic airway inflammation</style></title><secondary-title><style face="normal" font="default">J Mycol Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Mycol Med</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">Neutrophils are the predominant inflammatory cells that infiltrate airways during acute exacerbation of asthma. The importance of A. fumigatus sensitization, and IgE response in the airways in patients with acute asthma is unclear. Rockefeller (RK) mice were sensitized with A. fumigatus extract protein. The animals were subsequently challenged with different degrees of A. fumigatus contamination in the cage bedding. All groups of mice were euthanized to obtain bronchoalveolar lavage fluid (BALF) for cytological and Elisa assays, and lung tissue for histological analysis. Moreover, several bioassays were conducted to determine whether BALF IgE antibodies can activate mast cells. In this study, we demonstrated that exposure of sensitized mice to a known concentration of A. fumigatus conidia produces bronchial hyperreactivity with marked neutrophilic bronchial infiltration and increased BALF IgE, capable of triggering mast cell degranulation. This study suggests that IgE may play a role in bronchial hyperreactivity associated to A. fumigatus exposure in mice. Mice sensitized and challenged with this fungus showed characteristics of severe asthma, with an increase of BALF neutrophils, histological changes consistent with severe asthma and an increase of IgE capable of triggering type I hypersensitivity</style></abstract><notes><style face="normal" font="default">IS - 1773-0449 (Electronic)IS - 1156-5233 (Linking)LA - engPT - Journal ArticleCO - Chile -</style></notes><work-type><style face="normal" font="default">10.1016/j.mycmed.2017.11.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29233467">PM:29233467</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Mycol Med\20171221-MoranG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Mycol Med\20171221-MoranG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Moran G</style></custom2><misc3><style face="normal" font="default">10.1016/j.mycmed.2017.11.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87175</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sobhan,A.</style></author><author><style face="normal" font="default"> Oh,J.H.</style></author><author><style face="normal" font="default"> Park,M.K.</style></author><author><style face="normal" font="default"> Kim,S.W.</style></author><author><style face="normal" font="default"> Park,C.</style></author><author><style face="normal" font="default"> Lee,J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Single walled carbon nanotube based biosensor for detection of peanut allergy-inducing protein ara h1</style></title><secondary-title><style face="normal" font="default">Korean J Chem Eng</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Korean J Chem Eng</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Arachis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1975-7220</style></isbn><abstract><style face="normal" font="default">Food allergies are global trending issues in the food industry. Peanut allergy is an especially serious problem with emerging allergen symptoms because peanuts are utilized worldwide as a processing food source. Arachis hypogaea 1 (Ara h1) is a main seed storage protein from peanut materials that derives allergic medical symptoms. In this study, a single-walled carbon nanotube (SWCNT)-based biosensor was developed to detect Ara h1. The developed biosensor utilizes an Ara h1 antibody as a receptor for the target material, SWCNTs as a signal transfer, and 1-pyrenebutanoic acid succinimidyl ester (1-PBSE) as a linker between the SWCNTs and the receptors. SWCNTs dramatically transferred the biological reaction between the antibody and the antigen into measurable signals of electrical responses. The sensor capacity of the developed SWCNT-based biosensor, including the limit of detection (LOD, 1 ng/mL), the detection range (1-1,000 ng/mL), and the washing amounts (three times), was confirmed</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1007/s11814-017-0259-y</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s11814-017-0259-y</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Korean J Chem Eng\20171223-SobhanA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Korean J Chem Eng\20171223-SobhanA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Sobhan A</style></custom2><misc3><style face="normal" font="default">10.1007/s11814-017-0259-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87177</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Poulsen,L.K.</style></author></authors></contributors><titles><title><style face="normal" font="default">Food allergy: setting the scene for tolerance induction</style></title><secondary-title><style face="normal" font="default">Lancet Gastroenterol Hepatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Lancet Gastroenterol Hepatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2468-1253</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1016/S2468-1253(17)30391-6</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/S2468-1253(17)30391-6</url></web-urls><pdf-urls><url ppv-ref="no">lkpallgy@mail.dk</url></pdf-urls></urls><custom2><style face="normal" font="default">20171205, Poulsen LK</style></custom2><misc3><style face="normal" font="default">10.1016/S2468-1253(17)30391-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87178</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Andorf,S.</style></author><author><style face="normal" font="default"> Purington,N.</style></author><author><style face="normal" font="default"> Block,W.M.</style></author><author><style face="normal" font="default"> Long,A.J.</style></author><author><style face="normal" font="default"> Tupa,D.</style></author><author><style face="normal" font="default"> Brittain,E.</style></author><author><style face="normal" font="default"> Rudman Spergel,A.</style></author><author><style face="normal" font="default"> Desai,M.</style></author><author><style face="normal" font="default"> Galli,S.J.</style></author><author><style face="normal" font="default"> Nadeau,K.C.</style></author><author><style face="normal" font="default"> Chinthrajah,R.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Sean N Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, CA, USA</style></auth-address><titles><title><style face="normal" font="default">Anti-IgE treatment with oral immunotherapy in multifood allergic participants: a double-blind, randomised, controlled trial</style></title><secondary-title><style face="normal" font="default">Lancet Gastroenterol Hepatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Lancet Gastroenterol Hepatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status date="12/26/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Despite progress in single food oral immunotherapy, there is little evidence concerning the safety and efficacy of treating individuals with multiple food (multifood) allergies. We did a pilot study testing whether anti-IgE (omalizumab) combined with multifood oral immunotherapy benefited multifood allergic patients. METHODS: We did a blinded, phase 2 clinical trial at Stanford University. We enrolled participants, aged 4-15 years, with multifood allergies validated by double-blind, placebo-controlled food challenges to their offending foods. Inclusion criteria included a positive skin prick test of 6 mm or more (wheal diameter, above the negative control), a food-specific serum IgE concentration of more than 4 kU/L for each food, or both, and a positive double-blind, placebo-controlled food challenge at 500 mg or less of food protein. Exclusion criteria included eosinophilic oesophagitis and severe asthma. Participants were randomised (3:1) with a block size of four, to receive multifood oral immunotherapy to two to five foods, together with omalizumab (n=36) or placebo (n=12). 12 individuals who fulfilled the same inclusion and exclusion criteria were included as controls. These individuals were not randomised and received neither omalizumab nor oral immunotherapy. Omalizumab or placebo was administered subcutaneously for 16 weeks, with oral immunotherapy starting at week 8, and was stopped 20 weeks before the exit double-blind, placebo-controlled food challenge at week 36. The primary endpoint was the proportion of participants who passed double-blind, placebo-controlled food challenges to at least two of their offending foods. This completed trial is registered with ClinicalTrials.gov, number NCT02643862. FINDINGS: Between March 25, 2015, and Aug 18, 2016, 165 participants were assessed for eligibility, of whom 84 did not meet the inclusion criteria and 21 declined to participate. We enrolled and randomised 48 eligible participants and the remaining 12 patients were included as nonrandomised, untreated controls. At week 36, a significantly greater proportion of the omalizumab-treated (30 [83%] of 36) versus placebo (four [33%] of 12) participants passed double-blind, placebo-controlled food challenges to 2 g protein for two or more of their offending foods (odds ratio 10.0, 95% CI 1.8-58.3, p=0.0044). All participants completed the study. There were no serious or severe (grade 3 or worse) adverse events. Participants in the omalizumab group had a significantly lower median per-participant percentage of oral immunotherapy doses associated with any adverse events (27% vs 68%; p=0.0082). The most common adverse events in both groups were gastrointestinal events. INTERPRETATION: In multifood allergic patients, omalizumab improves the efficacy of multifood oral immunotherapy and enables safe and rapid desensitisation. FUNDING: US National Institutes of Health (NIH)</style></abstract><notes><style face="normal" font="default">IS - 2468-1253 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/S2468-1253(17)30392-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29242014">PM:29242014</url></web-urls><pdf-urls><url ppv-ref="no">schinths@stanford.edu</url></pdf-urls></urls><custom2><style face="normal" font="default">20171212, Andorf S</style></custom2><misc3><style face="normal" font="default">10.1016/S2468-1253(17)30392-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87188</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tophof,M.A.</style></author><author><style face="normal" font="default"> Hermanns,A.</style></author><author><style face="normal" font="default"> Adelt,T.</style></author><author><style face="normal" font="default"> Eberle,P.</style></author><author><style face="normal" font="default"> Gronke,C.</style></author><author><style face="normal" font="default"> Friedrichs,F.</style></author><author><style face="normal" font="default"> Knecht,R.</style></author><author><style face="normal" font="default"> Monter,E.</style></author><author><style face="normal" font="default"> Schopfer,H.</style></author><author><style face="normal" font="default"> Schwerk,N.</style></author><author><style face="normal" font="default"> Steinbach,J.</style></author><author><style face="normal" font="default"> Umpfenbach,H.U.</style></author><author><style face="normal" font="default"> Weisshaar,C.</style></author><author><style face="normal" font="default"> Wilmsmeyer,B.</style></author><author><style face="normal" font="default"> Bufe,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Experimental Pneumology, Ruhr-University Bochum, Bochum, GermanyAdelt T, Bramsche, GermanyNETSTAP e.V, Borstel, GermanyEberle P, Kassel, GermanyNETSTAP e.V, Borstel, GermanyGronke C, Ludwigsfelde, GermanyNETSTAP e.V, Borstel, GermanyFriedrichs F, Aachen, GermanyKnecht R, Bretten, GermanyNETSTAP e.V, Borstel, GermanyMonter E, Osnabruck, GermanyNETSTAP e.V, Borstel, GermanySchopfer H, Espelkamp, GermanyNETSTAP e.V, Borstel, GermanyHannover Medical School, Hannover, GermanySteinbach J, Bremen, GermanyNETSTAP e.V, Borstel, GermanyUmpfenbach HU, Dulken, GermanyWeisshaar C, Bielefeld, GermanyNETSTAP e.V, Borstel, GermanyWilmsmeyer B, Itzehoe, GermanyNETSTAP e.V, Borstel, GermanyDepartment of Experimental Pneumology, Ruhr-University Bochum, Bochum, GermanyNETSTAP e.V, Borstel, Germany</style></auth-address><titles><title><style face="normal" font="default">Side effects during subcutaneous immunotherapy (SCIT) in children with allergic diseases</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="16" Month="12" Year="2017">2017/12/16</year></dates><abstract><style face="normal" font="default">BACKGROUND: Allergen-specific immunotherapy (AIT) is the only causal form of therapy for IgE-mediated allergic diseases. Subcutaneous immunotherapy (SCIT) is considered safe and well tolerated in adults, yet there is less evidence of safety in the pediatric population. METHODS: A noninterventional prospective observing longitudinal study was carried out to determine the incidence of local and systemic side effects by SCIT, routinely performed in pediatric patients. A total of 581 pediatric patients were observed in 18 study centers between March 2012 and October 2014, recording 8,640 treatments and 10,015 injections. RESULTS: A total of 54.6% of the patients experienced immediate local side effects at least once; delayed local side effects were seen in 56.1%. Immediate systemic adverse reactions occurred in 2.2% of patients; 7.4% experienced delayed systemic side effects. However, severe systemic side effects (grade III in the classification of Ring and Messmer) were seen in 0.03% of all treatments, all appearing within 30 minutes after the injections. No grade IV reactions were observed. In addition, many potential risk factors were investigated, yet only a few were found to be associated with the occurrence of side effects. CONCLUSIONS: Subcutaneous immunotherapy is a safe form of therapy in pediatric patients, with similar rates of local side effects compared to adult patients and low rates of severe systemic side effects. However, local and systemic reactions occurring later than 30 minutes after injection were observed more often than expected, which makes it essential to be attentive on behalf of pediatricians, patients and parents. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12847</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247543">PM:29247543</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171220-TophofMA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171220-TophofMA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Tophof MA</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12847</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87189</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">EIgenmann,P.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">University Hospitals of Geneva, Department of Child and Adolescent Pediatric Allergy Unit, Geneva, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Do we still need oral food challenges for the diagnosis of food allergy?</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Diagnosis of food allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="14" Month="12" Year="2017">2017/12/14</year></dates><abstract><style face="normal" font="default">Food challenges are standard in the diagnosis in patients suspected of being allergic to food. However, their role is regularly questioned due to the time required to perform them, and to their cost and the inherent risk of severe reactions. Food challenges have been challenged by recent advances defining threshold values for food-specific IgE helping to predict the probability of having symptoms to the suspected food. Also, identification of major allergens to various highly allergenic foods such as peanuts or tree nuts have contributed to an increased accuracy of IgE testing. Altogether, these new data have contributed to a better definition of the role of oral food challenges in the diagnosis of food allergy. Oral food challenges are not outdated, and remain the gold standard in the diagnosis of food allergy. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12845</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29240247">PM:29240247</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171220-EigenmannPA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171220-EigenmannPA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Eigenmann PA</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12845</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87192</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chiu,C.Y.</style></author><author><style face="normal" font="default"> Su,K.W.</style></author><author><style face="normal" font="default"> Tsai,M.H.</style></author><author><style face="normal" font="default"> Hua,M.C.</style></author><author><style face="normal" font="default"> Liao,S.L.</style></author><author><style face="normal" font="default"> Lai,S.H.</style></author><author><style face="normal" font="default"> Chen,L.C.</style></author><author><style face="normal" font="default"> Yao,T.C.</style></author><author><style face="normal" font="default"> Yeh,K.W.</style></author><author><style face="normal" font="default"> Huang,J.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Chang Gung Memorial Hospital at Keelung and Chang Gung University College of Medicine, Taoyuan, Taiwan</style></auth-address><titles><title><style face="normal" font="default">Longitudinal vitamin D deficiency is inversely related to mite sensitization in early childhood</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="14" Month="12" Year="2017">2017/12/14</year></dates><abstract><style face="normal" font="default">BACKGROUND: There are few studies addressing the longitudinal analysis of vitamin D deficiency and its impact to the development of atopic diseases in early childhood. METHODS: We investigated 155 children who regularly followed up at our clinic for 5 years as subjects enrolled in a birth cohort study. The pattern of vitamin D levels from birth to 5 years of age was clustered using K-means method in R software. Absolute eosinophil count (AEC), total serum and specific immunoglobulin E antibodies against food (egg white, milk, and wheat) and inhalant allergens (D. pteronyssinus, D. farina, and C. herbarum) were measured at 1.5, 3, 4 and 5 years of age. RESULTS: A total of 137 children with serum samples obtained over at least 3 time-points during the follow-up period were recruited. By using K-means clustering, the dynamic changes in vitamin D levels was significantly stratified into 3 clusters (cluster A, >/= 30 ng/mL, n = 61; cluster B, 20 - 29.9 ng/mL, n = 53; cluster C, &lt; 20 ng/mL, n = 23). Despite no statistical association with atopic diseases, a persistent vitamin D deficiency appeared to be associated with eosinophilia at age 3, and total serum and mite-specific IgE levels at age 4. At which age, a higher prevalence of mite sensitization was significantly associated with the risk of allergic rhinitis and asthma. CONCLUSIONS: Vitamin D deficiency is inversely associated with AEC and mite-specific IgE levels, which may potentially increase susceptibility to develop allergies including rhinitis and asthma in early childhood. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleCO - Taiwan -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12846</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29240264">PM:29240264</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171220-ChiuCY.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\20171220-ChiuCY.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Chiu CY</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12846</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87193</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tamasauskiene,L.</style></author><author><style face="normal" font="default"> Sitkauskiene,B.</style></author></authors></contributors><titles><title><style face="normal" font="default">Role of Th22 and IL-22 in Pathogenesis of Allergic Airway Diseases: Pro-inflammatory or Anti-inflammatory Effect?</style></title><secondary-title><style face="normal" font="default">Pediatr Neonatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Neonatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IL-22</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Th22</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1875-9572</style></isbn><abstract><style face="normal" font="default">A new population of T cells known as Th22 was described for the first time in 2009. These cells are usually identified by the production of IL-22. However, this cytokine is also secreted by other cells such as Th1, Th2, Th17, natural killers, and innate lymphoid cells. Th22 is known as a pro-inflammatory agent in allergic skin diseases. Recently, more evidence has emerged showing associations between these cells and other diseases. The role of Th22 in asthma and allergic rhinitis is controversial: some authors suggest that Th22 has a pro-inflammatory effect, while others state that Th22 has anti-inflammatory properties. The aim of this article was to review the role of Th22 and IL-22 in allergic airway diseases based on the most recent literature. This review suggests that Th22 plays a significant role in the pathogenesis of allergic airway diseases and has predominantly anti-inflammatory properties. More studies are needed to clarify the role of Th22 in more detail</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Lithuania -</style></notes><work-type><style face="normal" font="default">10.1016/j.pedneo.2017.11.020</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29292068">PM:29292068</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Neonatol\20171204-TamasauskieneL.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Neonatol\20171204-TamasauskieneL.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Tamasauskiene L</style></custom2><misc3><style face="normal" font="default">10.1016/j.pedneo.2017.11.020</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87196</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wu,R.</style></author><author><style face="normal" font="default"> Wang,T.</style></author><author><style face="normal" font="default"> Warren,B.A.W.</style></author><author><style face="normal" font="default"> Thomson,S.J.</style></author><author><style face="normal" font="default"> Allan,A.C.</style></author><author><style face="normal" font="default"> Macknight,R.C.</style></author><author><style face="normal" font="default"> Varkonyi-Gasic,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">The New Zealand Institute for Plant and Food Research Limited (PFR) Mt Albert, Auckland Mail Centre, Private Bag 92169, Auckland, 1142, New Zealand</style></auth-address><titles><title><style face="normal" font="default">Kiwifruit SVP2 controls developmental and drought-stress pathways</style></title><secondary-title><style face="normal" font="default">Plant Mol Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Plant Mol Biol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> New Zealand</style></keyword></keywords><dates><year Day="8" Month="12" Year="2017">2017/12/8</year></dates><abstract><style face="normal" font="default">KEY MESSAGE: Genome-wide targets of Actinidia chinensis SVP2 confirm roles in ABA- and dehydration-mediated growth repression and reveal a conservation in mechanism of action between SVP genes of taxonomically distant Arabidopsis and a woody perennial kiwifruit. The molecular mechanisms underlying growth and dormancy in woody perennials are largely unknown. In Arabidopsis, the MADS-box transcription factor SHORT VEGETATIVE PHASE (SVP) plays a key role in the progression from vegetative to floral development, and in woody perennials SVP-like genes are also proposed to be involved in controlling dormancy. During kiwifruit development SVP2 has a role in growth inhibition, with high-chill kiwifruit Actinidia deliciosa transgenic lines overexpressing SVP2 showing suppressed bud outgrowth. Transcriptomic analyses of these plants suggests that SVP2 mimics the well-documented abscisic acid (ABA) effect on the plant dehydration response. To corroborate the growth inhibition role of SVP2 in kiwifruit development at the molecular level, we analysed the genome-wide direct targets of SVP2 using chromatin immunoprecipitation followed by high-throughput sequencing in kiwifruit A. chinensis. SVP2 was found to bind to at least 297 target sites in the kiwifruit genome, and potentially modulates 252 genes that function in a range of biological processes, especially those involved in repressing meristem activity and ABA-mediated dehydration pathways. In addition, our ChIP-seq analysis reveals remarkable conservation in mechanism of action between SVP genes of taxonomically distant plant species</style></abstract><notes><style face="normal" font="default">IS - 1573-5028 (Electronic)IS - 0167-4412 (Linking)LA - engPT - Journal ArticleCO - New Zealand -</style></notes><work-type><style face="normal" font="default">10.1007/s11103-017-0688-3</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29222611">PM:29222611</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM4_ESM.xlsxC:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM5_ESM.xlsxC:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM6_ESM.xlsxC:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM7_ESM.xlsxC:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM8_ESM.xlsxC:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM9_ESM.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM4_ESM.xlsxF:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM5_ESM.xlsxF:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM6_ESM.xlsxF:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM7_ESM.xlsxF:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM8_ESM.xlsxF:\A&amp;H HMW Papers\Plant Mol Biol\20171222-WuR_MOESM9_ESM.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20171222, Wu R</style></custom2><misc3><style face="normal" font="default">10.1007/s11103-017-0688-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87202</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vieira,G.C.</style></author><author><style face="normal" font="default"> Gadelha,F.A.A.F.</style></author><author><style face="normal" font="default"> Pereira,R.F.</style></author><author><style face="normal" font="default"> Ferreira Laercia,K.D.P.</style></author><author><style face="normal" font="default"> Barbosa-Filho,J.M.</style></author><author><style face="normal" font="default"> Bozza,P.T.</style></author><author><style face="normal" font="default"> Piuvezam,M.R.</style></author></authors></contributors><titles><title><style face="normal" font="default">Warifteine, an alkaloid of Cissampelos sympodialis, modulates allergic profile in a chronic allergic rhinitis model</style></title><secondary-title><style face="normal" font="default">Rev Bras Farmacogn</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Bras Farmacogn</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> Nasal tissues</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Warifteine</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0102-695X</style></isbn><abstract><style face="normal" font="default">Cissampelos sympodialis Eichler, Menispermaceae, a Brazilian medicinal plant and its alkaloid warifteine present immunomodulatory activity on asthma experimental model by reducing antigen-specific IgE levels, eosinophil infiltration and lung hyperactivity. Allergic rhinitis is a chronic inflammatory disorder of the nasal tissue that affect the quality of life and it is a risk factor for asthma exacerbation. This study evaluated the effect of inhaled warifteine in an allergic ovalbumin rhinitis model. Inhaled warifteine (2 mg/ml) treatment of ovalbumin-sensitized BALB/c mice significant decreased total and differential number of cells on the nasal cavity and decreased ovalbumin-specific IgE serum levels. Hematoxylin &amp;amp; eosin staining of histological preparations of ovalbumin nasal tissues showed changes such as congestion and a massive cell infiltration in the perivascular and subepithelial regions characterizing the nasal inflammatory process. However, inhaled warifteine or dexamethasone treatment decreased cell infiltration into the perivascular regions and it was observed an intact nasal tissue. Periodic acidic staining of nasal epithelium of ovalbumin animals demonstrated high amount of mucus production by goblet cells and inhaled warifteine or dexamethasone treatment modulated the mucus production. In addition, toluidine blue staining of the nasal epithelium of ovalbumin animals demonstrated an increase of mast cells on the tissue and inhaled warifteine or dexamethasone treatment decreased in average of 1.4 times the number of these cells on the nasal epithelium. Taken these data together we postulate that warifteine, an immunomodulatory alkaloid, can be a medicinal molecule prototype to ameliorate the allergic rhinitis conditions</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.bjp.2017.10.009</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.bjp.2017.10.009</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Bras Farmacogn\20171221-VieiraGC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Bras Farmacogn\20171221-VieiraGC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171221, Vieira GC</style></custom2><misc3><style face="normal" font="default">10.1016/j.bjp.2017.10.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87203</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dolgova,A.S.</style></author><author><style face="normal" font="default"> Sudina,A.E.</style></author><author><style face="normal" font="default"> Cherkashina,A.S.</style></author><author><style face="normal" font="default"> Stukolova,O.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Molecular Diagnostics and Epidemiology Department , Central Research Institute of Epidemiology , Moscow , Russia</style></auth-address><titles><title><style face="normal" font="default">Component-resolved microarray analysis of IgE sensitization profiles to Felis catus major allergen molecules in Russian cat-allergic patients</style></title><secondary-title><style face="normal" font="default">Scand J Clin Lab Invest</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Scand J Clin Lab Invest</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">We aimed to determine the profile of IgE reactivity to three major cat allergens, Fel d 1, Fel d 2 and Fel d 4, in cat-allergic patients in the Moscow region in Russia. sIgE levels to recombinant proteins expressed in Escherichia coli (Fel d 1 and Fel d 4) and to Fel d 2 protein purified from cat serum were measured using a microarray method developed in our laboratory. Sera from 174 anonymous subjects with a positive reaction (>/=0.35 IU/mL) to cat dander extract (e1, ImmunoCAP) and 56 negative controls were used for IgE testing. Fel d 1 was recognized by 92.5%, Fel d 2 by 29.9% and Fel d 4 by 39.1% of the tested patient sera. The sensitivity to these three proteins was approximately 98% compared to cat dander extract (correlation coefficient to ImmunoCAP is 0.94 with PPV = 0.99 and NPV = 0.95). These predictive values appeared to be even more statistically significant than the divergence between the ISAC IgE test and the extract-based singleplex ImmunoCAP. The combination of the three investigated proteins (Fel d 1, Fel d 2 and Fel d 4) is suitable for in vitro molecular (serological) diagnosis of cat allergy in this region as a complement to cat dander extract. Moreover, with this method, we found distinction between Fel d 2 and other Feline sIgEs formation</style></abstract><notes><style face="normal" font="default">IS - 1502-7686 (Electronic)IS - 0036-5513 (Linking)LA - engPT - Journal ArticleCO - Russia -</style></notes><work-type><style face="normal" font="default">10.1080/00365513.2017.1414955</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29228796">PM:29228796</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Scand J Clin Lab Invest\20171222-DolgovaAS.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Scand J Clin Lab Invest\20171222-DolgovaAS.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Dolgova AS</style></custom2><misc3><style face="normal" font="default">10.1080/00365513.2017.1414955</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87223</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Codispoti,C.D.</style></author><author><style face="normal" font="default"> Tapke,D.E.</style></author><author><style face="normal" font="default"> LoSavio,P.S.</style></author><author><style face="normal" font="default"> Batra,P.S.</style></author><author><style face="normal" font="default"> Mahdavinia,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immunology and Microbiology, Allergy/Immunology Section, Rush University Medical Center, Chicago, Illinois.</style></auth-address><titles><title><style face="normal" font="default">Living in lower income zip codes is associated with more severe chronic rhinosinusitis</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">immunology</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.025</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29290514">PM:29290514</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-CodispoliCD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-CodispoliCD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Codispoti CD</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.025</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87224</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cianferoni,A.</style></author><author><style face="normal" font="default"> Ruffner,M.A.</style></author><author><style face="normal" font="default"> Guzek,R.</style></author><author><style face="normal" font="default"> Guan,S.</style></author><author><style face="normal" font="default"> Brown-Whitehorn,T.</style></author><author><style face="normal" font="default"> Muir,A.</style></author><author><style face="normal" font="default"> Spergel,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia</style></auth-address><titles><title><style face="normal" font="default">Elevated expression of activated TH2 cells and milk-specific TH2 cells in milk-induced eosinophilic esophagitis</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">BACKGROUND: Eosinophilic esophagitis (EoE) is an allergic inflammatory disease that is triggered by food allergens and characterized by progressive esophageal dysfunction. Esophageal biopsy specimens are characterized by eosinophilia and expression of TH2 cytokines. OBJECTIVE: To ascertain whether TH2 cells can exist in the peripheral blood in patients with milk-induced EoE. METHODS: Peripheral blood mononuclear cells from 20 children with milk-induced EoE were collected during active EoE (EoE-A) while consuming milk and inactive EoE (EoE-I) while not consuming milk, and 8 healthy patients without EoE were used as controls. The samples were analyzed for T-cell phenotype, including intracellular cytokines before and after incubation with milk antigens and assessed by flow cytometry. RESULTS: We found a significant increase in CD4(+) TH2 cells in the peripheral blood of patients with EoE-A compared with the controls. Furthermore, we observed a significant mean (SD) increase in the activation marker of CD154(+) T cells (0.17% [0.047(%])) in patients with EoE-A compared with control patients (0.034% [0.007%]) and EoE-I (0.025% [0.008]). These CD4(+) T cells expressed significantly increase levels of TH2 cytokines (interleukins 4, 5, and 13) compared with the EoE-I and control groups. CD3(+)CD4(+)CD154(+)IL-5(+) cells were significantly increased by milk antigens in both milk-induced EoE-A (0.050% [0.008%] to 0.079% [0.017%]) and EoE-I (0.0045% [0.002%] to 0.014% [0.008%]) compared with the controls (0.008% [0.003%] to 0.003% [0.001%]). CONCLUSION: Our findings indicate that in EoE peripheral T cells have specific activation to milk allergens</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.11.006</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29289462">PM:29289462</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-CianferoniA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-CianferoniA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Cianferoni A</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.11.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87225</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Caruso,C.</style></author><author><style face="normal" font="default"> Gencarelli,G.</style></author><author><style face="normal" font="default"> Gaeta,F.</style></author><author><style face="normal" font="default"> Valluzzi,R.L.</style></author><author><style face="normal" font="default"> Rumi,G.</style></author><author><style face="normal" font="default"> Romano,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit, Policlinico Agostino Gemelli Hospital, Rome, Italy.</style></auth-address><titles><title><style face="normal" font="default">Efficacy of omalizumab treatment in a man with occupational asthma and eosinophilic granulomatosis with polyangioitis</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.034</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29290513">PM:29290513</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-CarusoC.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-CarusoC.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Caruso C</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.034</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87226</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shreffler,W.G.</style></author><author><style face="normal" font="default"> Baumert,J.L.</style></author><author><style face="normal" font="default"> Remington,B.C.</style></author><author><style face="normal" font="default"> Koppelman,S.J.</style></author><author><style face="normal" font="default"> Dinakar,C.</style></author><author><style face="normal" font="default"> Fleischer,D.M.</style></author><author><style face="normal" font="default"> Kim,E.</style></author><author><style face="normal" font="default"> Tilles,S.A.</style></author><author><style face="normal" font="default"> Spergel,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Massachusetts General Hospital, Boston, Massachusetts</style></auth-address><titles><title><style face="normal" font="default">The importance of reducing risk in peanut allergy: Current and future therapies</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.038</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29289463">PM:29289463</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-ShrefflerWG.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\20180103-ShrefflerWG.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Shreffler WG</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.038</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87261</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xu,J.</style></author><author><style face="normal" font="default"> Gao,L.</style></author><author><style face="normal" font="default"> Yao,H.</style></author><author><style face="normal" font="default"> Zhang,R.</style></author><author><style face="normal" font="default"> Liu,N.</style></author><author><style face="normal" font="default"> Wang,L.</style></author><author><style face="normal" font="default"> Liu,E.</style></author><author><style face="normal" font="default"> Dai,J.</style></author><author><style face="normal" font="default"> Fu,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Pediatrics Research Institute , Ministry of Education Key Laboratory of Child Development and Disorders , Children's Hospital of Chongqing Medical University , Chongqing , China</style></auth-address><titles><title><style face="normal" font="default">Characteristics of lower airway inflammatory changes in the minimal persistent inflammation of allergic rhinitis in mice</style></title><secondary-title><style face="normal" font="default">J Asthma</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Asthma</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="26" Month="12" Year="2017">2017/12/26</year></dates><abstract><style face="normal" font="default">OBJECTIVE: This study aims to establish an experimental mouse model of minimal persistent inflammation (MPI), observe the features of inflammation and hyper-responsiveness of the upper/lower airways, and explore the relationship between inflammation and hyper-responsiveness in the upper/lower airways. METHODS: Sixty-four female BALB/c mice were randomly divided into four groups: allergic rhinitis (AR) group as positive control, MPI group, negative control group and blank control group. Mice were given high and low-concentrated ovalbumin solution after basic and intensive sensitization to establish AR model and MPI model. Nasal mucosa and lung tissues were stained to observe eosinophil infiltration, goblet cell hyperplasia, and expression of intercellular adhesion molecule 1 (ICAM-1). Airway hyper-responsiveness was assessed. Levels of specific immunoglobulin E (sIgE), interleukin (IL)-4 and IL-5 in peripheral blood, nasal lavage fluid (NLF), and bronchoalveolar lavage fluid (BALF) were detected by Enzyme-linked immunosorbent assay. RESULTS: The eosinophil infiltration and expression of ICAM-1 on nasal mucosa and in lung tissues in the AR and MPI groups were significantly elevated compared to control groups. Goblet cells count increased only in the nasal mucosa and not in lung tissues. Eosinophil and neutrophil count of NLF and BALF in the AR and MPI groups increased significantly compared to control groups. Level of IL-4 did not increase significantly, but sIgE and IL-5 did. CONCLUSIONS: Mice in the MPI status exhibits lower airway inflammation and hyper-responsiveness with increase in eosinophil count, goblet cells, ICAM-1, IL-4, and IL-5. These results provide further evidence for the importance of MPI of AR in lower airway diseases</style></abstract><notes><style face="normal" font="default">IS - 1532-4303 (Electronic)IS - 0277-0903 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1080/02770903.2017.1410831</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29278941">PM:29278941</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Asthma\20171226-XuJ.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Asthma\20171226-XuJ.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171226, Xu J</style></custom2><misc3><style face="normal" font="default">10.1080/02770903.2017.1410831</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87263</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Deckers,J.</style></author><author><style face="normal" font="default"> Bougarne,N.</style></author><author><style face="normal" font="default"> Mylka,V.</style></author><author><style face="normal" font="default"> Desmet,S.</style></author><author><style face="normal" font="default"> Luypaert,A.</style></author><author><style face="normal" font="default"> Devos,M.</style></author><author><style face="normal" font="default"> Tanghe,G.</style></author><author><style face="normal" font="default"> Van Moorleghem,J.</style></author><author><style face="normal" font="default"> Vanheerswynghels,M.</style></author><author><style face="normal" font="default"> De Cauwer,L.</style></author><author><style face="normal" font="default"> Thommis,J.</style></author><author><style face="normal" font="default"> Vuylsteke,M.</style></author><author><style face="normal" font="default"> Tavernier,J.</style></author><author><style face="normal" font="default"> Lambrecht,B.</style></author><author><style face="normal" font="default"> Hammad,H.</style></author><author><style face="normal" font="default"> De Bosscher,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Nuclear Receptor Lab; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium</style></auth-address><titles><title><style face="normal" font="default">Co-activation of GR and PPARgamma in murine skin prevents worsening of atopic march</style></title><secondary-title><style face="normal" font="default">J Invest Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Invest Dermatol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword></keywords><dates><year Day="27" Month="12" Year="2017">2017/12/27</year></dates><abstract><style face="normal" font="default">Children with atopic dermatitis (AD) show an increased risk to develop asthma later in life, a phenomenon referred to as 'atopic march', which emphasizes the need for secondary prevention therapies. This study aimed to investigate whether relief of skin inflammation by glucocorticoids and PPARgamma-agonists might influence the subsequent development of asthma in a murine model for the atopic march in which mice were repeatedly exposed to house dust mite (HDM) via the skin, followed by exposure to HDM in lungs. To abrogate AD, mice received topical treatment with GR/PPARgamma-agonists. Nuclear receptor ligand effects were assessed on primary keratinocytes and dendritic cells, as central players in skin inflammation. Prior HDM-induced skin inflammation aggravates allergic airway inflammation and induces a mixed Th2/Th17 response in the lungs. Cutaneous combined activation of GR/PPARgamma reduced skin inflammation to a higher extent compared to single activation. Additive anti-inflammatory effects were more prominent in dendritic cells, as compared to keratinocytes. Alleviation of allergic skin inflammation by activation of GR/PPARgamma appeared insufficient to avoid the allergic immune response in the lungs but efficiently reduced asthma severity by counteracting the Th17 response. GR/PPARgamma co-activation represents a potent remedy against allergic skin inflammation and worsening of the atopic march</style></abstract><notes><style face="normal" font="default">IS - 1523-1747 (Electronic)IS - 0022-202X (Linking)LA - engPT - Journal ArticleCO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1016/j.jid.2017.12.023</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288652">PM:29288652</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171227, Deckers J</style></custom2><misc3><style face="normal" font="default">10.1016/j.jid.2017.12.023</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87267</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dutra,M.S.</style></author><author><style face="normal" font="default"> Roncada,C.</style></author><author><style face="normal" font="default"> da Silva,G.L.</style></author><author><style face="normal" font="default"> Ferla,N.J.</style></author><author><style face="normal" font="default"> Pitrez,P.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pontifical Catholic University of Rio Grande do Sul (PUCRS), Infant Center, Institute for Biomedical Research (IPB), Porto Alegre, Brazil</style></auth-address><titles><title><style face="normal" font="default">Mite Fauna Assessment in Houses of Two distinct Socioeconomic Groups From Southern Brazil</style></title><secondary-title><style face="normal" font="default">J Med Entomol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Med Entomol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="21" Month="12" Year="2017">2017/12/21</year></dates><abstract><style face="normal" font="default">House dust mites (HDM) are the main source of aeroallergens worldwide, yet epidemiological differences between socioeconomic factors in association with this medical condition have not been studied in the south region of Brazil. To assess the prevalence of HDM in two socioeconomically distinct populations of patients with allergic asthma or rhinitis, the differences between samples from houses of high-income families and low-income families were analyzed. Mite samples were collected between July and December 2015, in Porto Alegre, Brazil. The HDM were Dermatophagoides pteronyssinus and Dermatophagoides farinae (Hughes; Acari: Pyroglyphidae). Also, other non-pyroglyphid house mites were identified in dust samples: Tyrophagus putrescentiae (Schrank; Acari: Acaridae), Chortoglyphus arcuatus, and Cheyletus malaccensis. Identification of species was performed through morphological keys with a stereomicroscope and a phase optical microscope. A total of 104 homes was evaluated (low-income group: n = 53; high-income group, n = 51). We found a total of 721 mites, representing 11 species, in 93 (89%) houses. In the remaining houses, no mites were found. We observed no significant differences of species composition between the groups studied. However, the number of mites was significantly higher in the low-income group (P &lt; 0.001). D. pteronyssinus was the predominant species detected, with 286 mites (39.6%). D. farinae was not detected in any sample. Our results show that living-rooms from low-income families present higher numbers of HDM</style></abstract><notes><style face="normal" font="default">IS - 1938-2928 (Electronic)IS - 0022-2585 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1093/jme/tjx239</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29281052">PM:29281052</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171221, Dutra MS</style></custom2><misc3><style face="normal" font="default">10.1093/jme/tjx239</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87269</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lewis,R.D.</style></author><author><style face="normal" font="default"> Ong,K.H.</style></author><author><style face="normal" font="default"> Emo,B.</style></author><author><style face="normal" font="default"> Kennedy,J.</style></author><author><style face="normal" font="default"> Kesavan,J.</style></author><author><style face="normal" font="default"> Elliot,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Saint Louis University College for Public Health and Social Justice , 3545 Lafayette, St. Louis , MO , 63104</style></auth-address><titles><title><style face="normal" font="default">Resuspension of house dust and allergens during walking and vacuum cleaning</style></title><secondary-title><style face="normal" font="default">J Occup Environ Hyg</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Occup Environ Hyg</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">Conventional wisdom has been that hard, resilient surfaces resuspend less particles than carpeted surfaces, however, exceptions to this have been demonstrated and uncertainty remains about the factors that lead to this resuspension, notably, the effect of vacuum cleaning on either increasing or reducing resuspension from flooring. The purpose of this study was to determine how resuspension of house dust by aerodynamic size or particle type, including cat allergen and bacterial endotoxin, is affected by flooring, dust loading, embedding dust, and walking/cleaning activities. House dust was blown in and allowed to settle in a walk in chamber after overnight deposition followed by walking or a vacuumcleaning procedure. Using an aerosol particle sizer and large-volume air samplers at different heights in the chamber, concentrations of airborne particles, resuspension rates, and fractions were computed for four types of flooringconditions during six walking activities. Carpeting resulted in significantly more airborne cat allergen and airborne endotoxin than a laminate floor. Height does have an effect on measured allergen over carpet and this is apparent with concentrations at the infant and adult air samplers. Walking on laminate flooring resuspends less house dust than walking on an equally dusty carpeted floor, where dust is entirely on the surface of the carpet. However, vacuum cleaning a laminate floor resuspended more dust than vacuum cleaning carpets, at large particle sizes, 5 microm and 10 microm. Activities following a deep cleaning of hard resilient or a carpeted surface is likely to leave no differences in resuspended particles between them</style></abstract><notes><style face="normal" font="default">IS - 1545-9632 (Electronic)IS - 1545-9624 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1080/15459624.2017.1415438</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29283321">PM:29283321</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171228, Lewis RD</style></custom2><misc3><style face="normal" font="default">10.1080/15459624.2017.1415438</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87271</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tu,M.</style></author><author><style face="normal" font="default"> Liu,H.</style></author><author><style face="normal" font="default"> Chen,H.</style></author><author><style face="normal" font="default"> Fan,F.</style></author><author><style face="normal" font="default"> Shi,P.</style></author><author><style face="normal" font="default"> Xu,X.</style></author><author><style face="normal" font="default"> Lu,W.</style></author><author><style face="normal" font="default"> Du,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Food Science and Engineering, School of Chemistry and Chemical Engineering, Harbin Institute of Technology, Harbin, 150001, China</style></auth-address><titles><title><style face="normal" font="default">Bioactive hydrolysates from casein: Generation, identification, and in silico toxicity and allergenicity prediction of peptides</style></title><secondary-title><style face="normal" font="default">J Sci Food Agric</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Sci Food Agric</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> Hydrolysis</style></keyword><keyword><style face="normal" font="default"> Prediction</style></keyword></keywords><dates><year Day="27" Month="12" Year="2017">2017/12/27</year></dates><abstract><style face="normal" font="default">BACKGROUND: Bioactive casein peptides have attracted considerable attention for their applications in industry. However, there is little clarity regarding mass spectrometric profiles for peptides in enzymatic hydrolysates of casein produced under varying conditions. In this study, the compositions of the peptides from casein hydrolysates were compared for different E/S and hydrolysis times. The toxicity, allergenicity and bioactivity of the identified peptides were assessed in silico. RESULTS: A total of 70 unique peptides were identified, and there were 28, 21, 13 and 8 peptides from alphas1 -casein, alphas2 -casein, beta-casein and kappa-casein, respectively. The peptide number decreased with the increase in E/S and hydrolysis time. Moreover, peptides with molecular mass (Mr.) ranging from 1000 to 1500 Da occupied the highest proportion of 31.43%, and almost all of the peptides showed relative Mr. less than 5000 Da. In silico analysis showed that all of the peptides were non-toxic and non-allergenic, and several of them were assessed by PeptideRanker as having a relatively high likelihood of being bioactive peptides. CONCLUSIONS: Composition of the peptides in the casein hydrolysates varied with the enzymolysis conditions. This study's results may facilitate the production of target bioactive peptides by controlling E/S and hydrolysis time, which is beneficial for the application of casein peptides in the functional food industry</style></abstract><notes><style face="normal" font="default">IS - 1097-0010 (Electronic)IS - 0022-5142 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1002/jsfa.8854</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29280148">PM:29280148</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Sci Food Agric\20171227-TuM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Sci Food Agric\20171227-TuM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Tu M</style></custom2><misc3><style face="normal" font="default">10.1002/jsfa.8854</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87278</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Elaidy,S.M.</style></author><author><style face="normal" font="default"> Essawy,S.S.</style></author><author><style face="normal" font="default"> Hussain,M.A.</style></author><author><style face="normal" font="default"> El-Kherbetawy,M.K.</style></author><author><style face="normal" font="default"> Hamed,E.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Clinical Pharmacology, Faculty of Medicine, Suez Canal University, Ismailia, 41522, Egypt.</style></auth-address><titles><title><style face="normal" font="default">Modulation of the IL-23/IL-17 axis by fenofibrate ameliorates the ovalbumin/lipopolysaccharide-induced airway inflammation and bronchial asthma in rats</style></title><secondary-title><style face="normal" font="default">Naunyn Schmiedebergs Arch Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Naunyn Schmiedebergs Arch Pharmacol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="30" Month="12" Year="2017">2017/12/30</year></dates><abstract><style face="normal" font="default">The overlapping between asthmatic subtypes, including both CD4+ T helper (TH)2 and TH17 cells, is found in the natural course of allergic asthma, especially in exacerbations and severe and insensitive forms to steroids, which are in need of new molecular therapies. In the TH2-subset mediated asthma, fenofibrate displays therapeutic promises, besides evidenced therapeutic effects on TH17-mediated colitis and myocarditis. Therefore, the effects of fenofibrate versus dexamethasone on IL-23/IL-17 axis in ovalbumin (OVA)/lipopolysaccharide (LPS)-induced airway inflammation and bronchial asthma in rats were explored. The OVA/LPS sensitization and challenge were performed for 28 days in male Wistar rats. After sensitization, fenofibrate (100 mg/kg/day) or dexamethasone (2.5 mg/kg/day) was orally administered from the day 15 to 28. Either fenofibrate or dexamethasone attenuated the severity of OVA/LPS-induced airway inflammation and bronchial asthma through significant ameliorations in the total serum immunoglobulin (Ig)E assay; the total and differential leukocytic counts in the bronchoalveolar lavage (BAL) fluid; the lung inflammatory cytokines such as interleukin (IL)-4, IL-13, IL-17, and IL-23, transforming growth factor (TGF)-beta1, and tumor necrosis factor(TNF)-alpha levels; and the lung IL-17 and IL-23 expressions. In addition to the reduction in the inflammatory and fibrotic histopathological scores, fenofibrate significantly ameliorated the BAL neutrophilic count and the lung IL-17 and IL-23 expressions in comparison to dexamethasone. The suppression of IL-23/IL-17 axis could be considered a molecular therapeutic target for fenofibrate in OVA/LPS-induced airway inflammation and bronchial asthma. Combined therapeutic regimens of fenofibrate and steroids should be furtherly investigated in severe and resistant asthma</style></abstract><notes><style face="normal" font="default">IS - 1432-1912 (Electronic)IS - 0028-1298 (Linking)LA - engPT - Journal ArticleCO - Egypt -</style></notes><work-type><style face="normal" font="default">10.1007/s00210-017-1459-z</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288381">PM:29288381</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Naunyn Schmiedebergs Arch Pharmacol\20171230-ElaidySM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Naunyn Schmiedebergs Arch Pharmacol\20171230-ElaidySM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171230, Elaidy SM</style></custom2><misc3><style face="normal" font="default">10.1007/s00210-017-1459-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87289</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bidder,T.</style></author><author><style face="normal" font="default"> Sahota,J.</style></author><author><style face="normal" font="default"> Rennie,C.</style></author><author><style face="normal" font="default"> Lund,V.J.</style></author><author><style face="normal" font="default"> Robinson,D.S.</style></author><author><style face="normal" font="default"> Kariyawasam,H.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Thoracic Medicine, University College London Hospital NHS Foundation Trust, London, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Omalizumab treats chronic rhinosinusitis with nasal polyps and asthma together-a real life study</style></title><secondary-title><style face="normal" font="default">Rhinology</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rhinology</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="30" Month="12" Year="2017">2017/12/30</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Chronic rhinosinusitis with nasal polyps (CRSwNP) and asthma often coexist and thus treating both with one intervention is an attractive strategy. OBJECTIVE: To prospectively evaluate whether treatment with the monoclonal antibody against IgE Omalizumab for severe allergic asthma also effectively treats co-existent CRSwNP. METHODS: SNOT-22 and the ACQ-7 scores were recorded at 4 and 16 weeks of treatment in a cohort of patients with both CRSwNP and severe refractory allergic asthma treated with Omalizumab (n=13) according to UK guidelines for their severe asthma. SNOT-22 in a surgery only treated CRSwNP with asthma group (n=24) was compared. RESULTS: Rapid improvement was seen at 4 weeks and 16 weeks of treatment in both CRSwNP and asthma control. The improvement in CRSwNP with Omalizumab was similar to that seen in a group of patients who received upper airway surgery. CONCLUSION: Omalizumab treatment for severe allergic asthma also improves co-existent CRSwNP. Further clinical studies of current and emerging biological agents for severe asthma should include upper airway outcomes. These agents may be effective for severe CRSwNP and comparative studies with surgery are warranted</style></abstract><notes><style face="normal" font="default">IS - 0300-0729 (Print)IS - 0300-0729 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.4193/Rhin17.139</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288573">PM:29288573</url></web-urls><related-urls><url ppv-ref="no">presto - MedLine</url></related-urls></urls><custom2><style face="normal" font="default">20171230, Bidder T</style></custom2><misc3><style face="normal" font="default">10.4193/Rhin17.139</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87399</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Canavan,M.</style></author><author><style face="normal" font="default"> Mitchell,A.</style></author><author><style face="normal" font="default"> Sharkey,A.</style></author><author><style face="normal" font="default"> Whitethorn,C.</style></author><author><style face="normal" font="default"> McNicholl,B.</style></author><author><style face="normal" font="default"> Robinson,S.</style></author><author><style face="normal" font="default"> Ni,Riain U.</style></author><author><style face="normal" font="default"> Tormey,V.</style></author><author><style face="normal" font="default"> Mulkerrin,E.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Emergency Medicine, Galway University Hospitals, Galway, Ireland</style></auth-address><titles><title><style face="normal" font="default">Oral Mite Anaphylaxis</style></title><secondary-title><style face="normal" font="default">QJM</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">QJM</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Emergency medicine</style></keyword></keywords><dates><year Day="22" Month="12" Year="2017">2017/12/22</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1460-2393 (Electronic)IS - 1460-2393 (Linking)LA - engPT - Journal ArticleCO - Ireland -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1093/qjmed/hcx255</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29309668">PM:29309668</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\QJM\20171222-CanavanM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\QJM\20171222-CanavanM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Canavan M</style></custom2><misc3><style face="normal" font="default">10.1093/qjmed/hcx255</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87479</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Leffler,J.</style></author><author><style face="normal" font="default"> Mincham,K.T.</style></author><author><style face="normal" font="default"> Mok,D.</style></author><author><style face="normal" font="default"> Blank,F.</style></author><author><style face="normal" font="default"> Holt,P.G.</style></author><author><style face="normal" font="default"> Stumbles,P.A.</style></author><author><style face="normal" font="default"> Strickland,D.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Telethon Kids Institute, The University of Western Australia, WA, Australia</style></auth-address><titles><title><style face="normal" font="default">Functional differences in airway dendritic cells determine susceptibility to IgE-sensitisation</style></title><secondary-title><style face="normal" font="default">Immunol Cell Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Cell Biol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword></keywords><dates><year Day="30" Month="12" Year="2017">2017/12/30</year></dates><abstract><style face="normal" font="default">Respiratory IgE-sensitisation to innocuous antigens increases the risk for developing diseases such as allergic asthma. Dendritic cells (DC) residing in the airways orchestrate the immune response following antigen exposure and their ability to sample and present antigens to naive T cells in airway draining lymph nodes contributes to allergen-specific IgE-sensitisation. In order to characterise inhaled antigen capture and presentation by DC subtypes in vivo, we used an adjuvant-free respiratory sensitisation model using two genetically distinct rat strains, one of which is naturally resistant and the other naturally susceptible to allergic sensitisation. Upon multiple exposures to ovalbumin (OVA), the susceptible strain developed OVA-specific IgE and airway inflammation whereas the resistant strain did not. Using fluorescently tagged OVA and flow cytometry, we demonstrated significant differences in antigen uptake efficiency and presentation associated with either IgE-sensitisation or resistance to allergen exposures in respective strains. We further identified CD4(+) conventional DC (cDC) as the subset involved in airway antigen sampling in both strains, however CD4(+) cDC in the susceptible strain were less efficient in OVA sampling and displayed increased MHC-II expression compared to the resistant strain. This was associated with generation of an exaggerated Th2 response and a deficiency of airway regulatory T cells in the susceptible strain. These data suggest that subsets of cDC are able to induce either sensitisation or resistance to inhaled antigens as determined by genetic background, which may provide an underlying basis for genetically determined susceptibility to respiratory allergic sensitisation and IgE production in susceptible individuals. This article is protected by copyright. All rights reserved</style></abstract><notes><style face="normal" font="default">IS - 1440-1711 (Electronic)IS - 0818-9641 (Linking)LA - engPT - Journal ArticleCO - Australia -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1111/imcb.12005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29363184">PM:29363184</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171230, Leffler J</style></custom2><misc3><style face="normal" font="default">10.1111/imcb.12005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87480</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mussarat,A.</style></author><author><style face="normal" font="default"> Manohar,M.</style></author><author><style face="normal" font="default"> Verma,A.K.</style></author><author><style face="normal" font="default"> Upparahalli,V.S.</style></author><author><style face="normal" font="default"> Zaidi,A.</style></author><author><style face="normal" font="default"> Sanders,N.L.</style></author><author><style face="normal" font="default"> Zhu,X.</style></author><author><style face="normal" font="default"> Mishra,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, Tulane University School of Medicine, New Orleans, LA, 70112, USA</style></auth-address><titles><title><style face="normal" font="default">Intestinal overexpression of interleukin (IL)-15 promotes tissue eosinophilia and goblet cell hyperplasia</style></title><secondary-title><style face="normal" font="default">Immunol Cell Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Cell Biol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">Interleukin (IL)-15 overexpression in eosinophilic gastrointestinal disorders is reported, but IL-15's role in promoting eosinophilic gastroenteritis is largely unknown. Therefore, we generated enterocyte-overexpressed IL-15 transgenic mice using Fabpi promoter. The Fabpi-IL-15 (iIL-15) transgenic mice showed induced IL-15 levels in the jejunum with a marked increase in jejunum eosinophils. However, no induction of eosinophilia in the blood or any other gastrointestinal segment was observed. Eosinophilia in the jejunum villus was substantially higher in iIL-15 mice compared to wild-type mice. In addition, goblet cell hyperplasia was also observed in the jejunum of iIL-15 mice. Furthermore, a significant correlation between induced IL-15 transcript and the IL-18 transcripts was observed. Therefore, to further understand the role of IL-18 in IL-15 mice associated gastrointestinal disorders, we generated iIL-15/IL-18Ralpha(-/-) mice. Using these mice, we found that IL-18 has an important role in promoting IL-15-induced eosinophilia. As intestinal IL-15 overexpression is reported in food intolerance, we examined OVA intolerance in iIL-15 mice. The OVA-sensitized and challenged iIL-15 mice experienced weight loss, diarrhea and eosinophilia in the jejunum. Taken together, our findings demonstrate that intestinal IL-15 overexpression induces IL-18-dependent eosinophilia and immunoglobulins in the intestine that promotes food allergic responses</style></abstract><notes><style face="normal" font="default">IS - 1440-1711 (Electronic)IS - 0818-9641 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1111/imcb.1036</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29363170">PM:29363170</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171227, Mussarat A</style></custom2><misc3><style face="normal" font="default">10.1111/imcb.1036</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87481</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dubey,A.</style></author><author><style face="normal" font="default"> Izakelian,L.</style></author><author><style face="normal" font="default"> Ayaub,E.A.</style></author><author><style face="normal" font="default"> Ho,L.</style></author><author><style face="normal" font="default"> Stephenson,K.</style></author><author><style face="normal" font="default"> Wong,S.</style></author><author><style face="normal" font="default"> Kwofie,K.</style></author><author><style face="normal" font="default"> Austin,R.C.</style></author><author><style face="normal" font="default"> Botelho,F.</style></author><author><style face="normal" font="default"> Ask,K.</style></author><author><style face="normal" font="default"> Richards,C.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">McMaster Immunology Research Centre, McMaster University, Hamilton, Ontario, Canada</style></auth-address><titles><title><style face="normal" font="default">Separate roles of IL-6 and oncostatin M in mouse macrophage polarization in vitro and in vivo</style></title><secondary-title><style face="normal" font="default">Immunol Cell Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunol Cell Biol</style></abbr-1></periodical><pages end="" start="">-</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">Arginase-1 (Arg-1)-expressing M2-like macrophages are associated with Th2-skewed immune responses, allergic airway pathology, ectopic B16 melanoma cancer growth in murine models, and can be induced by Oncostatin M (OSM) transient overexpression in vivo. Here, we compare OSM to the gp130-cytokine IL-6 in mediating macrophage polarization, and find that IL-6 overexpression alone (Ad vector, AdIL-6) did not induce Arg-1 protein in mouse lungs at day 7, nor ectopic melanoma tumor growth at day 14, in contrast to overexpression of OSM (AdOSM). AdOSM elevated levels of IL-4, IL-5 and IL-13 in bronchoalveolar lavage fluid, whereas AdIL-6 did not. Bone marrow-derived macrophages respond with Arg-1 enzymatic activity to M2 stimuli (IL-4/IL-13), which was further elevated in combination with IL-6 stimulation; however, OSM or LIF had no detectable activity in vitro. Arg-1 mRNA expression induced by AdOSM was attenuated in IL-6-/- and STAT6-/- mice, suggesting requirements for both IL-6 and IL-4/IL-13 signaling in vivo. Ectopic B16 tumor burden was also reduced in IL-6-/- mice. Thus, OSM induces Arg-1+ macrophage accumulation indirectly through elevation of Th2 cytokines and IL-6 in vivo, whereas IL-6 acts directly on macrophages but requires a Th2 microenvironment, demonstrating distinct roles for OSM and IL-6 in M2 macrophage polarization</style></abstract><notes><style face="normal" font="default">IS - 1440-1711 (Electronic)IS - 0818-9641 (Linking)LA - engPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1111/imcb.1035</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29363180">PM:29363180</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171227, Dubey A</style></custom2><misc3><style face="normal" font="default">10.1111/imcb.1035</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86544</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Patel,D.S.</style></author><author><style face="normal" font="default"> Arunakirinathan,M.</style></author><author><style face="normal" font="default"> Stuart,A.</style></author><author><style face="normal" font="default"> Angunawela,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">Allergic eye disease</style></title><secondary-title><style face="normal" font="default">BMJ</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">BMJ</style></full-title></periodical><pages end="" start=" j4706"> j4706-</pages><volume><style face="normal" font="default">359</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">What you need to knowAllergic eye disease is usually bilateral and itching is the predominant symptomUncomplicated disease can be managed in primary care with one or more of cold compresses, lubricants, topical and/or oral antihistamines, and topical mast cell stabilisersTopical and oral steroids and immunomodulatory agents should be prescribed only under the care of an ophthalmologist in refractory casesAllergic eye diseases include conjunctivitis and occasionally keratitis in response to an allergen. The diseases affect 10%-20% of people globally12 and have a negative impact on quality of life and productivity.3456Early diagnosis and appropriate treatment is essential to reduce the frequency of relapses, to avoid complications that are potentially sight threatening, and to enhance patient self care. This article provides guidance on recognising the different forms of allergic eye disease and on their management.Children and adolescents are more commonly affected by atopic disease in general, which tends to diminish with age. People with asthma, eczema, and rhinitis often experience concurrent ocular allergy.7 Europe, North America, and Japan report higher prevalence than developing countries.1How do they present?Itching is the hallmark of allergic eye disease, which is accompanied by redness and watering of the eyes (fig 1</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">çô). Symptoms may occur in acute episodes which are generally recurrent or may be persistent in a chronic form.Fig 1-áSeasonal allergic conjunctivitis presenting acutely, with conjunctival redness and swelling (chemosis). Note that the cornea is clear, with no signs of keratitisWhat are the different types of allergic eye disease?Table 1</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">çô summarises the different types.View this table:In this windowIn a new windowTable 1 Clinical presentation and features of allergic eye disease subtypesCommon allergic eye diseasesSeasonal and perennial allergic conjunctivitis are the commonest forms of allergic eye disease and are associated with childhood atopy. Seasonal conjunctivitis is triggered by pollen and frequently occurs in spring and summer. It is often associated with nasal symptoms (rhinoconjunctivitis).Perennial </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çª</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1136/bmj.j4706</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1136/bmj.j4706</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMJ\2017-359- j4706.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMJ\2017-359- j4706.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Patel DS</style></custom2><misc3><style face="normal" font="default">10.1136/bmj.j4706</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86870</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Menzel,M.</style></author><author><style face="normal" font="default"> Akbarshahi,H.</style></author><author><style face="normal" font="default"> Mahmutovic,P.I.</style></author><author><style face="normal" font="default"> Puthia,M.</style></author><author><style face="normal" font="default"> Bjermer,L.</style></author><author><style face="normal" font="default"> Uller,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Respiratory Immunopharmacology, Dept of Experimental Medical Science, Lund University, Lund, Sweden</style></auth-address><titles><title><style face="normal" font="default">Caspase-1 deficiency reduces eosinophilia and interleukin-33 in an asthma exacerbation model</style></title><secondary-title><style face="normal" font="default">ERJ Open Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">ERJ Open Res</style></abbr-1></periodical><pages end="" start="00047-2017">00047-2017-</pages><volume><style face="normal" font="default">3</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">Rhinovirus infections are common triggers of asthma exacerbations. Viruses can activate the inflammasome, resulting in processing and activation of caspase-1. This recruitment triggers production of interleukin (IL)-1beta and IL-18, which have been implicated in asthma. Elucidating the involvement of the inflammasome and its compartments, such as caspase-1, in asthma exacerbations is warranted. Gene expression of caspase-1 was measured in rhinovirus-infected primary bronchial epithelial cells of asthmatic and healthy donors 24 h post-infection. In an in vivo exacerbation experiment C57BL/6 wild-type and caspase-1(-/-) mice were challenged with house dust mite followed by exposures to the viral mimic poly(I:C). General lung inflammatory parameters and levels of T-helper type 2 (Th2)-upstream cytokines IL-33, thymic stromal lymphopoietin (TSLP) and IL-25 were assessed. Caspase-1 expression was elevated after rhinoviral infection exclusively in bronchial epithelial cells from asthmatics. In a translational mouse model of asthma exacerbation effects of caspase-1 on airway inflammation and Th2-upstream cytokines were explored. Caspase-1 deficient mice exhibited no alterations of general lung inflammatory parameters, but showed markedly reduced eosinophilia. Furthermore, the Th2-upstream cytokines IL-33, TSLP and IL-25 were reduced at exacerbation in mice lacking caspase-1. Rhinovirus infection increases bronchial epithelial caspase-1 in asthma. Caspase-1 may induce production of lung Th2-upstream cytokines and eosinophilia at exacerbations. Further targeting of caspase-1 signalling is warranted to explore its role in asthma exacerbations</style></abstract><notes><style face="normal" font="default">IS - 2312-0541 (Print)IS - 2312-0541 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1183/23120541.00047-2017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29204432">PM:29204432</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\ERJ Open Res\2017-3-00047-2017.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\ERJ Open Res\2017-3-00047-2017.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171016, Menzel M</style></custom2><misc3><style face="normal" font="default">10.1183/23120541.00047-2017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86869</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gona-Hopler,M.</style></author><author><style face="normal" font="default"> Pfaller,B.</style></author><author><style face="normal" font="default"> Argeny,J.</style></author><author><style face="normal" font="default"> Kanolzer,S.</style></author><author><style face="normal" font="default"> Gruber,S.</style></author><author><style face="normal" font="default"> Schmidthaler,K.</style></author><author><style face="normal" font="default"> Renner,S.</style></author><author><style face="normal" font="default"> Nachbaur,E.</style></author><author><style face="normal" font="default"> Fucik,P.</style></author><author><style face="normal" font="default"> Glaser,A.G.</style></author><author><style face="normal" font="default"> Debiasi,M.</style></author><author><style face="normal" font="default"> Szepfalusi,Z.</style></author><author><style face="normal" font="default"> Crameri,R.</style></author><author><style face="normal" font="default"> Rhyner,C.</style></author><author><style face="normal" font="default"> Eiwegger,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dept of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Aspergillus fumigatus-specific immunoglobulin levels in BALF of CF patients</style></title><secondary-title><style face="normal" font="default">ERJ Open Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">ERJ Open Res</style></abbr-1></periodical><pages end="" start="00067-2017">00067-2017-</pages><volume><style face="normal" font="default">3</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Cystic fibrosis</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">IgE responses to Aspergillus fumigatus in cystic fibrosis lungs http://ow.ly/XXwv30furqs</style></abstract><notes><style face="normal" font="default">IS - 2312-0541 (Print)IS - 2312-0541 (Linking)LA - engPT - Journal ArticleCO - Austria -CO - Canada -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1183/23120541.00067-2017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29164145">PM:29164145</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\ERJ Open Res\2017-3-00067-2017.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\ERJ Open Res\2017-3-00067-2017.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Gona-Hopler M</style></custom2><misc3><style face="normal" font="default">10.1183/23120541.00067-2017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86592</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fletcher,E.A.K.</style></author><author><style face="normal" font="default"> Eltahir,M.</style></author><author><style face="normal" font="default"> Lindqvist,F.</style></author><author><style face="normal" font="default"> Rieth,J.</style></author><author><style face="normal" font="default"> Tornqvist,G.</style></author><author><style face="normal" font="default"> Leja-Jarblad,J.</style></author><author><style face="normal" font="default"> Mangsbo,S.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immuneed AB, Dag Hammarskjolds vag 13a, Uppsala, Sweden; Department of Immunology Genetics and Pathology, Science for Life Laboratory, Uppsala University, Rudbeck Laboratory C11 Floor 2, Dag Hammarskjoldsvag 20, 751 85 Uppsala, Sweden</style></auth-address><titles><title><style face="normal" font="default">Extracorporeal human whole blood in motion, as a tool to predict first-infusion reactions and mechanism-of-action of immunotherapeutics</style></title><secondary-title><style face="normal" font="default">Int Immunopharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Immunopharmacol</style></abbr-1></periodical><pages end="11" start="1">1-11</pages><volume><style face="normal" font="default">54</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">First infusion reactions along with severe anaphylactic responses can occur as a result of systemic administration of therapeutic antibodies. The underlying mechanisms by which monoclonal antibodies induce cytokine release syndrome (CRS) can involve direct agonistic effects via the drug target, or a combination of target-engagement along with innate receptor interactions. Despite the wide variety of pathways and cells that can play a role in CRS, many currently used assays are devoid of one or more components that must be present for these responses to occur. One assay that has not been assessed for its capacity to predict CRS is the modified Chandler loop model. Herein we evaluate a plethora of commercially available monoclonal antibodies to evaluate the modified Chandler loop model's potential in CRS prediction. We demonstrate that in a 4-hour loop assay, both the superagonistic antibodies, anti-CD3 (OKT3) and anti-CD28 (ANC28.1), display a clear cytokine response with a mixed adaptive/innate cytokine source. OKT3 induce TNFalpha and IFN-gamma release in 20 out of 23 donors tested, whereas ANC28.1 induce TNF-alpha, IL-2 and IFN-gamma release in all donors tested (n=18-22). On the other hand, non-agonistic antibodies associated with no or low infusion reactions in the clinic, namely cetuximab and natalizumab, neither induce cytokine release nor cause false positive responses. A TGN1412-like antibody also display a clear cytokine release with an adaptive cytokine profile (IFN-gamma and IL-2) and all donors (n=9) induce a distinct IL-2 response. Additionally, the value of an intact complement system in the assay is highlighted by the possibility to dissect out the mechanism-of-action of alemtuzumab and rituximab. The loop assay can either complement lymph node-like assays or stand-alone to investigate drug/blood interactions during preclinical development, or for individual safety screening prior to first-in-man clinical trial</style></abstract><notes><style face="normal" font="default">DA - 20171103IS - 1878-1705 (Electronic)IS - 1567-5769 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1016/j.intimp.2017.10.021</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29100032">PM:29100032</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Immunopharmacol\2017-54-1-11.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Immunopharmacol\2017-54-1-11.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171103, Fletcher EA</style></custom2><misc3><style face="normal" font="default">10.1016/j.intimp.2017.10.021</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86683</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vangipuram,R.</style></author><author><style face="normal" font="default"> Tyring,S.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Medicine, Department of Dermatology, The University of Texas Medical Branch, Galveston, TX, USA</style></auth-address><titles><title><style face="normal" font="default">Dupilumab for Moderate-to-Severe Atopic Dermatitis</style></title><secondary-title><style face="normal" font="default">Skin Therapy Lett</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Skin Therapy Lett</style></abbr-1></periodical><pages end="4" start="1">1-4</pages><volume><style face="normal" font="default">22</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Atopic dermatitis (AD) is the most common chronic inflammatory disease affecting 2-10% of adults and up to 15-30% of children. Despite a rising prevalence, effective and safe therapeutics for patients with moderate-to-severe AD are limited due to toxicity and side effects. Dupilumab, an interleukin (IL)-4 and IL-13 antagonist that limits type 2 T helper (Th2) driven inflammatory activity, is a promising therapeutic option. In clinical trials, it has demonstrated efficacy by reducing clinical activity and symptoms, and showed improvement in the AD genomic phenotype, including a significant reduction in Th2 chemokines and reversal of key epidermal markers of AD. It also has a favorable safety profile. This review discusses the role of dupilumab in treating Th2 related inflammation, and its efficacy and safety, as demonstrated in clinical trials. Dupilumab (Dupixent(R)) recently gained US FDA approval for patients with moderate-to-severe AD, and is poised to revolutionize the management of this chronic, relapsing condition</style></abstract><notes><style face="normal" font="default">DA - 20171101IS - 1201-5989 (Print)IS - 1201-5989 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29091379">PM:29091379</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Skin Therapy Lett\2017-22-1-4.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Skin Therapy Lett\2017-22-1-4.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171101, Vangipuram R</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86942</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Aquili,A.</style></author><author><style face="normal" font="default"> Farinelli,L.</style></author><author><style face="normal" font="default"> Bottegoni,C.</style></author><author><style face="normal" font="default"> Antonicelli,L.</style></author><author><style face="normal" font="default"> Gigante,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical Orthopaedics, Universita Politecnica delle Marche, Ancona, Italy</style></auth-address><titles><title><style face="normal" font="default">The effect of anti-IgE therapy in knee osteoarthritis: a pilot observational study</style></title><secondary-title><style face="normal" font="default">J Biol Regul Homeost Agents</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Biol Regul Homeost Agents</style></abbr-1></periodical><pages end="5" start="1">1-5</pages><volume><style face="normal" font="default">31</style></volume><number><style face="normal" font="default">4 Suppl. 1</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">Osteoarthritis is a whole-joint disease and its pathogenesis remains poorly understood. Recent evidence proposed the importance of the innate immune system as trigger of synovium inflammation following the degeneration of cartilage. Moreover, synovial mast cells (MCs) might be correlated with pain and disability reported by patients. Anti IgE therapy represents a new class of MCs stabilizing agent, licensed for people with asthma and chronic urticaria. Therefore, we studied if the stabilizing effect of anti IgE would improve the pain and disability in patients affected by knee osteoarthritis and atopic disease. This pilot study provides the first evidence that anti IgE treatment induces a short-term clinical improvement supporting the role of MCs in osteoarthritis</style></abstract><notes><style face="normal" font="default">IS - 0393-974X (Print)IS - 0393-974X (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29172299">PM:29172299</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171204, Aquili A</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87019</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bernard,A.</style></author><author><style face="normal" font="default"> Lheureux,F.</style></author><author><style face="normal" font="default"> Dirlewanger,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Walnut: past and future of genetic improvement</style></title><secondary-title><style face="normal" font="default">Tree Genet Genom</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Tree Genet Genom</style></full-title></periodical><pages end="" start="1">1-</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> ASIA</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1614-2950</style></isbn><abstract><style face="normal" font="default">Persian or English walnut (Juglans regia L.), the walnut species cultivated for nut production, is one of the oldest food sources known. Persian walnuts, native to the mountain valleys of Central Asia, are grown worldwide in temperate areas. World production exceeds three million tons since 2012, mostly provided by China, the USA, and Iran. Despite very ancient culture of walnut species (Juglans spp.), breeding actually started in the twentieth century. Using a range of methodologies, from morphological markers to the most recent advances in genome analysis, many genetic studies of walnut have been conducted during the past 30-áyears, including examination of diversity, determination of relationships within or among germplasm collections and populations, phylogenetic and origin elucidation, genetic map construction, and biotic or abiotic stress investigations. The genetic improvement of walnut has undergone great evolution. The producing countries of the Middle East have widely studied morphological characteristics of walnut. The USA and France, for example, are behind important cultivar releases such as </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Chandler</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ and </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Franquette.</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ Finally, genomics represents a major breakthrough in walnut improvement, in particular by recent sequencing of both chloroplast and nuclear genomes. This review summarizes worldwide molecular and </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£omics</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ studies and gives an overview of the main walnut breeding programs</style></abstract><notes><style face="normal" font="default">LA - ENGCO - France -</style></notes><work-type><style face="normal" font="default">10.1007/s11295-017-1214-0</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s11295-017-1214-0</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Tree Genet Genom\20171203-BernardA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Tree Genet Genom\20171203-BernardA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Bernard A</style></custom2><misc3><style face="normal" font="default">10.1007/s11295-017-1214-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86945</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Clark,S.</style></author><author><style face="normal" font="default"> Mora Garcia,M.B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Food Science and Human Nutrition, Iowa State University, Ames 50011-0152.</style></auth-address><titles><title><style face="normal" font="default">A 100-Year Review: Advances in goat milk research</style></title><secondary-title><style face="normal" font="default">J Dairy Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Dairy Sci</style></abbr-1></periodical><pages end="10044" start="10026">10026-10044</pages><volume><style face="normal" font="default">100</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Enzymes</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">In the century of research chronicled between 1917 and 2017, dairy goats have gone from simply serving as surrogates to cows to serving as transgenic carriers of human enzymes. Goat milk has been an important part of human nutrition for millennia, in part because of the greater similarity of goat milk to human milk, softer curd formation, higher proportion of small milk fat globules, and different allergenic properties compared with cow milk; however, key nutritional deficiencies limit its suitability for infants. Great attention has been given not only to protein differences between goat and cow milk, but also to fat and enzyme differences, and their effect on the physical and sensory properties of goat milk and milk products. Physiological differences between the species necessitate different techniques for analysis of somatic cell counts, which are naturally higher in goat milk. The high value of goat milk throughout the world has generated a need for a variety of techniques to detect adulteration of goat milk products with cow milk. Advances in all of these areas have been largely documented in the Journal of Dairy Science (JDS), and this review summarizes such advances</style></abstract><notes><style face="normal" font="default">IS - 1525-3198 (Electronic)IS - 0022-0302 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.3168/jds.2017-13287</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29153153">PM:29153153</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Dairy Sci\2017-100-10026-44.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Dairy Sci\2017-100-10026-44.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171130, Clark S</style></custom2><misc3><style face="normal" font="default">10.3168/jds.2017-13287</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87339</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kitaoka,M.</style></author><author><style face="normal" font="default"> Naritomi,A.</style></author><author><style face="normal" font="default"> Kawabe,Y.</style></author><author><style face="normal" font="default"> Kamihira,M.</style></author><author><style face="normal" font="default"> Kamiya,N.</style></author><author><style face="normal" font="default"> Goto,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dept. of Applied ChemistryKyushu University744 Moto-okaFukuoka819-0395Japan</style></auth-address><titles><title><style face="normal" font="default">Transcutaneous pollinosis immunotherapy using a solid-in-oil nanodispersion system carrying T cell epitope peptide and R848</style></title><secondary-title><style face="normal" font="default">Bioeng Transl Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Bioeng Transl Med</style></abbr-1></periodical><pages end="108" start="102">102-108</pages><volume><style face="normal" font="default">2</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="3" Year="2017">2017/3</year></dates><abstract><style face="normal" font="default">Antigen-specific immunotherapy is the only curative approach for the treatment of allergic diseases such as Japanese cedar pollinosis. Immunotherapy using a T cell epitope vaccine in combination with the adjuvant R848 is of particular interest as a safe and effective approach to treat allergic diseases. Herein, we propose a simple and easy to handle vaccine administration method using the original solid-in-oil (S/O) nanodispersion system that permeates through the skin. The S/O nanodispersion system is composed of nanoparticles of hydrophilic molecules surrounded with hydrophobic surfactants that are dispersed in an oil vehicle. The system has potential to carry and deliver both hydrophilic and hydrophobic bioactives. Hydrophilic T cell epitope peptide was efficiently delivered through mouse skin using the S/O nanodispersion system and lowered antigen-specific IgE levels in pollinosis model mice. Addition of the hydrophobic adju1vant R848 significantly lowered the antibody secretion and shifted the Th1/Th2-balance toward Th1-type immunity in the model mice, showing the potential to alleviate Japanese cedar pollinosis</style></abstract><notes><style face="normal" font="default">IS - 2380-6761 (Print)IS - 2380-6761 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1002/btm2.10048</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29313026">PM:29313026</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Bioeng Transl Med\2017-2-102-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Bioeng Transl Med\2017-2-102-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180103, Kitaoka M</style></custom2><misc3><style face="normal" font="default">10.1002/btm2.10048</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86730</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shaker,D.</style></author></authors></contributors><titles><title><style face="normal" font="default">An Analysis of "Natural" Food Litigation to Build a Sesame Allergy Consumer Class Action</style></title><secondary-title><style face="normal" font="default">Food Drug Law J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Drug Law J</style></abbr-1></periodical><pages end="140" start="103">103-140</pages><volume><style face="normal" font="default">72</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">In a world where food allergy is still an incurable disease, law and regulation stand as necessary mechanisms to provide food-allergic consumers with the information they need to protect their health. The Food Allergen Labeling and Consumer Protection Act of 2004 provided specific labeling requirements for the "Top Eight" allergens in the U.S.: milk, soy, gluten, egg, tree nut, peanut, fish, and Crustacean shellfish. Since then, sesame has become more prevalent as an allergen and remains just as dangerous, inducing anaphylactic shock in some sesame-allergic individuals. Yet sesame remains unregulated, despite advocates and congressional members arguing for its inclusion. This note entertains one solution to this problem by exploring the most strategic way to bring a sesame allergy class action against a private food company under California's consumer protection statutes. Because this kind of class action does not have much, if any, precedent, this note analyzes the basic, preliminary issues that any litigant would have to navigate around to certify a class, including preemption, standing, and the claim itself, by focusing on how courts have examined these issues in the recent "natural" class action litigation. It also analyzes the legal, moral, and practical aspects of choosing a type of relief, as well as whom to include in the class. Finally, this note briefly considers how FDA itself can ensure sesame is regulated on the labels of food products, given that some of the legal issues may well be insurmountable for this particular class action. This note explores the potential solutions to difficult legal hurdles in constructing a sesame allergy class action, arguing that litigating a sesame allergy class action-even if it is not ultimately successful-could start a productive conversation that might lead Congress or FDA to provide greater public health and consumer protection for those with sesame allergy</style></abstract><notes><style face="normal" font="default">DA - 20171115IS - 1064-590X (Print)IS - 1064-590X (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29140656">PM:29140656</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Drug Law J\2017-72-103-40.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Drug Law J\2017-72-103-40.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171115, Shaker D</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87364</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mazarakis,N.</style></author><author><style face="normal" font="default"> Vongsvivut,J.</style></author><author><style face="normal" font="default"> Bambery,K.R.</style></author><author><style face="normal" font="default"> Snibson,K.J.</style></author><author><style face="normal" font="default"> Royce,S.G.</style></author><author><style face="normal" font="default"> Karagiannis,T.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Central Clinical School, Department of Diabetes, Monash University, Alfred Centre, 99 Commercial Rd, Melbourne 3004, Victoria, Australia. tom.karagiannis@monash.edu</style></auth-address><titles><title><style face="normal" font="default">Synchrotron-Fourier transform infrared maps of ovalbumin-induced murine chronic allergic airways disease: Correlation with conventional histology</style></title><secondary-title><style face="normal" font="default">Hell J Nucl Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Hell J Nucl Med</style></abbr-1></periodical><pages end="113" start="103">103-113</pages><volume><style face="normal" font="default">20 Suppl</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="9" Year="2017">2017/9</year></dates><abstract><style face="normal" font="default">Asthma is a chronic respiratory disease characterised by airway inflammation, remodeling and hyperresponsiveness. The ability to replicate these asthma traits in the well-established ovalbumin induced chronic model of allergic airways disease is an important tool for asthma research and preclinical drug development. Here, spectra derived from focal plane array and Synchrotron-Fourier transform infrared maps were used to analyse biochemical changes in lung tissue from an ovalbumin-induced murine chronic allergic airways disease model. Analysis of the chemical maps resulted in distinct clusters and significant changes in the lipid and proteins regions of the spectra between the saline control and diseased lung tissue samples. Overall, the utilisation of conventional histological methodologies and Synchrotron infrared microspectroscopy has the ability to expand the characterisation of murine models of asthma</style></abstract><notes><style face="normal" font="default">IS - 1790-5427 (Print)IS - 1790-5427 (Linking)LA - engPT - Journal ArticleCO - Greece -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29324919">PM:29324919</url></web-urls></urls><custom2><style face="normal" font="default">20171221, Mazarakis N</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86756</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Porcaro,F.</style></author><author><style face="normal" font="default"> Paglietti,M.G.</style></author><author><style face="normal" font="default"> Diamanti,A.</style></author><author><style face="normal" font="default"> Petreschi,F.</style></author><author><style face="normal" font="default"> Schiavino,A.</style></author><author><style face="normal" font="default"> Negro,V.</style></author><author><style face="normal" font="default"> Pecora,V.</style></author><author><style face="normal" font="default"> Fiocchi,A.</style></author><author><style face="normal" font="default"> Cutrera,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Respiratory Unit, Academic Department of Pediatrics, Bambino Gesu Children's Hospital, IRCCS, Rome, Italy.</style></auth-address><titles><title><style face="normal" font="default">Anaphylactic shock with methylprednisolone sodium succinate in a child with short bowel syndrome and cow's milk allergy</style></title><secondary-title><style face="normal" font="default">Ital J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ital J Pediatr</style></abbr-1></periodical><pages end="" start="104">104-</pages><volume><style face="normal" font="default">43</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">BACKGROUND: Medications with methyl-prednisolone sodium succinate containing lactose, which potentially contains traces of cow's milk proteins (CMP), could cause allergic reactions or compromise treatment of acute allergic reactions in sensitized patients. CASE PRESENTATION: We describe the unusual case of a one-year-old child affected by short bowel syndrome and history of severe cow's milk allergy (CMA) and anaphylactic reaction due to intravenous administration of methyl-prednisolone sodium succinate (Solu-Medrol 40 mg, Pfizer). He was admitted to our hospital for severe respiratory failure and was initially treated with methyl-prednisolone (Urbason 40 mg, Sanofi Aventis), then with methyl-prednisolone sodium succinate (Solu-Medrol 40 mg, Pfizer). After the intravenous administration of second steroid, immediate anaphylaxis was recorded and treatment was stopped. Antihistamine and epinephrine were required and symptom resolution occurred. CONCLUSION: Children who are highly sensitive to milk may have severe allergic reactions also after exposure to CMP through a different administration route than the oral one. Patients who have food allergies need to pay particular attention to the prescription of drugs and their formulation</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1824-7288 (Electronic)IS - 1720-8424 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1186/s13052-017-0422-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29149860">PM:29149860</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ital J Pediatr\2017-43-104.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ital J Pediatr\2017-43-104.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Porcaro F</style></custom2><misc3><style face="normal" font="default">10.1186/s13052-017-0422-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86886</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chung,S.Y.</style></author><author><style face="normal" font="default"> Mattison,C.P.</style></author><author><style face="normal" font="default"> Grimm,C.C.</style></author><author><style face="normal" font="default"> Reed,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">United States Department of AgricultureAgricultural Research ServiceSouthern Regional Research CenterNew OrleansLAUSA</style></auth-address><titles><title><style face="normal" font="default">Simple methods to reduce major allergens Ara h 1 and Ana o 1/2 in peanut and cashew extracts</style></title><secondary-title><style face="normal" font="default">Food Sci Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Sci Nutr</style></abbr-1></periodical><pages end="1071" start="1065">1065-1071</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Flour</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Whole peanut or cashew extracts are usually used in immunotherapy. Reducing major allergen(s) in the extracts may lessen their side effects. Three methods were evaluated to reduce major allergens in peanut extracts: (1) p-aminobenzamidine; (2) magnetic agarose beads; and (3) extraction of a commercial peanut flour at pH 7, respectively. The first two methods were also used to reduce major allergens in cashew extracts. After treatments, samples were evaluated by SDS-PAGE. pABA-treated samples were also analyzed for IgE binding in western blot. We found that the methods resulted in peanut extracts lacking detectable Ara h 1 but containing Ara h 2/6 and cashew extract lacking Ana o 1/2, but containing Ana o 3. Consequently, reduced IgE binding was observed. We conclude that the methods are useful for producing peanut or cashew extract with little Ara h 1 or Ana o 1/2</style></abstract><notes><style face="normal" font="default">IS - 2048-7177 (Print)IS - 2048-7177 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1002/fsn3.491</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29188033">PM:29188033</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Sci Nutr\2017-5-1065-71.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Sci Nutr\2017-5-1065-71.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170725, Chung SY</style></custom2><misc3><style face="normal" font="default">10.1002/fsn3.491</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87384</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xu,X.</style></author><author><style face="normal" font="default"> Zheng,Y.</style></author><author><style face="normal" font="default"> Zhang,X.</style></author><author><style face="normal" font="default"> He,Y.</style></author><author><style face="normal" font="default"> Li,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Neurosurgery, Chinese PLA General Hospital, Beijing, China</style></auth-address><titles><title><style face="normal" font="default">Efficacy and safety of dupilumab for the treatment of moderate-to-severe atopic dermatitis in adults</style></title><secondary-title><style face="normal" font="default">Oncotarget</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Oncotarget</style></abbr-1></periodical><pages end="108491" start="108480">108480-108491</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">65</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="12" Month="12" Year="2017">2017/12/12</year></dates><abstract><style face="normal" font="default">Objective: Atopic dermatitis is a chronic, relapsing inflammatory skin disease characterized by intense pruritus, excoriations and limited therapies. Dupilumab, a monoclonal antibody against interleukin-4 receptor alpha, is a promising new treatment option for atopic dermatitis. We sought to systematically summarize the efficacy, safety, and influence on quality of life of dupilumab for the treatment of moderate-to-severe atopic dermatitis in adults. Results: A total of 7 RCTs containing 2705 subjects were identified. Significantly more patients receiving dupilumab (611/1789) achieved Investigator's Global Assessment response compared with the control (89/916; RR, 3.95; P &lt; 0.001). Dupilumab was significantly more effective in reducing Eczema Area and Severity Index, peak pruritus numerical rating scale score, and body surface area. Treatment duration rather than administration frequency slightly influenced the efficacy. Dupilumab treatment also contributed to marked improvement in patients' quality of life and psychological symptoms. Incidence of adverse events was similar in dupilumab group and control group. Conclusions: Dupilumab is effective and safe for the treatment of moderate-to-severe atopic dermatitis in adults. This meta-analysis supports the role of dupilumab as a primary targeted biologic therapy in adult patients with moderate-to-severe atopic dermatitis. Materials and Methods: We searched Pubmed, Embase, and the Cochrane Library for eligible trials. Only double-blinded randomized controlled trials (RCTs) investigating the efficacy and safety of dupilumab in treating moderate-to-severe atopic dermatitis were included in this analysis. We made a comparison of dupilumab with control based on the pooled relative risk (RR), weighted mean difference, and their corresponding 95% confidence intervals of different measurements</style></abstract><notes><style face="normal" font="default">IS - 1949-2553 (Electronic)IS - 1949-2553 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.18632/oncotarget.22499</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29312544">PM:29312544</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Oncotarget\2017-8-108480-91.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Oncotarget\2017-8-108480-91.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Xu X</style></custom2><misc3><style face="normal" font="default">10.18632/oncotarget.22499</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86669</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bartuzi,Z.</style></author><author><style face="normal" font="default"> Kaczmarski,M.</style></author><author><style face="normal" font="default"> Czerwionka-Szaflarska,M.</style></author><author><style face="normal" font="default"> Malaczynska,T.</style></author><author><style face="normal" font="default"> Krogulska,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Position Paper of Food Allergy Section the Polish Society of Allergology on the diagnosis and management of food allergies</style></title><secondary-title><style face="normal" font="default">Pol J Allergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pol J Allergol</style></abbr-1></periodical><pages end="122" start="109">109-122</pages><volume><style face="normal" font="default">4</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Food allergy</style></keyword><keyword><style face="normal" font="default"> Diagnosis of food allergy</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2353-3854</style></isbn><abstract><style face="normal" font="default">The paper concerns the current position of the Polish Society of Allergology Food Allergy Section on the diagnosis and management of food allergies. The aim of this position is to provide evidence-based recommendations on the diagnosis and management of patients with allergic hypersensitivity to foods. This position statement includes a systematic review of studies in three areas, namely the epidemiology, diagnosis and management of food allergies. While taking into account the specific Polish setting, we also used in this publication the current European Academy of Allergy and Clinical Immunology (EAACI) position paper and other current position statements, including those of the United States National Institute of Allergy and Infectious Diseases (NIAID)</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1016/j.alergo.2017.09.002</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.alergo.2017.09.002</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pol J Allergol\2017-4-109-22.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pol J Allergol\2017-4-109-22.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Bartuzi Z</style></custom2><misc3><style face="normal" font="default">10.1016/j.alergo.2017.09.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86885</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fawale,O.S.</style></author><author><style face="normal" font="default"> Gbadamosi,S.O.</style></author><author><style face="normal" font="default"> Ige,M.M.</style></author><author><style face="normal" font="default"> Kadiri,O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Nigerian Institute for Oceanography and Marine ResearchLagosNigeria</style></auth-address><titles><title><style face="normal" font="default">Effects of cooking and fermentation on the chemical composition, functional, and antinutritional properties of kariya (Hildergardia barteri) seeds</style></title><secondary-title><style face="normal" font="default">Food Sci Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Sci Nutr</style></abbr-1></periodical><pages end="1115" start="1106">1106-1115</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Cooking</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">The effects of natural fermentation and cooking on kariya seeds functional properties, chemical composition, and antinutritional properties were evaluated. Result showed a reduction in antinutritional properties and improvement in protein content which were observed to increase with cooking (at 100 degrees C) and fermentation period (24-96 hr). Functional analyses showed an increase in foaming and emulsion properties, while water absorption capacity and swelling power were observed to likewise increase with an increasing temperature between 60 degrees C and 90 degrees C. There was also an improvement in foaming properties with increase in salt (NaCl) concentration, while emulsifying property decreases with an increase in salt (NaCl) concentration. Based on the result of the findings of this study, it can be stated that the cooking and fermentation processes employed in this study can enhance the domestic and industrial utilization of these seeds</style></abstract><notes><style face="normal" font="default">IS - 2048-7177 (Print)IS - 2048-7177 (Linking)LA - engPT - Journal ArticleCO - Nigeria -</style></notes><work-type><style face="normal" font="default">10.1002/fsn3.501</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29188038">PM:29188038</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Sci Nutr\2017-5-1106-115.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Sci Nutr\2017-5-1106-115.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170725, Fawale OS</style></custom2><misc3><style face="normal" font="default">10.1002/fsn3.501</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87009</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ruiz Oropeza,A.</style></author><author><style face="normal" font="default"> Lassen,A.</style></author><author><style face="normal" font="default"> Halken,S.</style></author><author><style face="normal" font="default"> Bindslev-Jensen,C.</style></author><author><style face="normal" font="default"> Mortz,C.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Allergy Center, Odense Research Center for Anaphylaxis (ORCA), Odense University Hospital, Klovervaenget 15, entrance 142, 5000, Odense, Denmark.</style></auth-address><titles><title><style face="normal" font="default">Anaphylaxis in an emergency care setting: a one year prospective study in children and adults</style></title><secondary-title><style face="normal" font="default">Scand J Trauma Resusc Emerg Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Scand J Trauma Resusc Emerg Med</style></abbr-1></periodical><pages end="" start="111">111-</pages><volume><style face="normal" font="default">25</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="22" Month="11" Year="2017">2017/11/22</year></dates><abstract><style face="normal" font="default">BACKGROUND: Current data on anaphylaxis is based on retrospective and register based studies. The objective of this study was to describe the epidemiology of anaphylaxis in a 1 year prospective study at the emergency care setting, Odense University Hospital, Denmark (2013-2014). METHODS: Prospective study at the emergency care setting, Odense University Hospital, Denmark (2013-2014). To identify anaphylaxis cases, records from all patients with clinical suspicion on anaphylaxis or a related diagnosis according to the International Classification of Diseases 10 and from patients treated at the emergency care setting or at prehospital level with adrenaline, antihistamines or glucocorticoids were reviewed daily. The identified cases were referred to the Allergy Center, where a standardized interview regarding the anaphylactic reaction was conducted. International guidelines were applied for the assessment of anaphylaxis and its pharmacological treatment. Severity of the anaphylactic reaction was evaluated according to Sampson's severity score. RESULTS: We identified 180 anaphylactic patients. Anaphylaxis represented 0.3%-0.4% of all contacts in the emergency care setting with an incidence rate of 26.8 cases per 100,000 person years (95% CI: 14.3-45.8) in children and 40.4 cases per 100,000 person years (95% CI: 32.8-49.3) in adults. Moderate to severe anaphylaxis was registered in 96% of the cases. Skin (96%) and respiratory (79%) symptoms were the most frequent registered, but 7% of cases in adults occurred without skin manifestations. The most common elicitor in children was food (61%), while drugs (48%) and venom (24%) were the main suspected elicitors in adults. Adrenaline was administered in 25% of the cases and it was significantly less administered than glucocorticoids (83%) and antihistamines (91%). The mortality rate during our study period was 0.3 cases per 100,000 person years. DISCUSSION: This is one of the first prospective studies on the epidemiology of anaphylaxis in children and adults, where the patients are identified not only based on diagnosis codes but also on history, symptoms and treatment and thereafter classified according to international diagnosis criteria for anaphylaxis. A limitation of this study is that only patients who gave consent to participate in the study were included. Furthermore, patients may have attended other hospitals during the study period. Therefore, the estimates are minimum figures. CONCLUSION: The prospective study design with a broad search profile yield a higher incidence than previously reported. Adrenaline was administered in a low proportion of the patients with moderate to severe anaphylaxis. Standardized diagnosis criteria among physicians treating anaphylaxis are needed</style></abstract><notes><style face="normal" font="default">IS - 1757-7241 (Electronic)IS - 1757-7241 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1186/s13049-017-0402-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29166906">PM:29166906</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Scand J Trauma Resusc Emerg Med\20171122-RuizOropezaA.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Scand J Trauma Resusc Emerg Med\20171122-RuizOropezaA.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171122, Ruiz Oropeza A</style></custom2><misc3><style face="normal" font="default">10.1186/s13049-017-0402-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86659</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Edwards,T.S.</style></author><author><style face="normal" font="default"> Wise,S.K.</style></author></authors></contributors><titles><title><style face="normal" font="default">Clinical Applications of Sublingual Immunotherapy</style></title><secondary-title><style face="normal" font="default">Otolaryngol Clin North Am</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Otolaryngol Clin North Am</style></full-title></periodical><pages end="1134" start="1121">1121-1134</pages><volume><style face="normal" font="default">50</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Sublingual immunotherapy</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><isbn><style face="normal" font="default">0030-6665</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.otc.2017.08.010</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.otc.2017.08.010</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Otolaryngol Clin North Am\2017-50-1121-34.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Otolaryngol Clin North Am\2017-50-1121-34.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Edwards RS</style></custom2><misc3><style face="normal" font="default">10.1016/j.otc.2017.08.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86719</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ito,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of General Pediatrics, Aichi Children's Health and Medical Center</style></auth-address><titles><title><style face="normal" font="default">[JAPANESE PEDIATRIC GUIDELINE FOR FOOD ALLERGY 2016-DIETARY INSTRUCTION AND ORAL IMMUNOTHERAPY]</style></title><secondary-title><style face="normal" font="default">Arerugi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arerugi</style></abbr-1></periodical><pages end="1154" start="1149">1149-1154</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">9</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 0021-4884 (Print)IS - 0021-4884 (Linking)LA - jpnPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129884">PM:29129884</url></web-urls></urls><custom2><style face="normal" font="default">20171113, Ito K</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87333</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Arslan,S.</style></author><author><style face="normal" font="default"> Caliskener,A.Z.</style></author></authors></contributors><titles><title><style face="normal" font="default">High Serum Immunoglobulin E Level Is Not Always Connected To Allergy: Etiological Evaluation Tips</style></title><secondary-title><style face="normal" font="default">Asthma Allergy Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Asthma Allergy Immunol</style></full-title></periodical><pages end="122" start="115">115-122</pages><volume><style face="normal" font="default">15</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The constant progress of medical science has made it necessary to specialize on various fields. There are now many new disciplines in internal medicine and surgery.However, some beliefs continue with little change despite this specialization. A good example to these is considering allergy first in patients with significant eosinophilia or high IgE levels.In this article, we discuss the differential diagnosis of high IgE levels with information on the causes, when it should be investigated, and the relevant clinical findings and evaluations.</style></abstract><notes><style face="normal" font="default">LA - TURCO - Turkey -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://www.aai.org.tr/index.php/aai/article/view/49</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-115-22.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-115-22.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Arslan S</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86720</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kikkawa,S.</style></author><author><style face="normal" font="default"> Kamijo,A.</style></author><author><style face="normal" font="default"> Nakagome,K.</style></author><author><style face="normal" font="default"> Soma,T.</style></author><author><style face="normal" font="default"> Kobayashi,T.</style></author><author><style face="normal" font="default"> Uchida,Y.</style></author><author><style face="normal" font="default"> Morita,E.</style></author><author><style face="normal" font="default"> Nagata,M.</style></author><author><style face="normal" font="default"> Inoue,T.</style></author><author><style face="normal" font="default"> Kase,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otorhinolaryngology, Saitama Medical University</style></auth-address><titles><title><style face="normal" font="default">[ANALYSIS OF BACKGROUNDS AND LEVEL OF UNDERSTANDING OF TREATMENT OF POOR ADHERENCE AND DROPOUT CASES ON SUBLINGUAL IMMUNOTHERAPY FOR JAPANESE CEDAR POLLINOSIS IN THE FIRST FOLLOW-UP YEAR]</style></title><secondary-title><style face="normal" font="default">Arerugi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arerugi</style></abbr-1></periodical><pages end="1171" start="1165">1165-1171</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">9</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: We considered the factors of poor adherence to and dropout from sublingual immunotherapy (SLIT) by verifying patient backgrounds 1 year after start of treatment. METHODS: We recruited 38 patients who began SLIT between November 2014 and September 2015. We analyzed their attributes and level of understanding of the treatment, and conducted a self-reported survey on factors behind dropout cases and poor adherence cases. RESULTS: Four patients dropped out 1 year after start of treatment. Three left for reasons related to anxiety about side effects. There were five cases of poor adherence. There was no significant difference between good adherence, poor adherence, and dropout regarding level of understanding of the treatment (p=0.59). In the comparison between good and poor adherence groups, except four dropout patients, the adherence tended to be poor in patients with short duration of disease, smoking patients, and young patients. Continuous rate of SLIT achieved about 90%, suggesting relatively high level of adherence. CONCLUSION: It appears possible that anxiety related to side effects could be a factor affecting dropout from SLIT. There was no significant difference regarding level of understanding of the treatment. The adherence tended to be poor in patients with short duration of disease, smoking patients, and young patients</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 0021-4884 (Print)IS - 0021-4884 (Linking)LA - jpnPT - English AbstractPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129887">PM:29129887</url></web-urls></urls><custom2><style face="normal" font="default">20171113, Kikkawa S</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86717</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yuta,A.</style></author><author><style face="normal" font="default"> Ogawa,Y.</style></author><author><style face="normal" font="default"> Suzuki,Y.</style></author><author><style face="normal" font="default"> Ogihara,H.</style></author><author><style face="normal" font="default"> Ohta,N.</style></author><author><style face="normal" font="default"> Kozaki,H.</style></author><author><style face="normal" font="default"> Shimizu,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Yuta Clinic</style></auth-address><titles><title><style face="normal" font="default">[CLINICAL EFFICACY OF SUBLINGUAL IMMUNOTHERAPY IN THE THIRD TREATED YEAR WITH JAPANESE CEDAR POLLINOSIS IN 2017]</style></title><secondary-title><style face="normal" font="default">Arerugi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arerugi</style></abbr-1></periodical><pages end="1180" start="1172">1172-1180</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">9</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">It past 3 years in 2017 after the first purchase of the drug for sublingual immunotherapy (SLIT) for Japanese Cedar pollinosis (JCP). We reported the clinical efficacy of SLIT in the first and the second treated year. PURPOSE: The purpose of this study is to clear the clinical efficacy of SLIT in the third treated year by comparing with other therapies, such as subcutaneous immunotherapy (SCIT), or other pharmacotherapy. METHODS: We compared the clinical efficacy in 2017, of 112 SLIT in the third treated year with 38 SCIT, 364 primary pharmacotherapy that started therapies before pollen dispersal, 254 pharmacotherapy that started therapies after pollen disposal, or 333 non-treatment. The clinical efficacy was evaluated with symptom scores, total nasal symptom scores and combined total nasal symptom-medication scores (TNSMS), symptoms of nose and eye by visual analog scale (VAS), quality of life (QOL) scores by Japanese rhino-conjunctivitis QOL questionnaire (JRQLQ No1). RESULTS: Both SCIT and SLIT showed good clinical efficacy without significant difference in every assessment. Both SCIT and SLIT were significantly better than other pharmacotherapy in most assessment. Patients, whose symptom scores of nose and eye were 0 and 1 point without any rescue drugs, accounted for 9 and 24% of total SLIT, respectively. CONCLUSION: SLIT in the third treated year showed good clinical efficacy in reducing symptoms and TNSMS of JCP, and in improving QOL. SLIT was significantly effective compared with other pharmacotherapies</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 0021-4884 (Print)IS - 0021-4884 (Linking)LA - jpnPT - English AbstractPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129888">PM:29129888</url></web-urls></urls><custom2><style face="normal" font="default">20171113, Yuta A</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86658</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,S.E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Management of Anaphylaxis</style></title><secondary-title><style face="normal" font="default">Otolaryngol Clin North Am</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Otolaryngol Clin North Am</style></full-title></periodical><pages end="1184" start="1175">1175-1184</pages><volume><style face="normal" font="default">50</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><isbn><style face="normal" font="default">0030-6665</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.otc.2017.08.013</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.otc.2017.08.013</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Otolaryngol Clin North Am\2017-50-1175-84.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Otolaryngol Clin North Am\2017-50-1175-84.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Lee SE</style></custom2><misc3><style face="normal" font="default">10.1016/j.otc.2017.08.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86718</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yamazaki,M.</style></author><author><style face="normal" font="default"> Isozaki,A.</style></author><author><style face="normal" font="default"> Tanaka,A.</style></author><author><style face="normal" font="default"> Ando,E.</style></author><author><style face="normal" font="default"> Nakamura,Y.</style></author><author><style face="normal" font="default"> Kurihara,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Yokohama City Minato Red Cross Hospital</style></auth-address><titles><title><style face="normal" font="default">[AN ADULT CASE OF EGG ALLERGY TREATED WITH RUSH ORAL IMMUNOTHERAPY]</style></title><secondary-title><style face="normal" font="default">Arerugi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arerugi</style></abbr-1></periodical><pages end="1184" start="1181">1181-1184</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">9</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">A 26-year-old female patient exhibited symptoms associated with egg allergy, which had been present since early childhood. The patient requested the treatment of egg allergy and was admitted to our hospital for rush oral immunotherapy. The threshold was determined by an oral food challenge test, after positive results on a double-blind food challenge test. The patient ingested dry powder of raw egg-white 5 times per day starting with a tenth of the threshold dose (3.0mg), followed by a 1.2-times increase every time. When the amount of powder reached 1g, it was replaced with 8g of scrambled egg, after then subsequent doses were increased 1.5 times every time. The target of one chicken egg (60g) was reached on the 18th day. During treatment, minor allergic symptoms of urticarial and dyspnea were observed on two occasions, but they disappeared after oral administration of antihistamines. The result of an exercise challenge test after ingestion of egg was negative, and no allergic symptoms were observed by the ingestion of processed foods that contained egg. The patient currently receives ongoing maintenance treatment, consisting of the ingestion of one chicken egg per day; no allergic symptoms have been observed during a period of 2 year while receiving this treatment. Rush oral immunotherapy is a treatment option to be considered for adults with food allergy who were not able to acquire immune tolerance during childhood</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 0021-4884 (Print)IS - 0021-4884 (Linking)LA - jpnPT - English AbstractPT - Journal ArticleCO - Jpan -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129889">PM:29129889</url></web-urls></urls><custom2><style face="normal" font="default">20171113, Yamazaki M</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86799</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhu,K.</style></author><author><style face="normal" font="default"> Hou,X.L.</style></author><author><style face="normal" font="default"> Huang,H.J.</style></author><author><style face="normal" font="default"> Wang,Y.R.</style></author><author><style face="normal" font="default"> Ren,Y.X.</style></author><author><style face="normal" font="default"> Ni,X.</style></author><author><style face="normal" font="default"> Xiang,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy, Beijing Children's Hospital, Capital Medical University/National Center for Children's Health, Beijing 100045, China.</style></auth-address><titles><title><style face="normal" font="default">Distribution characteristics of serum specific IgE for inhaled allergens in children with different airway allergic diseases</style></title><secondary-title><style face="normal" font="default">Zhongguo Dang Dai Er Ke Za Zhi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Zhongguo Dang Dai Er Ke Za Zhi</style></abbr-1></periodical><pages end="1190" start="1185">1185-1190</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To investigate the distribution characteristics of serum specific IgE (sIgE) for inhaled allergens in children with different airway allergic diseases. METHODS: Fluorescent enzyme-linked immunosorbent assay on the UniCAP250 system was performed to measure serum sIgE for 9 common inhaled allergens in 256 children aged 3-14 years with different airway allergic diseases. According to the clinical diagnosis, these children were divided into rhinitis group (37 children with allergic rhinitis), asthma group (82 children with bronchial asthma), and rhinitis-asthma group (137 children with allergic rhinitis complicated by bronchial asthma). The three groups were compared in terms of the detection rates of 9 inhaled allergens, sensitization level, and number of allergens. RESULTS: The detection rate of serum sIgE for inhaled allergens was 57.3% (47/82) in the asthma group, 86.5% (32/37) in the rhinitis group, and 82.5% (113/137) in the rhinitis-asthma group (P&lt;0.05). The most common allergen in the asthma, rhinitis, and the rhinitis-asthma groups was mould fungi (32.9%, 54.1%, and 48.9% respectively), followed by dust mites (30.5%, 45.9%, and 46.0% respectively), pollen (26.8%, 35.1%, and 32.8% respectively), pets (12.2%, 27.0%, and 18.2% respectively), and cockroach (9.8%, 5.4%, and 5.8% respectively). The rhinitis group and the rhinitis-asthma group had a significantly higher detection rate of mould fungi (mx2) than the asthma group (P&lt;0.0166). There were no significant differences in the sensitization level of 9 allergens and number of allergens between the three groups. CONCLUSIONS: In children with either bronchial asthma, allergic rhinitis, or bronchial asthma complicated by allergic rhinitis, the three most common inhaled allergens are mould fungi, dust mites, and pollens. Compared with bronchial asthma, allergic rhinitis may be more closely associated with sensitization by mould fungi. The three common airway allergic diseases have similar distribution characteristics of inhaled allergens</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1008-8830 (Print)IS - 1008-8830 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132467">PM:29132467</url></web-urls></urls><custom2><style face="normal" font="default">20171114, Zhu K</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86691</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Deleanu,D.</style></author><author><style face="normal" font="default"> Nedelea,I.</style></author></authors></contributors><titles><title><style face="normal" font="default">Hypersensitivity reactions to biological agents</style></title><secondary-title><style face="normal" font="default">Alergologia</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Alergologia</style></full-title></periodical><pages end="18" start="12">12-18</pages><volume><style face="normal" font="default">1</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">As a result of immunomodulatory therapy, the last decade was marked by spectacular results in the targeted treatment of inflammatory, autoimmune, neoplastic, and other diseases. The widespread use of biological agents is affected by the increased number of drug and immunologically mediated adverse reactions, which justifies the need to explore the subject. The present paper is a presentation of adverse reactions to biological agents.</style></abstract><notes><style face="normal" font="default">LA - ROMCO - Romania -</style></notes><work-type><style face="normal" font="default">10.26416/Aler.1.1.2017.1238</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.26416/Aler.1.1.2017.1238</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Alergologia\20171120-DeleanuD.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Alergologia\20171120-DeleanuD.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Deleanu D</style></custom2><misc3><style face="normal" font="default">10.26416/Aler.1.1.2017.1238</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86792</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Perisson,C.</style></author><author><style face="normal" font="default"> Destruys,L.</style></author><author><style face="normal" font="default"> Grenet,D.</style></author><author><style face="normal" font="default"> Bassinet,L.</style></author><author><style face="normal" font="default"> Derelle,J.</style></author><author><style face="normal" font="default"> Sermet-Gaudelus,I.</style></author><author><style face="normal" font="default"> Thumerelle,C.</style></author><author><style face="normal" font="default"> Prevotat,A.</style></author><author><style face="normal" font="default"> Rosner,V.</style></author><author><style face="normal" font="default"> Clement,A.</style></author><author><style face="normal" font="default"> Corvol,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Omalizumab treatment for allergic bronchopulmonary aspergillosis in young patients with cystic fibrosis</style></title><secondary-title><style face="normal" font="default">Respir Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Med</style></abbr-1></periodical><pages end="15" start="12">12-15</pages><volume><style face="normal" font="default">133</style></volume><number><style face="normal" font="default">Supplement C</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Allergic bronchopulmonary aspergillosis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Cystic fibrosis</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0954-6111</style></isbn><abstract><style face="normal" font="default">Allergic bronchopulmonary aspergillosis (ABPA) is a severe lung disease complication caused by an Aspergillus fumigatus-induced hypersensitivity that affects 2</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô15% of patients with cystic fibrosis (CF). The mainstay treatment consists of a combination of corticosteroids and antifungals. However, repeated or long-term corticosteroid therapies can lead to serious side effects. The monoclonal anti-IgE antibody, omalizumab, has demonstrated its efficacy in allergic asthma. As ABPA results from a hypersensitivity to a specific allergen, omalizumab might benefit CF patients with ABPA. Therefore, we conducted a retrospective study to investigate the effects of omalizumab on ABPA in CF patients. We retrospectively analyzed the clinical records of young patients with CF treated with omalizumab for an ABPA in several French CF centers. The clinical data were collected 3 months before the start of omalizumab treatment, at initiation, and every 3 months up to 12 following initiation. These data comprised clinical, biological, nutritional, and functional parameters. Eighteen patients were included (mean age: 17.1-á-¦-á5.2-áyrs). Under omalizumab was observed a stabilization of the lung function decline associated with a significant decrease in the corticosteroid daily dose (p-á=-á0.0007) and an improvement in the nutritional status (p-á=-á0.01). No serious side effect of omalizumab was reported. This study suggests that omalizumab might be an interesting therapeutic strategy in ABPA, associated with less side effects compared to long-term corticosteroids. Further randomized-controlled trials are needed to ascertain the efficacy of omalizumab in CF patients with ABPA</style></abstract><notes><style face="normal" font="default">LA - ENGCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.rmed.2017.11.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29173443">PM:29173443</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Med\2017-133SC-12-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Med\2017-133SC-12-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Perisson C</style></custom2><misc3><style face="normal" font="default">10.1016/j.rmed.2017.11.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87186</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gutowska-Owsiak,D.</style></author><author><style face="normal" font="default"> Ogg,G.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">MRC Human Immunology Unit, NIHR Biomedical Research Centre, Radcliffe Department of Medicine, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.grid.4991.5MRC Human Immunology Unit, NIHR Biomedical Research Centre, Radcliffe Department of Medicine, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.grid.4991.5</style></auth-address><titles><title><style face="normal" font="default">Therapeutic vaccines for allergic disease</style></title><secondary-title><style face="normal" font="default">NPJ Vaccines</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">NPJ Vaccines</style></abbr-1></periodical><pages end="" start="12">12-</pages><volume><style face="normal" font="default">2</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Allergic diseases are highly prevalent worldwide and affect all age groups, contributing to a high personal and socioeconomic burden. Treatment with an "allergy vaccine" or allergen immunotherapy aims to provide long-lasting benefits by inducing unresponsiveness to the relevant antigen. The consequences of the therapy are considered disease modifying and range from dampening of the immediate immune responses to the reduction of secondary tissue remodeling. Furthermore, allergen immunotherapy interventions have a potential to slow or cease the development of additional allergic manifestations with a long-term overall effect on morbidity and quality of life. Here, we review proposed mechanisms underlying the therapeutic effects of immunotherapy for allergic diseases. Further, we discuss both standard and novel approaches and possible future directions in the development of allergen immunotherapy</style></abstract><notes><style face="normal" font="default">IS - 2059-0105 (Print)IS - 2059-0105 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1038/s41541-017-0014-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29263869">PM:29263869</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\NPJ Vaccines\2017-2-12.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\NPJ Vaccines\2017-2-12.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Gutowska-Owsiak D</style></custom2><misc3><style face="normal" font="default">10.1038/s41541-017-0014-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87030</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Barnes,A.C.</style></author><author><style face="normal" font="default"> Blandford,A.D.</style></author><author><style face="normal" font="default"> Perry,J.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Cole Eye Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/i-13, Cleveland, OH 44195, United States</style></auth-address><titles><title><style face="normal" font="default">Cicatricial ectropion in a patient treated with dupilumab</style></title><secondary-title><style face="normal" font="default">Am J Ophthalmol Case Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Ophthalmol Case Rep</style></abbr-1></periodical><pages end="122" start="120">120-122</pages><volume><style face="normal" font="default">7</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword></keywords><dates><year Day="0" Month="9" Year="2017">2017/9</year></dates><abstract><style face="normal" font="default">Purpose: To describe a case of bilateral conjunctivitis and cicatricial ectropion associated with dupilumab therapy for atopic dermatitis. Observations: Severe hyperemia of the conjunctiva and eyelid margins, as well as cicatricial ectropion, began two months after starting weekly dupilumab injections for atopic dermatitis. The findings worsened over the next several months and improved after discontinuing dupilumab. Conclusions and importance: Dupilumab is a promising intervention in the management of atopic dermatitis and asthma, however, little is known about its potential ocular adverse effects. We report the first case of dupilumab-associated ocular inflammation leading to cicatricial ectropion</style></abstract><notes><style face="normal" font="default">IS - 2451-9936 (Print)IS - 2451-9936 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.ajoc.2017.06.017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29260094">PM:29260094</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Am J Ophthalmol Case Rep\2017-7-120-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Am J Ophthalmol Case Rep\2017-7-120-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Barnes AC</style></custom2><misc3><style face="normal" font="default">10.1016/j.ajoc.2017.06.017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86748</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gamazo,C.</style></author><author><style face="normal" font="default"> Garcia-Azpiroz,M.</style></author><author><style face="normal" font="default"> Souza Reboucas,J.</style></author><author><style face="normal" font="default"> Gastaminza,G.</style></author><author><style face="normal" font="default"> Ferrer,M.</style></author><author><style face="normal" font="default"> Irache,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Microbiology, University of Navarra, Instituto de Investigacion Sanitaria de Navarra (Idisna), C/Irunlarrea, 1; 31</style></auth-address><titles><title><style face="normal" font="default">Oral immunotherapy using polymeric nanoparticles loaded with peanut proteins in a murine model of fatal anaphylaxis</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1217" start="1205">1205-1217</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Peanut allergy is the most common cause of anaphylaxis and food-related death. However, there is currently no approved immunotherapy treatment. Hence, this warrants the need for relevant and convenient animal models to test for adequate immunotherapies. MATERIALS &amp; METHODS: In this study, we compared three mouse strains: CD1, BALB/c and C57, to select a model of peanut allergy. After that, we conducted then a therapeutic study using an immunogenic peanut extract encapsulated in nanoparticles made with polymer Gantrez(R) following the solvent displacement method. RESULTS &amp; CONCLUSION: After implementing a dosing schedule with oral commercial peanut butter, the antibody responses, cytokine profiles and, above all, the anaphylaxis induced after a challenge with peanut proteins, showed that the outbred CD1 strain was the most susceptible to peanut sensitization. CD1 sensitized mice were orally immunized with three doses of the nanoparticle formulation capable of protecting them against the severe anaphylactic symptoms induced by the peanut challenge</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - Spain -CO - Brazil -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0111</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130802">PM:29130802</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171113, Gamazo C</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0111</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87109</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tsuda,M.</style></author><author><style face="normal" font="default"> Arakawa,H.</style></author><author><style face="normal" font="default"> Ishii,N.</style></author><author><style face="normal" font="default"> Ubukata,C.</style></author><author><style face="normal" font="default"> Michimori,M.</style></author><author><style face="normal" font="default"> Noda,M.</style></author><author><style face="normal" font="default"> Takahashi,K.</style></author><author><style face="normal" font="default"> Kaminogawa,S.</style></author><author><style face="normal" font="default"> Hosono,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Food Bioscience and Biotechnology, College of Bioresource Sciences, Nihon University, Fujisawa, Japan</style></auth-address><titles><title><style face="normal" font="default">Dietary Fructo-Oligosaccharides Attenuate Early Activation of CD4+ T Cells Which Produce both Th1 and Th2 Cytokines in the Intestinal Lymphoid Tissues of a Murine Food Allergy Model</style></title><secondary-title><style face="normal" font="default">Int Arch Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Arch Allergy Immunol</style></abbr-1></periodical><pages end="132" start="121">121-132</pages><volume><style face="normal" font="default">174</style></volume><number><style face="normal" font="default">3-4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: Fructo-oligosaccharides (FOS) are prebiotic agents with immunomodulatory effects involving improvement of the intestinal microbiota and metabolome. In this study, we investigated the cellular mechanisms through which FOS modulate intestinal antigen-specific CD4+ T cell responses in food allergy, using OVA23-3 mice. METHODS: OVA23-3 mice were fed an experimental diet containing either ovalbumin (OVA) or OVA and FOS for 1 week. Body weight and mucosal mast cell protease 1 in the serum were measured as the indicator of intestinal inflammation. Single-cell suspensions were prepared from intestinal and systemic lymphoid tissues for cellular analysis. Cytokine production was measured by ELISA. Activation markers and intracellular cytokines in CD4+ T cells were analyzed by flow cytometry. Activated CD4+ T cells were purified to examine cytokine production. RESULTS: Dietary intake of FOS provided moderate protection from the intestinal inflammation induced by the OVA-containing diet. FOS significantly reduced food allergy-induced Th2 cytokine responses in intestinal tissues but not in systemic tissues. FOS decreased OVA diet-induced IFN-gamma+IL-4+ double-positive CD4+ T cells and early-activated CD45RBhighCD69+CD4+ T cells in the mesenteric lymph nodes. Furthermore, we confirmed that these CD45RBhighCD69+CD4+ T cells are able to produce high levels of IFN-gamma and moderate level of IL-4, IL-10, and IL-13. CONCLUSIONS: Dietary intake of FOS during the development of food allergy attenuates the induction of intestinal Th2 cytokine responses by regulating early activation of naive CD4+ T cells, which produce both Th1 and Th2 cytokines. Our results suggest FOS might be a potential food agent for the prevention of food allergy by modulating oral sensitization to food antigens</style></abstract><notes><style face="normal" font="default">IS - 1423-0097 (Electronic)IS - 1018-2438 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1159/000481984.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29145201">PM:29145201</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-121-32.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-121-32.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Tsuda M</style></custom2><misc3><style face="normal" font="default">10.1159/000481984.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86607</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cruz,A.A.</style></author><author><style face="normal" font="default"> Cooper,P.J.</style></author><author><style face="normal" font="default"> Figueiredo,C.A.</style></author><author><style face="normal" font="default"> Alcantara-Neves,N.M.</style></author><author><style face="normal" font="default"> Rodrigues,L.C.</style></author><author><style face="normal" font="default"> Barreto,M.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">ProAR-Faculdade de Medicina da Universidade Federal da Bahia, Salvador, Brazil</style></auth-address><titles><title><style face="normal" font="default">Global issues in allergy and immunology: Parasitic infections and allergy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="1228" start="1217">1217-1228</pages><volume><style face="normal" font="default">140</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Allergic diseases are on the increase globally in parallel with a decrease in parasitic infection. The inverse association between parasitic infections and allergy at an ecological level suggests a causal association. Studies in human subjects have generated a large knowledge base on the complexity of the interrelationship between parasitic infection and allergy. There is evidence for causal links, but the data from animal models are the most compelling: despite the strong type 2 immune responses they induce, helminth infections can suppress allergy through regulatory pathways. Conversely, many helminths can cause allergic-type inflammation, including symptoms of "classical" allergic disease. From an evolutionary perspective, subjects with an effective immune response against helminths can be more susceptible to allergy. This narrative review aims to inform readers of the most relevant up-to-date evidence on the relationship between parasites and allergy. Experiments in animal models have demonstrated the potential benefits of helminth infection or administration of helminth-derived molecules on chronic inflammatory diseases, but thus far, clinical trials in human subjects have not demonstrated unequivocal clinical benefits. Nevertheless, there is sufficiently strong evidence to support continued investigation of the potential benefits of helminth-derived therapies for the prevention or treatment of allergic and other inflammatory diseases</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Brazil -CO - Ecuador -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.09.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29108604">PM:29108604</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\2017-140-1217-28.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\2017-140-1217-28.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Cruz AA</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.09.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86745</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ciprandi,G.</style></author><author><style face="normal" font="default"> Puccinelli,P.</style></author><author><style face="normal" font="default"> Incorvaia,C.</style></author><author><style face="normal" font="default"> Passalacqua,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy &amp; Respiratory Diseases, Ospedale Policlinico San Martino, Largo R. Benzi 10, 16132 Genoa, Italy</style></auth-address><titles><title><style face="normal" font="default">The relevance of house dust mites allergy in clinical practice: the epidemiological impact on allergen immunotherapy</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1224" start="1219">1219-1224</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">House dust mite (HDM) is the most common cause of respiratory allergy worldwide. The impact of HDM allergy is influenced by a number of factors, including local climate. We investigated such issue in Italy, using a real-life setting, including outpatients visited at allergy clinics. In 9143 patients (7873 adults and 1270 children) who were evaluated in 15 allergy clinics, investigating as well the rate of prescription of allergen immunotherapy. The present study confirms that Mediterranean climate is associated with a higher prevalence of mite allergy than continental climate. This significant difference may have an impact on allergen immunotherapy prescription, which should be more common in areas with higher prevalence of HDM allergy</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0086</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130801">PM:29130801</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunotherapy\2017-9-1219-24.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunotherapy\2017-9-1219-24.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Ciprandi G</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0086</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87054</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yoshimoto,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immunology, Hyogo College of Medicine</style></auth-address><titles><title><style face="normal" font="default">[MOLECULAR MECHANISMS FOR CUTANEOUSLY SENSITIZED FOOD ALLERGY : EXPERIMENTAL EVIDENCES FOR DUAL ALLERGEN EXPOSURE HYPOTHESIS]</style></title><secondary-title><style face="normal" font="default">Arerugi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arerugi</style></abbr-1></periodical><pages end="1229" start="1224">1224-1229</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">10</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 0021-4884 (Print)IS - 0021-4884 (Linking)LA - jpnPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.15036/arerugi.66.1224</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249755">PM:29249755</url></web-urls></urls><custom2><style face="normal" font="default">20171220, Yoshimoto T</style></custom2><misc3><style face="normal" font="default">10.15036/arerugi.66.1224</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86752</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mosges,R.</style></author><author><style face="normal" font="default"> Rohdenburg,C.</style></author><author><style face="normal" font="default"> Eichel,A.</style></author><author><style face="normal" font="default"> Zadoyan,G.</style></author><author><style face="normal" font="default"> Kasche,E.M.</style></author><author><style face="normal" font="default"> Shah-Hosseini,K.</style></author><author><style face="normal" font="default"> Lehmacher,W.</style></author><author><style face="normal" font="default"> Schmalz,P.</style></author><author><style face="normal" font="default"> Compalati,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Medical Statistics, Informatics and Epidemiology, Medical Faculty, University of Cologne, Cologne, Germany</style></auth-address><titles><title><style face="normal" font="default">Dose-finding study of carbamylated monomeric allergoid tablets in grass-allergic rhinoconjunctivitis patients</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1238" start="1225">1225-1238</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">AIM: To determine the optimal effective and safe dose of sublingual immunotherapy tablets containing carbamylated monomeric allergoids in patients with grass pollen-induced allergic rhinoconjunctivitis. METHODS: In this prospective, randomized, double-blind, active-controlled, multicenter, Phase II study, four different daily doses were applied preseasonally for 12 weeks. RESULTS: Of 158 randomized adults, 155 subjects (safety population) received 300 units of allergy (UA)/day (n = 36), 600 UA/day (n = 43), 1000 UA/day (n = 39), or 2000 UA/day (n = 37). After treatment, 54.3, 47.6, 59.0 and 51.4% of patients, respectively, ceased to react to the highest allergen concentration in a conjunctival provocation test. Furthermore, the response threshold improved in 70.4, 62.9, 76.7 and 66.7% of patients, respectively. No serious adverse events occurred. CONCLUSION: This study found 1000 UA/day to be the optimal effective and safe dose</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - Germany -CO - Italy -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0058</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130797">PM:29130797</url></web-urls></urls><custom2><style face="normal" font="default">20171113, Mosges R</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0058</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86670</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rogala,B.</style></author></authors></contributors><titles><title><style face="normal" font="default">Atopic dermatitis. Is it always an allergic disease?</style></title><secondary-title><style face="normal" font="default">Pol J Allergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pol J Allergol</style></abbr-1></periodical><pages end="125" start="123">123-125</pages><volume><style face="normal" font="default">4</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Hyper-IgE syndrome</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2353-3854</style></isbn><abstract><style face="normal" font="default">The article is aimed to provide a critical overview of the current knowledge regarding the differential diagnosis of atopic dermatitis being within the scope of interest of allergists. It points out the grounds of taking into account in clinical practice the recognition of hyper-IgE syndrome in patients with signs and symptoms of atopic dermatitis particularly in those suffering from severe one and with highly elevated serum IgE</style></abstract><notes><style face="normal" font="default">LA - POLCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1016/j.alergo.2017.08.004</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.alergo.2017.08.004</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pol J Allergol\2017-4-123-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pol J Allergol\2017-4-123-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Rogala B</style></custom2><misc3><style face="normal" font="default">10.1016/j.alergo.2017.08.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86746</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Datta,A.</style></author><author><style face="normal" font="default"> Moitra,S.</style></author><author><style face="normal" font="default"> Das,P.K.</style></author><author><style face="normal" font="default"> Mondal,S.</style></author><author><style face="normal" font="default"> Omar Faruk,S.M.</style></author><author><style face="normal" font="default"> Hazra,I.</style></author><author><style face="normal" font="default"> Tripathi,S.K.</style></author><author><style face="normal" font="default"> Chaudhuri,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Laboratory Medicine, School of Tropical Medicine, 108 C R Avenue, Kolkata 700073, West Bengal, India</style></auth-address><titles><title><style face="normal" font="default">Allergen immunotherapy modulates sensitivity of Treg cells to apoptosis in a rat model of allergic asthma</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1251" start="1239">1239-1251</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">AIM: To study the apoptosis of Foxp3+ Treg cells following Alstonia scholaris pollen sensitization-challenge and following allergen immunotherapy. MATERIALS &amp; METHODS: Wistar rats were sensitized-challenged with Alstonia scholaris pollen and were further given intranasal immunotherapy. For the analysis of the apoptotic proteins on Treg cells by flow cytometry, multiple gating procedures were followed. RESULTS: Allergen sensitization-challenge increases Annexin-V, Fas, FasL, caspases-8, 9, 3 cytochrome-C, APAF-1, Bax, perforin-1 and granzyme-B on Treg cells which is decreased following intranasal immunotherapy. On the other hand, Bcl-2 expression is decreased in allergy and increased by immunotherapy. CONCLUSION: Apoptosis of Treg cells is increased following allergen sensitization-challenge via extrinsic, intrinsic and perforin/granzyme pathways and allergen immunotherapy decreased the sensitivity to apoptosis of Treg cells</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0038</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130799">PM:29130799</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunotherapy\2017-9-1239-51.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunotherapy\2017-9-1239-51.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Datta A</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0038</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87056</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shingaki,T.</style></author><author><style face="normal" font="default"> Hiraguchi,Y.</style></author><author><style face="normal" font="default"> Gen,M.</style></author><author><style face="normal" font="default"> Yoshino,S.</style></author><author><style face="normal" font="default"> Kumagai,Y.</style></author><author><style face="normal" font="default"> Ebishima,Y.</style></author><author><style face="normal" font="default"> Owa,K.</style></author><author><style face="normal" font="default"> Otuji,K.</style></author><author><style face="normal" font="default"> Kondou,Y.</style></author><author><style face="normal" font="default"> Suehiro,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Center of Allergy and Clinical Immunology, Osaka Saiseikai Nakatsu Hospital</style></auth-address><titles><title><style face="normal" font="default">[A CASE OF HYPERSENSITIVITY REACTION TO ENOKITAKE (FLAMMULINA VELUTIPES) INGESTION]</style></title><secondary-title><style face="normal" font="default">Arerugi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arerugi</style></abbr-1></periodical><pages end="1243" start="1240">1240-1243</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">10</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">We experienced a case of 10-year-old girl who developed hypersensitivity reactions after eating enokitake. The patient had food allergy to egg until 5 years old. When she was 4 years old, she ate enokitake with a hot-pot dish. Later, she felt itching in her mouth. Therefore, she never ate enokitake since that time. At the age of 10, she drank only the soup of enokitake with school lunch. After that she felt discomfort and itching in her oral cavity. The result of enokitake and other mushrooms (siitake, simeji, and eringi) skin prick to prick test were all positive. We performed Western blotting with enokitake extracts and the patient's serum. Enokitake protein's band (75kDa) reacted specifically with the patient's IgE. At the same time Western blotting was performed with the patient's serum of previously reported enokitake anaphylaxis, but a 75kDa band showing specific reaction in this case was not observed. This band we identified was a novel enokitake allergen</style></abstract><notes><style face="normal" font="default">IS - 0021-4884 (Print)IS - 0021-4884 (Linking)LA - jpnPT - English AbstractPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.15036/arerugi.66.1240</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249758">PM:29249758</url></web-urls></urls><custom2><style face="normal" font="default">20171220, Shingaki T</style></custom2><misc3><style face="normal" font="default">10.15036/arerugi.66.1240</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87055</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Uno,H.</style></author><author><style face="normal" font="default"> Sekimoto,H.</style></author><author><style face="normal" font="default"> Kitamura,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Nippon Kokan Fukuyama Hospital</style></auth-address><titles><title><style face="normal" font="default">[A CASE OF A 7-YEAR-OLD GIRL WITH ANAPHYLAXIS CAUSED BY PECTIN IN ALBEDO OF CITRUS UNSHIU BUT NOT BY THE FRUIT ITSELF]</style></title><secondary-title><style face="normal" font="default">Arerugi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arerugi</style></abbr-1></periodical><pages end="1247" start="1244">1244-1247</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">10</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Pectin is used in several foods as an additive and a thickner. But some cases of anaphylaxis have been reported. Most of these are induced by occasional exposures; however, no cases of anaphylaxis after eating a Citrus unshiu, the albedo of which is rich in pectin, have been reported.A 7-year-old girl developed barking cough and pruritus approximately two hours after eating a frozen Citrus unshiu. She had a history of anaphylaxis induced by consuming cashew nuts. Skin testing and basophil activation tests were performed using a commercially available pectin product. Both tests were positive. In an oral food challenge test, she felt abdominal pain and nausea only after eating fruit, along with the albedo, of Citrus unshiu. We concluded that this case was induced by pectin present in the albedo of Citrus unshiu, but not by the fruit itself. We should consider that patients with cashew nut allergies have a possibility of pectin allergies as well, and that pectin in the albedo of Citrus unshiu may induce anaphylaxis</style></abstract><notes><style face="normal" font="default">IS - 0021-4884 (Print)IS - 0021-4884 (Linking)LA - jpnPT - English AbstractPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.15036/arerugi.66.1244</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249759">PM:29249759</url></web-urls></urls><custom2><style face="normal" font="default">20171220, Uno H</style></custom2><misc3><style face="normal" font="default">10.15036/arerugi.66.1244</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86751</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Schulze,J.</style></author><author><style face="normal" font="default"> Leberkuehne,L.</style></author><author><style face="normal" font="default"> Salzmann-Manrique,E.</style></author><author><style face="normal" font="default"> Schubert,R.</style></author><author><style face="normal" font="default"> Zielen,S.</style></author><author><style face="normal" font="default"> Rosewich,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy, Pulmonology &amp; Cystic Fibrosis, Children's Hospital, Goethe University, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany</style></auth-address><titles><title><style face="normal" font="default">Comparison of two different assays and the predictive value of allergen components in house dust mite allergy</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1262" start="1253">1253-1262</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Cystic fibrosis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">AIM: In house dust mite (HDM) allergy diagnostics, the IMMULITE, ImmunoCAP and assays for allergen components (nDer p 1 and rDer p 2) are available. METHODS: Serum sIgE levels were compared and the predictive values for the detection of an early asthmatic response (EAR) were calculated with receiver operating characteristics and a log-logistic regression model. RESULTS: sIgE levels of IMMULITE and ImmunoCAP were similar (Dermatophagoides pteronyssinus [D. pter.] 47.3 +/- 35.7 and 42.9 +/- 34.4 kU.l-1; p = 0.23). ImmunoCAP slgEs exhibited similar accuracy in detecting an EAR, area under the curves (AUCs): D. pter. (0.76); Dermatophagoides farinae (0.79); nDer p 1 (0.69); and rDer p 2 (0.72). At low sIgE concentrations (3.5 kU.l-1), rDer p 2 was more specific and better predicted an EAR (probability rDer p 2: 62%; D. pter.: 19%)</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0084</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130795">PM:29130795</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171113, Schulze J</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0084</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86747</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nadir Bahceciler,N.</style></author><author><style face="normal" font="default"> Galip,N.</style></author><author><style face="normal" font="default"> Babayigit,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pediatric Allergy &amp; Immunology, Faculty of Medicine, Near East University, Nicosia, North Cyprus</style></auth-address><titles><title><style face="normal" font="default">Steroid sparing effect of sublingual immunotherapy: real life study in mono/polisensitized children with asthma</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1269" start="1263">1263-1269</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">AIM: Steroid-sparing effect of sublingual immunotherapy (SLIT) in mono/polisensitized asthmatic children were evaluated. MATERIALS AND METHODS: Children undergoing allergen-specific SLIT between 2010 and 2014 were included. Asthma control and usage/dose of inhaled corticosteroid (ICS) in the previous year was determined. Asthma control without ICS need >/=6 months was defined as 'ICS avoidance'. RESULTS: 90 children (mean +/- SD age 8.92 +/- 4.17 years) were enrolled, 56.7% (n = 60) being polysensitized. Mono, 2-simultaneous and multiple-pollen-mix allergen SLIT were prescribed in 84.4, 17.8 and 7.8%, respectively. ICS was avoided in 70%, with no significant difference in mono- versus poly-sensitized patients. ICS-avoidance rates in mono-allergen, pollen-mixture and 2-simultaneous-allergen SLIT were 93.6, 83.3 and 73.7%, respectively. Longer-duration SLIT resulted in significantly more ICS-avoidance (p:0.0001). CONCLUSION: SLIT with mono/multiple-mixed/simultaneous allergens in childhood asthma resulted in retained-avoidance of ICS. Steroid-sparing effect of SLIT in polysensitized children warrants further investigation</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - Cyprus -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0110</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130803">PM:29130803</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171113, Nadir Bahceciler N</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0110</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86749</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Incorvaia,C.</style></author><author><style face="normal" font="default"> Ridolo,E.</style></author><author><style face="normal" font="default"> Mauro,M.</style></author><author><style face="normal" font="default"> Russello,M.</style></author><author><style face="normal" font="default"> Pastorello,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Cardiac/Pulmonary Rehabilitation, ASST Pini/CTO, Milan, Italy</style></auth-address><titles><title><style face="normal" font="default">Allergen immunotherapy for birch-apple syndrome: what do we know?</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1278" start="1271">1271-1278</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Apple allergy is common in patients allergic to birch pollen, and this is defined as 'birch-apple syndrome'. Allergens responsible for cross-reactivity belong to the pathogenesis-related-10 family, and high homology in the amino acid sequences of the major allergens Bet v 1 from birch and Mal d 1 from apple has been demonstrated. Here we review the literature on the treatment of birch-apple syndrome by allergen immunotherapy. The only allergen immunotherapy method available thus far is based on the administration of birch-pollen extracts, through the subcutaneous or sublingual route, to induce tolerance to Bet v1 and to the homologous allergen Mal d 1. However, the studies performed thus far show modest efficacy, and thus other methods of immunotherapy should be investigated</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0040</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130794">PM:29130794</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunotherapy\2017-9-1271-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunotherapy\2017-9-1271-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Incorvaia C</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0040</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86890</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Laffleur,B.</style></author><author><style face="normal" font="default"> Debeaupuis,O.</style></author><author><style face="normal" font="default"> Dalloul,Z.</style></author><author><style face="normal" font="default"> Cogne,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY, United StatesFaculte de Pharmacie, Universite Paris-Descartes, Paris, FranceUMR 7276 Centre National de la Recherche Scientifique: Controle de la Reponse Immune B et des Lymphoproliferations, Universite de Limoges, Limoges, FranceUMR 7276 Centre National de la Recherche Scientifique: Controle de la Reponse Immune B et des Lymphoproliferations, Universite de Limoges, Limoges, FranceInstitut Universitaire de France, Paris, France</style></auth-address><titles><title><style face="normal" font="default">B Cell Intrinsic Mechanisms Constraining IgE Memory</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1277">1277-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Memory B cells and long-lived plasma cells are key elements of adaptive humoral immunity. Regardless of the immunoglobulin class produced, these cells can ensure long-lasting protection but also long-lasting immunopathology, thus requiring tight regulation of their generation and survival. Among all antibody classes, this is especially true for IgE, which stands as the most potent, and can trigger dramatic inflammatory reactions even when present in minute amounts. IgE responses and memory crucially protect against parasites and toxic components of venoms, conferring selective advantages and explaining their conservation in all mammalian species despite a parallel broad spectrum of IgE-mediated immunopathology. Long-term memory of sensitization and anaphylactic responses to allergens constitute the dark side of IgE responses, which can trigger multiple acute or chronic pathologic manifestations, some punctuated with life-threatening events. This Janus face of the IgE response and memory, both necessary and potentially dangerous, thus obviously deserves the most elaborated self-control schemes</style></abstract><notes><style face="normal" font="default">IS - 1664-3224 (Print)IS - 1664-3224 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -CO - France -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01277</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29180995">PM:29180995</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1277.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1277.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Laffleur B</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01277</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>44686</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhu,X.H.</style></author><author><style face="normal" font="default"> Li,Q.G.</style></author><author><style face="normal" font="default"> Wang,J.</style></author><author><style face="normal" font="default"> Hu,G.Z.</style></author><author><style face="normal" font="default"> Liu,Z.Q.</style></author><author><style face="normal" font="default"> Hu,Q.H.</style></author><author><style face="normal" font="default"> Wu,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Medicine, Nanchang University, Nanchang 330006, China.</style></auth-address><titles><title><style face="normal" font="default">[Mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice]</style></title><secondary-title><style face="normal" font="default">Zhongguo Dang Dai Er Ke Za Zhi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Zhongguo Dang Dai Er Ke Za Zhi</style></abbr-1></periodical><pages end="1284" start="1278">1278-1284</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To investigate the molecular mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice. METHODS: A total of 24 mice were randomly divided into control group, ovalbumin (OVA)-induced asthma group (OVA group), and JQ1 intervention group (JQ1+OVA group), with 8 mice in each group. OVA sensitization/challenge was performed to establish a mouse model of asthma. At 1 hour before challenge, the mice in the JQ1+OVA group were given intraperitoneal injection of JQ1 solution (50 mug/g). Bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at 24 hours after the last challenge, and the total number of cells and percentage of eosinophils in BALF were calculated. Pathological staining was performed to observe histopathological changes in lung tissue. RT-PCR and Western blot were used to measure the mRNA and protein expression of E-cadherin and vimentin during epithelial-mesenchymal transition (EMT). RESULTS: Compared with the control group, the OVA group had marked infiltration of inflammatory cells in the airway, thickening of the airway wall, increased secretion of mucus, and increases in the total number of cells and percentage of eosinophils in BALF (P&lt;0.01). Compared with the OVA group, the JQ1+OVA group had significantly alleviated airway inflammatory response and significant reductions in the total number of cells and percentage of eosinophils in BALF (P&lt;0.01). Compared with the control group, the OVA group had significant reductions in the mRNA and protein expression of E-cadherin and significant increases in the mRNA and protein expression of vimentin (P&lt;0.01); compared with the OVA group, the JQ1+OVA group had significant increases in the mRNA and protein expression of E-cadherin and significant reductions in the mRNA and protein expression of vimentin (P&lt;0.01); there were no significant differences in these indices between the JQ1+OVA group and the control group (P>0.05). CONCLUSIONS: Mice with OVA-induced asthma have airway remodeling during EMT. BET bromodomain inhibitor JQ1 can reduce airway inflammation, inhibit EMT, and alleviate airway remodeling, which provides a new direction for the treatment of asthma</style></abstract><notes><style face="normal" font="default">IS - 1008-8830 (Print)IS - 1008-8830 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29237530">PM:29237530</url></web-urls></urls><custom2><style face="normal" font="default">20171214, Zhu XH</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86750</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Molnar,V.</style></author><author><style face="normal" font="default"> Nagy,A.</style></author><author><style face="normal" font="default"> Tamasi,L.</style></author><author><style face="normal" font="default"> Galffy,G.</style></author><author><style face="normal" font="default"> Bocskei,R.</style></author><author><style face="normal" font="default"> Bikov,A.</style></author><author><style face="normal" font="default"> Czaller,I.</style></author><author><style face="normal" font="default"> Csoma,Z.</style></author><author><style face="normal" font="default"> Krasznai,M.</style></author><author><style face="normal" font="default"> Csaki,C.</style></author><author><style face="normal" font="default"> Zsigmond,G.</style></author><author><style face="normal" font="default"> Csontos,Z.</style></author><author><style face="normal" font="default"> Kurucz,A.</style></author><author><style face="normal" font="default"> Kurucz,E.</style></author><author><style face="normal" font="default"> Fabos,B.</style></author><author><style face="normal" font="default"> Balint,B.L.</style></author><author><style face="normal" font="default"> Sasvari-Szekely,M.</style></author><author><style face="normal" font="default"> Szekely,A.</style></author><author><style face="normal" font="default"> Kotyuk,E.</style></author><author><style face="normal" font="default"> Kozma,G.T.</style></author><author><style face="normal" font="default"> Cserta,G.</style></author><author><style face="normal" font="default"> Farkas,A.</style></author><author><style face="normal" font="default"> Gal,Z.</style></author><author><style face="normal" font="default"> Gezsi,A.</style></author><author><style face="normal" font="default"> Millinghoffer,A.</style></author><author><style face="normal" font="default"> Antal,P.</style></author><author><style face="normal" font="default"> Szalai,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Csertex Research Laboratory, 1037 Budapest, Becsi ut 224, HungaryDepartment of Genetics, Cell- &amp; Immunobiology, Semmelweis University, 1089 Budapest, Nagyvarad ter 4, Hungary</style></auth-address><titles><title><style face="normal" font="default">From genomes to diaries: a 3-year prospective, real-life study of ragweed-specific sublingual immunotherapy</style></title><secondary-title><style face="normal" font="default">Immunotherapy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Immunotherapy</style></abbr-1></periodical><pages end="1294" start="1279">1279-1294</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">15</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">During the last decades, the prevalence of allergy has dramatically increased. Allergen-specific immunotherapy is the only currently available medical intervention that has the potential to affect the natural course of the disease, but there are still many questions and unmet needs hindering its widespread use to fulfill its treatment potential and maximize its benefits for the society. To provide a comprehensive phenome-wide overview in sublingual immunotherapy, using ragweed allergy as a target, we planned and carried out a longitudinal, prospective, observational, open-label study (DesensIT). In this paper we present challenges of using deep and comprehensive phenotypes embracing biological, clinical and patient-reported outcomes in allergen-specific immunotherapy and show how we designed the DesensIT project to optimize data collection, processing and evaluation</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1750-7448 (Electronic)IS - 1750-743X (Linking)LA - engPT - Journal ArticleCO - Hungary -</style></notes><work-type><style face="normal" font="default">10.2217/imt-2017-0093</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130793">PM:29130793</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Immunotherapy\2017-9-1279-94.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Immunotherapy\2017-9-1279-94.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Molnar V</style></custom2><misc3><style face="normal" font="default">10.2217/imt-2017-0093</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87335</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Topal,E.</style></author><author><style face="normal" font="default"> Kaplan,F.</style></author><author><style face="normal" font="default"> Turker,K.</style></author><author><style face="normal" font="default"> Kutluturk,K.</style></author><author><style face="normal" font="default"> Gozukara Bag,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">The Prevalence of Allergic Diseases and Associated Risk Factors in the 6-7 Age Children Who are Living in Malatya, Turkey</style></title><secondary-title><style face="normal" font="default">Asthma Allergy Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Asthma Allergy Immunol</style></full-title></periodical><pages end="134" start="129">129-134</pages><volume><style face="normal" font="default">15</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Cockroaches</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Objective: The prevalence of allergic disease in children has been increasing in the recent years. There is no previous study on the prevalence of allergic disease in Malatya, Turkey. We aimed to investigate the prevalence of allergic disease and related risk factors among children aged 6-7 years in Malatya.Materials and Methods: We administered the questionnaire of the International Study of Asthma and Allergies in Childhood (ISAAC) translated into the Turkish language to 480 children aged 6-7 years living in Malatya. The questionnaires were completed by the parents for 413 (86%) of the children.Results: There were 210 (50.8%) males and the overall mean age was 6.6±0.49 years. The lifetime prevalence of wheezing, rhinitis and eczema was 20.3%, 37% and 7.5% respectively and the reported prevalence for the last 12 months was 12.3%, 32% and 6.5% respectively. When the risk factors associated with allergic disease were analyzed; male gender (p=0.001), history of parental asthma (p=0.002), doctor's diagnosis of allergic rhinitis (p=0.025) and having cockroaches at the home (p=0.002) were associated with asthma. A history of doctor's diagnosis of asthma (p&lt;0.001) and atopic eczema (p=0.001) were associated with rhinitis as risk factors. History of parental atopic eczema (p&lt;0.001) and doctor's diagnosis of asthma (p=0.006) were associated with atopic eczema as risk factors.Conclusion: This study is the first to investigate the prevalence of allergic disease in the 6-7 years age group in Malatya using the ISAAC questionnaire. The current study shows the prevalence of allergic diseases is considerable in children living in Malatya.</style></abstract><notes><style face="normal" font="default">LA - TURCO - Turkey -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://www.aai.org.tr/index.php/aai/article/view/348</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-129-34.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-129-34.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Topal E</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87021</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xu,J.</style></author><author><style face="normal" font="default"> Wang,Y.</style></author><author><style face="normal" font="default"> Chen,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Children's Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, China</style></auth-address><titles><title><style face="normal" font="default">[Lung injury in ovalbumin-challenged asthma mice induced by high-dose PM2.5 and its mechanism]</style></title><secondary-title><style face="normal" font="default">Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi</style></abbr-1></periodical><pages end="1302" start="1297">1297-1302</pages><volume><style face="normal" font="default">33</style></volume><number><style face="normal" font="default">10</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">Objective To investigate the degree of lung injury induced by different doses of particulate matter with diameters &lt;/=2.5 microm (PM2.5) in asthmatic mice. Methods Male BALB/c mice were randomly divided into normal control group, ovalbumin (OVA) asthma group, 1, 5, 15 mg/mL PM2.5 treated OVA asthma group. The bronchoalveolar lavage fluid (BALF) was collected and the number of white blood cells was observed by Gimsa staining. ELISA was used to determine the concentrations of serum cytokines interferon gamma (IFN-gamma), interleukin 17 (IL-17) and IL-10 in the peripheral blood of mice. Real-time quantitative PCR was performed to detect the mRNA expression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappaB (NF-kappaB) in peripheral blood mononuclear cells (PBMCs). The levels of T-bet, RORgammat and FOXP3 were tested by Western blotting. The lung tissues were collected and the pathological changes were observed by HE staining. Results Compared with the normal control group, the OVA asthma group showed thickened alveolar septum, enlarged alveolar cavity and more obvious inflammatory cell infiltration, as well as significantly increased white blood cells associated with inflammatory response in the BALF. Whereas, compared with the OVA asthma group, the above mentioned changes in 15 mg/mL PM2.5 treated OVA asthma group were extremely obvious. ELISA showed that the levels of IFN-gamma and IL-10 in the serum of the OVA asthma group were significantly lower than those in the control group, while IL-17 significantly increased. Compared with the OVA asthma group, the levels of IFN-gamma and IL-10 in 15 mg/mL PM2-treated OVA asthma group significantly decreased, while the content of IL-17 significantly increased. Real-time quantitative PCR showed that the expressions of TLR4 and NF-kappaB in PBMCs of the OVA asthma group were significantly higher than those in the control group. In 15 mg/mL PM2.5-treated OVA asthma group, the levels of TLR4 and NF-kappaB increased significantly as compared with the OVA asthma group. Compared with the control group, the expressions of T-bet and FOXP3 proteins in the OVA asthma group were significantly lower than those in the control group, and the expression of RORgammat protein was significantly increased. Compared with the OVA asthma group, the levels of T-bet and FOXP3 proteins were reduced a lot in 15 mg/mL PM2.5-treated OVA asthma group, while RORgammat protein level was remarkably elevated. Conclusion The 15 mg/mL PM2.5 can obviously promote OVA-induced asthma and even lung injury by activating the TLR4/NF-kappaB signaling pathway</style></abstract><notes><style face="normal" font="default">IS - 1007-8738 (Print)IS - 1007-8738 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29169411">PM:29169411</url></web-urls></urls><custom2><style face="normal" font="default">20171201, Xu J</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87180</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Christopoulou,S.</style></author><author><style face="normal" font="default"> Karaiskou,S.</style></author><author><style face="normal" font="default"> Kalogianni,D.P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Microbead-based simultaneous fluorometric detection of three nut allergens</style></title><secondary-title><style face="normal" font="default">Microchimica Acta</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Microchimica Acta</style></abbr-1></periodical><pages end="" start="13">13-</pages><volume><style face="normal" font="default">185</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1436-5073</style></isbn><abstract><style face="normal" font="default">A microbead-based method is developed for the detection of three nut allergens that can occur in food. The bead array constitutes of a suspension of spectrally distinct fluorescent polystyrene microbeads and has been applied for the simultaneous detection of three main and serious allergens (hazelnut, peanut and walnut). The method is based on the simultaneous identification of specific DNA sequences after PCR. The PCR products are biotinylated and hybridized to nut-specific oligonucleotide probes attached to the microbeads. The hybrids are finally detected by a streptavidin-phycoerythrin conjugate and flow cytometric analysis. As low as 0.01% content of the three nuts in processed food (cookies) can be detected by this method</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Greece -</style></notes><work-type><style face="normal" font="default">10.1007/s00604-017-2559-7</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s00604-017-2559-7</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Microchimica Acta\2017-185-13.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Microchimica Acta\2017-185-13.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Christopoulou S</style></custom2><misc3><style face="normal" font="default">10.1007/s00604-017-2559-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86521</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhou,C.</style></author><author><style face="normal" font="default"> Ibanez,G.</style></author><author><style face="normal" font="default"> Miramont,V.</style></author><author><style face="normal" font="default"> Steinecker,M.</style></author><author><style face="normal" font="default"> Baiz,N.</style></author><author><style face="normal" font="default"> Banerjee,S.</style></author><author><style face="normal" font="default"> Just,J.</style></author><author><style face="normal" font="default"> Annesi-Maesano,I.</style></author><author><style face="normal" font="default"> Chastang,J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Prenatal maternal depression related to allergic rhinoconjunctivitis in the first 5 years of life in children of the EDEN mother-child cohort study</style></title><secondary-title><style face="normal" font="default">Allergy Rhinol (Providence)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Rhinol (Providence)</style></abbr-1></periodical><pages end="138" start="132">132-138</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="10" Year="2017">2017/10/1</year></dates><abstract><style face="normal" font="default">Backgroud: Evidence about the relationship between prenatal maternal depression and the development of childhood asthma and allergies in early life is scarce. We aimed to examine this relationship by using data set of EDEN mother-child cohort study. A total of 1139 children were followed-up until the age of 5 years. METHODS: Prenatal maternal depression was self-reported by using the Centre for Epidemiological Studies-Depression scale (CES-D) questionnaire and was classified into binary variable (maternal depression [CES-D score of >/=16] and no maternal depression [CES-D score of &lt;16]). Asthma and allergies in the first 5 years were assessed by using the questionnaire of the International Study of Asthma and Allergies in Childhood (ISAAC). Adjusted odds ratio (aOR) was estimated for the relationship between prenatal maternal depression and early life asthma and allergies by marginal models through the method of generalized estimating equation (GEE) when adjusting for the confounders. RESULTS: In our study population, 13.67 % of the mothers had clinical significant depression (the total scores for CES-D >/=16) during pregnancy. For children ages 5 years, the prevalence of wheezing, physician-diagnosed asthma, physician-diagnosed eczema and allergic rhinoconjunctivitis were 46.78, 20.99, 29.17, and 22.54%, respectively. Prenatal maternal depression was associated with ever allergic rhinoconjunctivitis (aOR 1.87 [95% confidence interval {CI}, 1.33-2.62]). No significant relationships were found between prenatal maternal depression and wheezing, physician-diagnosed asthma and physician-diagnosed eczema (aOR 1.12 [95% CI, 0.91-1.39], aOR 1.23 [95% CI, 0.81-1.85] and aOR 1.17 [95% CI, 0.86-1.61], respecitvely). CONCLUSION: Prenatal maternal depression was related to ever allergic rhinoconjunctivitis in the first 5 years of life in children of EDEN mother-child cohort study</style></abstract><notes><style face="normal" font="default">DA - 20171026IS - 2152-6575 (Print)IS - 2152-6567 (Linking)LA - engPT - Journal ArticleCO - China -CO - France -</style></notes><work-type><style face="normal" font="default">10.2500/ar.2017.8.0213</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29070270">PM:29070270</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Rhinol (Providence)\2017-8-132-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Rhinol (Providence)\2017-8-132-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171026, Zhou C</style></custom2><misc3><style face="normal" font="default">10.2500/ar.2017.8.0213</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86641</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vajravijayan,S.</style></author><author><style face="normal" font="default"> Nandhagopal,N.</style></author><author><style face="normal" font="default"> Gunasekaran,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre of Advanced Study in Crystallography and Biophysics, University of Madras, Guindy Campus, Chennai 600 025, India</style></auth-address><titles><title><style face="normal" font="default">Crystal structure determination and analysis of 11S coconut allergen: Cocosin</style></title><secondary-title><style face="normal" font="default">Mol Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Immunol</style></abbr-1></periodical><pages end="135" start="132">132-135</pages><volume><style face="normal" font="default">92</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="27" Month="10" Year="2017">2017/10/27</year></dates><abstract><style face="normal" font="default">Allergy is an abnormal immune response against an innocuous target. Food allergy is an adverse reaction caused by common foods most well-known being those involving peanuts. Apart from mono sensitized food allergy, cross-reactivity with other food allergens is also commonly observed. To understand the phenomenon of cross-reactivity related to immune response, three dimensional structures of the allergens and their antigenic epitopes has to be analysed in detail. The X-ray crystal structure of Cocosin, a common 11S food allergen from coconut, has been determined at 2.2A resolution using molecular replacement technique. The monomer of 52kDa is composed of two beta-jelly roll domains, one with acidic and the other with basic character. The structure shows hexameric association with two trimers facing each other. Though the overall structure of Cocosin is similar to other 11S allergens, the occurrence of experimentally determined epitopes of the peanut allergen Ara h 3 at flexible as well as variable regions could be the reason for the clinically reported result of cross-reactivity that the peanut allergic patients are not sensitized with coconut allergen</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 1872-9142 (Electronic)IS - 0161-5890 (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.1016/j.molimm.2017.10.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29096167">PM:29096167</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Immunol\2017-92-132-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Immunol\2017-92-132-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Vajravijayan S</style></custom2><misc3><style face="normal" font="default">10.1016/j.molimm.2017.10.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87108</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Farioli,L.</style></author><author><style face="normal" font="default"> Losappio,L.M.</style></author><author><style face="normal" font="default"> Giuffrida,M.G.</style></author><author><style face="normal" font="default"> Pravettoni,V.</style></author><author><style face="normal" font="default"> Micarelli,G.</style></author><author><style face="normal" font="default"> Nichelatti,M.</style></author><author><style face="normal" font="default"> Scibilia,J.</style></author><author><style face="normal" font="default"> Mirone,C.</style></author><author><style face="normal" font="default"> Cavallarin,L.</style></author><author><style face="normal" font="default"> Lamberti,C.</style></author><author><style face="normal" font="default"> Balossi,L.G.</style></author><author><style face="normal" font="default"> Pastorello,E.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Laboratory Medicine, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy</style></auth-address><titles><title><style face="normal" font="default">Mite-Induced Asthma and IgE Levels to Shrimp, Mite, Tropomyosin, Arginine Kinase, and Der p 10 Are the Most Relevant Risk Factors for Challenge-Proven Shrimp Allergy</style></title><secondary-title><style face="normal" font="default">Int Arch Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Arch Allergy Immunol</style></abbr-1></periodical><pages end="143" start="133">133-143</pages><volume><style face="normal" font="default">174</style></volume><number><style face="normal" font="default">3-4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Tropomyosin</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: Shrimp sensitization is common in the general population, but the presence of symptoms is only moderately related to sensitization. A point still at issue is which in vivo and/or in vitro tests (food challenge, component-resolved diagnosis, house dust mite [HDM] sensitization) can help in distinguishing shrimp-allergic subjects from subjects that are sensitized but tolerant. METHODS: The aim of this study was to evaluate the role of IgE to the different shrimp and mite allergens in distinguishing shrimp challenge-positive from challenge-negative patients. Subjects with suspected hypersensitivity reactions to shrimp, positive skin prick tests (SPTs), and/or anti-shrimp IgE were submitted to open and double-blind placebo-controlled food challenges (DBPCFC). Specific IgE to shrimp, mites, and the recombinants rPen a 1, rDer p 1, 2, and 10 were tested using ImmunoCAP-FEIA. IgE immunoblotting was performed to identify the patients' allergenic profiles. RESULTS: In total, 13 out of 51 (25.5%) patients with reported reactions to shrimp were truly shrimp allergic (7 DBPCFC positive and 6 with documented severe reactions). These patients had significantly higher skin test wheal diameters than nonallergic patients, as well as higher levels of IgE to rPen a 1 and rDer p 10. HDM-induced asthma and the simultaneous presence of anti-nDer p 1, 2, and 10 IgE levels increased the risk of true shrimp allergy. CONCLUSION: Food challenge tests are mandatory for the diagnosis of shrimp allergy. Tropomyosin is associated with clinical reactivity. HDM-induced asthma and anti-mite IgE are risk factors for shrimp allergy</style></abstract><notes><style face="normal" font="default">IS - 1423-0097 (Electronic)IS - 1018-2438 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1159/000481985</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29169170">PM:29169170</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-133-43.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-133-43.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Farioli L</style></custom2><misc3><style face="normal" font="default">10.1159/000481985</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86839</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Geng,G.</style></author><author><style face="normal" font="default"> Du,Y.</style></author><author><style face="normal" font="default"> Dai,J.</style></author><author><style face="normal" font="default"> Tian,D.</style></author><author><style face="normal" font="default"> Xia,Y.</style></author><author><style face="normal" font="default"> Fu,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiration, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing 400014, China</style></auth-address><titles><title><style face="normal" font="default">KIF3A knockdown sensitizes bronchial epithelia to apoptosis and aggravates airway inflammation in asthma</style></title><secondary-title><style face="normal" font="default">Biomed Pharmacother</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biomed Pharmacother</style></abbr-1></periodical><pages end="1355" start="1349">1349-1355</pages><volume><style face="normal" font="default">97</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="15" Month="11" Year="2017">2017/11/15</year></dates><abstract><style face="normal" font="default">BACKGROUND: KIF3A expression was decreased in asthmatic child patients and animal. Impaired KIF3A expression resulted in increased Th2 inflammation in mice and apoptosis in renal tubular epithelium and photoreceptor cells. This work aimed to investigate the role of KIF3A in epithelium apoptosis and bronchial inflammation in asthma. METHODS: After establishment of ovalbumin induced asthma, the mice were infected with KIF3A adenovirus through nasal cavity inhalation. KIF3A expression and apoptosis in epithelia of nasal mucosa and bronchia were determined using qRT-PCR, western blotting, immunohistochemistry and TUNEL staining. The mRNA expression of COX-2, IL-4, IL-5, IL-13, IL-6, IL-10 and TNF-alpha was also measured. In vitro, human bronchial epithelial cell line 16HBE 14o- was stimulated with IL-4, IL-13 and TNF-alpha, accompanied by KIF3A knockdown or overexpression using siRNA or KIF3A adenovirus respectively. Apoptosis, mRNA expression of CCL17, CCL26, IL-5 and IL-8, and protein expression of COX-2 and beta-catenin were determined using flow cytometry, qRT-PCR and western blotting. RESULTS: KIF3A expression was reduced in epithelia of nasal mucosa and bronchia of asthmatic mice, and overexpression of KIF3A ameliorated epithelial cell apoptosis and bronchial inflammation in asthmatic mice. In vitro, KIF3A knockdown significantly promoted epithelium apoptosis, facilitated the transcription of CCL17, CCL26, IL-5 and IL-8, and increased the protein levels of COX-2 and beta-catenin translocation, whereas overexpression of KIF3A exhibited the opposite effect. CONCLUSION: KIF3A plays an important role in epithelium apoptosis and bronchial inflammation in asthma, and may be a potential target for asthma treatment</style></abstract><notes><style face="normal" font="default">IS - 1950-6007 (Electronic)IS - 0753-3322 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.biopha.2017.10.160</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29156524">PM:29156524</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biomed Pharmacother\2017-97-1349-55.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biomed Pharmacother\2017-97-1349-55.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Geng G</style></custom2><misc3><style face="normal" font="default">10.1016/j.biopha.2017.10.160</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87337</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ozceker,D.</style></author><author><style face="normal" font="default"> Durak,C.</style></author><author><style face="normal" font="default"> Kardelen,A.D.</style></author><author><style face="normal" font="default"> Guler,N.</style></author><author><style face="normal" font="default"> Tamay,Z.</style></author></authors></contributors><titles><title><style face="normal" font="default">Atopic Dermatitis in Children: How Much Atopic?</style></title><secondary-title><style face="normal" font="default">Asthma Allergy Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Asthma Allergy Immunol</style></full-title></periodical><pages end="139" start="135">135-139</pages><volume><style face="normal" font="default">15</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Inhalant allergen</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Objective: One of the many factors that involved with the pathogenesis of atopic dermatitis (AD) is sensitivity to allergens. Food allergy is a known etiological factor and evidence connecting sensitivity to inhalant allergens with atopic dermatitis also keeps increasing. Our study aimed to investigate allergen hypersensitivity together with clinical features and allergic parameters of children with atopic dermatitis who live in Istanbul.Materials and Methods: A total of 826 children aged 2-18 years who had been followed-up with an AD diagnosis at the Istanbul University Medical School's Allergy and Immunology Department between January 2010 and December 2013 were included in our study. Age, gender, atopy history in the family, serum levels of total IgE, presence of additional allergic disease, eosinophil percentage in total blood count and the results of skin prick tests were recorded for these patients.Results: Among the patients included in the study, 41.2% (n:340) were female and 58.8% (n=486) were male, and the mean age was 6.48±3.50 years. Atopic children made up 80% and non-atopic children 20% of the patient population. Patients whose Ig E level was >100 were found to be more sensitive to allergens (p&lt;0.001). As age increased, sensitivity to allergens also increased (p&lt;0.001). Accompanying respiratory allergic diseases were not found to be related with sensitivity to allergens (p=0.07). The most frequent allergens in this study were house dust mite, sweet vernal grass, and cynodon dactylon.Conclusion: We found that 80% of the children with atopic dermatitis who lived in Istanbul were atopic and the most frequent allergen we came across was house dust mite. When dealing with AD patients who are resistant to therapy, house dust mite allergy should be considered and relevant precautions may be clinically useful.</style></abstract><notes><style face="normal" font="default">LA - TURCO - Turkey -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://www.aai.org.tr/index.php/aai/article/view/333</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-135-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-135-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Ozceker D</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86552</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Roberts,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Faculty of Medicine, Clinical and Experimental Sciences and Human Development and Health, University of Southampton, Southampton, UK</style></auth-address><titles><title><style face="normal" font="default">Towards safer oral immunotherapy for food allergy and allergic asthma is still increasing in prevalence</style></title><secondary-title><style face="normal" font="default">Clin Exp Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Exp Allergy</style></abbr-1></periodical><pages end="1361" start="1360">1360-1361</pages><volume><style face="normal" font="default">47</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171027IS - 1365-2222 (Electronic)IS - 0954-7894 (Linking)LA - engPT - EditorialCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1111/cea.13046</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29076600">PM:29076600</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Exp Allergy\2017-47-1360-1.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Exp Allergy\2017-47-1360-1.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171027, Roberts G</style></custom2><misc3><style face="normal" font="default">10.1111/cea.13046</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86944</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Planque,M.</style></author><author><style face="normal" font="default"> Arnould,T.</style></author><author><style face="normal" font="default"> Dieu,M.</style></author><author><style face="normal" font="default"> Delahaut,P.</style></author><author><style face="normal" font="default"> Renard,P.</style></author><author><style face="normal" font="default"> Gillard,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">CER Groupe, Health Department, Rue du Point du Jour, 8, 6900 Marloie, Belgium; Laboratory of Biochemistry and Cell Biology (URBC)-Namur Research Institute for Life Sciences (NARILIS), University of Namur, 61, rue de Bruxelles, 5000 Namur, Belgium</style></auth-address><titles><title><style face="normal" font="default">Liquid chromatography coupled to tandem mass spectrometry for detecting ten allergens in complex and incurred foodstuffs</style></title><secondary-title><style face="normal" font="default">J Chromatogr A</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Chromatogr A</style></abbr-1></periodical><pages end="151" start="138">138-151</pages><volume><style face="normal" font="default">1530</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="29" Month="12" Year="2017">2017/12/29</year></dates><abstract><style face="normal" font="default">Food allergy is a considerable heath problem, as undesirable contaminations by allergens during food production are still widespread and may be dangerous for human health. To protect the population, laboratories need to develop reliable analytical methods in order to detect allergens in various food products. Currently, a large majority of allergen-related food recalls concern bakery products. It is therefore essential to detect allergens in unprocessed and processed foodstuffs. In this study, we developed a method for detecting ten allergens in complex (chocolate, ice cream) and processed (cookie, sauce) foodstuffs, based on ultra-high performance liquid chromatography coupled to tandem mass spectrometry (UHPLC-MS/MS). Using a single protocol and considering a signal-to-noise ratio higher than 10 for the most abundant multiple reaction monitoring (MRM) transition, we were able to detect target allergens at 0.5mg/kg for milk proteins, 2.5mg/kg for peanut, hazelnut, pistachio, and cashew proteins, 3mg/kg for egg proteins, and 5mg/kg for soy, almond, walnut, and pecan proteins. The ability of the method to detect 10 allergens with a single protocol in complex and incurred food products makes it an attractive alternative to the ELISA method for routine laboratories</style></abstract><notes><style face="normal" font="default">IS - 1873-3778 (Electronic)IS - 0021-9673 (Linking)LA - engPT - Journal ArticleCO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1016/j.chroma.2017.11.039</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29169644">PM:29169644</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Chromatogr A\2017-1530-138-51.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Chromatogr A\2017-1530-138-51.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Planque m</style></custom2><misc3><style face="normal" font="default">10.1016/j.chroma.2017.11.039</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86788</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Romero-Sandoval,K.</style></author><author><style face="normal" font="default"> Costa,A.A.</style></author><author><style face="normal" font="default"> Teixeira Sousa,M.G.</style></author><author><style face="normal" font="default"> Furucho,C.R.</style></author><author><style face="normal" font="default"> Valente,N.</style></author><author><style face="normal" font="default"> Criado,P.R.</style></author><author><style face="normal" font="default"> Aoki,V.</style></author><author><style face="normal" font="default"> Benard,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Hospital das Clinicas da Faculdade de Medicina da Universidade de Sao Paulo. Avenue Dr. Eneas de Carvalho Aguiar 255, CEP 05403-000 Sao Paulo, Brazil.</style></auth-address><titles><title><style face="normal" font="default">Recurrent and disseminated pityriasis versicolor: A novel clinical form consequent to Malassezia-host interaction?</style></title><secondary-title><style face="normal" font="default">Med Hypotheses</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Med Hypotheses</style></abbr-1></periodical><pages end="144" start="139">139-144</pages><volume><style face="normal" font="default">109</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Pityriasis versicolor is a superficial fungal infection caused by Malassezia spp. The aim of this study is to propose the definition of a new clinical entity: the recurrent and disseminated pityriasis versicolor (RDPV). All patients with RDPV were enrolled over an eight-month period. Clinical and epidemiological data were obtained, Malassezia (M.) species were isolated in cultures and identified by phenotypic and molecular characterization, skin biopsies were taken from active lesions, serum levels of immunoglobulin E were obtained and therapeutic schemes were evaluated. A total of 16 patients were included (11 male, 5 female). The most frequently isolated species were M. japonica (n=3) and M. furfur (n=3). This is the first study that isolates M. japonica in patients with pityriasis versicolor; interestingly, those were recalcitrant patients. Seven patients (43.8%) had no cure with any of the proposed treatments; among those, 5 (71.4%) had increased serum IgE levels. The most effective treatment was itraconazole 200mg daily for 28days. The RDPV has very different features from the classic form, including a poor response to treatment, and the isolation of different Malassezia species; therefore, we propose a hypothesis for the definition of a new clinical condition (RDPV), which could be a result of the interaction Malassezia-host</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1532-2777 (Electronic)IS - 0306-9877 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.mehy.2017.10.013</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150273">PM:29150273</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Med Hypotheses\2017-109-139-44.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Med Hypotheses\2017-109-139-44.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Romero-Sandoval K</style></custom2><misc3><style face="normal" font="default">10.1016/j.mehy.2017.10.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87391</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Buczylko,K.</style></author><author><style face="normal" font="default"> Majsiak,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Upper aero- and digestive tract allergy - selected cross reactivity</style></title><secondary-title><style face="normal" font="default">Pol J Allergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pol J Allergol</style></abbr-1></periodical><pages end="145" start="139">139-145</pages><volume><style face="normal" font="default">4</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Bet v 1-2</style></keyword><keyword><style face="normal" font="default"> Components</style></keyword><keyword><style face="normal" font="default"> Der p 1- 36</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Laryngitis</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Oesophagitis</style></keyword><keyword><style face="normal" font="default"> Oral allergy syndrome</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> Pharyngitis</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sal s 1-8</style></keyword><keyword><style face="normal" font="default"> sIgE</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2353-3854</style></isbn><abstract><style face="normal" font="default">Allergic rhinitis, stomatitis, pharyngitis, laryngitis and oesophagitis are characterized by IgE-mediated reactions. There was a strong correlation between mites component resolved diagnostic (CRD) and chronic allergic rhinitis. CRD had important influence on cross- reaction's diagnostics. The majority of birch allergic patients are IgE-sensitized to the major birch pollen allergen Bet v 1 as well as to the major apple CRD Mal d 1 and soy bean allergen Gly m 4. Birch pollen-related oral allergy syndrome (OAS) is a common type of food allergy, transient and mild in nature. More information is discovered about the possible causal association between allergy and vocal pathologies or eosinophilic eosophagitis (EoE). Cross-reactivity of the wheat CRD may be important. Allergenic extracts and molecular components are available at present in FABER test. Allergen molecular diagnostics may represent a useful way in allergy work-up. Many data suggest that components resolved diagnostics constitutes a reliable tool for the diagnosis of pollen-food syndromes or other form of cross-reactivity</style></abstract><notes><style face="normal" font="default">LA - POLCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1016/j.alergo.2017.09.003</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.alergo.2017.09.003</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pol J Allergol\2017-4-139-45.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pol J Allergol\2017-4-139-45.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170920, Buczylko K</style></custom2><misc3><style face="normal" font="default">10.1016/j.alergo.2017.09.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86882</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jonsson,K.</style></author><author><style face="normal" font="default"> Barman,M.</style></author><author><style face="normal" font="default"> Brekke,H.K.</style></author><author><style face="normal" font="default"> Hesselmar,B.</style></author><author><style face="normal" font="default"> Johansen,S.</style></author><author><style face="normal" font="default"> Sandberg,A.S.</style></author><author><style face="normal" font="default"> Wold,A.E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Food and Nutrition Science, Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden</style></auth-address><titles><title><style face="normal" font="default">Late introduction of fish and eggs is associated with increased risk of allergy development - results from the FARMFLORA birth cohort</style></title><secondary-title><style face="normal" font="default">Food Nutr Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Nutr Res</style></abbr-1></periodical><pages end="" start="1393306">1393306-</pages><volume><style face="normal" font="default">61</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The prevalence of allergy is markedly low in children growing up on farms. An increasing number of studies indicate that the timing of food introduction may affect allergy development. We aimed to investigate if protection against allergy in farm environments may be mediated through differences in food-introduction practices between farm and non-farm families, using an explorative approach. Twenty-eight farm and 37 non-farm children were included in the FARMFLORA birth cohort. Practices of breastfeeding and introduction of formulas and complementary foods were collected by questionnaires at 6, 12, and 18 months of age. Allergy was diagnosed by pediatricians at 3 years of age. The only difference in food-introduction practices observed between farm and non-farm children was an earlier introduction of nuts in farmers (median month: 11 [IQR: 8-6] in farmers, 15 [12-19] in non-farmers). One farm child (4%) and 10 non-farm children (27%) were allergic at 3 years of age. Lower risk of allergy development was associated with early exclusive breastfeeding (continuous variable; OR = 0.59, 95% CI: 0.39-0.89), but also having received eggs (OR = 0.08, 95% CI: 0.13-0.54) and fish (logistic regression not applicable, P = 0.01 in likelihood ratio testing [chi(2)]) at 10 months of age or earlier compared to later. Our results were not affected by reverse causation, as judged by a questionnaire sent to the families in retrospect. Timing of introduction of complementary foods is unlikely to contribute to the lower risk of allergy among farm children. Although early exclusive breastfeeding was associated with a lower rate of allergy development, postponed introduction of complementary foods might increase the risk of developing allergy. Owing to the limited sample size, our results are only indicative, but support prior findings</style></abstract><notes><style face="normal" font="default">IS - 1654-661X (Print)IS - 1654-661X (Linking)LA - engPT - Journal ArticleCO - Sweden -CO - Norway -</style></notes><work-type><style face="normal" font="default">10.1080/16546628.2017.1393306</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29151834">PM:29151834</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Nutr Res\2017-61-1393306.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Nutr Res\2017-61-1393306.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171206, Jonsson K</style></custom2><misc3><style face="normal" font="default">10.1080/16546628.2017.1393306</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86883</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lee,S.Y.</style></author><author><style face="normal" font="default"> Bae,C.S.</style></author><author><style face="normal" font="default"> Choi,Y.H.</style></author><author><style face="normal" font="default"> Seo,N.S.</style></author><author><style face="normal" font="default"> Na,C.S.</style></author><author><style face="normal" font="default"> Yoo,J.C.</style></author><author><style face="normal" font="default"> Cho,S.S.</style></author><author><style face="normal" font="default"> Park,D.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">College of Oriental Medicine, Dongshin University, Naju, Jeonnam, Korea</style></auth-address><titles><title><style face="normal" font="default">Opuntia humifusa modulates morphological changes characteristic of asthma via IL-4 and IL-13 in an asthma murine model</style></title><secondary-title><style face="normal" font="default">Food Nutr Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Nutr Res</style></abbr-1></periodical><pages end="" start="1393307">1393307-</pages><volume><style face="normal" font="default">61</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Asthma is a chronic pulmonary disease that affects an estimated 235 million people worldwide, but asthma drugs have many adverse effects. Opuntia humifusa (eastern prickly pear) has been used as a food and traditional medicine worldwide; however, its anti-asthmatic effects have not been reported. We evaluated O. humifusa as a potential therapeutic or preventive component of anti-asthmatic drugs. We divided ovalbumin-sensitized mice into the following groups: normal control, asthma-induced control, dexamethasone-treated group (positive control), 50 mg/kg O. humifusa-treated group, 100 mg/kg O. humifusa-treated group, and 500 mg/kg O. humifusa-treated group. Levels of Th1/Th2/Th17-related cytokines were evaluated using RT-PCR, ELISA, and immunohistochemistry. O. humifusa dose-dependently suppressed the morphological changes typically observed in asthma, such as goblet cell hyperplasia, inflammatory cell infiltration, mucous hypersecretion, and relative basement membrane thickening in the respiratory system. These results may be attributable to regulation of Th1-/Th2-/Th17-related factors, especially interleukin (IL)-4 and IL-13. We conclude that O. humifusa is a potential anti-asthmatic functional food. Abbreviations: O. humifusa: Opuntia humifusa; Th: helper T; RT-PCR: real-time polymerase chain reaction; ELISA: enzyme-linked immunosorbent assay; IL: interleukin; WHO: World Health Organization; IFN-gamma: interferon gamma; TNF-alpha: tumor necrosis factor-alpha; IgE: immunoglobulin E; CD: cluster of differentiation; OVA: ovalbumin; DEX: dexamethasone; BALF: bronchoalveolar fluid; H&amp;E: hematoxylin and eosin; PAS: periodic acid-schiff; PBS: phosphate-buffered saline; BM: basement membrane; cDNA: complementary deoxyribonucleic acid; RNA: ribo nucleic acid; RIPA: radioimmunoprecipitation assay; IHC: immunohistochemistry; HPLC: high-performance liquid chromatography; SD: standard deviation; WBC: white blood cells; APCs: antigen-presenting cells</style></abstract><notes><style face="normal" font="default">IS - 1654-661X (Print)IS - 1654-661X (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1080/16546628.2017.1393307</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29151835">PM:29151835</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Nutr Res\2017-61-1393307.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Nutr Res\2017-61-1393307.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Lee SY</style></custom2><misc3><style face="normal" font="default">10.1080/16546628.2017.1393307</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87336</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bicakci,A.</style></author><author><style face="normal" font="default"> Saatcioglu,G.</style></author><author><style face="normal" font="default"> Tosunoglu,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Allergenic Betula (Birch) Pollen Concentrations in Turkey</style></title><secondary-title><style face="normal" font="default">Asthma Allergy Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Asthma Allergy Immunol</style></full-title></periodical><pages end="151" start="140">140-151</pages><volume><style face="normal" font="default">15</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Aeroallergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Oral allergy syndrome</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Objective: Pollen grains belonging to some plants have an important place among aeroallergens that present in the air and cause allergies by entering the body via the respiratory tract. These include Betula (birch - birch tree) pollen belonging to the family of Betulaceae.Materials and Methods: In this study, we reviewed studies on the monthly variation and annual proportions of Betula pollen in 51 different regions in Turkey with the volumetric method using a Lanzoni/Burkard sampler or with the gravimetric method using a Durham sampler together with the daily distribution of Betula pollen in m3 air in Bursa province in 2012. Furthermore, the authors reviewed studies on Betula pollen sensitivities in Europe and our country.Results: According to the atmospheric pollen studies, Birch tree pollen was found in the air for 3-5 months at many centers. It was most intensely observed in March-April. A total of 454 birch pollens were found in m3 air in 2012 in Bursa. The birch tree main pollen season lasted 86 days and birch pollen grains were most intensely encountered in March.Conclusion: Symptoms can develop in people who are sensitive to birch tree pollen in the spring due to widespread planting for decorative purposes especially in parks and gardens and along the streets in recent years and the resultant production of large amounts of pollen, especially in April and May. In addition, it must not forgotten that some food allergies of vegetable origin (oral allergy syndrome) can be accompanied by pollen allergy in these individuals.</style></abstract><notes><style face="normal" font="default">LA - TURCO - Turkey -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://www.aai.org.tr/index.php/aai/article/view/367</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-140-51.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-140-51.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Bicakci A</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86543</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Venturini,C.L.</style></author><author><style face="normal" font="default"> Macho,A.</style></author><author><style face="normal" font="default"> Arunachalam,K.</style></author><author><style face="normal" font="default"> de Almeida,D.A.T.</style></author><author><style face="normal" font="default"> Rosa,S.I.G.</style></author><author><style face="normal" font="default"> Pavan,E.</style></author><author><style face="normal" font="default"> Balogun,S.O.</style></author><author><style face="normal" font="default"> Damazo,A.S.</style></author><author><style face="normal" font="default"> Martins,D.T.O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Area de Farmacologia, Departamento de Ciencias Basicas em Saude, Faculdade de Medicina, Universidade Federal de Mato Grosso, Cuiaba, Mato Grosso, Brazil</style></auth-address><titles><title><style face="normal" font="default">Vitexin inhibits inflammation in murine ovalbumin-induced allergic asthma</style></title><secondary-title><style face="normal" font="default">Biomed Pharmacother</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biomed Pharmacother</style></abbr-1></periodical><pages end="151" start="143">143-151</pages><volume><style face="normal" font="default">97</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">Vitexin is an important component of various medicinal plants frequently used to treat asthma, such as Crataegus spp., Vitex spp., Passiflora spp., and Echinodorus spp. However, there is no information about the vitexin potential as anti-asthmatic. The aim of the present work was to evaluate the anti-hypersensitive activity of vitexin in a murine ovalbumin (OVA)-induced allergic asthma model. Mice were sensitized to OVA by i.p. injection on days 1st and 10th, followed by a daily challenge with OVA using a nebulizer, from days 19th to 24th. Vitexin or dexamethasone were orally administered 1h before each OVA challenge. Vitexin attenuates migration induced by OVA-hypersensitivity of eosinophil, neutrophil, and mononuclear cells in bronchoalveolar lavage fluid (BALF). Histological analysis of the lungs shows that vitexin suppressed leukocyte infiltration, mucus production and pulmonary edema. Increases in Th2 cytokines in BALF in OVA-induced asthma is also attenuated by vitexin, as well as plasma levels of IgE. Overall, these results suggest that vitexin can suppress OVA-induced allergic inflammation in mice and provide a strong rationale for further developing vitexin as a candidate treatment for allergic hypersensitivity. These data corroborate the popular use of vitexin-rich plants for asthma treatment</style></abstract><notes><style face="normal" font="default">DA - 20171101IS - 1950-6007 (Electronic)IS - 0753-3322 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.biopha.2017.10.073</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29091859">PM:29091859</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biomed Pharmacother\2017-97-143-51.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biomed Pharmacother\2017-97-143-51.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171101, Venturini CL</style></custom2><misc3><style face="normal" font="default">10.1016/j.biopha.2017.10.073</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86801</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dubakiene,R.</style></author><author><style face="normal" font="default"> Rubinaite,V.</style></author><author><style face="normal" font="default"> Petronyte,M.</style></author><author><style face="normal" font="default"> Dalgediene,I.</style></author><author><style face="normal" font="default"> Rudzeviciene,O.</style></author><author><style face="normal" font="default"> Dubakaite,D.</style></author><author><style face="normal" font="default"> Rudaleviciene,P.</style></author><author><style face="normal" font="default"> Zvirbliene,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Faculty of Medicine, Vilnius University, Vilnius, Lithuania</style></auth-address><titles><title><style face="normal" font="default">Investigation of markers of allergic sensitization and viral infections in children with allergy and asthma</style></title><secondary-title><style face="normal" font="default">Acta Med Litu</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Acta Med Litu</style></abbr-1></periodical><pages end="152" start="145">145-152</pages><volume><style face="normal" font="default">24</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: Allergic diseases are the most prevalent chronic diseases in the developed countries. It is believed that early allergic sensitization and respiratory viral infections play an important role in the development of allergic diseases and asthma. Methods: The current study investigated the correlation between asthma, allergy, and various markers - allergen-specific IgE, IgG4 and IgA, ECP, IgM, and IgG antibodies against respiratory viruses hRSV and hPIV1-4 - in blood serum samples from 80 children (mean age 5.2 years) recruited from the Lithuanian birth cohort. Children were divided into three groups according to their diagnosis: asthma (n = 25), allergy without asthma (n = 14), and control group (n = 41). Results: Based on retrospective data, airway infections and bronchitis by the age of two years were associated with asthma in later childhood. The presence of IgM and IgG antibodies against hRSV and hPIV1-4 at the age of five years were not associated with asthma and allergy: a high rate of persistent or past respiratory viral infections was revealed in all three groups. Among allergic children, increased levels of allergen-specific IgE and d1-specific IgG4 were determined. Conclusion: The current study provides new insights into the relationships between allergic sensitization and respiratory virus infections in children</style></abstract><notes><style face="normal" font="default">IS - 1392-0138 (Print)IS - 1392-0138 (Linking)LA - engPT - Journal ArticleCO - Lithuania -</style></notes><work-type><style face="normal" font="default">10.6001/actamedica.v24i3.3548</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29217968">PM:29217968</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Med Litu\2017-24-145.52.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Med Litu\2017-24-145.52.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Dubakiene R</style></custom2><misc3><style face="normal" font="default">10.6001/actamedica.v24i3.3548</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86640</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shi,T.</style></author><author><style face="normal" font="default"> Li,R.</style></author><author><style face="normal" font="default"> Chen,Q.</style></author><author><style face="normal" font="default"> Li,Y.</style></author><author><style face="normal" font="default"> Pan,F.</style></author><author><style face="normal" font="default"> Chen,Q.</style></author></authors></contributors><titles><title><style face="normal" font="default">De novo sequencing of seed transcriptome and development of genic-SSR markers in common buckwheat (Fagopyrum esculentum)</style></title><secondary-title><style face="normal" font="default">Mol Breed</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Mol Breed</style></full-title></periodical><pages end="" start="147">147-</pages><volume><style face="normal" font="default">37</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1572-9788</style></isbn><abstract><style face="normal" font="default">Large-scale identification of simple sequence repeat (SSR) markers has not been reported in the genus Fagopyrum due to a lack of genomic resources. High-throughput transcriptomic sequencing can provide a rich resource for development of genic-SSR markers. In our study, the immature seeds transcriptome of common buckwheat (Fagopyrum esculentum) was sequenced using the Illumina HiSeq</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">äó 2000 platform. We obtained a total of 21 million paired-end reads after filtering. The reads were assembled into 54,947 transcripts with an average length of 1235-ábp. In total, 46,126 (83.95%) transcripts showed significant hits to known proteins or domains. Among these, 43,647 (79.43%) transcripts was assigned at least one gene ontology (GO) term. A total of 12,677 (23.07%) transcripts were mapped to the 141 Kyoto Encyclopedia of Genes and Genome (KEGG) pathways. Overall, 2326 transcripts contained at least one SSR with a frequency of one SSR per 1.17-ákb. Mono-nucleotide repeats were the most abundant type (45.48%) followed by tri-nucleotide repeats (35.17%). Of the 150 SSRs chosen randomly, 36 markers showed polymorphism among 24 common buckwheat accessions, and 141 genic-SSRs (94.0%) were transferable to tartary buckwheat. A low level of genetic diversity was found among 35 registered tartary buckwheat varieties in China assessed using 31 polymorphic SSR markers. Genic-SSR markers developed herein will be valuable for construction of linkage maps, genetic diversity studies, and marker-assisted selection in Fagopyrum species</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s11032-017-0743-4</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s11032-017-0743-4</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Breed\2017-32-147.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Breed\2017-32-147.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Shi T</style></custom2><misc3><style face="normal" font="default">10.1007/s11032-017-0743-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86731</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Castells,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Drug Hypersensitivity and Anaphylaxis in Cancer and Chronic Inflammatory Diseases: The Role of Desensitizations</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1472">1472-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1664-3224</style></isbn><abstract><style face="normal" font="default">Drug Allergy is a rising problem in the XXI century which affects all populations and races, children and adults, and for which the recognition, diagnosis, management and treatment is still not well standardized. Classical and new chemotherapy drugs, monoclonal antibodies and small molecules to treat cancer and chronic inflammatory diseases are aimed at improving quality of life and life expectancy of patients, but an increasing number of reactions including anaphylaxis precludes their use in targeted populations. Women are more affected by drug allergy and up to 27 % of women with ovarian and breast cancer develop carboplatin allergy after multiple cycles of treatment. Carriers of BRCA genes develop drug allergy after fewer exposures and can present with severe reactions, including anaphylaxis. Atopic patients are at increased risk for chemotherapy and monoclonal antibodies drug allergy and the current patterns of treatment with recurrent and intermittent drug exposures may favor the development of drug allergies. To overcome drug allergy, desensitization has been developed, a novel approach which provides a unique opportunity to protect against anaphylaxis and to improve clinical outcomes. There is evidence that inhibitory mechanisms blocking IgE/antigen mast cell activation are active during desensitization, enhancing safety. Whether desensitization modulates drug allergic and anaphylactic responses facilitating tolerance is currently being investigated. This review provides insight into the current knowledge of drug allergy and anaphylaxis to cancer and chronic inflammatory diseases drugs, the mechanisms of drug desensitization and its applications to personalized medicine</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01472</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29163536">PM:29163536</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1472.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1472.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Castells M</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01472</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86599</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Boguniewicz,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy-Immunology, Department of Pediatrics, National Jewish Health and University of Colorado School of Medicine, Denver, Colo.</style></auth-address><titles><title><style face="normal" font="default">Biologic Therapy for Atopic Dermatitis: Moving Beyond the Practice Parameter and Guidelines</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1487" start="1477">1477-1487</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Atopic dermatitis (AD), a common chronic pruritic inflammatory skin disease, impacts the quality of life of patients and caregivers and has become a global health problem. It is increasingly recognized as a disease not only of children but also of adults who may have a persistent or relapsing course from childhood or who develop new-onset adult disease. Besides well-established atopic comorbidities, associations with a number of nonatopic comorbidities have been reported. AD is characterized by both immune dysregulation and epidermal barrier dysfunction. The findings that nonlesional skin in AD has both terminal keratinocyte differentiation defects and immune abnormalities as well as multiple markers of immune and inflammatory activation in the circulation point to the systemic nature of the disease and have important translational implications. Although AD is predominantly associated with type 2 immune responses, activation of other cytokine pathways including TH1, TH22, and TH17/IL-23 has been reported, suggesting potential therapeutic targets and provide a rationale for treatment with novel biologics. Dupilumab, a fully human mAb targeting the IL-4 Ralpha subunit, blocks signaling of both IL-4 and IL-13 and is the first biologic to be approved for the treatment of moderate-to-severe AD in adult patients. Other biologics in current trials for AD are targeting the IL-31 receptor, IL-13, and the common p40 subunit of IL-12/IL-23</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.08.031</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122151">PM:29122151</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1477-87.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1477-87.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Boguniewicz M</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.08.031</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87340</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ujiie,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Hokkaido University Graduate School of Medicine, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan</style></auth-address><titles><title><style face="normal" font="default">IgE autoantibodies in bullous pemphigoid</style></title><secondary-title><style face="normal" font="default">Br J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Br J Dermatol</style></abbr-1></periodical><pages end="1482" start="1481">1481-1482</pages><volume><style face="normal" font="default">177</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">IgE</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1365-2133 (Electronic)IS - 0007-0963 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1111/bjd.16034</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29313925">PM:29313925</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Br J Dermatol\2017-177-1481-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Br J Dermatol\2017-177-1481-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171212, Ujiie H</style></custom2><misc3><style face="normal" font="default">10.1111/bjd.16034</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87131</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shamji,M.H.</style></author><author><style face="normal" font="default"> Durham,S.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunomodulation and Tolerance Group</style></auth-address><titles><title><style face="normal" font="default">Mechanisms of allergen immunotherapy for inhaled allergens and predictive biomarkers</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol</style></abbr-1></periodical><pages end="1498" start="1485">1485-1498</pages><volume><style face="normal" font="default">140</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">Allergen immunotherapy is effective in patients with IgE-dependent allergic rhinitis and asthma. When immunotherapy is given continuously for 3 years, there is persistent clinical benefit for several years after its discontinuation. This disease-modifying effect is both antigen-specific and antigen-driven. Clinical improvement is accompanied by decreases in numbers of effector cells in target organs, including mast cells, basophils, eosinophils, and type 2 innate lymphoid cells. Immunotherapy results in the production of blocking IgG/IgG4 antibodies that can inhibit IgE-dependent activation mediated through both high-affinity IgE receptors (FcepsilonRI) on mast cells and basophils and low-affinity IgE receptors (FcepsilonRII) on B cells. Suppression of TH2 immunity can occur as a consequence of either deletion or anergy of antigen-specific T cells; induction of antigen-specific regulatory T cells; or immune deviation in favor of TH1 responses. It is not clear whether the altered long-term memory resides within the T-cell or the B-cell compartment. Recent data highlight the role of IL-10-producing regulatory B cells and "protective" antibodies that likely contribute to long-term tolerance. Understanding mechanisms underlying induction and persistence of tolerance should identify predictive biomarkers of clinical response and discover novel and more effective strategies for immunotherapy</style></abstract><notes><style face="normal" font="default">IS - 1097-6825 (Electronic)IS - 0091-6749 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United KIngdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaci.2017.10.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29221580">PM:29221580</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol\2017-140-1485-98.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol\2017-140-1485-98.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171217, Shamji MH</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaci.2017.10.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87016</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Menzella,F.</style></author><author><style face="normal" font="default"> Galeone,C.</style></author><author><style face="normal" font="default"> Lusuardi,M.</style></author><author><style face="normal" font="default"> Simonazzi,A.</style></author><author><style face="normal" font="default"> Castagnetti,C.</style></author><author><style face="normal" font="default"> Ruggiero,P.</style></author><author><style face="normal" font="default"> Facciolongo,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medical Specialties, Pneumology Unit, Arcispedale Santa Maria Nuova - IRCCS, Azienda USL di Reggio Emilia, Reggio Emilia</style></auth-address><titles><title><style face="normal" font="default">Near-fatal asthma responsive to mepolizumab after failure of omalizumab and bronchial thermoplasty</style></title><secondary-title><style face="normal" font="default">Ther Clin Risk Manag</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ther Clin Risk Manag</style></abbr-1></periodical><pages end="1493" start="1489">1489-1493</pages><volume><style face="normal" font="default">13</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Severe asthma affects between 5% and 10% of patients with asthma worldwide and requires best standard therapies at maximal doses, but there is a subgroup of patients refractory to all treatments. We share a case report of a 53-year-old woman with a history of severe allergic asthma that progressively worsened over the years despite the best therapy. She had been hospitalized 35 times, including nine admissions to the respiratory intensive care unit due to severe exacerbations. To rule out other possible diagnoses, several investigations were performed, such as computed tomography scan of the chest and neck, fiberoptic laryngoscopy, antineutrophil cytoplasmic antibodies, and complete blood cell count. The patient was first treated with omalizumab, which was completely ineffective, and then with bronchial thermoplasty (BT), again without clinical benefit. The situation remained critical for about 3 months during the last hospitalization, but in February 2017, the Italian Medicines Agency approved the treatment of severe refractory eosinophilic asthma with mepolizumab (Nucala((R))). Given a blood eosinophil count of 300 cells/muL, our patient was started on 100 mg mepolizumab treatment. After the second administration, symptoms improved progressively, with a reduction in the number and severity of exacerbations, so the patient could finally be discharged from hospital. At follow-up, it was possible to reduce and then suspend oral corticosteroids by continuing only with inhaled corticosteroids/long-acting beta-agonists and montelukast. No further asthmatic exacerbations occurred; symptom control and quality of life improved significantly. To our knowledge, this is the first case of a patient unresponsive to omalizumab and BT but with excellent clinical response to mepolizumab. She is also the first patient to be treated with an anti-IL5 agent in Italy in a real-life clinical setting. The availability of new effective biological agents will allow many patients to resume as normal a life as possible, with a positive outcome also from a social and economic point of view</style></abstract><notes><style face="normal" font="default">IS - 1176-6336 (Print)IS - 1176-6336 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.2147/TCRM.S149775</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29184413">PM:29184413</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ther Clin Risk Manag\2017-13-1489-93.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ther Clin Risk Manag\2017-13-1489-93.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Menzella F</style></custom2><misc3><style face="normal" font="default">10.2147/TCRM.S149775</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86842</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kwizera,R.</style></author><author><style face="normal" font="default"> Parkes-Ratanshi,R.</style></author><author><style face="normal" font="default"> Page,I.D.</style></author><author><style face="normal" font="default"> Sekaggya-Wiltshire,C.</style></author><author><style face="normal" font="default"> Musaazi,J.</style></author><author><style face="normal" font="default"> Fehr,J.</style></author><author><style face="normal" font="default"> Castelnuovo,B.</style></author><author><style face="normal" font="default"> Kambugu,A.</style></author><author><style face="normal" font="default"> Denning,D.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Infectious Diseases Institute, College of Health Sciences, Makerere University, P.O.BOX 22418, Kampala, Uganda.</style></auth-address><titles><title><style face="normal" font="default">Elevated Aspergillus-specific antibody levels among HIV infected Ugandans with pulmonary tuberculosis</style></title><secondary-title><style face="normal" font="default">BMC Pulm Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMC Pulm Med</style></abbr-1></periodical><pages end="" start="149">149-</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">methods</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">BACKGROUND: The incidence of tuberculosis (TB) is high among human immunodeficiency virus (HIV) infected Ugandans. Recent evidence suggests that Chronic Pulmonary Aspergillosis and Aspergillus sensitisation might be responsible for significant mortality in patients treated for tuberculosis in Uganda. METHODS: We retrieved and tested paired serum aliquots for 101 HIV-TB co-infected patients at the beginning and week 24 of TB treatment. We tested samples for Aspergillus-specific immunoglobulin G (IgG) and immunoglobulin E (IgE) using ImmunoCAP(R); and Aspergillus-specific IgG and total serum IgE using Immulite(R) immunoassays. We compared antibody levels between baseline and week 24, relating them to selected baseline characteristics. RESULTS: 10% of the patients had elevated Aspergillus-specific IgE (Aspergillus sensitization) and Aspergillus-specific IgG antibodies were elevated in 9% of the patients at the end of TB treatment. There was a significant fall in the Aspergillus-specific IgG antibody levels between baseline and week 24 (P = 0.02). Patients with cluster of differentiation 4 (CD4) T-cell count &lt;100 cells/mul and those who were not on anti-retroviral therapy at baseline had more elevated Aspergillus-specific IgG antibodies (P = 0.01, P = 0.03). The ImmunoCAP(R) Aspergillus-specific IgG antibody titres were higher at week 24 than baseline with more positives at week 24; even though the difference in means was small. However, this difference was statistically significant (P = 0.02). Pulmonary infiltrates were the commonest x-ray abnormality and only 5% of the patients had pulmonary cavities on chest x-ray at week 24. CONCLUSION: These results suggest that Aspergillus infection may complicate active pulmonary TB and further studies including fungal culture and thoracic imaging may now be indicated to measure the prevalence of pulmonary aspergillosis complicating tuberculosis. TRIAL REGISTRATION: The SOUTH trial was registered prospectively. ClinicalTrials.gov Identifier: NCT01782950 ; Registration date: 4th February 2013; Last verified: 13th April 2015</style></abstract><notes><style face="normal" font="default">IS - 1471-2466 (Electronic)IS - 1471-2466 (Linking)LA - engPT - Journal ArticleCO - Uganda -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1186/s12890-017-0500-9</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29162063">PM:29162063</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMC Pulm Med\2017-17-149.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMC Pulm Med\2017-17-149.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Kwizera R</style></custom2><misc3><style face="normal" font="default">10.1186/s12890-017-0500-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86615</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kuang,F.L.</style></author><author><style face="normal" font="default"> Klion,A.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Human Eosinophil Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Md</style></auth-address><titles><title><style face="normal" font="default">Biologic Agents for the Treatment of Hypereosinophilic Syndromes</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1509" start="1502">1502-1509</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Hypereosinophilic syndromes (HES) are a heterogeneous group of rare disorders defined by the presence of marked peripheral or tissue eosinophilia resulting in end-organ damage. Although conventional therapies, including glucocorticoids, hydroxyurea, and IFN-alpha, are initially effective in reducing eosinophilia and symptoms in a majority of patients with platelet-derived growth factor mutation-negative HES, the development of resistance and treatment-related toxicity are common. In contrast, targeted therapy with the tyrosine kinase inhibitor, imatinib, is well tolerated but effective only in the subset of patients with HES with a primary myeloid disorder. Eosinophil-targeted biotherapeutics offer the potential of improved efficacy with few, if any, adverse effects. The aims of this review are to provide an overview of current approaches to the use of conventional HES therapies and a discussion of existing biotherapeutics that target eosinophils and their potential use in the treatment of HES. With the continuing expansion of eosinophil-targeted biotherapeutics, the future for patients with eosinophilic disorders is promising</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 2213-2201 (Electronic)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.08.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122152">PM:29122152</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1502-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1502-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Kuang FL</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.08.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86681</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,Y.</style></author><author><style face="normal" font="default"> Wu,Y.</style></author><author><style face="normal" font="default"> Qi,H.</style></author><author><style face="normal" font="default"> Gong,H.</style></author><author><style face="normal" font="default"> Zhang,Y.</style></author><author><style face="normal" font="default"> Xu,E.</style></author><author><style face="normal" font="default"> Li,S.</style></author><author><style face="normal" font="default"> Ma,D.</style></author><author><style face="normal" font="default"> Xiao,J.</style></author><author><style face="normal" font="default"> Wang,Y.</style></author><author><style face="normal" font="default"> Li,W.</style></author><author><style face="normal" font="default"> Shen,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immunology, School of Basic Medical Sciences, Key Laboratory of Immunology, Ministry of Health, Peking University Health Science Center, Beijing, 100191, China</style></auth-address><titles><title><style face="normal" font="default">A new antagonist for CCR4 attenuates allergic lung inflammation in a mouse model of asthma</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="15038">15038-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">CCR4 is highly expressed on Th2 cells. CCR4 ligands include CCL22 and CCL17. Chemokine-like factor 1 can also mediate chemotaxis via CCR4. We designed and synthetized novel CCR4 antagonists, which were piperazinyl pyridine derivatives, for disrupting the interaction between three ligands and CCR4. We also determined whether these novel CCR4 antagonists could alleviate allergic asthma in a mouse. For identifying the potent compounds in vitro, we used chemotaxis inhibition and competition binding assays induced by CCL22, CCL17 and one of CKLF1's C-terminal peptides, C27. We found compound 8a which showed excellent potency in blocking the interaction of CCR4 and its three ligands. For studying the specificity of compounds, we chose chemotaxis inhibition assays with different receptors and ligands. We found compound 8a had excellent receptor specificity and exerted few influence on the interaction of other receptors and their ligands. In the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, compound 8a had no obvious cytotoxicity till the higher concentration (16 muM). For determining the potency of compounds in blocking the interaction of CCR4 in vivo, we used the ovalbumin induced allergic asthma model in mice. Our study demonstrated that CCR4 blockaded by compound 8a effectively attenuated airway hyperresponsiveness, airway eosinophilia and Th2 cytokines</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-11868-9</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29118379">PM:29118379</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-15038.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-15038.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Zhang Y</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-11868-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86604</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Busse,W.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wis.</style></auth-address><titles><title><style face="normal" font="default">Are Biotherapeutics Revolutionizing Treatment of "Allergic" Diseases?</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1518" start="1517">1517-1518</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 2213-2201 (Electronic)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.08.017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122153">PM:29122153</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1517-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1517-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Busse WW</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.08.017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86679</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nunez,N.K.</style></author><author><style face="normal" font="default"> Bennett,E.</style></author><author><style face="normal" font="default"> Chen,L.</style></author><author><style face="normal" font="default"> Pitrez,P.M.</style></author><author><style face="normal" font="default"> Zosky,G.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Medicine, Faculty of Health, University of Tasmania, Hobart, Tasmania, Australia.</style></auth-address><titles><title><style face="normal" font="default">The independent effects of vitamin D deficiency and house dust mite exposure on lung function are sex-specific</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="15198">15198-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">Vitamin D deficiency is increasing around the world and has been associated with the development of asthma. This study aims to evaluate the effect of dietary vitamin D deficiency at different life stages on lung function using a murine model of allergic airways disease. BALB/c mice were challenged intranasally with HDM or saline alone for 10 days. Twenty four hours after the last challenge, mice were anesthetized and lung function was measured using the forced oscillation technique (FOT). Mice were euthanized for assessment of inflammation in the bronchoalveolar lavage (BAL) and total collagen content in lung homogenates by ELISA. Vitamin D deficiency impaired lung function in both male and female mice, increasing tissue damping and elastance, however had no effect on HDM induced inflammation. The impact of vitamin D deficiency was more evident in females. HDM also decreased airway distensibility, but only in females and this response was not altered by vitamin D deficiency. Our data suggest that vitamin D deficiency and HDM exposure have independent effects on lung mechanics and that females are more susceptible to these effects. Vitamin D deficiency may exacerbate lung function deficits by having a direct, but independent, effect on parenchymal mechanics</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Australia -CO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-15517-z</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29123222">PM:29123222</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-15198.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-15198.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Nunez NK</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-15517-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86680</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hu,X.</style></author><author><style face="normal" font="default"> Li,X.</style></author><author><style face="normal" font="default"> Hu,C.</style></author><author><style face="normal" font="default"> Qin,L.</style></author><author><style face="normal" font="default"> He,R.</style></author><author><style face="normal" font="default"> Luo,L.</style></author><author><style face="normal" font="default"> Tang,W.</style></author><author><style face="normal" font="default"> Feng,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Medicine (Department of Respiratory and Critical Care Medicine), Key Cite of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China</style></auth-address><titles><title><style face="normal" font="default">Respiratory Syncytial Virus Exacerbates OVA-mediated asthma in mice through C5a-C5aR regulating CD4+T cells Immune Responses</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="15207">15207-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">Asthma exacerbation could be induced by respiratory syncytial virus (RSV), and the underlying pathogenic mechanism is related to complement activation. Although complement might regulate CD4+T cells immune responses in asthma model, this regulation existed in RSV-induced asthma model remains incompletely characterrized. In this study, we assessed the contribution of C5a-C5aR to CD4+T cell immune responses in RSV-infected asthma mice. Female BALB/C mice were sensitized and challenged with ovalbumin (OVA) while treated with RSV infection and C5a receptor antagonist (C5aRA) during challenge period. RSV enhanced lung damage, airway hyperresponsiveness, and C5aR expressions in asthma mice, while C5aRA alleviated these pathologic changes. The percentages of Th1, Th2 and Th17 cells were increased, while the percentage of Treg cells was decreased in RSV-infected asthma mice compared with asthma mice. IFN-gamma, IL-4, IL-10 and IL-17A levels have similar trend with Th1, Th2, Th17 and Treg cells. Notably, above changes of CD4+T cells and their related cytokines were reversed by C5aRA. Together, the data indicates that RSV infection could apparently increase C5a and C5aR expression in the pathogenesis of RSV-infected asthma mice, meanwhile C5aRA prevents some of the CD4+T cells immune changes that are induced by RSV</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-15471-w</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29123203">PM:29123203</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-15207.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-15207.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Hu X</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-15471-w</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86678</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Drinic,M.</style></author><author><style face="normal" font="default"> Wagner,A.</style></author><author><style face="normal" font="default"> Sarate,P.</style></author><author><style face="normal" font="default"> Zwicker,C.</style></author><author><style face="normal" font="default"> Korb,E.</style></author><author><style face="normal" font="default"> Loupal,G.</style></author><author><style face="normal" font="default"> Peschke,R.</style></author><author><style face="normal" font="default"> Joachim,A.</style></author><author><style face="normal" font="default"> Wiedermann,U.</style></author><author><style face="normal" font="default"> Schabussova,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Specific Prophylaxis and Tropical Medicine, Medical University of Vienna, Vienna, Austria</style></auth-address><titles><title><style face="normal" font="default">Toxoplasma gondii tachyzoite-extract acts as a potent immunomodulator against allergic sensitization and airway inflammation</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="15211">15211-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">Epidemiological and experimental studies have shown an inverse relationship between infections with certain parasites and a reduced incidence of allergic diseases. We and others have shown that infection with Toxoplasma gondii prevents the development of allergy in mice. To establish whether this beneficial effect could be recapitulated by soluble products of this parasite, we tested an extract derived from T. gondii tachyzoites. Immunization of BALB/c mice with tachyzoites lysate antigen (TLA) elicited mixed Th1/Th2 responses. When TLA was applied together with the sensitizing ovalbumin (OVA), the development of allergic airway inflammation was reduced, with decreased airway hyperresponsiveness associated with reduced peribronchial and perivascular cellular infiltration, reduced production of OVA-specific Th2 cytokines in lungs and spleens and reduced levels of serum OVA-specific IgG1 as well as IgE-dependent basophil degranulation. Of note, TLA retained its immunomodulatory properties, inducing high levels of IL-6, TNFalpha, IL-10 and IL-12p70 in bone marrow-derived dendritic cells after heat-inactivation or proteinase K-treatment for disruption of proteins, but not after sodium metaperiodate-treatment that degrades carbohydrate structures, suggesting that carbohydrates may play a role in immunomodulatory properties of TLA. Here we show that extracts derived from parasites may replicate the benefits of parasitic infection, offering new therapies for immune-mediated disorders</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-15663-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29123241">PM:29123241</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-15211.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-15211.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Drinic M</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-15663-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86889</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fu,L.</style></author><author><style face="normal" font="default"> Song,J.</style></author><author><style face="normal" font="default"> Wang,C.</style></author><author><style face="normal" font="default"> Fu,S.</style></author><author><style face="normal" font="default"> Wang,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Food Safety Key Laboratory of Zhejiang Province, School of Food Science and Biotechnology, Zhejiang Gongshang University, Hangzhou, China</style></auth-address><titles><title><style face="normal" font="default">Bifidobacterium infantis Potentially Alleviates Shrimp Tropomyosin-Induced Allergy by Tolerogenic Dendritic Cell-Dependent Induction of Regulatory T Cells and Alterations in Gut Microbiota</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1536">1536-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Tropomyosin</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Shellfish is one of the major allergen sources worldwide, and tropomyosin (Tm) is the predominant allergic protein in shellfish. Probiotics has been appreciated for its beneficial effects on the host, including anti-allergic and anti-inflammatory effects, although the underlying mechanisms were not fully understood. In this study, oral administration of probiotic strain Bifidobacterium infantis 14.518 (Binf) effectively suppressed Tm-induced allergic response in a mouse model by both preventive and therapeutic strategies. Further results showed that Binf stimulated dendritic cells (DCs) maturation and CD103(+) tolerogenic DCs accumulation in gut-associated lymphoid tissue, which subsequently induced regulatory T cells differentiation for suppressing Th2-biased response. We also found that Binf regulates the alterations of gut microbiota composition. Specifically, the increase of Dorea and decrease of Ralstonia is highly correlated with Th2/Treg ratio and may contribute to alleviating Tm-induced allergic responses. Our findings provide molecular insight into the application of Binf in alleviating food allergy and even gut immune homeostasis</style></abstract><notes><style face="normal" font="default">IS - 1664-3224 (Print)IS - 1664-3224 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01536</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29176981">PM:29176981</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1536.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1536.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Fu L</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01536</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86888</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Matsuba,S.</style></author><author><style face="normal" font="default"> Yabe-Wada,T.</style></author><author><style face="normal" font="default"> Takeda,K.</style></author><author><style face="normal" font="default"> Sato,T.</style></author><author><style face="normal" font="default"> Suyama,M.</style></author><author><style face="normal" font="default"> Takai,T.</style></author><author><style face="normal" font="default"> Kikuchi,T.</style></author><author><style face="normal" font="default"> Nukiwa,T.</style></author><author><style face="normal" font="default"> Nakamura,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immunology, Kanazawa Medical University, Kahoku Uchinada, Ishikawa, Japan</style></auth-address><titles><title><style face="normal" font="default">Identification of Secretory Leukoprotease Inhibitor As an Endogenous Negative Regulator in Allergic Effector Cells</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1538">1538-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Eosinophil</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Mast cells, basophils, and eosinophils are central effectors in allergic inflammatory disorders. These cells secrete abundant serine proteases as well as chemical mediators and cytokines; however, the expression profiles and functions of their endogenous inhibitors remain elusive. We found that murine secretory leukoprotease inhibitor (SLPI) is expressed in basophils and eosinophils but in not in mast cells. SLPI-deficient (Slpi(-/-)) basophils produce more cytokines than wild-type mice after IgE stimulation. Although the deletion of SLPI in basophils did not affect the release of chemical mediators upon IgE stimulation, the enzymatic activity of the serine protease tryptase was increased in Slpi(-/-) basophils. Mice transferred with Slpi(-/-) basophils were highly sensitive to IgE-mediated chronic allergic inflammation. Eosinophils lacking SLPI showed greater interleukin-6 secretion and invasive activity upon lipopolysaccharide stimulation, and the expression of matrix metalloproteinase-9 by these eosinophils was increased without stimulation. The absence of SLPI increases JNK1 phosphorylation at the steady state, and augments the serine phosphorylation of JNK1-downstream ETS transcriptional factor Elk-1 in eosinophils upon stimulation. Of note, SLPI interacts with a scaffold protein, JNK-interacting protein 3 (JIP3), that constitutively binds to the cytoplasmic domain of toll-like receptor (TLR) 4, suggesting that SLPI controls Elk-1 activation via binding to JIP3 in eosinophils. Mice transferred with Slpi(-/-) eosinophils showed the exacerbation of chitin-induced allergic inflammation. These findings showed that SLPI is a negative regulator in allergic effector cells and suggested a novel inhibitory role of SLPI in the TLR4 signaling pathways</style></abstract><notes><style face="normal" font="default">IS - 1664-3224 (Print)IS - 1664-3224 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01538</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29181004">PM:29181004</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1538.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1538.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Matsuba S</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01538</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86613</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bingemann,T.</style></author><author><style face="normal" font="default"> Khan,D.A.</style></author><author><style face="normal" font="default"> Markovics,S.</style></author><author><style face="normal" font="default"> Weinstein,A.G.</style></author><author><style face="normal" font="default"> Sharma,H.P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Rochester Regional Health, University of Rochester School of Medicine &amp; Dentistry, Rochester, NY</style></auth-address><titles><title><style face="normal" font="default">Feeling Burned Out? Half of Us Are: The Urgent Need to Address Provider Health and Wellness in Allergy and Immunology</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1550" start="1549">1549-1550</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 2213-2201 (Electronic)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.08.040</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122154">PM:29122154</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1549-50.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1549-50.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171110, Bingemann T</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.08.040</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86598</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ameratunga,R.</style></author><author><style face="normal" font="default"> Gillis,D.</style></author><author><style face="normal" font="default"> Gold,M.</style></author><author><style face="normal" font="default"> Linneberg,A.</style></author><author><style face="normal" font="default"> Elwood,J.M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Evidence Refuting the Existence of Autoimmune/Autoinflammatory Syndrome Induced-áby Adjuvants (ASIA)</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1555" start="1551">1551-1555</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">ASIA</style></keyword><keyword><style face="normal" font="default"> SLE</style></keyword><keyword><style face="normal" font="default"> Autoimmunity</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">Autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA) was described in 2011. Over time the condition and its triggers have broadened to include several autoimmune disorders, the macrophagic myofasciitis syndrome, the Gulf war syndrome, the sick building syndrome, siliconosis, and the chronic fatigue syndrome. The aluminum-containing adjuvants in the hepatitis B vaccine and the human papillomavirus vaccine in particular have been stated to be the major causes of the disorder. Here, we review the specificity of the diagnostic criteria for ASIA. We also examine relevant human data, pertaining to causation, particularly from patients undergoing allergen-specific immunotherapy (IT). Patients undergoing allergen-specific IT receive 100 to 500 times more injected aluminum over 3 to 5 years, compared with hepatitis B and human papillomavirus vaccine recipients. In a large pharmacoepidemiological study, in contrast to case series of ASIA, patients receiving aluminum-containing allergen IT preparations were shown to have a lower incidence of autoimmune disease. In another clinical trial, there were no increases in exacerbations in a cohort of patients with systemic lupus erythematosus immunized with the hepatitis B vaccine. Current data do not support the causation of ASIA by vaccine adjuvants containing aluminum, which should be of reassurance to patients undergoing routine immunizations as well as to those undergoing allergen-specific IT</style></abstract><notes><style face="normal" font="default">LA - ENGCO - New Zealand -CO - Australia -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.06.033</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.06.033</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1551-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1551-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Ameratunga R</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.06.033</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86796</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Harmon,B.</style></author><author><style face="normal" font="default"> Chylek,L.A.</style></author><author><style face="normal" font="default"> Liu,Y.</style></author><author><style face="normal" font="default"> Mitra,E.D.</style></author><author><style face="normal" font="default"> Mahajan,A.</style></author><author><style face="normal" font="default"> Saada,E.A.</style></author><author><style face="normal" font="default"> Schudel,B.R.</style></author><author><style face="normal" font="default"> Holowka,D.A.</style></author><author><style face="normal" font="default"> Baird,B.A.</style></author><author><style face="normal" font="default"> Wilson,B.S.</style></author><author><style face="normal" font="default"> Hlavacek,W.S.</style></author><author><style face="normal" font="default"> Singh,A.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Systems Biology, Sandia National Laboratories, Livermore, CA, USA</style></auth-address><titles><title><style face="normal" font="default">Timescale Separation of Positive and Negative Signaling Creates History-Dependent Responses to IgE Receptor Stimulation</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="15586">15586-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="in-file"/><keywords/><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">The high-affinity receptor for IgE expressed on the surface of mast cells and basophils interacts with antigens, via bound IgE antibody, and triggers secretion of inflammatory mediators that contribute to allergic reactions. To understand how past inputs (memory) influence future inflammatory responses in mast cells, a microfluidic device was used to precisely control exposure of cells to alternating stimulatory and non-stimulatory inputs. We determined that the response to subsequent stimulation depends on the interval of signaling quiescence. For shorter intervals of signaling quiescence, the second response is blunted relative to the first response, whereas longer intervals of quiescence induce an enhanced second response. Through an iterative process of computational modeling and experimental tests, we found that these memory-like phenomena arise from a confluence of rapid, short-lived positive signals driven by the protein tyrosine kinase Syk; slow, long-lived negative signals driven by the lipid phosphatase Ship1; and slower degradation of Ship1 co-factors. This work advances our understanding of mast cell signaling and represents a generalizable approach for investigating the dynamics of signaling systems</style></abstract><notes><style face="normal" font="default">DA - 20171115IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-15568-2</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29138425">PM:29138425</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-15586.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-15586.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171115, Harmon B</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-15568-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86892</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Alnahas,S.</style></author><author><style face="normal" font="default"> Hagner,S.</style></author><author><style face="normal" font="default"> Raifer,H.</style></author><author><style face="normal" font="default"> Kilic,A.</style></author><author><style face="normal" font="default"> Gasteiger,G.</style></author><author><style face="normal" font="default"> Mutters,R.</style></author><author><style face="normal" font="default"> Hellhund,A.</style></author><author><style face="normal" font="default"> Prinz,I.</style></author><author><style face="normal" font="default"> Pinkenburg,O.</style></author><author><style face="normal" font="default"> Visekruna,A.</style></author><author><style face="normal" font="default"> Garn,H.</style></author><author><style face="normal" font="default"> Steinhoff,U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Medical Microbiology and Hospital Hygiene, University of Marburg, Marburg, Germany</style></auth-address><titles><title><style face="normal" font="default">IL-17 and TNF-alpha Are Key Mediators of Moraxella catarrhalis Triggered Exacerbation of Allergic Airway Inflammation</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1562">1562-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Alterations of the airway microbiome are often associated with pulmonary diseases. For example, detection of the bacterial pathogen Moraxella catarrhalis in the upper airways is linked with an increased risk to develop or exacerbate asthma. However, the mechanisms by which M. catarrhalis augments allergic airway inflammation (AAI) remain unclear. We here characterized the cellular and soluble mediators of M. catarrhalis triggered excacerbation of AAI in wt and IL-17 deficient as well as in animals treated with TNF-alpha and IL-6 neutralizing antibodies. We compared the type of inflammatory response in M. catarrhalis infected, house dust mite (HDM)-allergic and animals infected with M. catarrhalis at different time points of HDM sensitization. We found that airway infection of mice with M. catarrhalis triggers a strong inflammatory response with massive neutrophilic infiltrates, high amounts of IL-6 and TNF-alpha and moderate levels of CD4(+) T-cell-derived IFN-gamma and IL-17. If bacterial infection occurred during HDM allergen sensitization, the allergic airway response was exacerbated, particularly by the expansion of Th17 cells and increased TNF-alpha levels. Neutralization of IL-17 or TNF-alpha but not IL-6 resulted in accelerated clearance of M. catarrhalis and effectively prevented infection-induced exacerbation of AAI. Taken together, our data demonstrate an essential role for TNF-alpha and IL-17 in infection-triggered exacerbation of AAI</style></abstract><notes><style face="normal" font="default">IS - 1664-3224 (Print)IS - 1664-3224 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01562</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29184554">PM:29184554</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1562.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1562.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Alnahas S</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01562</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86522</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Meglio,P.</style></author><author><style face="normal" font="default"> Giampietro,P.G.</style></author><author><style face="normal" font="default"> Carello,R.</style></author><author><style face="normal" font="default"> Galli,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Oral immunotherapy in children with IgE-mediated hen's egg allergy: Follow-ups at 2.5 and 7 years</style></title><secondary-title><style face="normal" font="default">Allergy Rhinol (Providence)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Rhinol (Providence)</style></abbr-1></periodical><pages end="169" start="157">157-169</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="10" Year="2017">2017/10/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: The present report was a follow-up investigation at 2.5- and 7-year intervals of a previous study of 20 children with moderate-to-severe immunoglobulin E (IgE) mediated hen's egg (HE) allergy who received oral immunotherapy (OIT) with raw HE. The study design of the previous study divided the 20 subjects into two groups of 10 each: (1) group 1, the OIT group (OIT-G), and, (2) group 2, an age-matched control group (C-G). In that study, 8 of 10 of the children in the OIT-G were successfully desensitized, one child was partially desensitized, and desensitization failed in one child. The aims of the present study were to evaluate the long-term effectiveness and safety profile of OIT with raw HE, and to assess the course and prognostic value of skin-prick tests (SPT) and serum-specific HE-IgEs in this study population. METHODS: Of the 20 children who were recalled, 2 dropped out, which left 18 to be evaluated. Information on their HE intake was recorded, and SPTs with HE allergen extracts and with raw and hard-boiled HE were performed. Ovomucoid- and ovalbumin-specific IgE levels were also measured. RESULTS: At the first (2.5-year) and second (7-year) follow-ups, 87.5% of the children in the OIT-G who tolerated raw HE were still tolerant, whereas the children in the C-G were significantly less tolerant. Overall, cutaneous sensitivity to HE significantly decreased after the 6-month desensitization period and at both follow-ups with regard to the OIT-G but not with regard to the C-G. A significant reduction in serum ovomucoid- and ovalbumin-specific IgE levels was seen in both the OIT-G and the C-G. CONCLUSION: Clinical raw HE tolerance induced by OIT persists over time. Negativization of SPTs could be considered a more reliable prognostic indicator of clinical tolerance to raw HE than the reduction in specific-HE IgE levels. Raw-HE OIT would seem to be a promising method to treat HE allergy</style></abstract><notes><style face="normal" font="default">DA - 20171026IS - 2152-6575 (Print)IS - 2152-6567 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.2500/ar.2017.8.0211</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29070273">PM:29070273</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Rhinol (Providence)\2017-8-157-69.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Rhinol (Providence)\2017-8-157-69.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171026, Meglio P</style></custom2><misc3><style face="normal" font="default">10.2500/ar.2017.8.0211</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86597</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Murphy,K.</style></author><author><style face="normal" font="default"> Jacobs,J.</style></author><author><style face="normal" font="default"> Bjermer,L.</style></author><author><style face="normal" font="default"> Fahrenholz,J.M.</style></author><author><style face="normal" font="default"> Shalit,Y.</style></author><author><style face="normal" font="default"> Garin,M.</style></author><author><style face="normal" font="default"> Zangrilli,J.</style></author><author><style face="normal" font="default"> Castro,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Long-term Safety and Efficacy of Reslizumab in Patients with Eosinophilic Asthma</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1581" start="1572">1572-1581</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Reslizumab</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Anti-IL-5</style></keyword><keyword><style face="normal" font="default"> Long-term safety</style></keyword><keyword><style face="normal" font="default"> Open-label extension study</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">In placebo-controlled trials, reslizumab, an anti-IL-5 monoclonal antibody, significantly reduced asthma exacerbations and improved lung function and asthma control in patients with eosinophilic asthma. This open-label extension study evaluated safety and efficacy of reslizumab for up to 24 months. After participation in 1 of 3 placebo-controlled, phase III trials in moderate-to-severe eosinophilic asthma, patients received reslizumab 3.0 mg/kg intravenously every 4 weeks for up to 24 months. Adverse events (AEs), lung function, and patient-reported asthma control were evaluated. In the open-label extension, 1,051 patients received </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ1 reslizumab dose (480 reslizumab-na+»ve, 571 reslizumab-experienced); median (range) exposure was 319 (36-840) and 343-á(36-863) days in reslizumab-na+»ve and reslizumab-experienced patients, respectively. Continuous exposure, including during the placebo-controlled studies, was </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ12 months for 740 patients and </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ëÑ24 months for 249 patients. The most common AEs were worsening of asthma and nasopharyngitis. Serious AEs affected-á78-áof 1,051 (7%) patients; 18 of 1,051 (2%) discontinued treatment because of AEs; and there were 3 deaths (all non-treatment-related). Fifteen adult patients (15 of 1,023; 1%) had malignancies of diverse tissue types. Reslizumab-experienced patients maintained improved lung function and asthma control;-áreslizumab-na+»ve patients had improvements in these measures throughout open-label treatment. Blood eosinophil counts appeared to be returning to baseline after reslizumab discontinuation. In patients with moderate-to-severe eosinophilic asthma, intravenous reslizumab 3.0 mg/kg displays favorable long-term safety and sustained long-term efficacy. Initial improvements in lung function and asthma control were maintained for up to 2 years. These findings substantially add to our understanding of the long-term safety and efficacy of anti-IL-5 strategies</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -CO - Sweden -CO - Israel -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.08.024</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.08.024</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1572-81.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1572-81.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Murphy K</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.08.024</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86841</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cloots,R.H.E.</style></author><author><style face="normal" font="default"> Sankaranarayanan,S.</style></author><author><style face="normal" font="default"> Poynter,M.E.</style></author><author><style face="normal" font="default"> Terwindt,E.</style></author><author><style face="normal" font="default"> van Dijk,P.</style></author><author><style face="normal" font="default"> Lamers,W.H.</style></author><author><style face="normal" font="default"> Kohler,E.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Anatomy &amp; Embryology and NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, P.O. Box 616, 6200, MD, Maastricht, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">Arginase 1 deletion in myeloid cells affects the inflammatory response in allergic asthma, but not lung mechanics, in female mice</style></title><secondary-title><style face="normal" font="default">BMC Pulm Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMC Pulm Med</style></abbr-1></periodical><pages end="" start="158">158-</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">BACKGROUND: (Over-)expression of arginase may limit local availability of arginine for nitric oxide synthesis. We investigated the significance of arginase1 (ARG1) for the development of airway hyperresponsiveness (AHR) and lung inflammation in female mice with ovalbumin (OVA)-induced allergic asthma. METHODS: Arg1 was ablated in the lung by crossing Arg1 (fl/fl) and Tie2Cre (tg/-) mice. OVA sensitization and challenge were conducted, and AHR to methacholine was determined using the Flexivent system. Changes in gene expression, chemokine and cytokine secretion, plasma IgE, and lung histology were quantified using RT-qPCR, ELISA, and immunohistochemistry, respectively. RESULTS: Arg1 ablation had no influence on the development of OVA-induced AHR, but attenuated OVA-induced increases in expression of Arg2 and Nos2, Slc7a1, Slc7a2, and Slc7a7 (arginine transporters), Il4, Il5 and Il13 (TH2-type cytokines), Ccl2 and Ccl11 (chemokines), Ifng (TH1-type cytokine), Clca3 and Muc5ac (goblet cell markers), and OVA-specific IgE. Pulmonary IL-10 protein content increased, but IL-4, IL-5, IL-13, TNFalpha and IFNgamma content, and lung histopathology, were not affected. Arg1 elimination also decreased number and tightness of correlations between adaptive changes in lung function and inflammatory parameters in OVA/OVA-treated female mice. OVA/OVA-treated female mice mounted a higher OVA-IgE response than males, but the correlation between lung function and inflammation was lower. Arg1-deficient OVA/OVA-treated females differed from males in a more pronounced decline of arginine-metabolizing and -transporting genes, higher plasma arginine levels, a smaller OVA-specific IgE response, and no improvement of peripheral lung function. CONCLUSION: Complete ablation of Arg1 in the lung affects mRNA abundance of arginine-transporting and -metabolizing genes, and pro-inflammatory genes, but not methacholine responsiveness or accumulation of inflammatory cells</style></abstract><notes><style face="normal" font="default">IS - 1471-2466 (Electronic)IS - 1471-2466 (Linking)LA - engPT - Journal ArticleCO - Netherlands -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1186/s12890-017-0490-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29183288">PM:29183288</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMC Pulm Med\2017-17-158.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMC Pulm Med\2017-17-158.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Cloots RH</style></custom2><misc3><style face="normal" font="default">10.1186/s12890-017-0490-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87334</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sami Metin,M.</style></author><author><style face="normal" font="default"> Kizilyel,O.</style></author><author><style face="normal" font="default"> Elmas,O.F.</style></author><author><style face="normal" font="default"> Ozdemir,S.</style></author><author><style face="normal" font="default"> Bilen,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Acute Acneiform Eruption Related to Cetuximab Treated Successfully with Oral Tetracycline</style></title><secondary-title><style face="normal" font="default">Asthma Allergy Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Asthma Allergy Immunol</style></full-title></periodical><pages end="161" start="158">158-161</pages><volume><style face="normal" font="default">15</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The most common known causes of acneiform lesions secondary to chemotherapy are epidermal growth factor receptor (EGFR) inhibitors. Cetuximab and panitumumab which are monoclonal antibodies and gefitinib and erlotinib which are tyrosine kinase inhibitors are the major drugs in this group. An acneiform lesion is the most common and the earliest reaction among the dermatological side effects related to EGFR inhibitors. Acneiform eruption, asthenia, stomach ache and nausea-vomiting are side effects related to cetuximab. We reported a 59-year-old man who presented with sudden acneiform lesions on his face, neck and chest at the 8th day of cetuximab treatment which was used for metastatic colon cancer. We reported this case to share that it is possible to treat acneiform eruption related to cetuximab with oral tetracycline, topical ketoconazole, local clindamycin phosphate and benzoyl peroxide.</style></abstract><notes><style face="normal" font="default">LA - TURCO - Turkey -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://www.aai.org.tr/index.php/aai/article/view/23</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-158-61.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asthma Allergy Immunol\2017-15-158-61.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Sami Mein M</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86595</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Naclerio,R.M.</style></author><author><style face="normal" font="default"> Baroody,F.M.</style></author><author><style face="normal" font="default"> Pinto,J.M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Nasal Polyps and Biomarkers</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1590" start="1589">1589-1590</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.05.007</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.05.007</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1589-90.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1589-90.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Naclerio RM</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.05.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86596</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Giavina-Bianchi,P.</style></author><author><style face="normal" font="default"> Kalil,J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Diagnosis of Allergic Bronchopulmonary Aspergillosis Exacerbations</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="1600" start="1599">1599-1600</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.06.024</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.06.024</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1599-600.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1599-600.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Giavina-Bianchi P</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.06.024</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87110</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Calus,L.</style></author><author><style face="normal" font="default"> Derycke,L.</style></author><author><style face="normal" font="default"> Dullaers,M.</style></author><author><style face="normal" font="default"> Van Zele,T.</style></author><author><style face="normal" font="default"> De Ruyck,N.</style></author><author><style face="normal" font="default"> Perez-Novo,C.</style></author><author><style face="normal" font="default"> Holtappels,G.</style></author><author><style face="normal" font="default"> De Vos,G.</style></author><author><style face="normal" font="default"> Lambrecht,B.N.</style></author><author><style face="normal" font="default"> Bachert,C.</style></author><author><style face="normal" font="default"> Gevaert,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Upper Airways Research Laboratory, Department of Otorhinolaryngology, Ghent University Hospital, Ghent, Belgium</style></auth-address><titles><title><style face="normal" font="default">IL-21 Is Increased in Nasal Polyposis and after Stimulation with Staphylococcus aureus Enterotoxin B</style></title><secondary-title><style face="normal" font="default">Int Arch Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Arch Allergy Immunol</style></abbr-1></periodical><pages end="169" start="161">161-169</pages><volume><style face="normal" font="default">174</style></volume><number><style face="normal" font="default">3-4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: Chronic rhinosinusitis with nasal polyposis (CRSwNP) is an inflammatory disease associated with lymphoid aggregates and local IgE production related to Staphylococcus aureus enterotoxins. T-follicular helper cells and their effector cytokine interleukin (IL)-21 play an important role in germinal center proliferation. METHODS: IL-21 was determined on the mRNA level by qPCR in nasal tissue of 3 groups of patients: control (n = 17), chronic rhinosinusitis without nasal polyposis (CRSsNP; n = 23), and CRSwNP (n = 35). The expression of IL-21 by CD4+ T cells was analyzed in tissue at baseline and after 24-h stimulation of tissue fragments with S. aureus enterotoxin B (SEB) using flow cytometry. Finally, human nasal IL-21+CXCR5+CD4+ T cells were isolated and coincubated with human blood naive B cells to investigate their functionality. RESULTS: IL-21 mRNA expression was increased in the CRSwNP group (p &lt; 0.05) compared to the control group, and B-cell lymphoma-6 and B-lymphocyte-induced maturation protein-1 were upregulated in CRSwNP versus CRSsNP. Furthermore, SEB was able to increase IL-21 mRNA expression significantly (p &lt; 0.01) in nasal polyps. Flow cytometry revealed that the source of IL-21 was predominantly CD4+ T cells and that IL-21+CD4+ T cells were significantly increased in polyp tissue and further increased after SEB stimulation. Finally, tissue CXCR5+CD4+ T cells derived from nasal polyp tissue were able to induce maturation of human naive B cells. CONCLUSIONS: IL-21- and IL-21-producing CD4+ T cells were increased in CRSwNP. In addition, SEB induced an increase in IL-21 and IL-21+CD4+ T cells, suggesting that S. aureus can modulate the function of Tfh cells in nasal polyps. We speculate that T-follicular helper cells and IL-21 are important in the pathophysiology of CRSwNP</style></abstract><notes><style face="normal" font="default">IS - 1423-0097 (Electronic)IS - 1018-2438 (Linking)LA - engPT - Journal ArticleCO - Belgium -</style></notes><work-type><style face="normal" font="default">10.1159/000481435</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29131072">PM:29131072</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-161-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-161-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Calus L</style></custom2><misc3><style face="normal" font="default">10.1159/000481435</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86891</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sparber,F.</style></author><author><style face="normal" font="default"> LeibundGut-Landmann,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Section of Immunology, Vetsuisse Faculty, University of Zurich, Zurich, SwitzerlandSection of Immunology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Host Responses to Malassezia spp. in the Mammalian Skin</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1614">1614-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The skin of mammalian organisms is home for a myriad of microbes. Many of these commensals are thought to have beneficial effects on the host by critically contributing to immune homeostasis. Consequently, dysbiosis can have detrimental effects for the host that may manifest with inflammatory diseases at the barrier tissue. Besides bacteria, fungi make an important contribution to the microbiota and among these, the yeast Malassezia widely dominates in most areas of the skin in healthy individuals. There is accumulating evidence that Malassezia spp. are involved in a variety of skin disorders in humans ranging from non- or mildly inflammatory conditions such as dandruff and pityriasis versicolor to more severe inflammatory skin diseases like seborrheic eczema and atopic dermatitis. In addition, Malassezia is strongly linked to the development of dermatitis and otitis externa in dogs. However, the association of Malassezia spp. with such diseases remains poorly characterized. Until now, studies on the fungus-host interaction remain sparse and they are mostly limited to experiments with isolated host cells in vitro. They suggest a multifaceted crosstalk of Malassezia spp. with the skin by direct activation of the host via conserved pattern recognition receptors and indirectly via the release of fungus-derived metabolites that can modulate the function of hematopoietic and/or non-hematopoietic cells in the barrier tissue. In this review, we discuss our current understanding of the host response to Malassezia spp. in the mammalian skin</style></abstract><notes><style face="normal" font="default">IS - 1664-3224 (Print)IS - 1664-3224 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01614</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29213272">PM:29213272</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1614.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1614.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Sparber F</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01614</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87010</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Strasser,L.</style></author><author><style face="normal" font="default"> Dang,H.H.</style></author><author><style face="normal" font="default"> Schwarz,H.</style></author><author><style face="normal" font="default"> Asam,C.</style></author><author><style face="normal" font="default"> Ferreira,F.</style></author><author><style face="normal" font="default"> Horejs-Hoeck,J.</style></author><author><style face="normal" font="default"> Huber,C.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Molecular Biology, Division of Chemistry and Bioanalytics, University of Salzburg, Hellbrunner Strasse 34, 5020, Salzburg, Austria</style></auth-address><titles><title><style face="normal" font="default">Unbiased Quantitative Proteomics Reveals a Crucial Role of the Allergen Context for the Activation of Human Dendritic Cells</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="16638">16638-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword></keywords><dates><year Day="30" Month="11" Year="2017">2017/11/30</year></dates><abstract><style face="normal" font="default">Worldwide, more than 1 billion people suffer from allergic diseases. However, until now it is not fully understood how certain proteins can induce allergic immune responses, while others cannot. Studies suggest that allergenicity is a process not only determined by properties of the allergen itself but also by costimulatory factors, that are not classically associated with allergic reactions. To investigate the allergenicity of the major birch pollen allergen Bet v 1 and the impact of adjuvants associated with pollen, e.g. lipopolysaccharide (LPS), we performed quantitative proteome analysis to study the activation of monocyte-derived dendritic cells (moDCs). Thus, we treated cells with birch pollen extract (BPE), recombinant Bet v 1, and LPS followed by proteomic profiling via high-performance liquid chromatography and tandem mass spectrometry (HPLC-MS/MS) using isobaric labelling. Enrichment and pathway analysis revealed the influence of regulated proteins especially in cytokine signalling and dendritic cell activation. We found highly regulated, but differentially expressed proteins after treatment with BPE and LPS, whereas the cellular response to Bet v 1 was limited. Our findings lead to the conclusion that Bet v 1 needs a specific "allergen context" involving cofactors apart from LPS to induce an immune response in human moDCs</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-16726-2</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29192156">PM:29192156</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-16638.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-16638.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171130, Strasser L</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-16726-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87098</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,B.W.S.</style></author><author><style face="normal" font="default"> Stadhouders,R.</style></author><author><style face="normal" font="default"> de Bruijn,M.J.W.</style></author><author><style face="normal" font="default"> Lukkes,M.</style></author><author><style face="normal" font="default"> Beerens,D.M.J.M.</style></author><author><style face="normal" font="default"> Brem,M.D.</style></author><author><style face="normal" font="default"> KleinJan,A.</style></author><author><style face="normal" font="default"> Bergen,I.</style></author><author><style face="normal" font="default"> Vroman,H.</style></author><author><style face="normal" font="default"> Kool,M.</style></author><author><style face="normal" font="default"> van IJcken,W.F.J.</style></author><author><style face="normal" font="default"> Rao,T.N.</style></author><author><style face="normal" font="default"> Fehling,H.J.</style></author><author><style face="normal" font="default"> Hendriks,R.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pulmonary Medicine, Rotterdam, Netherlands</style></auth-address><titles><title><style face="normal" font="default">Group 2 Innate Lymphoid Cells Exhibit a Dynamic Phenotype in Allergic Airway Inflammation</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1684">1684-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Group 2 innate lymphoid cells (ILC2) are implicated in allergic asthma as an early innate source of the type 2 cytokines IL-5 and IL-13. However, their induction in house dust mite (HDM)-mediated airway inflammation additionally requires T cell activation. It is currently unknown whether phenotypic differences exist between ILC2s that are activated in a T cell-dependent or T cell-independent fashion. Here, we compared ILC2s in IL-33- and HDM-driven airway inflammation. Using flow cytometry, we found that surface expression levels of various markers frequently used to identify ILC2s were dependent on their mode of activation, highly variable over time, and differed between tissue compartments, including bronchoalveolar lavage (BAL) fluid, lung, draining lymph nodes, and spleen. Whereas in vivo IL-33-activated BAL fluid ILC2s exhibited an almost uniform CD25(+)CD127(+)T1/ST2(+)ICOS(+)KLRG1(+) phenotype, at a comparable time point after HDM exposure BAL fluid ILC2s had a very heterogeneous surface marker phenotype. A major fraction of HDM-activated ILC2s were CD25(low)CD127(+)T1/ST2(low) ICOS(low)KLRG1(low), but nevertheless had the capacity to produce large amounts of type 2 cytokines. HDM-activated CD25(low) ILC2s in BAL fluid and lung rapidly reverted to CD25(high) ILC2s upon in vivo stimulation with IL-33. Genome-wide transcriptional profiling of BAL ILC2s revealed ~1,600 differentially expressed genes: HDM-stimulated ILC2s specifically expressed genes involved in the regulation of adaptive immunity through B and T cell interactions, whereas IL-33-stimulated ILC2s expressed high levels of proliferation-related and cytokine genes. In both airway inflammation models ILC2s were present in the lung submucosa close to epithelial cells, as identified by confocal microscopy. In chronic HDM-driven airway inflammation ILC2s were also found inside organized cellular infiltrates near T cells. Collectively, our findings show that ILC2s are phenotypically more heterogeneous than previously thought, whereby their surface marker and gene expression profile are highly dynamic</style></abstract><notes><style face="normal" font="default">IS - 1664-3224 (Print)IS - 1664-3224 (Linking)LA - engPT - Journal ArticleCO - Netherlands -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01684</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29250067">PM:29250067</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1684.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1684.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Li WS</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01684</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87099</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Petursdottir,D.H.</style></author><author><style face="normal" font="default"> Nordlander,S.</style></author><author><style face="normal" font="default"> Qazi,K.R.</style></author><author><style face="normal" font="default"> Carvalho-Queiroz,C.</style></author><author><style face="normal" font="default"> Ahmed,O.O.</style></author><author><style face="normal" font="default"> Hell,E.</style></author><author><style face="normal" font="default"> Bjorkander,S.</style></author><author><style face="normal" font="default"> Haileselassie,Y.</style></author><author><style face="normal" font="default"> Navis,M.</style></author><author><style face="normal" font="default"> Kokkinou,E.</style></author><author><style face="normal" font="default"> Lio,I.Z.L.</style></author><author><style face="normal" font="default"> Hennemann,J.</style></author><author><style face="normal" font="default"> Brodin,B.</style></author><author><style face="normal" font="default"> Huseby,D.L.</style></author><author><style face="normal" font="default"> Nilsson,C.</style></author><author><style face="normal" font="default"> Hughes,D.</style></author><author><style face="normal" font="default"> Udekwu,K.I.</style></author><author><style face="normal" font="default"> Sverremark-Ekstrom,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Molecular Biosciences, The Wenner-Gren Institute, Arrhenius Laboratories for Natural Sciences, Stockholm University, Stockholm, Sweden</style></auth-address><titles><title><style face="normal" font="default">Early-Life Human Microbiota Associated With Childhood Allergy Promotes the T Helper 17 Axis in Mice</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1699">1699-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The intestinal microbiota influences immune maturation during childhood, and is implicated in early-life allergy development. However, to directly study intestinal microbes and gut immune responses in infants is difficult. To investigate how different types of early-life gut microbiota affect immune development, we collected fecal samples from children with different allergic heredity (AH) and inoculated germ-free mice. Immune responses and microbiota composition were evaluated in the offspring of these mice. Microbial composition in the small intestine, the cecum and the colon were determined by 16S rRNA sequencing. The intestinal microbiota differed markedly between the groups of mice, but only exposure to microbiota associated with AH and known future allergy in children resulted in a T helper 17 (Th17)-signature, both systemically and in the gut mucosa in the mouse offspring. These Th17 responses could be signs of a particular microbiota and a shift in immune development, ultimately resulting in an increased risk of allergy</style></abstract><notes><style face="normal" font="default">IS - 1664-3224 (Print)IS - 1664-3224 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01699</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29250074">PM:29250074</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1699.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1699.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Petursdottir DH</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01699</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86520</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Peterson,M.R.</style></author><author><style face="normal" font="default"> Coop,C.A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Long-term omalizumab use in the treatment of exercise-induced anaphylaxis</style></title><secondary-title><style face="normal" font="default">Allergy Rhinol (Providence)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Rhinol (Providence)</style></abbr-1></periodical><pages end="172" start="170">170-172</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="10" Year="2017">2017/10/1</year></dates><abstract><style face="normal" font="default">Reported is a case of a 39-year-old male who was diagnosed with exercise-induced anaphylaxis (EIA). He was initially treated prophylactically with fexofenadine, montelukast, and ranitidine. He also used an epinephrine autoinjector as needed. He was refractory to these medications and continued to have episodes of EIA. He was then started on a trial of omalizumab, an immunoglobulin E monoclonal antibody, and had resolution of the EIA episodes. After discontinuation of the omalizumab, the EIA episodes returned. He was restarted on omalizumab and since that time, has had 5 years free of EIA episodes and can now exercise without any symptoms. To our knowledge, this is only the third case in the literature of successful treatment of EIA by using omalizumab. This case was unique because it provided successful long-term use of omalizumab for EIA. Further studies are recommended for the use of omalizumab in the treatment of EIA</style></abstract><notes><style face="normal" font="default">DA - 20171026IS - 2152-6575 (Print)IS - 2152-6567 (Linking)LA - engPT - Journal ArticleCO - United states -</style></notes><work-type><style face="normal" font="default">10.2500/ar.2017.8.0204</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29070274">PM:29070274</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Rhinol (Providence)\2017-8-170-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Rhinol (Providence)\2017-8-170-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171026, Peterson MR</style></custom2><misc3><style face="normal" font="default">10.2500/ar.2017.8.0204</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87011</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kumeta,H.</style></author><author><style face="normal" font="default"> Nakayama,H.</style></author><author><style face="normal" font="default"> Ogura,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Global Station for Soft Matter, Global Institution for Collaborative Research and Education, Hokkaido University, Kita 21 Nishi 11, Kita, Sapporo, 0110021, Japan</style></auth-address><titles><title><style face="normal" font="default">Solution structure of the major fish allergen parvalbumin Sco j 1 derived from the Pacific mackerel</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="17160">17160-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Fish allergen</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">Although fish is an important part of the human diet, it is also a common source of food allergy. The major allergen in fish is parvalbumin, a well-conserved Ca(2+)-binding protein found in the white muscle of many fish species. Here, we studied the solution structure of the parvalbumin Sco j 1, derived from the Pacific mackerel, using nuclear magnetic resonance spectroscopy. We mapped the IgE-binding epitope proposed in a recent study onto the present structure. Interestingly, three of four residues, which were elucidated as key residues of the IgE-binding epitope, were exposed to solvent, whereas one residue faced the inside of the molecule. We expect that this solution structure can be used in future studies attempting to analyze the various IgE-binding modes of these allergens</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-17281-6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29215073">PM:29215073</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-17160.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-17160.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Kumeta H</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-17281-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87207</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Andre,D.M.</style></author><author><style face="normal" font="default"> Calixto,M.C.</style></author><author><style face="normal" font="default"> Sollon,C.</style></author><author><style face="normal" font="default"> Alexandre,E.C.</style></author><author><style face="normal" font="default"> Tavares,E.B.G.</style></author><author><style face="normal" font="default"> Naime,A.C.A.</style></author><author><style face="normal" font="default"> Anhe,G.F.</style></author><author><style face="normal" font="default"> Antunes,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pharmacology, Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, Sao Paulo, Brazil</style></auth-address><titles><title><style face="normal" font="default">High-fat diet-induced obesity impairs insulin signaling in lungs of allergen-challenged mice: Improvement by resveratrol</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="17296">17296-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">Insulin resistance plays an important role in obesity-associated asthma exacerbations. Using a murine model of allergic airway inflammation, we evaluated the insulin signaling transmission in lungs of obese compared with lean mice. We further evaluated the effects of the polyphenol resveratrol in the pulmonary insulin signaling. In lean mice, insulin stimulation significantly increased phosphorylations of AKT, insulin receptor substrate 1 (IRS-1) and insulin receptor beta (IRbeta) in lung tissue and isolated bronchi (p &lt; 0.05), which were impaired in obese group. Instead, obese mice displayed increased tyrosine nitrations of AKT, IRbeta and IRS-1 (p &lt; 0.05). Two-week therapy of obese mice with resveratrol (100 mg/kg/day) restored insulin-stimulated AKT, IRS-1 and IRbeta phosphorylations, and simultaneously blunted the tyrosine nitration of these proteins. Additionally, the c-Jun N-terminal kinase (JNK) and inhibitor of NF-kappaB Kinase (IkappaK) phosphorylations were significantly increased in obese group, an effect normalized by resveratrol. In separate experiments, the inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (20 mg/kg/day, three weeks) mimicked the protective effects exerted by resveratrol in lungs of obese mice. Lungs of obese mice display nitrosative-associated impairment of insulin signaling, which is reversed by resveratrol. Polyphenols may be putative drugs to attenuate asthma exacerbations in obese individuals</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-17558-w.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29229986">PM:29229986</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-17296.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-17296.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171218, Andre DM</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-17558-w.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87205</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Takahashi,M.</style></author><author><style face="normal" font="default"> Soejima,K.</style></author><author><style face="normal" font="default"> Taniuchi,S.</style></author><author><style face="normal" font="default"> Hatano,Y.</style></author><author><style face="normal" font="default"> Yamanouchi,S.</style></author><author><style face="normal" font="default"> Ishikawa,H.</style></author><author><style face="normal" font="default"> Irahara,M.</style></author><author><style face="normal" font="default"> Sasaki,Y.</style></author><author><style face="normal" font="default"> Kido,H.</style></author><author><style face="normal" font="default"> Kaneko,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Kansai Medical University, Osaka, 573-1191, Japan</style></auth-address><titles><title><style face="normal" font="default">Oral immunotherapy combined with omalizumab for high-risk cow's milk allergy: a randomized controlled trial</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="17453">17453-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="12" Month="12" Year="2017">2017/12/12</year></dates><abstract><style face="normal" font="default">We evaluated the efficacy and safety of oral immunotherapy (OIT) combined with 24 weeks of omalizumab (OMB) at inducing desensitization in children with cow's milk allergy (CM) compared with an untreated group. The present study was a prospective randomized controlled trial. Sixteen patients (age, 6-14 years) with high IgE levels to CM were enrolled in the present study. Patients were randomized 1:1 to receive OMB-OIT group or untreated group. The primary outcome was the induction of desensitization at 8 weeks after OMB was discontinued in OMB-OIT treated group and at 32 weeks after study entry. None of the 6 children in the untreated group developed desensitization to CM while all of the 10 children in the OIT-OMB treated group achieved desensitization (P &lt; 0.001). A significantly decreased wheal diameter in response to a skin prick test using CM was found in the OMB-OIT treated group (P &lt; 0.05). These data suggest that OIT combined with OMB using microwave heated CM may help to induce desensitization for children with high-risk CM allergy. This prospective randomized controlled trial was intended for 50 participants but was prematurely discontinued due to overwhelming superiority of OMB combined with microwave heated OIT over CM avoidance</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-16730-6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29234055">PM:29234055</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-17453.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-17453.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171218, Takahashi M</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-16730-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87247</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hellman,L.T.</style></author><author><style face="normal" font="default"> Akula,S.</style></author><author><style face="normal" font="default"> Thorpe,M.</style></author><author><style face="normal" font="default"> Fu,Z.</style></author></authors></contributors><titles><title><style face="normal" font="default">Tracing the Origins of IgE, Mast Cells, and Allergies by Studies of Wild Animals</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1749">1749-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Enzymes</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1664-3224</style></isbn><abstract><style face="normal" font="default">In most industrialized countries allergies have increased in frequency quite dramatically during the past 50 years. Estimates show that 20-30% of the populations are affected. Allergies have thereby become one of the major medical challenges of the 21st century. Despite several theories including the hygiene hypothesis there are still very few solid clues concerning the causes of this increase. To trace the origins of allergies we have studied cells and molecules of importance for the development of IgE mediated allergies, including when they have appeared during vertebrate evolution. By studying the immunoglobulin repertoire in the three extant mammalian lineages we have been able to show that IgE and IgG most likely appeared by a gene duplication of IgY in an early mammal, possibly 220-300 million years ago. Receptors specific for IgE and IgG subsequently appeared in parallel with the increase in Ig isotypes from a subfamily of the recently identified Fc receptor-like molecules. Circulating IgE levels are generally very low in humans and laboratory rodents. However, when dogs and Scandinavian wolfs were analyzed, IgE levels were found to be 100-200 times higher compared to humans, indicating a generally much more active IgE synthesis in free-living animals, most likely connected to intestinal parasite infections. One of the major effector molecules released upon IgE-mediated activation by mast cells are serine proteases. These proteases, which belong to the large family of hematopoietic serine proteases, are extremely abundant and can account for up to 35% of the total cellular protein. Recent studies show that several of these enzymes, including the chymases and tryptases, have been part of the mast cell granule repertoire for more than 200 million years. The first members of the larger family of hematopoietic serine proteases seemed to have appeared with the jawed vertebrates. The aim is now to continue these studies of mast cell biology and IgE to obtain additional clues to their evolutionary conserved functions. A focus concerns why the humoral immune response involving IgE and mast cells have become so dysregulated in humans as well as several of our domestic companion animals</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01749</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29312297">PM:29312297</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1749.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1749.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Hellman LT</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01749</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87204</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,W.H.</style></author><author><style face="normal" font="default"> An,H.J.</style></author><author><style face="normal" font="default"> Kim,J.Y.</style></author><author><style face="normal" font="default"> Gwon,M.G.</style></author><author><style face="normal" font="default"> Gu,H.</style></author><author><style face="normal" font="default"> Jeon,M.</style></author><author><style face="normal" font="default"> Sung,W.J.</style></author><author><style face="normal" font="default"> Han,S.M.</style></author><author><style face="normal" font="default"> Pak,S.C.</style></author><author><style face="normal" font="default"> Kim,M.K.</style></author><author><style face="normal" font="default"> Park,K.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu, Korea</style></auth-address><titles><title><style face="normal" font="default">Beneficial effects of melittin on ovalbumin-induced atopic dermatitis in mouse</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="17679">17679-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="15" Month="12" Year="2017">2017/12/15</year></dates><abstract><style face="normal" font="default">Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus and relapsable eczematous lesions. The hallmarks of AD are defects in the epidermal barrier and immunoglobulin E (IgE)-mediated sensitization to several environmental allergens, as well as an immune disorder mediated by an imbalance toward T-helper-2 response. Melittin, a major component of bee venom, has been studied in various inflammatory diseases. However, the beneficial effects of melittin on mouse with AD-like symptoms have not been explored. Therefore, we investigated the anti-allergic effects of melittin. AD was induced by ovalbumin (OVA) patch. After agent treatment, skin tissues and sera were extracted from the sacrificed mice were used to demonstrate the effects of melittin through various molecular biological methods. The results showed that OVA-induced skin thickening and inflammatory infiltration were decreased in the melittin-treated group. Melittin prevented OVA-induced filaggrin deficiency and imbalanced inflammatory mediators. Furthermore, melittin inhibited IL-4/IL-13-induced filaggrin downregulation through the blockade of STAT3 activation in human keratinocytes. In summary, this study has shown that melittin ameliorated OVA-induced AD-like symptoms from various perspectives. The findings of this study may be the first evidence of the anti-inflammatory effects of melittin on OVA-induced AD</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - South Korea -CO - Australia -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-17873-2.</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247241">PM:29247241</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-17679.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-17679.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Kim WH</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-17873-2.</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87206</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Maeda,S.</style></author><author><style face="normal" font="default"> Nakamura,T.</style></author><author><style face="normal" font="default"> Harada,H.</style></author><author><style face="normal" font="default"> Tachibana,Y.</style></author><author><style face="normal" font="default"> Aritake,K.</style></author><author><style face="normal" font="default"> Shimosawa,T.</style></author><author><style face="normal" font="default"> Yatomi,Y.</style></author><author><style face="normal" font="default"> Murata,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Animal Radiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan</style></auth-address><titles><title><style face="normal" font="default">Prostaglandin D2 metabolite in urine is an index of food allergy</style></title><secondary-title><style face="normal" font="default">Sci Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Rep</style></abbr-1></periodical><pages end="" start="17687">17687-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="15" Month="12" Year="2017">2017/12/15</year></dates><abstract><style face="normal" font="default">Food allergy is immediate hypersensitive reactions to ingested foods. Since early diagnosis is effective for disease control, development of an objective diagnostic index is required. Using mediator-lipidomics, we found that levels of the urinary prostaglandin D2 (PGD2) metabolite, tetranor-PGDM, reflected the severity of the allergic symptoms and intestinal mast cell hyperplasia in mice. Repeated oral challenges with ovalbumin promoted allergic symptoms in sensitized mice. Particularly, the allergic mice presented with increased numbers of intestinal mast cells, which strongly expressed hematopoietic PGD synthase (H-PGDS). The levels of urinary tetranor-PGDM increased as the disease progressed. Treatment with a mast cell inactivator or an anti-inflammatory steroid attenuated these symptoms and decreased the tetranor-PGDM urinary levels. The levels of urinary tetranor-PGDM did not correlate with the disease severity in murine models of colitis, asthma, or allergic dermatitis. Furthermore, we have shown that urinary levels of tetranor-PGDM were significantly higher in patients with food allergy than those in healthy volunteers and patients with other types of allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis. These findings suggest that urinary tetranor-PGDM is a useful diagnostic index of food allergy in both mice and humans</style></abstract><notes><style face="normal" font="default">IS - 2045-2322 (Electronic)IS - 2045-2322 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1038/s41598-017-17798-w</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29247205">PM:29247205</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Rep\2017-7-17687.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Rep\2017-7-17687.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171218, Maeda S</style></custom2><misc3><style face="normal" font="default">10.1038/s41598-017-17798-w</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86787</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sampson,H.A.</style></author><author><style face="normal" font="default"> Shreffler,W.G.</style></author><author><style face="normal" font="default"> Yang,W.H.</style></author><author><style face="normal" font="default"> Sussman,G.L.</style></author><author><style face="normal" font="default"> Brown-Whitehorn,T.F.</style></author><author><style face="normal" font="default"> Nadeau,K.C.</style></author><author><style face="normal" font="default"> Cheema,A.S.</style></author><author><style face="normal" font="default"> Leonard,S.A.</style></author><author><style face="normal" font="default"> Pongracic,J.A.</style></author><author><style face="normal" font="default"> Sauvage-Delebarre,C.</style></author><author><style face="normal" font="default"> Assa'ad,A.H.</style></author><author><style face="normal" font="default"> de Blay,F.</style></author><author><style face="normal" font="default"> Bird,J.A.</style></author><author><style face="normal" font="default"> Tilles,S.A.</style></author><author><style face="normal" font="default"> Boralevi,F.</style></author><author><style face="normal" font="default"> Bourrier,T.</style></author><author><style face="normal" font="default"> Hebert,J.</style></author><author><style face="normal" font="default"> Green,T.D.</style></author><author><style face="normal" font="default"> Gerth van Wijk,R.</style></author><author><style face="normal" font="default"> Knulst,A.C.</style></author><author><style face="normal" font="default"> Kanny,G.</style></author><author><style face="normal" font="default"> Schneider,L.C.</style></author><author><style face="normal" font="default"> Kowalski,M.L.</style></author><author><style face="normal" font="default"> Dupont,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Icahn School of Medicine at Mount Sinai, New York, New York</style></auth-address><titles><title><style face="normal" font="default">Effect of Varying Doses of Epicutaneous Immunotherapy vs Placebo on Reaction to Peanut Protein Exposure Among Patients With Peanut Sensitivity: A Randomized Clinical Trial</style></title><secondary-title><style face="normal" font="default">JAMA</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">JAMA</style></abbr-1></periodical><pages end="1809" start="1798">1798-1809</pages><volume><style face="normal" font="default">318</style></volume><number><style face="normal" font="default">18</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">Importance: Epicutaneous immunotherapy may have potential for treating peanut allergy but has been assessed only in preclinical and early human trials. Objective: To determine the optimal dose, adverse events (AEs), and efficacy of a peanut patch for peanut allergy treatment. Design, Setting, and Participants: Phase 2b double-blind, placebo-controlled, dose-ranging trial of a peanut patch in peanut-allergic patients (6-55 years) from 22 centers, with a 2-year, open-label extension (July 31, 2012-July 31, 2014; extension completed September 29, 2016). Patients (n = 221) had peanut sensitivity and positive double-blind, placebo-controlled food challenges to an eliciting dose of 300 mg or less of peanut protein. Interventions: Randomly assigned patients (1:1:1:1) received an epicutaneous peanut patch containing 50 mug (n = 53), 100 mug (n = 56), or 250 mug (n = 56) of peanut protein or a placebo patch (n = 56). Following daily patch application for 12 months, patients underwent a double-blind, placebo-controlled food challenge to establish changes in eliciting dose. Main Outcomes and Measures: The primary efficacy end point was percentage of treatment responders (eliciting dose: >/=10-times increase and/or reaching >/=1000 mg of peanut protein) in each group vs placebo patch after 12 months. Secondary end points included percentage of responders by age strata and treatment-emergent adverse events (TEAEs). Results: Of 221 patients randomized (median age, 11 years [quartile 1, quartile 3: 8, 16]; 37.6% female), 93.7% completed the trial. A significant absolute difference in response rates was observed at month 12 between the 250-mug (n = 28; 50.0%) and placebo (n = 14; 25.0%) patches (difference, 25.0%; 95% CI, 7.7%-42.3%; P = .01). No significant difference was seen between the placebo patch vs the 100-mug patch. Because of statistical testing hierarchical rules, the 50-mug patch was not compared with placebo. Interaction by age group was only significant for the 250-mug patch (P = .04). In the 6- to 11-year stratum, the response rate difference between the 250-mug (n = 15; 53.6%) and placebo (n = 6; 19.4%) patches was 34.2% (95% CI, 11.1%-57.3%; P = .008); adolescents/adults showed no difference between the 250-mug (n = 13; 46.4%) and placebo (n = 8; 32.0%) patches: 14.4% (95% CI, -11.6% to 40.4%; P = .40). No dose-related serious AEs were observed. The percentage of patients with 1 or more TEAEs (largely local skin reactions) was similar across all groups in year 1: 50-mug patch = 100%, 100-mug patch = 98.2%, 250-mug patch = 100%, and placebo patch = 92.9%. The overall median adherence was 97.6% after 1 year; the dropout rate for treatment-related AEs was 0.9%. Conclusions and Relevance: In this dose-ranging trial of peanut-allergic patients, the 250-mug peanut patch resulted in significant treatment response vs placebo patch following 12 months of therapy. These findings warrant a phase 3 trial. Trial Registration: clinicaltrials.gov Identifier: NCT01675882</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1538-3598 (Electronic)IS - 0098-7484 (Linking)LA - engPT - Journal ArticlePT - Research Support, Non-U.S. Gov'tCO - United States -CO - France -CO - Canada -CO - Netherlands -CO - Poland -</style></notes><work-type><style face="normal" font="default">10.1001/jama.2017.16591</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29136445">PM:29136445</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\JAMA\2017-318-1798-809.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\JAMA\2017-318-1798-809.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Sampson HA</style></custom2><misc3><style face="normal" font="default">10.1001/jama.2017.16591</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86555</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">van Odijk,J.</style></author><author><style face="normal" font="default"> Sjolander,S.</style></author><author><style face="normal" font="default"> Brostedt,P.</style></author><author><style face="normal" font="default"> Borres,M.P.</style></author><author><style face="normal" font="default"> Englund,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dept of Respiratory Medicine and Allergology, Sahlgrenska Academy at Goteborg University, Goteborg, Sweden</style></auth-address><titles><title><style face="normal" font="default">High frequency of IgE sensitization towards kiwi seed storage proteins among peanut allergic individuals also reporting allergy to kiwi</style></title><secondary-title><style face="normal" font="default">Clin Mol Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Mol Allergy</style></abbr-1></periodical><pages end="" start="18">18-</pages><volume><style face="normal" font="default">15</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: IgE sensitization to storage proteins from nuts and seed is often related to severe allergic symptoms. There is a risk of immunological IgE cross-reactivity between storage proteins from different species. The potential clinical implication of such cross-reactivity is that allergens other than the known sensitizer can cause allergic symptoms. Previous studies have suggested that kiwi seed storage proteins may constitute hidden food allergens causing cross-reactive IgE-binding with peanut and other tree nut homologs, thereby mediating a potential risk of causing allergy symptoms among peanut ant tree nut allergic individuals. The objective of this study was to investigate the degree of sensitization towards kiwi fruit seed storage proteins in a cohort of peanut allergic individuals. Methods: A cohort of 59 adolescents and adults with peanut allergy was studied, and self reported allergies to a number of additional foods were collected. Quantitative IgE measurements to seed storage proteins from kiwi and peanut were performed. Results: In the cohort, 23 out of the 59 individuals were reporting kiwi fruit allergy (39%). The frequency of IgE sensitization to kiwi fruit and to any kiwi seed storage protein was higher among peanut allergic individuals also reporting kiwi fruit allergy (P = 0.0001 and P = 0.01). A positive relationship was found between IgE levels to 11S globulin (r = 0.65) and 7S globulin (r = 0.48) allergens from kiwi and peanut, but IgE levels to 2S albumin homologs did not correlate. Patients reporting kiwi fruit allergy also reported allergy to hazelnut (P = 0.015), soy (P &lt; 0.0001), pea (P = 0.0002) and almond (P = 0.016) to a higher extent than peanut allergic individuals without kiwi allergy. Conclusions: Thirty-nine percent of the peanut allergic patients in this cohort also reported kiwi fruit allergy, they displayed a higher degree of sensitization to kiwi storage proteins from both kiwi and peanut, and they also reported a higher extent of allergy to other nuts and legumes. On the molecular level, there was a correlation between IgE levels to 11S and 7S storage proteins from kiwi and peanut. Taken together, reported symptoms and serological findings to kiwi in this cohort of patients with concurrent allergy to peanut and kiwi fruit, could be explained by a combination of cross-reactivity between the 11S and 7S globulins and co-sensitization to the 2S albumin Act d 13</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 1476-7961 (Print)IS - 1476-7961 (Linking)LA - engPT - Journal ArticleCO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1186/s12948-017-0073-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29118674">PM:29118674</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Mol Allergy\2017-15-18.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Mol Allergy\2017-15-18.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, van odijk J</style></custom2><misc3><style face="normal" font="default">10.1186/s12948-017-0073-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86642</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,F.</style></author><author><style face="normal" font="default"> Huang,Y.</style></author><author><style face="normal" font="default"> Huang,Y.Y.</style></author><author><style face="normal" font="default"> Kuang,Y.S.</style></author><author><style face="normal" font="default"> Wei,Y.J.</style></author><author><style face="normal" font="default"> Xiang,L.</style></author><author><style face="normal" font="default"> Zhang,X.J.</style></author><author><style face="normal" font="default"> Jia,Z.C.</style></author><author><style face="normal" font="default"> Jiang,S.</style></author><author><style face="normal" font="default"> Li,J.Y.</style></author><author><style face="normal" font="default"> Wan,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Biomedical Analysis Center, Third Military Medical University, Chongqing 400038, China; Chongqing Key Laboratory of Cytomics, Chongqing 400038, China</style></auth-address><titles><title><style face="normal" font="default">MicroRNA-146a promotes IgE class switch in B cells via upregulating 14-3-3sigma expression</style></title><secondary-title><style face="normal" font="default">Mol Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Immunol</style></abbr-1></periodical><pages end="189" start="180">180-189</pages><volume><style face="normal" font="default">92</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="11" Year="2017">2017/11/1</year></dates><abstract><style face="normal" font="default">B cells play a critical role in immune responses both in physiological and pathological conditions, and microRNAs have been shown to play important roles in regulating B cell proliferation and function. MiR-146a has been shown to modulate T cell immunity, but its function in regulating B cell response remains partially understood. Our previous studies indicated that germinal center (GC) B cells are significantly expanded in miR-146a-overexpressing (TG) mice. In this study, we further characterized the roles of miR-146a in regulating humoral immune responses to specific antigens. We found that the production of IgE antibody were significantly elevated in TG mice, while the antibody affinity maturation of IgM and IgG were similar between TG mice and the normal controls. We further found higher IgE antibody levels in TG B cell culture supernatant than that in normal controls. A global protein expression comparison of B cells from TG mice and the normal controls through TMT proteomic assay showed that 14-3-3sigma, a key factor of immunoglobulin class switch DNA recombination (CSR) in B cells, was highly up-regulated in B cells with overexpression of miR-146a, while Smad4, the target of miR-146a, was decreased. Using an asthma model induced by OVA immunization, we further confirmed the increased level of OVA specific IgE antibodies in TG mice. These results demonstrate that miR-146a enhances class switch and secretion of IgE in B cells by upregulating 14-3-3sigma expression, and suggest that miR-146a may be a potential target for asthma therapy</style></abstract><notes><style face="normal" font="default">DA - 20171104IS - 1872-9142 (Electronic)IS - 0161-5890 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.molimm.2017.10.023</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29101850">PM:29101850</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Immunol\2017-92-180-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Immunol\2017-92-180-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171104, Li F</style></custom2><misc3><style face="normal" font="default">10.1016/j.molimm.2017.10.023</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86600</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mendoza,J.</style></author><author><style face="normal" font="default"> Waibel,K.H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Meals-Ready-to-Eat by Almost Everyone: A Quick Reference Guide for Individuals with Food Allergy</style></title><secondary-title><style face="normal" font="default">J Allergy Clin Immunol Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Allergy Clin Immunol Pract</style></abbr-1></periodical><pages end="" start="1801">1801-</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="11/16/2017" status="on-request"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2213-2198</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.jaip.2017.09.013</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.jaip.2017.09.013</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1801.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Allergy Clin Immunol Pract\2017-5-1801.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Mendoza J</style></custom2><misc3><style face="normal" font="default">10.1016/j.jaip.2017.09.013</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87246</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mohamud,R.</style></author><author><style face="normal" font="default"> LeMasurier,J.S.</style></author><author><style face="normal" font="default"> Boer,J.C.</style></author><author><style face="normal" font="default"> Sieow,J.L.</style></author><author><style face="normal" font="default"> Rolland,J.M.</style></author><author><style face="normal" font="default"> O'Hehir,R.E.</style></author><author><style face="normal" font="default"> Hardy,C.L.</style></author><author><style face="normal" font="default"> Plebanski,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Synthetic Nanoparticles That Promote Tumor Necrosis Factor Receptor 2 Expressing Regulatory T Cells in the Lung and Resistance to Allergic Airways Inflammation</style></title><secondary-title><style face="normal" font="default">Front Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Front Immunol</style></full-title></periodical><pages end="" start="1812">1812-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1664-3224</style></isbn><abstract><style face="normal" font="default">Synthetic glycine coated 50 nm polystyrene nanoparticles (PS50G), unlike ambient nanoparticles, do not promote pulmonary inflammation, but instead render lungs resistant to the development of allergic airway inflammation (AAI). In this study we show that PS50G modulate the frequency and phenotype of regulatory T cells (Treg) in the lung, specifically increasing the proportion of tumour necrosis factor 2 (TNFR2) expressing Treg. Mice pre-exposed to PS50G, which were sensitised and then challenged with an allergen a month later, preferentially expanded TNFR2+Foxp3+ Treg, which further expressed enhanced levels of latency associated peptide (LAP) and cytotoxic T-lymphocyte associated molecule-4 (CTLA-4). Moreover, PS50G CD103+ dendritic cell (DC) activation in the lung was associated with the proliferative expansion of TNFR2+Foxp3+ Treg. These findings provide the first evidence that engineered nanoparticles can promote the selective expansion of maximally suppressing TNFR2+Foxp3+ Treg, and further suggest a novel mechanism by which nanoparticles may promote healthy lung homeostasis</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Australia -CO - Malaysia -</style></notes><work-type><style face="normal" font="default">10.3389/fimmu.2017.01812</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29312323">PM:29312323</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Immunol\2017-8-1812.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Immunol\2017-8-1812.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Mohamud R</style></custom2><misc3><style face="normal" font="default">10.3389/fimmu.2017.01812</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86542</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Suzuki,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Faculty of Pharmaceutical Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University</style></auth-address><titles><title><style face="normal" font="default">The Emerging Picture of Mast Cell Activation: The Complex Regulatory Network of High-Affinity Receptor for Immunoglobulin E Signaling</style></title><secondary-title><style face="normal" font="default">Biol Pharm Bull</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Biol Pharm Bull</style></abbr-1></periodical><pages end="1832" start="1828">1828-1832</pages><volume><style face="normal" font="default">40</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">It is now well known that immunoglobulin E (IgE) and mast cells (MCs) are important participants in allergic diseases. MCs contain electron-dense secretory granules which are filled with inflammatory mediators. The interaction of an allergen (antigen) with an antigen-specific IgE-bound high-affinity receptor for IgE (FcepsilonRI) is an essential step in MC activation as well as subsequent downstream signaling events. What we know is that IgE and FcepsilonRI activate a complex regulatory network (i.e., signaling molecules and messengers) that governs both the type of MC activation and the symptoms of allergic disease. This review focuses on recent discoveries that shed new light on FcepsilonRI signaling networks, holding promise for the development of new therapeutic solutions in the treatment of allergic diseases</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 1347-5215 (Electronic)IS - 0918-6158 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1248/bpb.b17-00465</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29093329">PM:29093329</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Biol Pharm Bull\2017-40-1828-32.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Biol Pharm Bull\2017-40-1828-32.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Suzuki R</style></custom2><misc3><style face="normal" font="default">10.1248/bpb.b17-00465</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86538</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chang,Y.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Clinical Immunology, Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea</style></auth-address><titles><title><style face="normal" font="default">Autumn leaves: about aging and allergy</style></title><secondary-title><style face="normal" font="default">Asia Pac Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Asia Pac Allergy</style></abbr-1></periodical><pages end="184" start="183">183-184</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 2233-8276 (Print)IS - 2233-8276 (Linking)LA - engPT - EditorialCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.5415/apallergy.2017.7.4.183</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29094014">PM:29094014</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asia Pac Allergy\2017-7-183-4.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asia Pac Allergy\2017-7-183-4.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Cheng YS</style></custom2><misc3><style face="normal" font="default">10.5415/apallergy.2017.7.4.183</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87051</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jakubas-Zawalska,J.</style></author><author><style face="normal" font="default"> Asman,M.</style></author><author><style face="normal" font="default"> Solarz,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Parasitology, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia in Katowice, ul. Jednosci 8, 41-218 Sosnowiec, Poland</style></auth-address><titles><title><style face="normal" font="default">Sensitization to the storage mites Lepidoglyphus destructor and Tyrophagus putrescentiae (Acari, Sarcoptiformes, Astigmatina) in a suburban population in Southern Poland</style></title><secondary-title><style face="normal" font="default">Ann Parasitol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Ann Parasitol</style></full-title></periodical><pages end="188" start="183">183-188</pages><volume><style face="normal" font="default">63</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Mite infestation of stored products is a serious threat to food safety and public health. These stored product mites are not only serious pests of stored food but also cause allergies in humans. Thirty serum samples from patients living in suburban areas of Upper Silesia (South Poland) were tested for sensitization to two species of storage mites: Lepidoglyphus destructor [LD] and Tyrophagus putrescentiae [TP]. Patient antibodies against particular antigens were identified using anti-human anti-IgE monoclonal antibodies. Fifteen protein fractions from LD gave positive reactions with IgE antibodies and 18 from TP. Seven of the 30 samples showed positive reactions to a protein fraction measuring about 29 kDa from LD and six reacted with a fraction measuring about 25 kDa from TP. These findings may imply the existence of many protein fractions with allergenic properties besides the characterized allergens in the two tested species</style></abstract><notes><style face="normal" font="default">IS - 2299-0631 (Print)IS - 2299-0631 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.17420/ap6303.104</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29274211">PM:29274211</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Parasitol\2017-63-183-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Parasitol\2017-63-183-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171226, Jakubas-Zawalska J</style></custom2><misc3><style face="normal" font="default">10.17420/ap6303.104</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87107</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ha,E.K.</style></author><author><style face="normal" font="default"> Na,M.S.</style></author><author><style face="normal" font="default"> Lee,S.</style></author><author><style face="normal" font="default"> Baek,H.</style></author><author><style face="normal" font="default"> Lee,S.J.</style></author><author><style face="normal" font="default"> Sheen,Y.H.</style></author><author><style face="normal" font="default"> Jung,Y.H.</style></author><author><style face="normal" font="default"> Lee,K.S.</style></author><author><style face="normal" font="default"> Kim,M.A.</style></author><author><style face="normal" font="default"> Jee,H.M.</style></author><author><style face="normal" font="default"> Han,M.Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, CHA University School of Medicine, Seongnam, Korea</style></auth-address><titles><title><style face="normal" font="default">Prevalence and Clinical Characteristics of Local Allergic Rhinitis in Children Sensitized to House Dust Mites</style></title><secondary-title><style face="normal" font="default">Int Arch Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Arch Allergy Immunol</style></abbr-1></periodical><pages end="189" start="183">183-189</pages><volume><style face="normal" font="default">174</style></volume><number><style face="normal" font="default">3-4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">OBJECTIVE: The prevalence of local allergic rhinitis (LAR) in nonatopic children remains unknown. This study aimed to determine the prevalence, clinical characteristics, and severity of LAR in children in comparison to classical allergic rhinitis (AR) and nonallergic rhinitis (NAR). STUDY DESIGN: A total of 145 children (aged 1-18 years) were enrolled and classified into 3 groups (AR, NAR, and LAR) based on a skin prick test (SPT) and a nasal provocation test (NPT) with house dust mite, i.e., Dermatophagoides pteronyssinus. NPT positivity was defined as a symptom score >/=2 standard deviations (SDs) above the healthy control score. RESULTS: Eighty-one children had AR (55.9%), and 64 (44.1%) had symptoms of rhinitis with negative SPT; 59 NAR (40.7%) and 5 LAR (3.4%) children were identified. The kappa score for agreement between the SPT and the NPT results was 0.778 (95% CI 0.726-0.830, p &lt; 0.001). A significant correlation was observed between wheal diameter and maximum nasal symptom score provoked by D.pteronyssinus (rho = 0.589, p &lt; 0.001). Nasal severity according to the ARIA guideline did not show any differences in the 3 groups (p = 0.693). The AR group was older than the LAR and NAR groups (AR > LAR > NAR, p = 0.003). CONCLUSIONS: Despite the evidence to support the existence of LAR in pediatric populations, we found that its prevalence was relatively low, possibly due to the high rate of agreement between SPT and NPT. Further investigations are needed to identify immunological as well as clinical implications of LAR</style></abstract><notes><style face="normal" font="default">IS - 1423-0097 (Electronic)IS - 1018-2438 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1159/000481091</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130983">PM:29130983</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-183-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-183-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Ha EK</style></custom2><misc3><style face="normal" font="default">10.1159/000481091</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86537</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Song,W.J.</style></author><author><style face="normal" font="default"> Chang,Y.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Korea</style></auth-address><titles><title><style face="normal" font="default">Respiratory allergies in the elderly: findings from the Korean Longitudinal Study on Health and Aging phase I study (2005-2006)</style></title><secondary-title><style face="normal" font="default">Asia Pac Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Asia Pac Allergy</style></abbr-1></periodical><pages end="192" start="185">185-192</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">Population aging is a global issue, but is estimated to be more rapid and dramatic in Asian countries. In the past, allergy might have been a minor concern in the elderly (usually defined as >/=65 years). However, recent series of epidemiologic studies indicate that allergic diseases are more prevalent than expected in the aged population. Furthermore, they pose significant impact on quality of life and socioeconomic costs. The burden may also increase in the elderly, due to frequent comorbidities and treatment-related complications. The Korean Longitudinal Study on Health and Aging (KLoSHA) cohort study is one of major research projects on the epidemiology of common geriatric disease conditions in Korea. In this review, we summarized the baseline findings on the prevalence, risk factors, comorbidities and impact of geriatric respiratory allergic conditions in the phase I KLoSHA cohort study</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 2233-8276 (Print)IS - 2233-8276 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.5415/apallergy.2017.7.4.185</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29094015">PM:29094015</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asia Pac Allergy\2017-7-185-92.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asia Pac Allergy\2017-7-185-92.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Song WJ</style></custom2><misc3><style face="normal" font="default">10.5415/apallergy.2017.7.4.185</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86494</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hajas,L.</style></author><author><style face="normal" font="default"> Scherf,K.A.</style></author><author><style face="normal" font="default"> Bugyi,Z.</style></author><author><style face="normal" font="default"> Torok,K.</style></author><author><style face="normal" font="default"> Schall,E.</style></author><author><style face="normal" font="default"> Kohler,P.</style></author><author><style face="normal" font="default"> Tomoskozi,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">ELISA response and gliadin composition of different wheat cultivars grown in multiple harvest years</style></title><secondary-title><style face="normal" font="default">Acta Aliment</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Acta Aliment</style></full-title></periodical><pages end="195" start="187">187-195</pages><volume><style face="normal" font="default">46</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year><pub-dates><date Day="14" Month="11" Year="2017">2017/11/14</date></pub-dates></dates><publisher><style face="normal" font="default">Akad+®miai Kiad+¦</style></publisher><isbn><style face="normal" font="default">0139-3006</style></isbn><abstract><style face="normal" font="default">In special dietary products for people intolerant to gluten, gluten content is not supposed to exceed the regulatory thresholds. Enzyme-linked immunosorbent assays (ELISAs) are routinely used to quantitate gluten in these products. They measure gliadin/gluten with high specificity and sensitivity, but they have some limitations. Quantitative and qualitative variability of the target proteins among wheat cultivars is a factor that may cause inaccurate results. One of the aims of this work was to characterize the protein composition of five wheat cultivars grown in multiple harvest years and their blends by reversed-phase high-performance liquid chromatography (RP-HPLC). The gliadin/gluten content of these wheat flours was also analysed with two commercial ELISA kits. The effect of differences in protein profiles between the flours from an individual cultivar and the blend of five cultivars, harvest years, as well as processing procedures (dough forming and baking) on the results of two ELISA kits was investigated and their relative magnitude was determined. Among the factors investigated, the differences between flours had the greatest impact on gliadin recoveries</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Hungary -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1556/066.2016.0019</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1556/066.2016.0019</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Aliment\2017-46-187-95.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Aliment\2017-46-187-95.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Hajas L</style></custom2><misc3><style face="normal" font="default">10.1556/066.2016.0019</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87106</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Saulite,I.</style></author><author><style face="normal" font="default"> Hoetzenecker,W.</style></author><author><style face="normal" font="default"> Guenova,E.</style></author><author><style face="normal" font="default"> Schmid-Grendelmeier,P.</style></author><author><style face="normal" font="default"> Glatz,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit, Department of Dermatology, University and University Hospital of Zurich, Zurich, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Skin Test Reactivity to Hymenoptera Venom after Venom Immunotherapy Correlates Inversely with the IgG/IgE Ratio</style></title><secondary-title><style face="normal" font="default">Int Arch Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Arch Allergy Immunol</style></abbr-1></periodical><pages end="199" start="190">190-199</pages><volume><style face="normal" font="default">174</style></volume><number><style face="normal" font="default">3-4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Honeybee</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: Skin test reactivity to hymenoptera venom and venom-specific IgE are important for diagnosing venom allergy and deciding on the appropriate allergen for venom immunotherapy (VIT). Longitudinal data on skin test reactivity during VIT and their correlation with venom-specific immunoglobulin (Ig)E and IgG are scarce. METHODS: We retrospectively analyzed shifts in skin test reactivity and serum levels of venom-specific IgE and IgG in patients allergic to hymenoptera venom before the initiation of VIT with ultrarush therapy and after >/=3 years of VIT. RESULTS: Fifty-four patients received ultrarush desensitization and subsequent VIT with wasp venom, 26 with honeybee venom, and 8 with both wasp and honeybee venom. Hymenoptera-specific skin test reactivity decreased during VIT in most patients, and became negative in 8% of the wasp-allergic patients and in 25% of the honeybee-allergic patients. Serum levels of venom-specific IgE positively correlated to skin test reactivity before VIT, but did not change significantly during VIT. IgG serum levels and the IgG/IgE ratio increased during VIT in most patients. A high IgG/IgE ratio correlated with low skin test reactivity after >/=3 years of VIT. CONCLUSIONS: The correlation between a high venom-specific IgG/IgE ratio and low skin test reactivity after VIT may be interesting for future investigations that assess its role as a potential marker for VIT efficacy</style></abstract><notes><style face="normal" font="default">IS - 1423-0097 (Electronic)IS - 1018-2438 (Linking)LA - engPT - Journal ArticleCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1159/000481255</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130986">PM:29130986</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-190-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Arch Allergy Immunol\2017-174-190-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Saulite I</style></custom2><misc3><style face="normal" font="default">10.1159/000481255</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86793</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Deschildre,A.</style></author><author><style face="normal" font="default"> Pichavant,M.</style></author><author><style face="normal" font="default"> Engelmann,I.</style></author><author><style face="normal" font="default"> Langlois,C.</style></author><author><style face="normal" font="default"> Drumez,E.</style></author><author><style face="normal" font="default"> Pouessel,G.</style></author><author><style face="normal" font="default"> Boileau,S.</style></author><author><style face="normal" font="default"> Romero-Cubero,D.</style></author><author><style face="normal" font="default"> Decleyre-Badiu,I.</style></author><author><style face="normal" font="default"> Dewilde,A.</style></author><author><style face="normal" font="default"> Hober,D.</style></author><author><style face="normal" font="default"> Neve,V.</style></author><author><style face="normal" font="default"> Thumerelle,C.</style></author><author><style face="normal" font="default"> Lejeune,S.</style></author><author><style face="normal" font="default"> Mordacq,C.</style></author><author><style face="normal" font="default"> Gosset,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">University Lille, U1</style></auth-address><titles><title><style face="normal" font="default">Virus-triggered exacerbation in allergic asthmatic children: neutrophilic airway inflammation and alteration of virus sensors characterize a subgroup of patients</style></title><secondary-title><style face="normal" font="default">Respir Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Res</style></abbr-1></periodical><pages end="" start="191">191-</pages><volume><style face="normal" font="default">18</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">BACKGROUND: Viruses are important triggers of asthma exacerbations. They are also detected outside of exacerbation. Alteration of anti-viral response in asthmatic patients has been shown although the mechanisms responsible for this defect remain unclear. The objective of this study was to compare in virus-infected and not-infected allergic asthmatic children, aged 6 to 16 years, admitted to hospital for a severe exacerbation, the innate immune response and especially the expression of pattern recognition receptor (PRR) and their function. METHODS: Virus identification was performed both during the exacerbation and at steady state (eight weeks later). Data assessed at both periods included clinical features, anti-viral response and inflammation (in sputum and plasma), and PRR expression/function in blood mononuclear cells. RESULTS: Viruses were identified in 46 out of 72 children (median age 8.9 years) during exacerbation, and among them, in 17 at steady state. IFN-beta, IFN-gamma and IL-29 levels in sputum and plasma were similar between infected and not infected patients at both times, as well as the expression of TLR3, RIG-I and MDA5 in blood monocytes and dendritic cells. Airway inflammation in infected patients was characterized by significantly higher IL-5 concentration and eosinophil count. Compared to patients only infected at exacerbation, the re-infected children significantly exhibited lower levels of IFN-gamma in plasma and sputum at exacerbation associated with modifications in PRR expression and function in blood mononuclear cells. These re-infected patients also presented an airway neutrophilic inflammation at steady state. CONCLUSION: Our results reports in asthmatic children that impaired anti-viral response during virus-induced exacerbation is more pronounced in a subgroup of patients prone to re-infection by virus. This subgroup is characterized by altered PRR function and a different pattern of airway inflammation. TRIAL REGISTRATION: This multicenter prospective study was approved by the regional investigational review board (ref: 08/07)</style></abstract><notes><style face="normal" font="default">DA - 20171115IS - 1465-993X (Electronic)IS - 1465-9921 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1186/s12931-017-0672-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29137638">PM:29137638</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Res\2017-18-191.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Res\2017-18-191.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171115, Deschildre A</style></custom2><misc3><style face="normal" font="default">10.1186/s12931-017-0672-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86973</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Watson,C.T.</style></author><author><style face="normal" font="default"> Cohain,A.T.</style></author><author><style face="normal" font="default"> Griffin,R.S.</style></author><author><style face="normal" font="default"> Chun,Y.</style></author><author><style face="normal" font="default"> Grishin,A.</style></author><author><style face="normal" font="default"> Hacyznska,H.</style></author><author><style face="normal" font="default"> Hoffman,G.E.</style></author><author><style face="normal" font="default"> Beckmann,N.D.</style></author><author><style face="normal" font="default"> Shah,H.</style></author><author><style face="normal" font="default"> Dawson,P.</style></author><author><style face="normal" font="default"> Henning,A.</style></author><author><style face="normal" font="default"> Wood,R.</style></author><author><style face="normal" font="default"> Burks,A.W.</style></author><author><style face="normal" font="default"> Jones,S.M.</style></author><author><style face="normal" font="default"> Leung,D.Y.M.</style></author><author><style face="normal" font="default"> Sicherer,S.</style></author><author><style face="normal" font="default"> Sampson,H.A.</style></author><author><style face="normal" font="default"> Sharp,A.J.</style></author><author><style face="normal" font="default"> Schadt,E.E.</style></author><author><style face="normal" font="default"> Bunyavanich,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA</style></auth-address><titles><title><style face="normal" font="default">Integrative transcriptomic analysis reveals key drivers of acute peanut allergic reactions</style></title><secondary-title><style face="normal" font="default">Nat Commun</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nat Commun</style></abbr-1></periodical><pages end="" start="1943">1943-</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Mechanisms driving acute food allergic reactions have not been fully characterized. We profile the dynamic transcriptome of acute peanut allergic reactions using serial peripheral blood samples obtained from 19 children before, during, and after randomized, double-blind, placebo-controlled oral challenges to peanut. We identify genes with changes in expression triggered by peanut, but not placebo, during acute peanut allergic reactions. Network analysis reveals that these genes comprise coexpression networks for acute-phase response and pro-inflammatory processes. Key driver analysis identifies six genes (LTB4R, PADI4, IL1R2, PPP1R3D, KLHL2, and ECHDC3) predicted to causally modulate the state of coregulated networks in response to peanut. Leukocyte deconvolution analysis identifies changes in neutrophil, naive CD4(+) T cell, and macrophage populations during peanut challenge. Analyses in 21 additional peanut allergic subjects replicate major findings. These results highlight key genes, biological processes, and cell types that can be targeted for mechanistic study and therapeutic targeting of peanut allergy</style></abstract><notes><style face="normal" font="default">IS - 2041-1723 (Electronic)IS - 2041-1723 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1038/s41467-017-02188-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29203772">PM:29203772</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nat Commun\2017-8-1943.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nat Commun\2017-8-1943.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Watson CT</style></custom2><misc3><style face="normal" font="default">10.1038/s41467-017-02188-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87114</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Huang,N.</style></author><author><style face="normal" font="default"> Liu,K.</style></author><author><style face="normal" font="default"> Liu,J.</style></author><author><style face="normal" font="default"> Gao,X.</style></author><author><style face="normal" font="default"> Zeng,Z.</style></author><author><style face="normal" font="default"> Zhang,Y.</style></author><author><style face="normal" font="default"> Chen,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Emergency, Xi'an Children's Hospital, Xi'an 710003, Shaanxi, China</style></auth-address><titles><title><style face="normal" font="default">Interleukin-37 alleviates airway inflammation and remodeling in asthma via inhibiting the activation of NF-kappaB and STAT3 signalings</style></title><secondary-title><style face="normal" font="default">Int Immunopharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Immunopharmacol</style></abbr-1></periodical><pages end="204" start="198">198-204</pages><volume><style face="normal" font="default">55</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="18" Month="12" Year="2017">2017/12/18</year></dates><abstract><style face="normal" font="default">Asthma is a common respiratory inflammatory disorder disease of childhood, and airway smooth muscle cells (ASMCs) play an important role in this disease. Recently, studies have found that interleukin (IL)-37 inhibits allergic airway inflammation of asthmatic mouse models. The aim of this study was to investigate the exact mechanism of IL-37 in asthma. In this study, we found recombinant human IL-37 protein significantly reduced ovalbumin (OVA)-induced airway hyperresponsiveness, inflammatory cell infiltration, the epithelial-mesenchymal-transition (EMT) process, and levels of IL-4, IL-6 and IL-13, but increased interferon (IFN)-gamma expression. Moreover, IL-37 treatment remarkably inhibited transforming growth factor (TGF)-beta1-induced cell proliferation, migration, EMT, and inflammatory response in ASMCs. IL-37 notably upregulated IkappaB expression and downregulated levels of NF-kappaB p65, phospho-NF-kappaB p65, STAT3 and phospho-STAT3 both in OVA-induced mice and in TGF-beta1-stimulated ASMCs. The effects of IL-37 on TGF-beta1-induced ASMCs were abrogated by STAT3 upregulation. Additionally, PDTC, a NF-kappaB inhibitor, showed the similar effects as IL-37 in ASMCs. In conclusion, IL-37 may alleviate airway inflammation and remodeling in asthma through suppressing the activation of NF-kappaB and STAT3</style></abstract><notes><style face="normal" font="default">IS - 1878-1705 (Electronic)IS - 1567-5769 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.intimp.2017.12.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29268192">PM:29268192</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Immunopharmacol\2017-55-198-204.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Immunopharmacol\2017-55-198-204.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Huang N</style></custom2><misc3><style face="normal" font="default">10.1016/j.intimp.2017.12.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87001</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,Z.</style></author><author><style face="normal" font="default"> Zhuang,J.</style></author><author><style face="normal" font="default"> Zhao,L.</style></author><author><style face="normal" font="default"> Gao,X.</style></author><author><style face="normal" font="default"> Luo,Z.</style></author><author><style face="normal" font="default"> Liu,E.</style></author><author><style face="normal" font="default"> Xu,F.</style></author><author><style face="normal" font="default"> Fu,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatrics Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, No.136, Zhong Shan 2nd Road, Yuzhong District, Chongqing, 400014, ChinaDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing, China</style></auth-address><titles><title><style face="normal" font="default">Roles of Bronchopulmonary C-fibers in airway Hyperresponsiveness and airway remodeling induced by house dust mite</style></title><secondary-title><style face="normal" font="default">Respir Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Res</style></abbr-1></periodical><pages end="" start="199">199-</pages><volume><style face="normal" font="default">18</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="29" Month="11" Year="2017">2017/11/29</year></dates><abstract><style face="normal" font="default">BACKGROUND: Asthma is characterized by chronic airway inflammation, airway hyperresponsiveness (AHR), and airway remodeling. While exposure of house dust mites (HDM) is a common cause of asthma, the pathogenesis of the HDM-induced asthma is not fully understood. Bronchopulmonary C-fibers (PCFs) contribute to the neurogenic inflammation, viral infection induced-persistent AHR, and ovalbumin induced collagen deposition largely via releasing neuropeptides, such as substance P (SP). However, PCF roles in the pathogenesis of the HDM-induced asthma remain unexplored. The goal of this study was to determine what role PCFs played in generating these characteristics. METHODS: We compared the following variables among the PCF-intact and -degenerated BALB/c mice with and without chronic HDM exposure (four groups): 1) AHR and pulmonary SP; 2) airway smooth muscle (ASM) mass; 3) pulmonary inflammatory cells; and 4) epithelium thickening and mucus secretion. RESULTS: We found that HDM evoked AHR associated with upregulation of pulmonary SP and inflammation, ASM mass increase, epithelium thickenings, and mucus hypersecretion. PCF degeneration decreased the HDM-induced changes in AHR, pulmonary SP and inflammation, and ASM mass, but failed to significantly affect the epithelium thickening and mucus hypersecretion. CONCLUSION: Our data suggest an involvement of PCFs in the mechanisms by which HDM induces allergic asthma via airway inflammation, AHR, and airway remodeling</style></abstract><notes><style face="normal" font="default">IS - 1465-993X (Electronic)IS - 1465-9921 (Linking)LA - engPT - Journal ArticleCO - China -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1186/s12931-017-0677-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29187212">PM:29187212</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Res\2017-18-199.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Res\2017-18-199.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Yang Z</style></custom2><misc3><style face="normal" font="default">10.1186/s12931-017-0677-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87119</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Irigoitia,M.M.</style></author><author><style face="normal" font="default"> Braicovich,E.P.</style></author><author><style face="normal" font="default"> Lanfranchi,L.A.</style></author><author><style face="normal" font="default"> Farber,D.M.</style></author><author><style face="normal" font="default"> Timi,T.J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Distribution of anisakid nematodes parasitizing rajiform skates under commercial exploitation in the Southwestern Atlantic</style></title><secondary-title><style face="normal" font="default">Int J Food Microbiol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Int J Food Microbiol</style></full-title></periodical><pages end="28" start="20">20-28</pages><volume><style face="normal" font="default">267</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anisakis</style></keyword><keyword><style face="normal" font="default"> Anisakis berlandi</style></keyword><keyword><style face="normal" font="default"> Anisakis pegreffii</style></keyword><keyword><style face="normal" font="default"> Argentine Sea</style></keyword><keyword><style face="normal" font="default"> Atlantoraja castelanui</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Pseudoterranova cattani</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Sympterygia bonapartii</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword><keyword><style face="normal" font="default"> Zearaja chilensis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0168-1605</style></isbn><abstract><style face="normal" font="default">In order to evaluate the infestation by anisakids present in elasmobranchs and their distribution in the Argentine Sea, this study was carried at a regional scale with the following aims: 1) to identify those anisakid species present in skates under exploitation; 2) to characterize quantitatively these infestations and 3) to determine those factors driving the variability in parasite burdens across skate species. A total of 351 skates, belonging to 3 species (218 Sympterygia bonapartii, 86 Zearaja chilensis and 47 Atlantoraja castelnaui) and from different localities of the Argentine Sea were examined for anisakids. Parasites were found in the stomach wall at high prevalence in some samples. Based on morphology and mtDNA cox2 sequences analyses (from 24 larval worms), specimens were identified as Anisakis berlandi, A. pegreffii and Pseudoterranova cattani; the last two known as potentially pathogenic for humans. Differential distribution patterns were observed across parasite and hosts species. In general, fish caught in southern and deeper waters exhibited higher loads of Anisakis spp., whereas infestation levels by P. cattani increase in larger skates. Taking into account that the mere presence of worms or their antigens in fish meat can provoke allergic responses, information on distribution of parasites and their variability is essential for the implementation of food safety practices</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Argentina -</style></notes><work-type><style face="normal" font="default">10.1016/j.ijfoodmicro.2017.12.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29277002">PM:29277002</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Food Microbiol\20171209-IrigoitiaMM.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Food Microbiol\20171209-IrigoitiaMM.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171209, Irigoitia MM</style></custom2><misc3><style face="normal" font="default">10.1016/j.ijfoodmicro.2017.12.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87115</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Singh,V.P.</style></author><author><style face="normal" font="default"> Mabalirajan,U.</style></author><author><style face="normal" font="default"> Pratap,K.</style></author><author><style face="normal" font="default"> Bahal,D.</style></author><author><style face="normal" font="default"> Maheswari,D.</style></author><author><style face="normal" font="default"> Gheware,A.</style></author><author><style face="normal" font="default"> Bajaj,A.</style></author><author><style face="normal" font="default"> Panda,L.</style></author><author><style face="normal" font="default"> Jaiswal,A.</style></author><author><style face="normal" font="default"> Ram,A.</style></author><author><style face="normal" font="default"> Agrawal,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre of Excellence for Translational Research in Asthma &amp; Lung Disease, Council of Scientific &amp; Industrial Research-Institute of Genomics and Integrative Biology (CSIR-IGIB), Mall Road, Delhi 110007, India.</style></auth-address><titles><title><style face="normal" font="default">House dust mite allergen causes certain features of steroid resistant asthma in high fat fed obese mice</style></title><secondary-title><style face="normal" font="default">Int Immunopharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Immunopharmacol</style></abbr-1></periodical><pages end="27" start="20">20-27</pages><volume><style face="normal" font="default">55</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword></keywords><dates><year Day="4" Month="12" Year="2017">2017/12/4</year></dates><abstract><style face="normal" font="default">Obesity is a high risk factor for diseases such as cardiovascular, metabolic syndrome and asthma. Obese-asthma is another emerging phenotype in asthma which is typically refractive to steroid treatment due to its non-classical features such as non-eosinophilic cellular inflammation. The overall increased morbidity, mortality and economical burden in asthma is mainly due to steroid resistant asthma. In the present study, we used high fat diet induced obese mice which when sensitized with house dust mite (HDM) showed steroid resistant features. While the steroid, dexamethasone (DEX), treatment to high fat fed naive mice could not reduce the airway hyperresponsiveness (AHR) induced by high fat, DEX treatment to high fat fed allergic mice could not reduce the HDM allergen induced airway remodeling features though it reduced airway inflammation. Further, these HDM induced high fat fed mice with or without DEX treatment had shown the increased activity and expression of arginase as well as the inducible nitric oxide synthase (iNOS) expression. However, DEX treatment had reduced the expressions of high iNOS and arginase I in control chow diet fed mice. Thus, we speculate that the steroid resistance seen in human obese asthmatics could be stemming from altered NO metabolism and its induced airway remodeling and with further investigations, it would encourage new treatments specific to obese-asthma phenotype</style></abstract><notes><style face="normal" font="default">IS - 1878-1705 (Electronic)IS - 1567-5769 (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.1016/j.intimp.2017.11.014</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29220719">PM:29220719</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Immunopharmacol\2017-55-20-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Immunopharmacol\2017-55-20-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Singh VP</style></custom2><misc3><style face="normal" font="default">10.1016/j.intimp.2017.11.014</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86630</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ahn,J.Y.</style></author><author><style face="normal" font="default"> Hong,S.J.</style></author><author><style face="normal" font="default"> Choi,B.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Kyungpook National University School of Medicine, Daegu, Korea</style></auth-address><titles><title><style face="normal" font="default">Clinical Evaluation of Techniques for Measuring Nasal-Specific Immunoglobulin E in Pediatric Patients</style></title><secondary-title><style face="normal" font="default">J Korean Med Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Korean Med Sci</style></abbr-1></periodical><pages end="2008" start="2005">2005-2008</pages><volume><style face="normal" font="default">32</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">Currently used methods for collecting nasal-specific immunoglobulin E (IgE) require administration of a large amount of saline into the nostrils, which is difficult in children. We designed two methods that are easy to use in children. We measured nasal-specific IgE and evaluated clinical characteristics of nasal-specific IgE in pediatric rhinitis. This study included 82 patients who visited Kyungpook National University Children's Hospital from December 2014 to July 2016 with rhinitis symptoms. Thirty patients used the spray method, and 52 patients used the swab method. We examined nasal-specific IgE to Dermatophagoides farinae, Dermatophagoides pteronyssinus, Alternaria, birch, and weed mix. Thirty patients had nasal-specific IgE concentrations of >/= 0.35 kIU/L. There was a positive correlation between nasal-specific IgE and serum-specific IgE to D. farinae and D. pteronyssinus (r = 0.548, P &lt; 0.001; r = 0.656, P &lt; 0.001). If we regard positivity of skin prick test as standard, cutoff point of nasal-specific IgE to D. farinae was 0.11 kIU/L and to D. pteronyssinus was 0.12 kIU/L. Based on these cutoff points, five patients would be considered to have local allergic rhinitis. The methods showed relatively high positivity for nasal-specific IgE, which reflected the serum-specific IgE as well. These methods can be considered to diagnose local allergic rhinitis in children</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1598-6357 (Electronic)IS - 1011-8934 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.3346/jkms.2017.32.12.2005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29115083">PM:29115083</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Korean Med Sci\2017-32-2005-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Korean Med Sci\2017-32-2005-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Ahn JY</style></custom2><misc3><style face="normal" font="default">10.3346/jkms.2017.32.12.2005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86577</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ahamad,M.N.U.</style></author><author><style face="normal" font="default"> Ali,M.E.</style></author><author><style face="normal" font="default"> Hossain,M.A.M.</style></author><author><style face="normal" font="default"> Asing,A.</style></author><author><style face="normal" font="default"> Sultana,S.</style></author><author><style face="normal" font="default"> Jahurul,M.H.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Nanotechnology and Catalysis Research Center, Institute of Graduate Studies , University of Malaya , Kuala Lumpur , Malaysia</style></auth-address><titles><title><style face="normal" font="default">Multiplex PCR assay discriminates rabbit, rat and squirrel meat in food chain</style></title><secondary-title><style face="normal" font="default">Food Addit Contam Part A Chem Anal Control Expo Risk Assess</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Addit Contam Part A Chem Anal Control Expo Risk Assess</style></abbr-1></periodical><pages end="2057" start="2043">2043-2057</pages><volume><style face="normal" font="default">34</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="in-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">Rabbit meat is receiving increasing attention because it contains a high level of proteins with relatively little fat. On the other hand, squirrel meat is served in upper-class meals in certain countries, so is sold at higher prices. The other side of the coin is rat meat, which has family ties with rabbit and squirrel but poses substantial threats to public health because it is a potential carrier of several zoonotic organisms. Recently, rat meat was mislabelled and sold as lamb after chemical modification. Thus, the chances of rabbit and squirrel meat substitution by rat meat cannot be ruled out. For the first time, a multiplex PCR assay was developed in Malaysia for the discriminatory identification of rat, rabbit and squirrel in the food chain. Rabbit (123 bp), rat (108 bp) and squirrel (243 bp) targets were amplified from ATP6 and cytb genes, along with a eukaryotic internal control (141bp). The products were sequenced and cross-tested against 22 species. A total of 81 reference samples and 72 meatball specimens were screened to validate the assay. Analyte stability was evaluated through boiling, autoclaving and micro-oven cooking. The tested lower limits of detection were 0.01 ng DNA for pure meat and 0.1% for meatballs</style></abstract><notes><style face="normal" font="default">DA - 20170727IS - 1944-0057 (Electronic)IS - 1944-0057 (Linking)LA - engPT - Journal ArticleCO - Malaysia -</style></notes><work-type><style face="normal" font="default">10.1080/19440049.2017.1359752</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28748739">PM:28748739</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Addit Contam Part A Chem Anal Control Expo Risk Assess\2017-34-2043-57.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Addit Contam Part A Chem Anal Control Expo Risk Assess\2017-34-2043-57.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170727, Ahamad MN</style></custom2><misc3><style face="normal" font="default">10.1080/19440049.2017.1359752</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86815</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cabezas-Cruz,A.</style></author><author><style face="normal" font="default"> de la Fuente,J.</style></author><author><style face="normal" font="default"> Fischer,J.</style></author><author><style face="normal" font="default"> Hebsaker,J.</style></author><author><style face="normal" font="default"> Lupberger,E.</style></author><author><style face="normal" font="default"> Blumenstock,G.</style></author><author><style face="normal" font="default"> Aichinger,E.</style></author><author><style face="normal" font="default"> Yazdi,A.S.</style></author><author><style face="normal" font="default"> Enkel,S.</style></author><author><style face="normal" font="default"> Oehme,R.</style></author><author><style face="normal" font="default"> Biedermann,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">UMR BIPAR, Animal Health Laboratory, INRA, ANSES, ENVA, Universite Paris-Est, Maisons Alfort Cedex, France</style></auth-address><titles><title><style face="normal" font="default">Prevalence of type I sensitization to alpha-gal in forest service employees and hunters: Is the blood type an overlooked risk factor in epidemiological studies of the alpha-Gal syndrome?</style></title><secondary-title><style face="normal" font="default">Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy</style></abbr-1></periodical><pages end="2047" start="2044">2044-2047</pages><volume><style face="normal" font="default">72</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1398-9995 (Electronic)IS - 0105-4538 (Linking)LA - engPT - LetterCO - France -CO - Czechia -CO - Spain -CO - United States -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1111/all.13206</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29159820">PM:29159820</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy\2017-72-2044-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">FD:\A&amp;H HMW Papers\Allergy\2017-72-2044-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Cabezas-Cruz A</style></custom2><misc3><style face="normal" font="default">10.1111/all.13206</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86572</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Made,D.</style></author><author><style face="normal" font="default"> Rohmberger,D.</style></author></authors></contributors><titles><title><style face="normal" font="default">Development of sensitive and specific real-time PCR systems for the detection of crustaceans in food</style></title><secondary-title><style face="normal" font="default">Eur Food Res Technol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Eur Food Res Technol</style></full-title></periodical><pages end="2113" start="2105">2105-2113</pages><volume><style face="normal" font="default">243</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1438-2385</style></isbn><abstract><style face="normal" font="default">Crustaceans are known allergens for a remarkable number of people. For the detection of traces of crustaceans in food, a specific and sensitive real-time PCR method was developed. An approximately 205-ábp long fragment of the mitochondrial 16S rRNA gene was chosen as molecular target region for the detection systems. The DNA sequence of this fragment was determined from 13 species belonging to different families and checked for homologies. Based on these data, primer</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çôprobe systems were developed for the economically relevant decapods within the class of Malacostraca belonging to the families Penaeidae, Palinuroidea, Astacoidea, Nephropoidea, Cancridae and Caridea. The specificity of the primer</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çôprobe systems was checked for inclusivity using DNA extracted from 17 different crustaceans. Exclusivity tests were carried out by analysing DNA samples derived from 21 mammals, six birds, 13 fishes, two molluscs and two insect species. Except for two systems, the molecular detection systems were optimised to be highly specific for the crustaceans. False positive signal was produced by DNA extracted from the hoverfly (Psilota rubra) in the system targeting the family Astacoidea and the common green lacewing (Chrysoperla carnea) in the systems targeting the family Astacoidea and Cancroidea. The LOD95% was close to the theoretical value of 2.96 copies per reaction. The sensitivity of the real-time PCR systems was determined using dilution series of crustacean DNA in rainbow trout DNA as animal matrix, and by artificial contamination of fish sticks and by artificial contamination of cassava-áchips with crustacean meat. The sensitivity ranging from 10 to 0.01-áppm is considered being appropriate for food analysis</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s00217-017-2911-5</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s00217-017-2911-5</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Food Res Technol\2017-243-2105-113.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Food Res Technol\2017-243-2105-113.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Made D</style></custom2><misc3><style face="normal" font="default">10.1007/s00217-017-2911-5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86858</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Masella,K.</style></author><author><style face="normal" font="default"> Aimuyo,O.C.</style></author><author><style face="normal" font="default"> Patadia,M.O.</style></author></authors></contributors><titles><title><style face="normal" font="default">Inhalant Allergy Evaluation in ENT Patients</style></title><secondary-title><style face="normal" font="default">Curr Otorhinolaryngol Rep</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Otorhinolaryngol Rep</style></full-title></periodical><pages end="219" start="212">212-219</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2167-583X</style></isbn><abstract><style face="normal" font="default">The purpose of this article is to educate the reader on the current trends in the evaluation of allergic rhinitis, with a focus on inhalant allergy, in otolaryngic patients</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s40136-017-0177-x</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40136-017-0177-x</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Otorhinolaryngol Rep\2017-5-212-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Otorhinolaryngol Rep\2017-5-212-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Masella K</style></custom2><misc3><style face="normal" font="default">10.1007/s40136-017-0177-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87082</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Antolin-Amerigo,D.</style></author><author><style face="normal" font="default"> Tabar,I.A.</style></author><author><style face="normal" font="default"> Del Mar Fernandez-Nieto,M.</style></author><author><style face="normal" font="default"> Callejo-Melgosa,A.M.</style></author><author><style face="normal" font="default"> Munoz-Bellido,F.J.</style></author><author><style face="normal" font="default"> Martinez-Alonso,J.C.</style></author><author><style face="normal" font="default"> Mendez-Alcalde,J.D.</style></author><author><style face="normal" font="default"> Reche,M.</style></author><author><style face="normal" font="default"> Rodriguez-Trabado,A.</style></author><author><style face="normal" font="default"> Rosado-Ingelmo,A.</style></author><author><style face="normal" font="default"> Alonso-Gomez,A.</style></author><author><style face="normal" font="default"> Blanco-Gonzalez,R.</style></author><author><style face="normal" font="default"> Alvarez-Fernandez,J.A.</style></author><author><style face="normal" font="default"> Botella,I.</style></author><author><style face="normal" font="default"> Valls,A.</style></author><author><style face="normal" font="default"> Cimarra,M.</style></author><author><style face="normal" font="default"> Blanco,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Servicio de Enfermedades del Sistema Inmune-Alergia, Hospital Universitario Principe de Asturias, Departamento de Medicina, Universidad de Alcala, Alcala de Henares, Madrid, Spain</style></auth-address><titles><title><style face="normal" font="default">Satisfaction and quality of life of allergic patients following sublingual five-grass pollen tablet immunotherapy in Spain</style></title><secondary-title><style face="normal" font="default">Drugs Context</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Drugs Context</style></abbr-1></periodical><pages end="" start="212309">212309-</pages><volume><style face="normal" font="default">6</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: Five-grass pollen tablet is an effective and well-tolerated therapy for patients with allergic rhinoconjunctivitis (ARC). This trial sought to determine the satisfaction and health-related quality of life (HRQoL) of patients undergoing this treatment. Methods: This was a cross-sectional, multicentre, observational, naturalistic study, following a discontinuous pre- and co-seasonal five-grass pollen regimen over two seasons in Spain (2012, 2013). The HRQoL of the patients was measured with the specific Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) for adults, adolescent (AdolRQLQ), or paediatric (PRQLQ) patients. Treatment satisfaction was assessed by the Satisfaction Scale for Patients Receiving Allergen Immunotherapy (ESPIA) questionnaire. Patients/investigators were surveyed on beliefs and attitudes towards the five-grass pollen tablet. ARC evolution according to allergic rhinitis and its impact on asthma (ARIA) criteria and treatment adherence were evaluated. Results: Among the 591 ARC patients included, the mean (SD) HRQoL scores were 1.40 (1.1) in adults, 1.33 (1.1) in adolescents, and 1.15 (1.1) in children, indicating low levels of impairment (scale 0-6). ESPIA answers showed high levels of satisfaction, with an average score of 69.2 (scale 0-100). According to ARIA criteria, 88.2% of patients reported improvement of ARC. Moreover, this was accompanied by a reduced use of symptomatic medication. Adherence to treatment was estimated at 96.8%. In general, both patients and specialists exhibited a positive attitude towards five-grass pollen tablet treatment. Conclusion: ARC patients treated with five-grass pollen tablet showed favourable levels of HRQoL and treatment satisfaction, with concomitant improvements in ARC and symptomatic medication use, which translated into high levels of treatment adherence and a positive attitude towards five-grass pollen tablet</style></abstract><notes><style face="normal" font="default">IS - 1745-1981 (Print)IS - 1740-4398 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.7573/dic.212309</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29225657">PM:29225657</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Drugs Context\2017-6-212309.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Drugs Context\2017-6-212309.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171206, Antolin-Amerigo D</style></custom2><misc3><style face="normal" font="default">10.7573/dic.212309</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87284</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bao,A.</style></author><author><style face="normal" font="default"> Yang,H.</style></author><author><style face="normal" font="default"> Ji,J.</style></author><author><style face="normal" font="default"> Chen,Y.</style></author><author><style face="normal" font="default"> Bao,W.</style></author><author><style face="normal" font="default"> Li,F.</style></author><author><style face="normal" font="default"> Zhang,M.</style></author><author><style face="normal" font="default"> Zhou,X.</style></author><author><style face="normal" font="default"> Li,Q.</style></author><author><style face="normal" font="default"> Ben,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China</style></auth-address><titles><title><style face="normal" font="default">Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model</style></title><secondary-title><style face="normal" font="default">Respir Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Res</style></abbr-1></periodical><pages end="" start="216">216-</pages><volume><style face="normal" font="default">18</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword></keywords><dates><year Day="29" Month="12" Year="2017">2017/12/29</year></dates><abstract><style face="normal" font="default">BACKGROUND: Exposure to ambient ozone (O3) increases the susceptivity to allergens and triggers exacerbations in patients with asthma. However, the detailed mechanisms of action for O3 to trigger asthma exacerbations are still unclear. METHODS: An ovalbumin (OVA)-established asthmatic mouse model was selected to expose to filtered air (OVA-model) or 1.0 ppm O3 (OVA-O3 model) during the process of OVA challenge. Next, the possible involvements of p38 MAPK and oxidative stress in the ozone actions on the asthma exacerbations were investigated on the mice of OVA-O3 model by treating them with SB239063 (a p38 MAPK inhibitor), and/or the alpha-tocopherol (antioxidant). Biological measurements were conducted including airway hyperresponsiveness (AHR), airway resistance (Raw), lung compliance (CL), inflammation in the airway lumen and lung parenchyma, the phosphorylation of p38 MAPK and heat shock protein (HSP) 27 in the tracheal tissues, and the malondialdehyde (MDA) content and the glutathione peroxidase (GSH-Px) activity in lung tissues. RESULTS: In OVA-allergic mice, O3 exposure deteriorated airway hyperresponsiveness (AHR), airway resistance (Raw), lung compliance (CL) and pulmonary inflammation, accompanied by the increased oxidative stress in lung tissues and promoted p38 MAPK and HSP27 phosphorylation in tracheal tissues. Administration of SB239063 (a p38 MAPK inhibitor) on OVA-O3 model exclusively mitigated the Raw, the CL, and the BAL IL-13 content, while alpha-tocopherol (antioxidant) differentially reduced the BAL number of eosinophils and macrophages, the content of BAL hyaluronan, the peribronchial inflammation, as well as the mRNA expression of TNF-alpha and IL-5 in the lung tissues of OVA-O3 model. Administration of these two chemical inhibitors similarly inhibited the AHR, the BAL IFN-gamma and IL-6 production, the perivascular lung inflammation and the lung IL-17 mRNA expression of OVA-O3 model. Interestingly, the combined treatment of both compounds together synergistically inhibited neutrophil counts in the BALF and CXCL-1 gene expression in the lung. CONCLUSIONS: O3 exposure during the OVA challenge process promoted exacerbation in asthma. Both p38 MAPK and oxidative stress were found to play a critical role in this process and simultaneous inhibition of these two pathways significantly reduced the O3-elicited detrimental effects on the asthma exacerbation</style></abstract><notes><style face="normal" font="default">IS - 1465-993X (Electronic)IS - 1465-9921 (Linking)LA - engPT - Journal ArticleCO - China -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1186/s12931-017-0697-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29284473">PM:29284473</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Res\2017-18-216.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Res\2017-18-216.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171229, Bao A</style></custom2><misc3><style face="normal" font="default">10.1186/s12931-017-0697-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87242</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mendy,A.</style></author><author><style face="normal" font="default"> Wilkerson,J.</style></author><author><style face="normal" font="default"> Salo,P.M.</style></author><author><style face="normal" font="default"> Cohn,R.D.</style></author><author><style face="normal" font="default"> Zeldin,D.C.</style></author><author><style face="normal" font="default"> Thorne,P.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Occupational and Environmental Health, University of Iowa, Iowa City, IA, United States</style></auth-address><titles><title><style face="normal" font="default">Endotoxin predictors and associated respiratory outcomes differ with climate regions in the U.S</style></title><secondary-title><style face="normal" font="default">Environ Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Environ Int</style></abbr-1></periodical><pages end="226" start="218">218-226</pages><volume><style face="normal" font="default">112</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Inhalant allergen</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="22" Month="12" Year="2017">2017/12/22</year></dates><abstract><style face="normal" font="default">RATIONALE: Although endotoxin is a recognized cause of environmental lung disease, how its relationship with respiratory outcomes varies with climate is unknown. OBJECTIVE: To examine the endotoxin predictors as well as endotoxin association with asthma, wheeze, and sensitization to inhalant allergens in various US climate regions. METHODS: We analyzed data on 6963 participants in the National Health and Nutrition Examination Survey. Endotoxin measurements of house dust from bedroom floor and bedding were performed at the University of Iowa. Linear and logistic regression analyses were used to identify endotoxin predictors and assess endotoxin association with health outcomes. RESULTS: The overall median house dust endotoxin was 16.2 EU/mg; it was higher in mixed-dry/hot-dry regions (19.7 EU/mg) and lower in mixed-humid/marine areas (14.8 EU/mg). Endotoxin predictors and endotoxin association with health outcomes significantly differed across climate regions. In subarctic/very cold/cold regions, log10-endotoxin was significantly associated with higher prevalence of wheeze outcomes (OR:1.48, 95% CI:1.19-1.85 for any wheeze, OR:1.48, 95% CI:1.22-1.80 for exercise-induced wheeze, OR:1.50, 95% CI:1.13-1.98 for prescription medication for wheeze, and OR:1.95, 95% CI:1.50-2.54 for doctor/ER visit for wheeze). In hot-humid regions, log10-endotoxin was positively associated with any wheeze (OR:1.66, 95% CI:1.04-2.65) and current asthma (OR:1.56, 95% CI:1.11-2.18), but negatively with sensitization to any inhalant allergens (OR:0.83, 95% CI:0.74-0.92). CONCLUSION: Endotoxin predictors and endotoxin association with asthma and wheeze differ across U.S. climate regions. Endotoxin is associated positively with wheeze or asthma in cold and hot-humid regions, but negatively with sensitization to inhalant allergens in hot-humid climates</style></abstract><notes><style face="normal" font="default">IS - 1873-6750 (Electronic)IS - 0160-4120 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.envint.2017.12.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29277065">PM:29277065</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Environ Int\2017-112-218-26.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Environ Int\2017-112-218-26.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Mendy A</style></custom2><misc3><style face="normal" font="default">10.1016/j.envint.2017.12.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86726</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gupta,R.K.</style></author><author><style face="normal" font="default"> Gupta,K.</style></author><author><style face="normal" font="default"> Dwivedi,P.D.</style></author></authors></contributors><titles><title><style face="normal" font="default">Pathophysiology of IL-33 and IL-17 in allergic disorders</style></title><secondary-title><style face="normal" font="default">Cytokine Growth Factor Rev</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Cytokine Growth Factor Rev</style></abbr-1></periodical><pages end="36" start="22">22-36</pages><volume><style face="normal" font="default">38</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IL-17</style></keyword><keyword><style face="normal" font="default"> IL-33</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1359-6101</style></isbn><abstract><style face="normal" font="default">Allergic diseases are among common clinical conditions, affecting millions of children and adults throughout the world. Food allergies, skin allergies (atopic dermatitis), and respiratory allergies (allergic rhinitis and asthma) are the common types of allergies. Recently discovered cytokines IL-17 and IL-33 have been found to play an important role in the pathogenicity of various hypersensitive disorders. After exposure to allergens or infection with parasites or viruses, IL-17 and IL-33 producing cells, such as Th17 and specialized epithelial cells respectively, become activated and trigger the pathogenic immune responses in different susceptible conditions. Potent inhibitors of these cytokines have been identified recently that may represent potential therapeutic agents to overcome the clinical complications of allergies. In the present review, we have discussed the cellular sources, modes of action and regulation of IL-17 and IL-33 in the context of hypersensitive diseases. We have also assessed the therapeutic potential of inhibitory molecules that may alter production of both these cytokines, and thus modulate susceptible conditions</style></abstract><notes><style face="normal" font="default">LA - ENGCO - India -</style></notes><work-type><style face="normal" font="default">10.1016/j.cytogfr.2017.09.005</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29153708">PM:29153708</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Cytokine Growth Factor Rev\20171119-GuptaRK.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Cytokine Growth Factor Rev\20171119-GuptaRK.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171119, Gupta RK</style></custom2><misc3><style face="normal" font="default">10.1016/j.cytogfr.2017.09.005</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87241</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Licari,A.</style></author><author><style face="normal" font="default"> Castagnoli,R.</style></author><author><style face="normal" font="default"> Panfili,E.</style></author><author><style face="normal" font="default"> Marseglia,A.</style></author><author><style face="normal" font="default"> Brambilla,I.</style></author><author><style face="normal" font="default"> Marseglia,G.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy</style></auth-address><titles><title><style face="normal" font="default">An Update on Anti-IgE Therapy in Pediatric Respiratory Diseases</style></title><secondary-title><style face="normal" font="default">Curr Respir Med Rev</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Respir Med Rev</style></abbr-1></periodical><pages end="29" start="22">22-29</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="3" Year="2017">2017/3</year></dates><abstract><style face="normal" font="default">Anti-IgE treatment represents a major breakthrough in the therapeutic management of severe allergic asthma. Omalizumab is the unique biologic treatment registered for asthma therapy in children. The clinical efficacy and safety of omalizumab treatment in the pediatric population has been extensively documented in specific trials and consistently expanded from real-life studies. In addition, new experimental evidence suggests that omalizumab may also interfere with the cellular and molecular mechanisms underlying airway remodeling. Novel investigational anti-IgE monoclonal antibodies with improved pharmacodynamic properties are in the pipeline, potentially offering alternative mechanisms of modulating IgE pathway. The aim of this review is to update current knowledge on anti-IgE therapy in pediatric respiratory diseases</style></abstract><notes><style face="normal" font="default">IS - 1573-398X (Print)IS - 1573-398X (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Italy -</style></notes><work-type><style face="normal" font="default">10.2174/1573398X13666170616110738</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29290750">PM:29290750</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Respir Med Rev\2017-13-22-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Respir Med Rev\2017-13-22-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170523, Licari A</style></custom2><misc3><style face="normal" font="default">10.2174/1573398X13666170616110738</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86859</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Moscato,G.</style></author></authors></contributors><titles><title><style face="normal" font="default">Occupational Allergic Airway Disease</style></title><secondary-title><style face="normal" font="default">Curr Otorhinolaryngol Rep</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Otorhinolaryngol Rep</style></full-title></periodical><pages end="228" start="220">220-228</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2167-583X</style></isbn><abstract><style face="normal" font="default">The purpose of this paper was to review recent advances on causal agents, diagnosis and management of occupational allergic airway diseases</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1007/s40136-017-0170-4</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40136-017-0170-4</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Otorhinolaryngol Rep\2017-5-220-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Otorhinolaryngol Rep\2017-5-220-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Moscato G</style></custom2><misc3><style face="normal" font="default">10.1007/s40136-017-0170-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86648</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xu,J.</style></author><author><style face="normal" font="default"> Zhang,F.</style></author><author><style face="normal" font="default"> Gao,C.</style></author><author><style face="normal" font="default"> Ma,X.</style></author><author><style face="normal" font="default"> Peng,X.</style></author><author><style face="normal" font="default"> Kong,D.</style></author><author><style face="normal" font="default"> Hao,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China</style></auth-address><titles><title><style face="normal" font="default">Microarray Analysis of lncRNA and mRNA Expression Profiles in Patients with Neuromyelitis Optica</style></title><secondary-title><style face="normal" font="default">Mol Neurobiol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Neurobiol</style></abbr-1></periodical><pages end="2208" start="2201">2201-2208</pages><volume><style face="normal" font="default">54</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="4" Year="2017">2017/4</year></dates><abstract><style face="normal" font="default">For the epigenetic characterization of neuromyelitis optica (NMO), we determined whether messenger RNAs (mRNAs) and long noncoding RNAs (lncRNAs) are expressed differentially in subjects with and without NMO. lncRNA and mRNA expression profiles of NMO patients and healthy controls were generated by using microarray analysis. For comparison, the differentially expressed mRNA functions were annotated by using gene ontology (GO) and pathway analyses. The microarray revealed that 1310 lncRNAs and 743 mRNAs differed in NMO patients from those in healthy controls. Pathway analysis then demonstrated that IL23-mediated signaling events, interferon gamma signaling, natural killer (NK)-kappaB signaling pathway, chemokine receptors that bind chemokines, GPCR ligand binding, and metabolic disorders of biological oxidation enzyme pathways play important roles in NMO. Several GO terms including cytokine stimulus, response to cytokine, immune response, cytokine-mediated signaling pathway, and response to chemical cytokine activity were enriched in gene lists, suggesting a potential correlation with NMO. Co-expression network analysis indicated that 183 lncRNAs and 458 mRNAs were included in the co-expression network. Our present study showed that these differentially expressed mRNAs and lncRNAs may play important roles in NMO and could provide basic information for new biomarkers or treatment targets to alleviate NMO</style></abstract><notes><style face="normal" font="default">DA - 20160304IS - 1559-1182 (Electronic)IS - 0893-7648 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s12035-016-9754-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="26941100">PM:26941100</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Neurobiol\2017-54-2201-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Neurobiol\2017-54-2201-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20160304, Xu J</style></custom2><misc3><style face="normal" font="default">10.1007/s12035-016-9754-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87008</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Takei,T.</style></author><author><style face="normal" font="default"> Ishida,T.</style></author><author><style face="normal" font="default"> Ikeda,M.</style></author><author><style face="normal" font="default"> Shingaki,S.</style></author><author><style face="normal" font="default"> Miyazaki,K.</style></author><author><style face="normal" font="default"> Yoshiki,Y.</style></author><author><style face="normal" font="default"> Abe,Y.</style></author><author><style face="normal" font="default"> Okazuka,K.</style></author><author><style face="normal" font="default"> Iki,S.</style></author><author><style face="normal" font="default"> Tsukada,N.</style></author><author><style face="normal" font="default"> Suzuki,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Hematology, Japanese Red Cross Medical Center</style></auth-address><titles><title><style face="normal" font="default">[IgE-kappa type multiple myeloma achieving complete response with novel agents]</style></title><secondary-title><style face="normal" font="default">Rinsho Ketsueki</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rinsho Ketsueki</style></abbr-1></periodical><pages end="2237" start="2232">2232-2237</pages><volume><style face="normal" font="default">58</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">IgE</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">IgE multiple myeloma (MM) is a rare subtype of MM characterized by an aggressive and poor prognosis. Although novel agents have improved the prognosis of MM, there are few case reports of IgE MM treated with these agents. A 53-year-old male patient presented with pain in the right rib and was diagnosed with IgE-kappa MM. He was treated with multidrug chemotherapy, including bortezomib and lenalidomide, and underwent autologous stem-cell transplantation (ASCT). Finally, he achieved a complete response after the initiation of pomalidomide. In previous reports, majority of patients with refractory IgE MM treated with novel agents had a poor prognosis. In contrast, patients who were treated with novel agents from the beginning and underwent ASCT had a long-term survival. Overall, the use of novel agents as the first-line therapy is expected to improve IgE MM prognosis</style></abstract><notes><style face="normal" font="default">IS - 0485-1439 (Print)IS - 0485-1439 (Linking)LA - jpnPT - English AbstractPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.11406/rinketsu.58.2232</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29212974">PM:29212974</url></web-urls></urls><custom2><style face="normal" font="default">20171130, Takei T</style></custom2><misc3><style face="normal" font="default">10.11406/rinketsu.58.2232</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87072</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Manjra,A.I.</style></author><author><style face="normal" font="default"> Prescott,P.R.</style></author><author><style face="normal" font="default"> Potter,P.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Cockroach allergy in Durban</style></title><secondary-title><style face="normal" font="default">Curr Allergy Clin Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Allergy Clin Immunol</style></full-title></periodical><pages end="232" start="230">230-232</pages><volume><style face="normal" font="default">30</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Cockroaches</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Africa -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">https://www.allergysa.co.za/Journal/December2017</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-230-2.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-230-2.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Manjra,A.I.</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86539</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sakai,K.</style></author><author><style face="normal" font="default"> Sasaki,K.</style></author><author><style face="normal" font="default"> Furuta,T.</style></author><author><style face="normal" font="default"> Sugiura,S.</style></author><author><style face="normal" font="default"> Watanabe,Y.</style></author><author><style face="normal" font="default"> Kobayashi,T.</style></author><author><style face="normal" font="default"> Kawabe,T.</style></author><author><style face="normal" font="default"> Morishita,M.</style></author><author><style face="normal" font="default"> Nakanishi,K.</style></author><author><style face="normal" font="default"> Ito,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy, Aichi Children's Health and Medical Center, Obu 474-8710, Japan</style></auth-address><titles><title><style face="normal" font="default">Evaluation of the results of oral food challenges conducted in specialized and general hospitals</style></title><secondary-title><style face="normal" font="default">Asia Pac Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Asia Pac Allergy</style></abbr-1></periodical><pages end="242" start="234">234-242</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">Background: Oral food challenge (OFC) tests are conducted in both specialized institutions and general hospitals. We aimed to compare the severity of the conditions of the patients between these 2 types of institutions in order to consider the role of such institutions in society. Objective: We evaluated the results of OFC tests for hen's egg, cow's milk, and wheat that were conducted in a specialized institution (Aichi Children's Health and Medical Center [ACHMC], n = 835) and in 4 general hospitals (n = 327) in Aichi prefecture, Japan. Methods: The symptoms provoked were scored using the total score (TS) of the Anaphylaxis Scoring Aichi scoring system in combination with the total ingested protein dose (Pro) before the appearance of allergic symptoms. Results: The total ingested dose of the challenge-positive patients in ACHMC was significantly less than that in the general hospitals (p &lt; 0.01). The median TS of the provoked symptoms in ACHMC and the general hospitals did not differ to a statistically significant extent in the hen's egg or cow's milk challenges; however, the median TS in ACHMC was significantly lower than that in the general hospitals for the wheat challenge (p = 0.02). The median TS/Pro values in ACHMC were almost identical to the upper 25% of the TS/Pro values in the general hospitals, suggesting that the specialized institution usually managed more severe patients. Conclusion: The specialized institution performed OFC tests at a lower threshold dose, but provoked similar TSs to the general hospitals. This evaluation may help in optimizing the distribution of patients to general hospitals and specialized institutions</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 2233-8276 (Print)IS - 2233-8276 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.5415/apallergy.2017.7.4.234</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29094022">PM:29094022</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Asia Pac Allergy\2017-7-234-42.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Asia Pac Allergy\2017-7-234-42.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Sakai K</style></custom2><misc3><style face="normal" font="default">10.5415/apallergy.2017.7.4.234</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87075</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lopata,A.L.</style></author><author><style face="normal" font="default"> Fenemore,B.</style></author><author><style face="normal" font="default"> Potter,C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Crustacean allergy in South Africa</style></title><secondary-title><style face="normal" font="default">Curr Allergy Clin Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Allergy Clin Immunol</style></full-title></periodical><pages end="238" start="234">234-238</pages><volume><style face="normal" font="default">30</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Africa -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">https://www.allergysa.co.za/Journal/December2017</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-234-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-234-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Lopata AL</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87076</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Johar,A.</style></author><author><style face="normal" font="default"> Lim,D.L.</style></author><author><style face="normal" font="default"> Mad Arif,S.A.</style></author><author><style face="normal" font="default"> Hawarden,D.</style></author><author><style face="normal" font="default"> du Toit,G.</style></author><author><style face="normal" font="default"> Weinberg,E.G.</style></author><author><style face="normal" font="default"> Motala,C.</style></author><author><style face="normal" font="default"> Fieggen,G.</style></author><author><style face="normal" font="default"> Yeet Yeang,H.</style></author><author><style face="normal" font="default"> Potter,P.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Low Prevalence of latex sensitivity in South African Spina Bifida Children in Cape Town</style></title><secondary-title><style face="normal" font="default">Curr Allergy Clin Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Allergy Clin Immunol</style></full-title></periodical><pages end="244" start="239">239-244</pages><volume><style face="normal" font="default">30</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Studies from Europe and the United States report that spina bifida children have a high prevalence of latex allergy. This study investigated the prevalence of latex allergy in a cohort of 24 spina bifida children at the Red Cross War Memorial Children's Hospital in Cape Town,South Africa. The children were investigated using adetailed questionnaire, skin-prick tests (ALK-Abello),ImmunoCap RASTs, Western blotting and ELISA, using the purified latex proteins Hev b1 and Hev b3 and whole latex preparation. A low overall prevalence of latex sensitisation of 16.7% was found in the children. Children who were sensitive reacted to water-insoluble Hev b1 and Hev b3 proteins. The low prevalence of latex sensitisation in the South African children may not be explained by stringent latex avoidance. The children were from a low socio-economic social status and 'hygiene' and other factors should be considered.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Malaysia -CO - Singapore -CO - South Africa -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">https://www.allergysa.co.za/Journal/December2017</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-239-44.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-239-44.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Johar A</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87057</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Thompson,D.</style></author></authors></contributors><titles><title><style face="normal" font="default">RELIABLE ALLERGY RESOURCES</style></title><secondary-title><style face="normal" font="default">Aust Nurs Midwifery J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Aust Nurs Midwifery J</style></abbr-1></periodical><pages end="" start="24">24-</pages><volume><style face="normal" font="default">24</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="2" Year="2017">2017/2</year></dates><abstract><style face="normal" font="default">Allergic conditions now affect 20% of the Australian population (Mullins et al. 2015). This means that nurses in different clinical practice fields will be involved in involved in caring for patients who may also have an allergic condition</style></abstract><notes><style face="normal" font="default">IS - 2202-7114 (Print)IS - 2202-7114 (Linking)LA - engPT - Journal ArticleCO - Australia -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29257365">PM:29257365</url></web-urls></urls><custom2><style face="normal" font="default">20171214, Thompson D</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86496</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rengganis,I.</style></author><author><style face="normal" font="default"> Susanto,A.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Clinical Immunology, Department of Internal Medicine, Faculty of Medicine, University of Indonesia - dr. Cipto Mangunkusumo Hospital, Jakarta, Indonesia.. irisrengganis@yahoo.com</style></auth-address><titles><title><style face="normal" font="default">Pollen Serum Specific IgE Sensitization in Respiratory Allergic Patients in Jakarta, Indonesia</style></title><secondary-title><style face="normal" font="default">Acta Med Indones</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Acta Med Indones</style></abbr-1></periodical><pages end="248" start="243">243-248</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="7" Year="2017">2017/7</year></dates><abstract><style face="normal" font="default">BACKGROUND: pollens from trees or grasses in Indonesia have a perennial distribution due to the tropical climate. However, pollen allergy has not been well studied. This study aimed to evaluate the profile of pollen IgE sensitization in respiratory allergic patients in Jakarta. METHODS: this was a cross-sectional study in patients with a history of respiratory allergy in Jakarta, Indonesia between September and December 2016. Adult asthmatic patients aged 19-60 years were invited to undergo serum specific IgE testing at the Allergy and Immunology Clinic, Cipto Mangunkusumo Hospital, Jakarta. Patients were included if they showed at least one positive skin prick test with environmental allergens. Quantitative determination of specific IgE in serum was carried out by multiple allergosorbent (MAST) assays (Polycheck Allergy(R), Biocheck GmbH, Munster, Germany). Serum specific IgE levels of more than 0.35 kU/L or Class 1 was considered positive. RESULTS: a total of 106 cases were eligible for analysis; 81 (76.4%) were women. Patients' mean age was 38.8+12.1 (range 19-59) years old. 59.4% of patients have both asthma and allergic rhinitis. There are 9 (8.5%) patients positive for IgE-pollen sensitization; 8 among them showed sensitization to at least 2 pollens. Sensitivity to goosefoot pollen is the highest (5.7%), followed by rye pollen (4.7%), plantain pollen (4.7%), wall pellitory pollen (4.7%), and Bermuda grass pollen (3.8%). CONCLUSION: although most pollens tested are not originated from native plants to Indonesia, a small number of patients showed specific IgE-sensitizations. Allergic persons planning to travel to the endemic areas of the relevant pollen should be advised. A panel of pollen allergens from local plants is highly desired</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 0125-9326 (Print)IS - 0125-9326 (Linking)LA - engPT - Journal ArticleCO - Indonesia -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29093235">PM:29093235</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Med Indones\2017-49-243-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Med Indones\2017-49-243-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Rengganis I</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87287</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Amaral,L.</style></author></authors></contributors><titles><title><style face="normal" font="default">Biological therapeutics in Immunoallergology</style></title><secondary-title><style face="normal" font="default">Rev Port Imunoalergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Port Imunoalergol</style></full-title></periodical><pages end="248" start="243">243-248</pages><volume><style face="normal" font="default">25</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Allergic diseases affect millions worldwide, and there is growing evidence of an increase in the occurrence of allergic diseases over the past few decades. Current treatments for allergy include corticosteroids to reduce inflammation and allergen immunotherapy (AIT). However, some individuals experience treatment-resistant inflammation or adverse reactions. There is a dire need for new therapeutic approaches for individuals with poorly controlled atopic diseases and to improve the safety and effectiveness of AIT. A better understanding of allergic mechanisms through animal models and clinical trials has unveiled potential targets for new therapies, leading to the development of several biologics to treat allergic diseases.</style></abstract><notes><style face="normal" font="default">LA - PORCO - Portugal -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://www.spaic.pt/rpia/arquivos?ano_publicacao=2017&amp;volume_publicacao=25&amp;numero_publicacao=4</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Port Imunoalergol\2017-25-243-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Port Imunoalergol\2017-25-243-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Amaral L</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87088</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chatain,C.</style></author><author><style face="normal" font="default"> Pin,I.</style></author><author><style face="normal" font="default"> Pralong,P.</style></author><author><style face="normal" font="default"> Jacquier,J.P.</style></author><author><style face="normal" font="default"> Leccia,M.T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Allergology and Photobiology, Centre Hospitalier Universitaire de Grenoble, Grenoble, France.</style></auth-address><titles><title><style face="normal" font="default">Medicinal bioactivites and allergenic properties of pumpkin seeds: review upon a pediatric food anaphylaxis case report</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="251" start="244">244-251</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Food allergy to pumpkin seed is considered very rare, and only some isolated case reports have so far been published. We report here a case of food anaphylaxis to pumpkin seed in an eight-year-old boy, who tolerated all other edible seeds, peanut and tree nuts, as well as pulp of different kinds of pumpkins and other fruits of the Cucurbitaceae family. From this observation, a review of the botanical, historical, medicinal and allergenic aspects of pumpkin and its seeds is proposed. With the advent of diets rich in omega-3 and omega-6 polyunsaturated fatty acids, edible seeds like pumpkin seed have been incorporated in the modern diet. Their incremental use in the food-processing industry might contribute to an increase in food allergy to pumpkin seed in the future</style></abstract><notes><style face="normal" font="default">IS - 1764-1489 (Print)IS - 1764-1489 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.19</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249131">PM:29249131</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-244-51.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-244-51.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Chatain C</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.19</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87074</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Berman,D.</style></author></authors></contributors><titles><title><style face="normal" font="default">Regional-specific pollen and fungal-spore allergens in South Africa</style></title><secondary-title><style face="normal" font="default">Curr Allergy Clin Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Allergy Clin Immunol</style></full-title></periodical><pages end="250" start="245">245-250</pages><volume><style face="normal" font="default">30</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The selection of skin-prick and ImmunoCAP radio-allergosorbent test (RAST) testing panels for tree, grass, weed and fungal-spore aeroallergens is an easiertask when pollen and fungal-spore levels for the particular geographic area are accessible to the allergologist. In South Africa, long-term pollen and fungal-spore level information exists for the Western Cape, where several areas in the greater Cape Town Metropole have been monitored. In Gauteng, sporadic pollen-sampling studies have been carried out in the vicinity of Johannesburg and Pretoria. In KwaZulu-Natal, short-term studies have sampled airspora in Durban and Richards Bay, and a three-year pollen and fungal-spore assessment has been conducted in Secunda, Mpumalanga. These findings are examined in relation to the choice of allergen-testing panels. There are vast unsampled areas of South Africa -containing major cities - where the major pollen allergens and their levels in the atmosphere are not known and, in addition, there is great variation in climate across these areas. Climate dictates the vegetation biome as well as the flowering times of allergenic plants. Guidelines for the selection of allergen-testing panels in clinical settings, where no pollen monitoring exists, are discussed.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Africa -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">https://www.allergysa.co.za/Journal/December2017</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-245-50.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-245-50.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Berman D</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86493</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bekes,F.</style></author><author><style face="normal" font="default"> Acs,K.</style></author><author><style face="normal" font="default"> Gell,G.</style></author><author><style face="normal" font="default"> Lantos,C.</style></author><author><style face="normal" font="default"> Kovacs,A.M.</style></author><author><style face="normal" font="default"> Birinyi,Z.</style></author><author><style face="normal" font="default"> Pauk,J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Towards breeding less allergenic spelt-wheat with low fodmap content </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çö A review</style></title><secondary-title><style face="normal" font="default">Acta Aliment</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Acta Aliment</style></full-title></periodical><pages end="258" start="246">246-258</pages><volume><style face="normal" font="default">46</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="29" Month="4" Year="2017">2017/4/29</year><pub-dates><date Day="14" Month="11" Year="2017">2017/11/14</date></pub-dates></dates><isbn><style face="normal" font="default">0139-3006</style></isbn><abstract><style face="normal" font="default">Consumption of "gluten-containing" diet causes disease for a significant minority of people who consume foods derived from wheat, rye, barley, and possibly oat. The fact is, however, that in several types of diseases related to the consumption of "gluten-containing" cereals, the trigger compounds are not components of gluten. The current view of medical experts is that, excluding people suffering from celiac disease, the majority of individuals who are feeling better on the "wheat-free" or "gluten-free" diet could select a food containing much healthier, low level of fermentable oligosaccharides (often called as FODMAP). To satisfy the specific health related demands of certain consumer groups, the challenge is in front of cereal breeding to develop new, "healthier" germplasms, suitable to produce such products by the food industry. This report aims to give an overview of some aspects of recent developments in this booming area, (i) summarizing the up-to-date knowledge on cereals-related health disorders; (ii) reporting on the status of developing celiac-safe cereals, and finally (iii) highlighting the potential of developing "healthier" spelt-based cereal products through the progress in an ongoing spelt breeding program.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Australia -CO - Ungary -</style></notes><work-type><style face="normal" font="default">10.1556/066.2017.46.2.15</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1556/066.2017.46.2.15</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Aliment\2016-46-246-58.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Aliment\2016-46-246-58.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Bekes F</style></custom2><misc3><style face="normal" font="default">10.1556/066.2017.46.2.15</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87360</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,I.</style></author><author><style face="normal" font="default"> Pletcher,S.D.</style></author><author><style face="normal" font="default"> Goldberg,A.N.</style></author><author><style face="normal" font="default"> Barker,B.M.</style></author><author><style face="normal" font="default"> Cope,E.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pathogen and Microbiome Institute, Northern Arizona University, Flagstaff, AZ, United States</style></auth-address><titles><title><style face="normal" font="default">Fungal Microbiota in Chronic Airway Inflammatory Disease and Emerging Relationships with the Host Immune Response</style></title><secondary-title><style face="normal" font="default">Front Microbiol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Front Microbiol</style></abbr-1></periodical><pages end="" start="2477">2477-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Cystic fibrosis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The respiratory tract is a complex system that is inhabited by niche-specific communities of microbes including bacteria, fungi, and viruses. These complex microbial assemblages are in constant contact with the mucosal immune system and play a critical role in airway health and immune homeostasis. Changes in the composition and diversity of airway microbiota are frequently observed in patients with chronic inflammatory diseases including chronic rhinosinusitis (CRS), cystic fibrosis, allergy, and asthma. While the bacterial microbiome of the upper and lower airways has been the focus of many recent studies, the contribution of fungal microbiota to inflammation is an emerging research interest. Within the context of allergic airway disease, fungal products are important allergens and fungi are potent inducers of inflammation. In addition, murine models have provided experimental evidence that fungal microbiota in peripheral organs, notably the gastrointestinal (GI) tract, influence pulmonary health. In this review, we explore the role of the respiratory and GI microbial communities in chronic airway inflammatory disease development with a specific focus on fungal microbiome interactions with the airway immune system and fungal-bacterial interactions that likely contribute to inflammatory disease. These findings are discussed in the context of clinical and immunological features of fungal-mediated disease in CRS, allergy, and asthmatic patients. While this field is still nascent, emerging evidence suggests that dysbiotic fungal and bacterial microbiota interact to drive or exacerbate chronic airway inflammatory disease</style></abstract><notes><style face="normal" font="default">IS - 1664-302X (Print)IS - 1664-302X (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.3389/fmicb.2017.02477</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29312187">PM:29312187</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Microbiol\2018-8-2477.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Microbiol\2018-8-2477.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171212, Zhang I</style></custom2><misc3><style face="normal" font="default">10.3389/fmicb.2017.02477</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87361</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shemesh,E.</style></author><author><style face="normal" font="default"> Hanf,B.</style></author><author><style face="normal" font="default"> Hagag,S.</style></author><author><style face="normal" font="default"> Attias,S.</style></author><author><style face="normal" font="default"> Shadkchan,Y.</style></author><author><style face="normal" font="default"> Fichtman,B.</style></author><author><style face="normal" font="default"> Harel,A.</style></author><author><style face="normal" font="default"> Kruger,T.</style></author><author><style face="normal" font="default"> Brakhage,A.A.</style></author><author><style face="normal" font="default"> Kniemeyer,O.</style></author><author><style face="normal" font="default"> Osherov,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Aspergillus and Antifungal Research Laboratory, Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel</style></auth-address><titles><title><style face="normal" font="default">Phenotypic and Proteomic Analysis of the Aspergillus fumigatus DeltaPrtT, DeltaXprG and DeltaXprG/DeltaPrtT Protease-Deficient Mutants</style></title><secondary-title><style face="normal" font="default">Front Microbiol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Front Microbiol</style></abbr-1></periodical><pages end="" start="2490">2490-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Enzymes</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Aspergillus fumigatus is the most common mold species to cause disease in immunocompromised patients. Infection usually begins when its spores (conidia) are inhaled into the airways, where they germinate, forming hyphae that penetrate and destroy the lungs and disseminate to other organs, leading to high mortality. The ability of hyphae to penetrate the pulmonary epithelium is a key step in the infectious process. A. fumigatus produces extracellular proteases that are thought to enhance penetration by degrading host structural barriers. This study explores the role of the A. fumigatus transcription factor XprG in controlling secreted proteolytic activity and fungal virulence. We deleted xprG, alone and in combination with prtT, a transcription factor previously shown to regulate extracellular proteolysis. xprG deletion resulted in abnormal conidiogenesis and formation of lighter colored, more fragile conidia and a moderate reduction in the ability of culture filtrates (CFs) to degrade substrate proteins. Deletion of both xprG and prtT resulted in an additive reduction, generating a mutant strain producing CF with almost no ability to degrade substrate proteins. Detailed proteomic analysis identified numerous secreted proteases regulated by XprG and PrtT, alone and in combination. Interestingly, proteomics also identified reduced levels of secreted cell wall modifying enzymes (glucanases, chitinases) and allergens following deletion of these genes, suggesting they target additional cellular processes. Surprisingly, despite the major alteration in the secretome of the xprG/prtT null mutant, including two to fivefold reductions in the level of 24 proteases, 18 glucanases, 6 chitinases, and 19 allergens, it retained wild-type virulence in murine systemic and pulmonary models of infection. This study highlights the extreme adaptability of A. fumigatus during infection based on extensive gene redundancy</style></abstract><notes><style face="normal" font="default">IS - 1664-302X (Print)IS - 1664-302X (Linking)LA - engPT - Journal ArticleCO - Israel -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.3389/fmicb.2017.02490</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29312198">PM:29312198</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Microbiol\2018-8-2490.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Microbiol\2018-8-2490.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Microbiol\2018-8-2490.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Microbiol\2018-8-2490.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20171212, Shemesh E</style></custom2><misc3><style face="normal" font="default">10.3389/fmicb.2017.02490</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87406</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Borisevich,I.V.</style></author><author><style face="normal" font="default"> Chemikova,N.K.</style></author><author><style face="normal" font="default"> Markov,V.I.</style></author><author><style face="normal" font="default"> Krasnianskiy,V.P.</style></author><author><style face="normal" font="default"> Borisevich,S.V.</style></author><author><style face="normal" font="default"> Rozhdestvenskiy,E.V.</style></author></authors></contributors><titles><title><style face="normal" font="default">An experience in the clinical use of specific immunoglobulin from horse blood serum for prophylaxis of Ebola haemorrhagic fever</style></title><secondary-title><style face="normal" font="default">Vopr Virusol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Vopr Virusol</style></abbr-1></periodical><pages end="29" start="25">25-29</pages><volume><style face="normal" font="default">62</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The aim of this work was to estimate the efficacy and safety of single intramuscular introduction of specific heterologous immunoglobulin as prophylactic drug against Ebola hemorrhagic fever. Materials and methods. The specific heterologous immunoglobulin was introduced as a special prophylactic drug to 28 patients in epidemic situations, after skin hurt with infectious materials or contact with infectious blood. Clinico-laboratory observation was performed in 24 subjects after single intramuscular introduction of heterologous immunoglobulin Ebola. The samples of blood serum were investigated for immunoglobulin Ebola and antibodies to horse gamma-globulin on the 30th and 60th days after prophylaxis. Results. None of the subjects of the study contracted Ebola fever. There were no anaphylactic reactions after special prophylaxis with specific heterologous immunoglobulin. Among the subjects with normal allergic state 31% responded with local reactions; 13%, with a general reaction (mild case of the serum disease). Almost no reaction was observed in patients with unfavorable allergic state subjected to desensitizing therapy; in the absence of desensitizing therapy, 50% of patients with unfavorable allergic state exhibited local reactions; 17%, mild cases of the serum disease; 33%, moderate cases of the serum disease. In summary, if the tactics of immunoglobulin application was right, the quantity of local allergic reactions was 28%; of wide spread reactions, 6%. Weak serum disease was observed in 11% of the subjects. The prognostic period of resistance to Ebola fever was less than 30 days. Conclusion. The prophylactic use of specific immunoglobulin from horse blood serum against hemorrhagic Ebola fever is effective and relatively safe in patients subjected to desensitizing therapy</style></abstract><notes><style face="normal" font="default">IS - 0507-4088 (Print)IS - 0507-4088 (Linking)LA - engPT - Journal ArticleCO - Russia -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29323843">PM:29323843</url></web-urls></urls><custom2><style face="normal" font="default">20170215, Borisevich IV</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86673</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Lopez-Marin,B.E.</style></author><author><style face="normal" font="default"> Rojano,B.</style></author><author><style face="normal" font="default"> Carvajal-de Pabon,L.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Universidad de Antioquia, Escuela de Nutricion y Dietetica, Medellin, Antoquia, Colombia.</style></auth-address><titles><title><style face="normal" font="default">[Determination of a new cow's milk-based formula allergenic capacity in 7 infants]</style></title><secondary-title><style face="normal" font="default">Rev Alerg Mex</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Alerg Mex</style></abbr-1></periodical><pages end="259" start="250">250-259</pages><volume><style face="normal" font="default">64</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="7" Year="2017">2017/7</year></dates><abstract><style face="normal" font="default">BACKGROUND: Cow's milk protein allergy is the main allergic problem during the first year of life, possibly owing to immune and gastrointestinal systems poor maturation. To prevent allergic reactions, the content and type of proteins in infant formulas resemble those of breast milk. We believe that reactions are due rather to the amount than to the type of protein. OBJECTIVE: To design a new formula with cow's milk that provides the infant with the main nutrients at an affordable cost and with lower risk for the development of allergies. METHODS: Three-phase project: product design, industrial production and ex vivo assay to assess for anemia and type I allergic reaction by CD63 expression in basophils. RESULTS: For every 100 calories, the content of protein was 2.0 g, carbohydrates 7.2 g and fat 0.5 g, which is higher than the indicated maximum value (4.5 g). Microbiologically, it was an innocuous food. CD63 expression was low in 57.1% of the babies and high in 42.9%. CONCLUSION: The new formula did not trigger any allergenic responses and can therefore be supplied to non-atopic infants</style></abstract><notes><style face="normal" font="default">DA - 20171019IS - 0002-5151 (Print)IS - 0002-5151 (Linking)LA - spaPT - English AbstractPT - Journal ArticleCO - Colombia -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29046023">PM:29046023</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Alerg Mex\2017-64-250-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Alerg Mex\2017-64-250-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171019, Lopez-Marin BE</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87071</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chongo-Faruk,V.</style></author></authors></contributors><titles><title><style face="normal" font="default">Skin exposure, symptoms and asthma in occupational settings - is there a link?</style></title><secondary-title><style face="normal" font="default">Curr Allergy Clin Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Allergy Clin Immunol</style></full-title></periodical><pages end="257" start="251">251-257</pages><volume><style face="normal" font="default">30</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Occupational contact with allergens through the dermatological and respiratory route can lead to various health effects, including allergic contact dermatitis, urticaria, rhinitis and asthma, which may result in a substantial disease burden in occupational settings. Inhalation is an obvious route for sensitisation and its pathophysiological mechanisms are relatively better defined. Recent studies have suggested that skin exposure may also play an important role in the sensitisation and development of respiratory outcomes in exposed workers. The review found that the evidence for such an association was limited and the immune mechanisms were not well understood. A better understanding of this association is required, more so for agents with a high molecular weight (protein), so as to identify important risk factors that may contribute to existing preventive efforts in reducing the incidence of allergy and asthma in occupational settings.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Africa -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">https://www.allergysa.co.za/Journal/December2017</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-251-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-251-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Chongo-Faruk V</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87087</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">El-Qutob,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Unit of Allergy, University Hospital of La Plana, Vila-Real, Spain</style></auth-address><titles><title><style face="normal" font="default">Shrimp allergy: beyond avoidance diet</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="256" start="252">252-256</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Currently, the management of people diagnosed with shellfish allergy relies on the avoidance of those foods. HDM immunotherapy has been reported to induce both shrimp allergy in non-allergic patients, and shrimp tolerance in shrimp-allergic patients. This article summarizes therapeutic options other than avoidance diet for shrimp allergic patients available once the diagnostic is established, such as production of hypoallergenic shrimp, use of immunotherapy with modified allergens, probiotics and Chinese herbal formulations</style></abstract><notes><style face="normal" font="default">IS - 1764-1489 (Print)IS - 1764-1489 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.16</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249132">PM:29249132</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-252-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-252-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, El-Qutob D</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.16</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86499</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tajmir-Riahi,A.</style></author><author><style face="normal" font="default"> Mahler,V.</style></author></authors></contributors><titles><title><style face="normal" font="default">Psychogenic nonepileptic seizure (PNES) mimicking acute anaphylactic reaction</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="257" start="255">255-257</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2197-0378</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0028-9</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40629-017-0028-9</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-255-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-255-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Tajmir-Riahi A</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0028-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86497</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Simon,D.</style></author><author><style face="normal" font="default"> Straumann,A.</style></author><author><style face="normal" font="default"> Schoepfer,A.M.</style></author><author><style face="normal" font="default"> Simon,H.U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Bern University Hospital, Inselspital, University of Bern, 3010 Bern, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Current concepts in eosinophilic esophagitis</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="266" start="258">258-266</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: Eosinophilic esophagitis (EoE) is a disease entity first described in the 1990s, but showing an increasing incidence that is characterized clinically by esophageal dysfunction and histologically by a striking eosinophil infiltration. Methods: This article discusses new aspects of the pathogenesis, symptoms, diagnosis, and treatment of EoE. Results: EoE affects both children and adults and is frequently associated with atopic disease and IgE sensitization. Barrier dysfunction and Thelper 2 inflammation are considered to be pathogenetically important factors. Recently, a proton pump inhibitor (PPI)-sensitive EoE subtype as well as an EoE-like disorder have been described. Conclusion: Research in recent years has contributed to a better understanding of the disease spectrum and pathogenesis of EoE, including genetic dispositions, thereby laying the foundation for innovative treatment approaches</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 2197-0378 (Print)IS - 2197-0378 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0037-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29104849">PM:29104849</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-258-66.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-258-66.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Simon D</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0037-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87073</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Coopasamy,K.</style></author><author><style face="normal" font="default"> Goldstone,E.</style></author><author><style face="normal" font="default"> Masekela,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">House-dust mites impact disease expression in children with chronic rhinitis: a retrospective study</style></title><secondary-title><style face="normal" font="default">Curr Allergy Clin Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Allergy Clin Immunol</style></full-title></periodical><pages end="263" start="258">258-263</pages><volume><style face="normal" font="default">30</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitisation</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: Asthma is the most common chronic childhood disease; it affects 10-20% of South African children, with allergic rhinitis (AR) being co-morbid in up to 80%. Data are lacking on the role of allergens in low- to middle-income countries, particularly in Durban, which is located in a sub-tropical region. Objectives: First, to determine the common allergens in children with asthma and/or AR. Secondly, to determine the prevalence of atopy and to compare disease severity in those with and without atopy. Methods: A retrospective chart review of asthmatic and AR children over a one-year period. The GINA2015 and ARIA guidelines were used for grading the disease severity. Laboratory tests included Phadiatop ® ;FX5; RAST ® for individual allergens. The Fisher's exact test and the Chi-squared test were used to test for associations between disease severity and atopy. The Kruskal-Wallis rank test was used to compare allergen load and disease severity. Ethical approval was granted. Results: One hundred children of mean age 5.5 ± 1.5 years with 60% males were enrolled. Of these, 66% were atopic, with common aeroallergens being D pteronyssinus (57%) and D farina (56%) There was an association between severity of AR and presence of D pteronyssinus and D farinae sensitisation (p = 0.012and p = 0.013), respectively. The persistence of AR was associated with the presence of D pteronyssinus andD farinae sensitisation (p = 0.007 and p = 0.009), respectively. There was no association between severity of asthma or the persistence of asthma and the presence of aeroallergens, all with p >0.05. (There was no correlation between severity or persistence of asthma based on aeroallergen sensitisation.) Conclusion: House-dust mites (HDM) are the commonest aeroallergens and conferred more severe and persistent AR in the sub-tropical region of Durban.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Africa -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">https://www.allergysa.co.za/Journal/December2017</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-258-63.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-258-63.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Coopasamy K</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87090</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Villalta,D.</style></author><author><style face="normal" font="default"> Cecchi,L.</style></author><author><style face="normal" font="default"> Farsi,A.</style></author><author><style face="normal" font="default"> Chiarini,F.</style></author><author><style face="normal" font="default"> Minale,P.</style></author><author><style face="normal" font="default"> Voltolini,S.</style></author><author><style face="normal" font="default"> Scala,E.</style></author><author><style face="normal" font="default"> Quercia,O.</style></author><author><style face="normal" font="default"> Muratore,L.</style></author><author><style face="normal" font="default"> Pravettoni,V.</style></author><author><style face="normal" font="default"> Calamari,A.M.</style></author><author><style face="normal" font="default"> Cortellini,G.</style></author><author><style face="normal" font="default"> Asero,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunologia e Allergologia, Ospedale "S. Maria degli Angeli", Via Montereale 24, 33170 Pordenone, Italy</style></auth-address><titles><title><style face="normal" font="default">Galactose-alpha-1,3-galactose syndrome: an Italian survey</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="269" start="263">263-269</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Background. The term of alpha-Gal syndrome, which includes the delayed allergy to red meat and the allergic reactions following the administration of cetuximab, is associated to the presence of specific IgE to alpha-Gal. In Italy, only anecdotal cases were reported so far. The Association of Italian Allergists (AAITO) carried out a survey with the aim of evaluating presence, characteristics, clinical features, and distribution of the syndrome in Italy. Methods. A web structured questionnaire was made available on the website of AAIITO from July 2016 to January 2017. It included 31 multiple-choice questions concerning different items, including the site of physicians, the number of patients diagnosed as having cetuximab allergy and/or delayed red meat allergy, recall of tick bites, symptoms, time to reactions, elicitor foods, reactions with foods other than meat, and in-vivo and in-vitro tests used for the diagnosis. Results. Seventy-nine physicians completed the questionnaire. Nine cases of allergy to cetuximab and 40 cases of delayed red meat allergy were recorded across Italy. 22.5% of patients with cetuximab allergy and 62.5% of those with delayed red meat allergy recalled a tick bite. 75% of patients with delayed red meat allergy experienced symptoms after eating beef (butcher's cut in 72.5%). Urticaria was the most frequent clinical manifestation (65% of cases). In 60.6% of cases symptoms appeared 2 - 4 hours after meat ingestion, while in 7.9% symptoms appeared after > 4 hours. The most used diagnostic methods were the intradermal test for cetuximab allergy (88.9%) and the detection of IgE to alpha-Gal (55.5%) for red meat allergy. Most case reports came from Northern Italy. Conclusions. alpha-Gal syndrome is present in Italy and beef is the most frequent offending food. In most cases symptoms were not severe</style></abstract><notes><style face="normal" font="default">IS - 1764-1489 (Print)IS - 1764-1489 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.35</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249134">PM:29249134</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-263-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-263-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Villalta D</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.35</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86540</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wegner,J.</style></author><author><style face="normal" font="default"> Weinmann-Menke,J.</style></author><author><style face="normal" font="default"> von Stebut,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, University Medical Center Mainz, Germany</style></auth-address><titles><title><style face="normal" font="default">Immunoadsorption for treatment of severe atopic dermatitis</style></title><secondary-title><style face="normal" font="default">Atheroscler Suppl</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Atheroscler Suppl</style></abbr-1></periodical><pages end="270" start="264">264-270</pages><volume><style face="normal" font="default">30</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Atopic dermatitis (AD) is a common disease affecting up to 10-20% of the population with the largest disease burden in childhood. Treatment options include basic emollient treatment, topical as well as systemic immunosuppressants. The pathogenesis is complex and among various triggers, genetic predisposition and immunological alterations contribute to development of disease. Atopy is common in patients with AD and many patients have high levels of Immunoglobulin E (IgE), some of which recognizes exogenous or auto/self-allergens. Treatment options targeting IgE such as specific immunotherapy against e.g. house dust mites or using anti-IgE antibodies (omalizumab) showed variable results that were not convincing. We now review recent data on the application of unspecific and IgE-selective immunoadsorption (IA) in AD. All in all, 53 patients have been treated with non-specific pan Ig IA and 28 patients with IgE-selective IA. Side effects were rarely seen. The efficacy of IgE depletion was generally high (&lt; approximately 80%) for each IA cycle, but transient and lasted only a few days/weeks. Of note, disease activity appeared to improve in almost all cases and lasted for several weeks. Although the evidence is still weak, these case studies suggest that IgE depletion in AD is effective and helped control the disease. The mechanism of action is not understood yet. Future controlled trials are needed to validate this observation</style></abstract><notes><style face="normal" font="default">DA - 20171103IS - 1878-5050 (Electronic)IS - 1567-5688 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.atherosclerosissup.2017.05.043</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29096848">PM:29096848</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Atheroscler Suppl\2017-30-264-70.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Atheroscler Suppl\2017-30-264-70.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171103, Wegner J</style></custom2><misc3><style face="normal" font="default">10.1016/j.atherosclerosissup.2017.05.043</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87077</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Adeniyi,T.A.</style></author><author><style face="normal" font="default"> Adeonipekun,P.A.</style></author><author><style face="normal" font="default"> Olowokudejo,J.D.</style></author></authors></contributors><titles><title><style face="normal" font="default">Allergenicity of dominant aeropollen in Nigeria: Part I</style></title><secondary-title><style face="normal" font="default">Curr Allergy Clin Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Allergy Clin Immunol</style></full-title></periodical><pages end="269" start="264">264-269</pages><volume><style face="normal" font="default">30</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Several pollen grains have been studied in detail for purification and characterisation of allergenic components in the advanced countries; however, many are yet to be studied in the tropics, including Nigeria. To close this gap, four pollen grains (Poaceae - Cynodon dactylon, Panicum maximum; Cyperaceae - Cyperus rotundus and Mariscus alternifolius) found dominant in the air from previous aeropalynological studies in Nigeria were selected. The pollen grains were harvested from fresh anthers and their proteins were extracted, quantified, separated and subjected to Western-blot analysis. The allergenic proteins were also identified. While C.dactylon had the highest protein content (17.09 mg/mL), M. alternifolius had the lowest (11.19 mg/mL).Western-blot analysis showed that individuals were most susceptible to the 35 kDa protein of C. dactylon(76%). Furthermore, only C. dactylon proteins of 14.5 kDa and 35 kDa were identified with their exact matches in the ProFound database (Cyn d 12 and Cyn d 1 respectively), where as the peptide sequencesof eight protein bands were newly added to the database. Of these, the Profilin protein group (14 kDa) is common to all studied pollen grains - an indication of veritable immunotherapeutic potential. This study is the first in Nigeria to record allergenic proteins in these pollen grains and to create a foundation for the development of immunotherapy drugs for allergy treatment in the country.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Nigeria -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">https://www.allergysa.co.za/Journal/December2017</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-264-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Clin Immunol\2017-30-264-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Adeniyi TA</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86500</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ring,J.</style></author><author><style face="normal" font="default"> Brockow,K.</style></author><author><style face="normal" font="default"> Kugler,C.</style></author><author><style face="normal" font="default"> Gebert,N.</style></author><author><style face="normal" font="default"> Grando,K.</style></author><author><style face="normal" font="default"> Gotz,D.</style></author><author><style face="normal" font="default"> Hutegger,I.</style></author><author><style face="normal" font="default"> Luthi,H.</style></author><author><style face="normal" font="default"> Munch,D.</style></author><author><style face="normal" font="default"> Spindler,T.</style></author><author><style face="normal" font="default"> Schmid-Grendelmeier,P.</style></author><author><style face="normal" font="default"> Gieler,U.</style></author></authors></contributors><titles><title><style face="normal" font="default">New aspects in allergy education with special emphasis on anaphylaxis</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="272" start="267">267-272</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2197-0378</style></isbn><abstract><style face="normal" font="default">Interdisciplinary anaphylaxis education programs have been performed in Germany and Austria since-á2007 according to the program of the Working Group on Anaphylaxis Training and Education (AGATE, </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£Arbeitsgemeinschaft Anaphylaxie Training und Edukation</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ), as well as in Switzerland with similar content. The basic units of education have been developed from a-ástandardized guideline-based manual, which is continuously updated and is currently being converted into a-ámodular system</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Switzerland -CO - Germany -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0032-0</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40629-017-0032-0</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-267-72.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-267-72.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Ring J</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0032-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87089</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Verga,M.C.</style></author><author><style face="normal" font="default"> Pastorino,R.</style></author><author><style face="normal" font="default"> Casani,A.</style></author><author><style face="normal" font="default"> Inturrisi,F.</style></author><author><style face="normal" font="default"> de Waure,C.</style></author><author><style face="normal" font="default"> Pugliese,A.</style></author><author><style face="normal" font="default"> Dello Iacono,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Primary Care Pediatrics, ASL Salerno, C.so Umberto I, 103 84019 Vietri sul Mare (SA), Italy</style></auth-address><titles><title><style face="normal" font="default">Prevalence, molecular characterization, and clinical relevance of sensitization to Anisakis simplex in children with sensitization and/or allergy to Dermatophagoides pteronyssinus</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="275" start="270">270-275</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anisakis</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Prevalence of the Anisakis Simplex's (AS) sensitization in children sensitized to Dermatophagoides pteronissynus (DP) is not known, neither it is to which percentage it might be due to cross-reactivity. The primary objective of the present retrospective cross-sectional study is to evaluate the prevalence of sensitization to AS in children sensitized or allergic to DP. Secondary outcomes were the prevalence of cross-reactivity and clinical relevance of the condition. The prevalence of sensitization to AS differs significantly among patients sensitized and not to DP (13.43% vs. 3.80%; p=0.019). The higher prevalence is mainly due to cross-reactivity with Der p10 (OR=8.86; 95% CI=4.33-40.74; p=0.0001). Currently, the sensitization to AS seems to have no clinical relevance in the pediatric population</style></abstract><notes><style face="normal" font="default">IS - 1764-1489 (Print)IS - 1764-1489 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.26</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249135">PM:29249135</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-270-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-270-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Verga MC</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.26</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86498</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Treudler,R.</style></author><author><style face="normal" font="default"> Simon,J.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Pollen-related food allergy: an update</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="282" start="273">273-282</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2197-0378</style></isbn><abstract><style face="normal" font="default">The vast majority of IgE-mediated food allergies in adults are based on sensitization to pollen, followed by reactions to structurally related, often unstable allergens, in particular in fruit (including edible nuts), vegetables, and spices</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0022-2</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40629-017-0022-2</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-273-82.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-273-82.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Treudler R</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0022-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87176</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">no authors</style></author></authors></contributors><titles><title><style face="normal" font="default">Artificial intelligence in health care: within touching distance</style></title><secondary-title><style face="normal" font="default">Lancet</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Lancet</style></full-title></periodical><pages end="" start="2739">2739-</pages><volume><style face="normal" font="default">390</style></volume><number><style face="normal" font="default">10114</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year><pub-dates><date Day="25" Month="12" Year="2017">2017/12/25</date></pub-dates></dates><publisher><style face="normal" font="default">Elsevier</style></publisher><isbn><style face="normal" font="default">0140-6736</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/S0140-6736(17)31540-4</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.1016/S0140-6736(17)31540-4</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Lancet\2017-390-2739.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Lancet\2017-390-2739.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171224, no authors</style></custom2><misc3><style face="normal" font="default">10.1016/S0140-6736(17)31540-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86880</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tong,P.</style></author><author><style face="normal" font="default"> Chen,S.</style></author><author><style face="normal" font="default"> Gao,J.</style></author><author><style face="normal" font="default"> Li,X.</style></author><author><style face="normal" font="default"> Wu,Z.</style></author><author><style face="normal" font="default"> Yang,A.</style></author><author><style face="normal" font="default"> Yuan,J.</style></author><author><style face="normal" font="default"> Chen,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, PR China</style></auth-address><titles><title><style face="normal" font="default">Caffeic acid-assisted cross-linking catalyzed by polyphenol oxidase decreases the allergenicity of ovalbumin in a Balb/c mouse model</style></title><secondary-title><style face="normal" font="default">Food Chem Toxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem Toxicol</style></abbr-1></periodical><pages end="283" start="275">275-283</pages><volume><style face="normal" font="default">111</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">Ovalbumin (OVA) is the most abundant egg white protein, but is also a major egg allergen. Desensitization of OVA may be a good way to control an egg allergy. In this study, caffeic acid-assisted cross-linked OVA catalyzed by polyphenol oxidase (PPO) was prepared, the effect of cross-linking on the allergenicity of OVA was tested in a Balb/c mouse model. Mice were orally sensitized with OVA or cross-linked OVA using cholera toxin as adjuvant. Clinical signs of allergy, specific antibody levels, serum histamine levels, mast cell protease-1 (mMCP-1) concentrations, morphological structure of duodenum, and cytokines were determined after mice were challenged with OVA or cross-linked OVA. Both OVA and cross-linked OVA induced allergic diarrhea in Balb/c mice, however, histological symptoms of small intestine were much milder in mice fed with cross-linked OVA than in those fed with OVA. A tendency toward decreased allergen-specific IgE, IgG, IgG1 and IgG2a levels, as well as serum histamine and mMCP-1 concentration were observed in cross-linked OVA group, accompanied by an inhibition of IL-4, IL-5, IL-13 and IFN-gamma production in the stimulated spleen cell. It could be concluded that caffeic acid-assisted PPO-catalyzed cross-linking significantly reduced the potential allergenicity of OVA, but may not completely eliminate it</style></abstract><notes><style face="normal" font="default">IS - 1873-6351 (Electronic)IS - 0278-6915 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.fct.2017.11.026</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29170047">PM:29170047</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem Toxicol\2017-111-275-83.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem Toxicol\2017-111-275-83.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Tong P</style></custom2><misc3><style face="normal" font="default">10.1016/j.fct.2017.11.026</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86541</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tselmin,S.</style></author><author><style face="normal" font="default"> Julius,U.</style></author><author><style face="normal" font="default"> Bornstein,S.R.</style></author><author><style face="normal" font="default"> Hohenstein,B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Extracorporeal Treatment and Lipoprotein Apheresis Center, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universitat Dresden, Fetscherstr. 74, 01307 Dresden, Germany.</style></auth-address><titles><title><style face="normal" font="default">Low rate of infectious complications following immunoadsorption therapy without regular substitution of intravenous immunoglobulins</style></title><secondary-title><style face="normal" font="default">Atheroscler Suppl</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Atheroscler Suppl</style></abbr-1></periodical><pages end="282" start="278">278-282</pages><volume><style face="normal" font="default">30</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Immunoadsorption (IA) is increasingly used instead of plasma exchange due to lower risk of side effects and a higher selectivity. As a consequence of the reduction of immunoglobulins (Ig), the rate of infectious complications might increase in those patients. We therefore aimed to investigate the infection rate following IA without intravenous IG (IVIG) substitution in our apheresis center, where patients do not receive IVIG on a regular basis. MATERIAL AND METHODS: We conducted a retrospective analysis of the IA treatments performed between 2010 and 2015 without IVIG substitution and collected data on patient age, diagnosis, number of IA treatments, serum levels of Ig, total protein, albumin, C-reactive protein (CRP) and infectious complications that occurred within 2 months after the IA treatment cycle. RESULTS: A total number of 52 patients (27 females) received at least 5 IA sessions using the following adsorbers: TheraSorb-Ig (n = 3), TheraSorb-Ig flex (n = 44), TheraSorb Ig pro (n = 1) and TheraSorb-IgE (n = 5). The median number of treatment sessions was 8.8 [range 5-16], the median IgG reduction was 82 [11-99] %. Serum albumin was decreased by 8%. The median CRP levels remained normal until the end of therapy and within 2 months after that (3.10 and 4.30 mg/L respectively). Only 4 patients had infections (7.7%). Three of them received additional immunosuppressive therapy. CONCLUSIONS: Immunoadsorption leads to a significant reduction of IgG. CRP as inflammatory marker is not affected. Even without substitution of IVIG the complication rate directly linked with IA is low and questionable</style></abstract><notes><style face="normal" font="default">DA - 20171103IS - 1878-5050 (Electronic)IS - 1567-5688 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.atherosclerosissup.2017.05.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29096850">PM:29096850</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Atheroscler Suppl\2017-30-278-82.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Atheroscler Suppl\2017-30-278-82.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171103, Tselmin S</style></custom2><misc3><style face="normal" font="default">10.1016/j.atherosclerosissup.2017.05.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86781</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Polyzoi,E.</style></author><author><style face="normal" font="default"> Polyzois,D.</style></author></authors></contributors><titles><title><style face="normal" font="default">Presence of Household Mold, Children's Respiratory Health, and School Absenteeism: Cause for Concern</style></title><secondary-title><style face="normal" font="default">J Environ Health</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Environ Health</style></abbr-1></periodical><pages end="35" start="28">28-35</pages><volume><style face="normal" font="default">79</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="3" Year="2017">2017/3</year></dates><abstract><style face="normal" font="default">A study examining the relationship between housing conditions, respiratory health, and school absenteeism was conducted in the city of Winnipeg in Manitoba, Canada. As part of this study, a survey was completed by 3,424 parents of children in grades 3 and 4 to determine the a) relationship between self-reported visible mold in homes and tested airborne mold; b) relationships of self-reported visible mold, tested airborne mold, and asthma and/or persistent colds; c) school absenteeism rates due to asthma and/or persistent colds; and d) children's socioeconomic status (SES) and incidence of asthma and/or persistent colds. In addition, a complete inspection of a subset of 715 homes was conducted, including the collection of over 1,400 indoor and 500 outdoor air samples for mold analysis. Results indicate a significant association between self-reported visible mold and airborne mold. Additionally, a significant association was found between Cladosporium levels from air samples (the most common genus type found) and children's asthma in combination with persistent colds. Children with persistent colds in combination with asthma miss significantly more school than children who have only asthma or only persistent colds. Children from poorer families reported more persistent colds than children from high-income families. No association was found between income and asthma. Furthermore, SES was not a significant factor for number of school days missed</style></abstract><notes><style face="normal" font="default">DA - 20171116IS - 0022-0892 (Print)IS - 0022-0892 (Linking)LA - engPT - Research Support, Non-U.S. Gov'tPT - Journal ArticleCO - Canada -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29144078">PM:29144078</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Environ Health\2017-79-28-35.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Environ Health\2017-79-28-35.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171116, Polyzoi E</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87086</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Vinas,M.</style></author><author><style face="normal" font="default"> Pineda,F.</style></author><author><style face="normal" font="default"> Izquierdo-Dominguez,A.</style></author><author><style face="normal" font="default"> Castillo,M.</style></author><author><style face="normal" font="default"> Castillo,M.J.</style></author><author><style face="normal" font="default"> Hernandez,N.</style></author><author><style face="normal" font="default"> Ibero,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Servicio de Alergia del Consorci Sanitari de Terrassa, Barcelona, Spain</style></auth-address><titles><title><style face="normal" font="default">Occupational allergy to Spagulax((R))(Plantago ovata seed)</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="283" start="281">281-283</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">We report the case of a 36-year-old male pharmaceutical laboratory worker. On handling Spagulax((R)) sachets whose content is a laxative called Plantago ovata, he immediately presented rhinoconjunctivitis. Methods. Specific allergy study included SDS-PAGE with Western Blot and specific nasal challenge to Plantago ovata extract. Results. Prick by prick for Spagulax((R)) was negative. Total IgE: 126.5 U/mL. Western Blot recognized two proteins of 15 and 20 kDa in the extract of Plantago ovata and three proteins of 15, 18 and 50 kDa in the extract of Plantago lanceolata. Conclusions. We present a case of occupational allergy due to inhalation of and/or contact with Plantago ovata seeds</style></abstract><notes><style face="normal" font="default">IS - 1764-1489 (Print)IS - 1764-1489 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.21</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249137">PM:29249137</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-281-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-281-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Vinas M</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.21</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87084</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Noshela,G.M.</style></author><author><style face="normal" font="default"> Thomsen,S.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Bispebjerg Hospital, Bispebjerg Bakke 23 DK-2400 Copenhagen NV Denmark</style></auth-address><titles><title><style face="normal" font="default">Transient hair loss in patients with chronic spontaneous urticaria treated with omalizumab</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="285" start="284">284-285</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Omalizumab (anti-IgE) is used as add-on therapy for antihistamine refractory chronic urticaria patients. The most commonly reported adverse effects were headache, arthralgia, upper respiratory infections, fatigue, nausea and injection-site reactions. However, lately a few cases of hair loss have been reported. We describe a case of transient hair loss in a young female patient after initiating treatment with omalizumab. Despite this side effect, the patient continued with omalizumab treatment for 10 months with good effect</style></abstract><notes><style face="normal" font="default">IS - 1764-1489 (Print)IS - 1764-1489 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.08</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249138">PM:29249138</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-284-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-284-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Noshela GM</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.08</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86806</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Trame,S.</style></author><author><style face="normal" font="default"> Roseler,S.</style></author><author><style face="normal" font="default"> Kluwig,D.</style></author><author><style face="normal" font="default"> Schreiter,C.</style></author><author><style face="normal" font="default"> Staub,J.</style></author><author><style face="normal" font="default"> Wurpts,G.</style></author><author><style face="normal" font="default"> Merk,H.F.</style></author><author><style face="normal" font="default"> Baron,J.M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Bird-egg syndrome: a-ávariant of secondary food allergies</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="286" start="285">285-286</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2197-0378</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0035-x</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40629-017-0035-x</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-285-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-285-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Trame S</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0035-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86897</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nguyet,T.M.N.</style></author><author><style face="normal" font="default"> Lomunova,M.</style></author><author><style face="normal" font="default"> Le,B.V.</style></author><author><style face="normal" font="default"> Lee,J.S.</style></author><author><style face="normal" font="default"> Park,S.K.</style></author><author><style face="normal" font="default"> Kang,J.S.</style></author><author><style face="normal" font="default"> Kim,Y.H.</style></author><author><style face="normal" font="default"> Hwang,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunology and Immunopharmacology Laboratory, College of Pharmacy, Chungnam National University, 99 Daekak-ro Yuseong-gu, Daejeon 34134, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">The mast cell stabilizing activity of Chaga mushroom critical for its therapeutic effect on food allergy is derived from inotodiol</style></title><secondary-title><style face="normal" font="default">Int Immunopharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Immunopharmacol</style></abbr-1></periodical><pages end="295" start="286">286-295</pages><volume><style face="normal" font="default">54</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="23" Month="11" Year="2017">2017/11/23</year></dates><abstract><style face="normal" font="default">While an anti-allergic effect of Chaga mushroom (Inonotus obliquus) has been indicated, its therapeutic effect on allergy and immunoregulatory mechanisms and chemical constituents directly responsible for that are hardly known. We examined the effect of 70% ethanol extract of Chaga mushroom (EE) and its dichloromethane (DF) and aqueous (AF) fractions using a mouse model of chicken ovalbumin (cOVA)-induced food allergy, and found that only EE and DF ameliorated allergy symptoms to a significant extent. The in vivo mast cell-stabilizing activity was also found only in EE and DF whereas the activities to suppress Th2 and Th17 immune responses and cOVA-specific IgE production in the small intestine were observed in all three treatment regimens, implying that inhibition of the mast cell function by lipophilic compounds was vital for the therapeutic effect. Results also indicated that inotodiol, a triterpenoid predominantly present in DF, played an active role as a mast cell stabilizer</style></abstract><notes><style face="normal" font="default">IS - 1878-1705 (Electronic)IS - 1567-5769 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1016/j.intimp.2017.11.025</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29175507">PM:29175507</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Immunopharmacol\2017-54-286-95.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Immunopharmacol\2017-54-286-95.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Nguyen TM</style></custom2><misc3><style face="normal" font="default">10.1016/j.intimp.2017.11.025</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87085</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Syrigos,N.</style></author><author><style face="normal" font="default"> Grapsa,D.</style></author><author><style face="normal" font="default"> Syrigou,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Department, "Sotiria" General Hospital, Athens, Greece</style></auth-address><titles><title><style face="normal" font="default">Omalizumab for refractory chronic spontaneous urticaria during concurrent immunomodulatory therapy for multiple sclerosis</style></title><secondary-title><style face="normal" font="default">Eur Ann Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur Ann Allergy Clin Immunol</style></abbr-1></periodical><pages end="287" start="286">286-287</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> multiple sclerosis</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Data derived from previous clinical trials and real-life studies have shown that omalizumab may represent an effective third-line treatment option for patients with chronic spontaneous urticaria (CSU) refractory to standard antihistamine treatment. Nevertheless, the safety and efficacy of omalizumab treatment for CSU, when administered concurrently with other immunomodulatory agents remains largely unknown. We herein present the case of a female patient with relapsing-remitting multiple sclerosis (RRMS), under treatment with interferon beta-1a, azathioprine and gabapentin, who was successfully treated with omalizumab for refractory CSU. To the best of our knowledge, this is the first reported case attesting to the safety and efficacy of omalizumab for CSU when administered concurrently with other immunomodulatory agents</style></abstract><notes><style face="normal" font="default">IS - 1764-1489 (Print)IS - 1764-1489 (Linking)LA - engPT - Journal ArticleCO - Greece -</style></notes><work-type><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.20</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249139">PM:29249139</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-286-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur Ann Allergy Clin Immunol\2017-49-286-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Syrigos N</style></custom2><misc3><style face="normal" font="default">10.23822/EurAnnACI.1764-1489.20</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86807</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Voegler,T.</style></author><author><style face="normal" font="default"> Goergen,F.</style></author><author><style face="normal" font="default"> Bergmann,K.C.</style></author><author><style face="normal" font="default"> Boelke,G.</style></author><author><style face="normal" font="default"> Salame,J.</style></author><author><style face="normal" font="default"> Gildemeister,J.</style></author><author><style face="normal" font="default"> Zuberbier,T.</style></author></authors></contributors><titles><title><style face="normal" font="default">Technical specifications of the Global Allergy and Asthma European Network (GA2LEN) chamber: a-ánovel mobile allergen exposure chamber</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="294" start="287">287-294</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2197-0378</style></isbn><abstract><style face="normal" font="default">Field trials are the traditional approach for clinical trials in allergy but are under criticism for lack of standardization as they are affected by uncontrollable parameters such as environmental conditions, pollen counts, or lifestyle. Stationary allergen exposure chambers with a-ádefined concentration of allergens under stable and standardized environmental conditions have been used to overcome these restrictions but have not allowed multicenter studies. We here describe the technical specifications and validation of a-ánovel mobile pollen chamber specifically designed for multicenter studies</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çöthe GA2LEN chamber</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0040-0</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40629-017-0040-0</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-287-94.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-287-94.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Voegler T</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0040-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86999</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nicholson,A.</style></author><author><style face="normal" font="default"> Pollard,S.L.</style></author><author><style face="normal" font="default"> Lima,J.J.</style></author><author><style face="normal" font="default"> Romero,K.M.</style></author><author><style face="normal" font="default"> Tarazona-Meza,C.</style></author><author><style face="normal" font="default"> Malpartida-Guzman,G.</style></author><author><style face="normal" font="default"> Mougey,E.</style></author><author><style face="normal" font="default"> Hansel,N.N.</style></author><author><style face="normal" font="default"> Checkley,W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, USA</style></auth-address><titles><title><style face="normal" font="default">Serum folate concentrations, asthma, atopy, and asthma control in Peruvian children</style></title><secondary-title><style face="normal" font="default">Respir Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Med</style></abbr-1></periodical><pages end="35" start="29">29-35</pages><volume><style face="normal" font="default">133</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">BACKGROUND: The relationship between folate status and asthma-related outcomes has not been carefully examined in low- and middle-income countries where folate deficiency is common. METHODS: Ancillary analysis of an unmatched case-control study in which we analyzed serum folate concentrations in 412 children with asthma and 342 controls living in peri-urban communities in Lima, Peru. We examined baseline associations between folate and asthma, atopy, total serum IgE, pulmonary function, and fractional exhaled nitric oxide. We then followed children with asthma longitudinally for 6-9 months and assessed associations between folate and odds of uncontrolled asthma (defined as Asthma Control Test score &lt;/= 19) and of >/=1 emergency visits during follow-up. RESULTS: A 10 ng/mL decrease in serum folate was associated with 45% higher adjusted odds of asthma (OR = 1.45, 95% CI 1.05-2.02). The folate-asthma relationship differed by atopic status: a 10 ng/mL decrease in serum folate was associated with a 2.4-fold higher odds of asthma among children without atopy (2.38, 1.20-4.72) and 23% higher odds of asthma in children with atopy (1.23, 0.85-1.80). Among children with asthma, a 10 ng/mL decrease in serum folate was associated with 62% higher odds of uncontrolled asthma (1.62, 1.02-2.56) and 73% higher odds of >/=1 emergency visits during follow-up (1.73, 1.05-2.85). CONCLUSIONS: Serum folate concentrations were inversely associated with asthma, but this effect was stronger in children without atopy. Among children with asthma, lower serum folate concentrations were associated with higher risk of uncontrolled asthma</style></abstract><notes><style face="normal" font="default">IS - 1532-3064 (Electronic)IS - 0954-6111 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Peru -</style></notes><work-type><style face="normal" font="default">10.1016/j.rmed.2017.10.026</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29173446">PM:29173446</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Med\2017-133-29-35.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Med\2017-133-29-35.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Nicholson A</style></custom2><misc3><style face="normal" font="default">10.1016/j.rmed.2017.10.026</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86672</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Camero-Martinez,H.</style></author><author><style face="normal" font="default"> Lopez-Garcia,A.I.</style></author><author><style face="normal" font="default"> Rivero-Yeverino,D.</style></author><author><style face="normal" font="default"> Caballero-Lopez,C.G.</style></author><author><style face="normal" font="default"> Arana-Munoz,O.</style></author><author><style face="normal" font="default"> Papaqui-Tapia,S.</style></author><author><style face="normal" font="default"> Rojas-Mendez,I.C.</style></author><author><style face="normal" font="default"> Vazquez-Rojas,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Hospital Universitario de Puebla, Servicio de Alergia e Inmunologia Clinica, Puebla, Puebla, Mexico.</style></auth-address><titles><title><style face="normal" font="default">[Frequency of skin reactivity to food allergens in allergic patients]</style></title><secondary-title><style face="normal" font="default">Rev Alerg Mex</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Alerg Mex</style></abbr-1></periodical><pages end="297" start="291">291-297</pages><volume><style face="normal" font="default">64</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="7" Year="2017">2017/7</year></dates><abstract><style face="normal" font="default">BACKGROUND: Food allergy is deemed to have a worldwide prevalence ranging from 2 to 10 %. OBJECTIVE: To determine the frequency of skin reactivity to food allergens by age groups. METHODS: Cross-sectional, descriptive, prolective, observational study. Patients aged from 2 to 64 years with symptoms consistent with allergic disease were included. Skin prick tests were carried out with food allergens. Frequencies and percentages were estimated. RESULTS: One-hundred and ninety-one patients were included, out of which 63.4% were females. Mean age was 22.5 years; 19.3 % showed positive skin reactivity to at least one food. Distribution by age group was as follows: preschool children 13.5 %, schoolchildren 24.3 %, adolescents 2.7 % and adults 59.5 %. Diagnoses included allergic rhinitis in 84.3 %, asthma in 19.4 %, urticaria in 14.1 % and atopic dermatitis in 8.4 %. Positive skin reactivity frequency distribution in descending order was: soybeans with 5.2 %, peach with 4.7 %, grapes, orange and apple with 3.6 %, nuts with 3.1 %, pineapple, avocado, tomato and tuna with 2.6 %. CONCLUSION: The frequency of skin reactivity to food allergens was similar to that reported in the national and Latin American literature, but sensitization to each specific allergen varied for each age group</style></abstract><notes><style face="normal" font="default">DA - 20171019IS - 0002-5151 (Print)IS - 0002-5151 (Linking)LA - spaPT - English AbstractPT - Journal ArticleCO - Mexico -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29046027">PM:29046027</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Alerg Mex\2017-64-291-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Alerg Mex\2017-64-291-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171019, Camero-Martinez H</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86794</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">MacDonald,S.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">The Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Room 3B.69, Baltimore, MD, 21224, USA.</style></auth-address><titles><title><style face="normal" font="default">History of Histamine-Releasing Factor (HRF)/Translationally Controlled Tumor Protein (TCTP) Including a Potential Therapeutic Target in Asthma and Allergy</style></title><secondary-title><style face="normal" font="default">Results Probl Cell Differ</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Results Probl Cell Differ</style></abbr-1></periodical><pages end="308" start="291">291-308</pages><volume><style face="normal" font="default">64</style></volume><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Histamine-releasing factor (HRF) also known as translationally controlled tumor protein (TCTP) is a highly conserved, ubiquitous protein that has both intracellular and extracellular functions. Here we will highlight the subcloning of the molecule, its clinical implications, as well as an inducible-transgenic mouse. Particular attention will be paid to its extracellular functioning and its potential role as a therapeutic target in asthma and allergy. The cells and the cytokines that are produced when stimulated or primed by HRF/TCTP will be detailed as well as the downstream signaling pathway that HRF/TCTP elicits. While it was originally thought that HRF/TCTP interacted with IgE, the finding that cells not binding IgE also respond to HRF/TCTP called this interaction into question. HRF/TCTP or at least its mouse counterpart appears to interact with some, but not all IgE and IgG molecules. HRF/TCTP has been shown to activate multiple human cells including basophils, eosinophils, T cells, and B cells. Since many of the cells that are activated by HRF/TCTP participate in the allergic response, the extracellular functions of HRF/TCTP could exacerbate the allergic, inflammatory cascade. Particularly exciting is that small molecule agonists of the phosphatase SHIP-1 have been shown to modulate the P13 kinase/AKT pathway and may control inflammatory disorders. This review discusses this possibility in light of HRF/TCTP</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 0080-1844 (Print)IS - 0080-1844 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/978-3-319-67591-6_16</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29149416">PM:29149416</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Results Probl Cell Differ\2017-64-291-308.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Results Probl Cell Differ\2017-64-291-308.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, MacDonald SM</style></custom2><misc3><style face="normal" font="default">10.1007/978-3-319-67591-6_16</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86622</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Aun,M.V.</style></author><author><style face="normal" font="default"> Bonamichi-Santos,R.</style></author><author><style face="normal" font="default"> Arantes-Costa,F.M.</style></author><author><style face="normal" font="default"> Kalil,J.</style></author><author><style face="normal" font="default"> Giavina-Bianchi,P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Animal models of asthma: utility and limitations</style></title><secondary-title><style face="normal" font="default">J Asthma Allergy</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Asthma Allergy</style></full-title></periodical><pages end="301" start="293">293-301</pages><volume><style face="normal" font="default">2017</style></volume><number><style face="normal" font="default">10</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Clinical studies in asthma are not able to clear up all aspects of disease pathophysiology. Animal models have been developed to better understand these mechanisms and to evaluate both safety and efficacy of therapies before starting clinical trials. Several species of animals have been used in experimental models of asthma, such as Drosophila, rats, guinea pigs, cats, dogs, pigs, primates and equines. However, the most common species studied in the last two decades is mice, particularly BALB/c. Animal models of asthma try to mimic the pathophysiology of human disease. They classically include two phases: sensitization and challenge. Sensitization is traditionally performed by intraperitoneal and subcutaneous routes, but intranasal instillation of allergens has been increasingly used because human asthma is induced by inhalation of allergens. Challenges with allergens are performed through aerosol, intranasal or intratracheal instillation. However, few studies have compared different routes of sensitization and challenge. The causative allergen is another important issue in developing a good animal model. Despite being more traditional and leading to intense inflammation, ovalbumin has been replaced by aeroallergens, such as house dust mites, to use the allergens that cause human disease. Finally, researchers should define outcomes to be evaluated, such as serum-specific antibodies, airway hyperresponsiveness, inflammation and remodeling. The present review analyzes the animal models of asthma, assessing differences between species, allergens and routes of allergen administration.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.2147/JAA.S121092</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.2147/JAA.S121092</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Asthma Allergy\2017-2017-293-301.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Asthma Allergy\2017-2017-293-301.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Aun MV</style></custom2><misc3><style face="normal" font="default">10.2147/JAA.S121092</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86804</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Worm,M.</style></author><author><style face="normal" font="default"> Sturm,G.</style></author><author><style face="normal" font="default"> Kleine-Tebbe,J.</style></author><author><style face="normal" font="default"> Cichocka-Jarosz,E.</style></author><author><style face="normal" font="default"> Cardona,V.</style></author><author><style face="normal" font="default"> Maris,I.</style></author><author><style face="normal" font="default"> Dolle,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">New trends in anaphylaxis</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="300" start="295">295-300</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2197-0378</style></isbn><abstract><style face="normal" font="default">This review presents the current trends in anaphylaxis management discussed at the fourth International Network for Online-Registration of Anaphylaxis (NORA) conference held in Berlin in April 2017. Current data from the anaphylaxis registry show that Hymenoptera venom, foods, and pharmaceutical drugs are still among the most frequent triggers of anaphylaxis. Rare triggers include chicory, cardamom, asparagus, and goji berries. A-ámeta-analysis on recent trends in insect venom anaphylaxis demonstrated for the first time that, although data on the efficacy of insect venom immunotherapy is limited, the occurrence of severe reactions upon repeated sting events can be prevented and patients</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖ quality of life improved. Molecular diagnostics of insect venom anaphylaxis have significantly improved diagnostic sensitivity and specificity. Self-treatment of anaphylaxis is of great importance. Recent data from the anaphylaxis registry show an increase (from 23% in 2012 to 29% in 2016) in the use of adrenaline as recommended in the guidelines. A-ásurvey on the implementation of guidelines conducted among the centers reporting to the anaphylaxis registry highlights the extent to which the guideline has been perceived and implemented. Reports on a-ávariety of cases in the anaphylaxis registry illustrate the diversity of this potentially life-threatening reaction. Component-resolved diagnostics can help to specify sensitization profiles in anaphylaxis, particularly in terms of the risk for severe reactions. Recent studies on anaphylaxis awareness show that training methods are effective; nevertheless, target groups and learning methods need to undergo further scientific investigation in coming years</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -CO - Austria -CO - Poland -CO - Spain -CO - Ireland -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0042-y</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40629-017-0042-y</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-295-300.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-295-300.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Worm M</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0042-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87412</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Susanto,A.J.</style></author><author><style face="normal" font="default"> Rengganis,I.</style></author><author><style face="normal" font="default"> Rumende,C.M.</style></author><author><style face="normal" font="default"> Harimurti,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Internal Medicine, Faculty of Medicine, University of Sebelas Maret - dr. Moewardi Hospital, Surakarta, Indonesia. agusjoko.susanto4@gmail.com</style></auth-address><titles><title><style face="normal" font="default">The Differences in Serum Quantitative Specific IgE Levels Induced by Dermatophagoides pteronyssinus, Dermatophagoides farinae and Blomia tropicalis Sensitization in Intermittent and Persistent Allergic Asthma</style></title><secondary-title><style face="normal" font="default">Acta Med Indones</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Acta Med Indones</style></abbr-1></periodical><pages end="306" start="299">299-306</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Inhalant allergen</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: house dust mites (HDM) are an important inhalant allergen in allergic asthma. However, molecular diagnostic study of specific IgE to HDM allergens has not been done in Indonesia. In addition, the association of quantitative specific IgE measurement with asthma severity has not been investigatedd. This study aimed to investigate the difference of serum quantitative specific IgE levels induced by Dermatophagoides (D.) pteronyssinus, D. farinae and Blomia tropicalis sensitization in intermittent and persistent allergic asthma. METHODS: this was a cross-sectional study on adult allergic asthma patients who were invited for serum specific IgE testing. This study was a part of a larger study within the Division of Allergy and Immunology, Cipto Mangunkusumo Hospital. Asthma severity was defined based on Global Initiative on Asthma (GINA) 2015 criteria and were grouped as intermittent or persistent. Quantitative specific IgE testing was done on blood serum using a multiple allergosorbent test (Polycheck Allergy, Biocheck GmbH, Munster, Germany). The HDM allergens tested were D. pteronyssinus, D. farinae, and Blomia tropicalis. Difference between two groups were analyze using Mann-Whitney test. RESULTS: a total of 87 subjects were enrolled in this study; 69 (79.3%) were women. Mean patients' age was 40, 2 years. Sixty-three (72.4%) subjects had asthma and allergic rhinitis. Fifty-eight (66.7%) subjects were classified as persistent asthma. The prevalence of sensitization was 62.1% for D. farinae, 51.7% for D. pteronyssinus, and 48.3% for Blomia tropicalis. The median of specific IgE levels were significantly higher in persistent asthma compares to intermittent asthma induced by D. farinae (median 1.30 vs. 0.0 kU/L; p=0.024) and B. tropicalis (median 0.57 vs. 0.0 kU/L; p=0.015) sensitization. Level of Specific IgE D. pteronyssinus was also to be higher in persistent asthma than the level measured in intermittent asthma (0.67 vs. 0.00 kU/L; p=0.066). CONCLUSION: Sensitization of HDM allergens was shown to be highest for D. farinae 62.1%, followed by D. pteronyssinus 51.7% and Blomia tropicalis 48.3%. Specific IgE level induced by D. farinae and Blomia tropicalis sensitization were significantly higher in patients with persistent asthma compared to intermittent asthma, whereas specific IgE level induced by D. pteronyssinus sensitization was higher in persistent asthma although not statistically significant</style></abstract><notes><style face="normal" font="default">IS - 0125-9326 (Print)IS - 0125-9326 (Linking)LA - engPT - Journal ArticleCO - Indonesia -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29348379">PM:29348379</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Med Indones\2017-49-299-306.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Med Indones\2017-49-299-306.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171129, Susanto AJ</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86693</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Prieto,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Seccion de Alergologia, Hospital Dr Peset and Universidad de Valencia, Spain.</style></auth-address><titles><title><style face="normal" font="default">Tablet-based sublingual immunotherapy for respiratory allergy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="35" start="30">30-35</pages><volume><style face="normal" font="default">45</style></volume><number><style face="normal" font="default">1S</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="13" Month="11" Year="2017">2017/11/13</year></dates><abstract><style face="normal" font="default">Allergic respiratory disease represents a significant and expanding health problem worldwide. The gold standard of therapeutic intervention is still grucocorticosteroids, although they are not effective in all patients and may cause side effects. Allergen Immunotherapy has been administrated as subcutaneous injections for treatment of allergic rhinoconjunctivitis and asthma and has been practiced for the past century. Sublingual immunotherapy (SLIT) tablets are now available for grass- or ragweed-induced rhinoconjunctivitis and will be available in Spain for house dust mite (HDM)-induced rhinoconjunctivitis and asthma in the next months. In this review, new developments in the field of tablet-based SLIT for respiratory allergy are summarized, with special emphasis on HDM-induced allergic rhinitis and asthma. SLIT tablets are the best-documented immunotherapy products on the market and represent a more patient-friendly concept because they can be self-administrated at home</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29146015">PM:29146015</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-30-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-30-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Prieto L</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87185</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zeltins,A.</style></author><author><style face="normal" font="default"> West,J.</style></author><author><style face="normal" font="default"> Zabel,F.</style></author><author><style face="normal" font="default"> El Turabi,A.</style></author><author><style face="normal" font="default"> Balke,I.</style></author><author><style face="normal" font="default"> Haas,S.</style></author><author><style face="normal" font="default"> Maudrich,M.</style></author><author><style face="normal" font="default"> Storni,F.</style></author><author><style face="normal" font="default"> Engeroff,P.</style></author><author><style face="normal" font="default"> Jennings,G.T.</style></author><author><style face="normal" font="default"> Kotecha,A.</style></author><author><style face="normal" font="default"> Stuart,D.I.</style></author><author><style face="normal" font="default"> Foerster,J.</style></author><author><style face="normal" font="default"> Bachmann,M.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Latvian Biomedical Research &amp; Study Centre, Ratsupites iela 1, Riga, LV 1067 Latvia.</style></auth-address><titles><title><style face="normal" font="default">Incorporation of tetanus-epitope into virus-like particles achieves vaccine responses even in older recipients in models of psoriasis, Alzheimer's and cat allergy</style></title><secondary-title><style face="normal" font="default">NPJ Vaccines</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">NPJ Vaccines</style></abbr-1></periodical><pages end="" start="30">30-</pages><volume><style face="normal" font="default">2</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aging</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Monoclonal antibodies are widely used to treat non-infectious conditions but are costly. Vaccines could offer a cost-effective alternative but have been limited by sub-optimal T-cell stimulation and/or weak vaccine responses in recipients, for example, in elderly patients. We have previously shown that the repetitive structure of virus-like-particles (VLPs) can effectively bypass self-tolerance in therapeutic vaccines. Their efficacy could be increased even further by the incorporation of an epitope stimulating T cell help. However, the self-assembly and stability of VLPs from envelope monomer proteins is sensitive to geometry, rendering the incorporation of foreign epitopes difficult. We here show that it is possible to engineer VLPs derived from a non human-pathogenic plant virus to incorporate a powerful T-cell-stimulatory epitope derived from Tetanus toxoid. These VLPs (termed CMVTT) retain self-assembly as well as long-term stability. Since Th cell memory to Tetanus is near universal in humans, CMVTT-based vaccines can deliver robust antibody-responses even under limiting conditions. By way of proof of concept, we tested a range of such vaccines against chronic inflammatory conditions (model: psoriasis, antigen: interleukin-17), neurodegenerative (Alzheimer's, beta-amyloid), and allergic disease (cat allergy, Fel-d1), respectively. Vaccine responses were uniformly strong, selective, efficient in vivo, observed even in old mice, and employing low vaccine doses. In addition, randomly ascertained human blood cells were reactive to CMVTT-VLPs, confirming recognition of the incorporated Tetanus epitope. The CMVTT-VLP platform is adaptable to almost any antigen and its features and performance are ideally suited for the design of vaccines delivering enhanced responsiveness in aging populations</style></abstract><notes><style face="normal" font="default">IS - 2059-0105 (Print)IS - 2059-0105 (Linking)LA - engPT - Journal ArticleCO - Latvia -CO - Switzerland -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1038/s41541-017-0030-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29263885">PM:29263885</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\NPJ Vaccines\2017-2-30.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\NPJ Vaccines\2017-2-30.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171204, Zeltins A</style></custom2><misc3><style face="normal" font="default">10.1038/s41541-017-0030-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87208</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Petras,K.E.</style></author><author><style face="normal" font="default"> Wells,R.J.</style></author><author><style face="normal" font="default"> Pronko,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Arizona Veterinary Emergency and Critical Care Center, USA. Colorado State University, USA</style></auth-address><titles><title><style face="normal" font="default">Suspected anaphylaxis and lack of clinical protection associated with envenomation in two dogs previously vaccinated with Crotalus atrox toxoid</style></title><secondary-title><style face="normal" font="default">Toxicon</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Toxicon</style></full-title></periodical><pages end="33" start="30">30-33</pages><volume><style face="normal" font="default">142</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Anaphylaxis</style></keyword></keywords><dates><year Day="14" Month="12" Year="2017">2017/12/14</year></dates><abstract><style face="normal" font="default">OBJECTIVE: to describe the clinical presentation of two canines present in anaphylactic shock secondary to rattlesnake envenomation. In both cases, there was no previous documented previous envenomation event and the initial sensitization required for anaphylactic response is believed to be secondary to Crotalus atrox toxoid vaccine. CASE DESCRIPTION: In the first case, a 12-year-old golden retriever present for collapse, severe hematochezia, and vomiting after first time envenomation from a suspected western diamondback rattlesnake. The patient presented in severe hypovolemic shock and required aggressive fluid therapy, antivenom, anti-emetics, and pain management. The patient made a full recovery within 24 hours. In the second case, an 8-year old English setter presented for acute collapse, vomiting, and facial swelling after suspected first time envenomation from a suspected Prairie rattlesnake. The patient presented in severe hypovolemic shock with cardiac arrhythmias and required aggressive fluid therapy, antivenom, pain control, anti-emetics, and antibiotics. The patient made a full recovery after three days of hospitalization. Both patients had been previously vaccinated with the C. atrox vaccine. CONCLUSION: This case report documents suspected anaphylaxis in two canine patients after first time envenomation by a rattlesnake. Both patients were previously vaccinated by the Crotalus atrox toxoid, which is hypothesized to be the initial inciting trigger</style></abstract><notes><style face="normal" font="default">IS - 1879-3150 (Electronic)IS - 0041-0101 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.toxicon.2017.12.044</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29248468">PM:29248468</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Toxicon\2017-142-30-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Toxicon\2017-142-30-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171219, Petras KE</style></custom2><misc3><style face="normal" font="default">10.1016/j.toxicon.2017.12.044</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86728</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shi,F.</style></author><author><style face="normal" font="default"> Zhang,Y.</style></author><author><style face="normal" font="default"> Qiu,C.</style></author><author><style face="normal" font="default"> Xiong,Y.</style></author><author><style face="normal" font="default"> Li,M.</style></author><author><style face="normal" font="default"> Shan,A.</style></author><author><style face="normal" font="default"> Yang,Y.</style></author><author><style face="normal" font="default"> Li,B.</style></author></authors></contributors><auth-address><style face="normal" font="default">a Emergency Department , Jinan University, The Second Clinical College , NO. 1017 Dongmen north Road, Shenzhen , China</style></auth-address><titles><title><style face="normal" font="default">Effects of inhaled corticosteroids on the expression of TNF family molecules in murine model of allergic asthma</style></title><secondary-title><style face="normal" font="default">Exp Lung Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Exp Lung Res</style></abbr-1></periodical><pages end="310" start="301">301-310</pages><volume><style face="normal" font="default">43</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: The tumor necrosis factor superfamily member LIGHT (the official gene symbol approved by NCBI Gene Database), an inflammatory factor secreted by T cells after allergen exposure, recently discovered to play crucial roles in asthmatic airway remodeling. However, it is unclear whether LIGHT could be controlled by inhaled corticosteroids, a key component of asthma management. This study was to investigate the effects and potential mechanisms of inhaled budesonide on the expressions of LIGHT and its receptors (LTbetaR and HVEM) of lung tissues in ovalbumin-sensitized mice. MATERIALS AND METHODS: Thirty-three BALB/c mice were randomly divided into the control, asthma model, and budesonide treatment groups (11 in each group). Mice were sensitized and challenged by OVA to develop mouse model of chronic asthma, and treated with aerosolized budesonide before OVA challenge. Bronchoalveolar lavage fluid (BALF) and lungs were obtained after the final OVA challenge. Protein and mRNA Levels of LIGHT, LTbetaR, and HVEM in the lungs were investigated by immunohistochemistry, image analysis, and real-time PCR. Expressions of IL-6 and IFN-gamma in BALF were measured by ELISA. RESULTS: Inhaled budesonide significantly reduced protein and mRNA levels of lung LIGHT, LTbetaR, and HVEM in asthmatic mice. Correspondingly, the number of eosinophils and neutrophils and IL-6 levels in BALF after budesonide treatment were found to be decreased, whereas the IFN-gamma levels in BALF were increased. Moreover, the expressions of LIGHT and HVEM mRNA showed positive correlation with IL-6 levels in the treatment group. CONCLUSIONS: Inhaled budesonide can down-regulate the expressions of LIGHT, LTbetaR, and HVEM in the lungs of asthmatic mice, and LIGHT/LTbetaR/HVEM interactions may be a potentially key target for asthma treatment</style></abstract><notes><style face="normal" font="default">DA - 20171115IS - 1521-0499 (Electronic)IS - 0190-2148 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1080/01902148.2017.1376129</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29140131">PM:29140131</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Exp Lung Res\2017-43-301-10.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Exp Lung Res\2017-43-301-10.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171115, Shi F</style></custom2><misc3><style face="normal" font="default">10.1080/01902148.2017.1376129</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86805</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Becker,S.</style></author><author><style face="normal" font="default"> Groger,M.</style></author><author><style face="normal" font="default"> Jakob,T.</style></author><author><style face="normal" font="default"> Klimek,L.</style></author></authors></contributors><titles><title><style face="normal" font="default">The benefit of molecular diagnostics in allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Allergo J Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergo J Int</style></abbr-1></periodical><pages end="310" start="301">301-310</pages><volume><style face="normal" font="default">26</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2197-0378</style></isbn><abstract><style face="normal" font="default">Molecular component-resolved diagnostics has established itself in recent years as an integral part of the routine diagnosis of allergic rhinitis</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s40629-017-0033-z</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40629-017-0033-z</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergo J Int\2017-26-301-10.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergo J Int\2017-26-301-10.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Becker S</style></custom2><misc3><style face="normal" font="default">10.1007/s40629-017-0033-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86898</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ou,Z.</style></author><author><style face="normal" font="default"> Chen,C.</style></author><author><style face="normal" font="default"> Chen,A.</style></author><author><style face="normal" font="default"> Yang,Y.</style></author><author><style face="normal" font="default"> Zhou,W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, First Affiliated Hospital of Chongqing Medical University, Chongqing, China.</style></auth-address><titles><title><style face="normal" font="default">Adverse events of Dupilumab in adults with moderate-to-severe atopic dermatitis: A meta-analysis</style></title><secondary-title><style face="normal" font="default">Int Immunopharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Int Immunopharmacol</style></abbr-1></periodical><pages end="310" start="303">303-310</pages><volume><style face="normal" font="default">54</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword></keywords><dates><year Day="25" Month="11" Year="2017">2017/11/25</year></dates><abstract><style face="normal" font="default">BACKGROUND: Dupilumab, a fully human monoclonal antibody against interleukin-4 receptor alpha, inhibits the signals of interleukin-4 and interleukin-13, and has also shown significant efficacy in patients with moderate-to-severe atopic dermatitis (AD), while the effect of it on adverse events remains controversial. OBJECTIVE: To assess the influence of dupilumab on adverse events in adults with moderate-to-severe AD. METHOD: Randomised controlled trials (RCTs) that compared dupilumab with a placebo for patients with moderate-to-severe AD were searched in the MEDLINE, EMBASE, Web of Science and Cochrane databases. The outcome of the study was the incidence of adverse events during the observation period. RESULTS: Eight RCTs were analysed in this study. Meta-analysis showed that patients treated with dupilumab had a lower risk of skin infection (risk ratio [RR] 0.54; 95% confidence interval [CI] 0.42-0.69) and exacerbation of AD (RR 0.44, 95% CI 0.34-0.59), but had a higher risk of injection-site reaction (RR 2.24, 95% CI 1.68-2.99), headache (RR 1.47, 95% CI 1.05-2.06), and conjunctivitis (RR 2.64, 95% CI 1.79-3.89) than did patients treated with a placebo. Nasopharyngitis, urinary tract infection, upper respiratory tract infection, and herpes virus infection were found balanced in dupilumab groups and placebo groups. CONCLUSION: Dupilumab moderately reduced the risk of skin infection and the exacerbation of AD, slightly increased the risk of headache, and moderately increased the risk of injection-site reaction and conjunctivitis, but had little effect on other infections in adults with moderate-to-severe AD</style></abstract><notes><style face="normal" font="default">IS - 1878-1705 (Electronic)IS - 1567-5769 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.intimp.2017.11.031</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29182975">PM:29182975</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int Immunopharmacol\2017-54-303-10.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int Immunopharmacol\2017-54-303-10.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Ou Z</style></custom2><misc3><style face="normal" font="default">10.1016/j.intimp.2017.11.031</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86629</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tyurin,Y.A.</style></author><author><style face="normal" font="default"> Lissovskaya,S.A.</style></author><author><style face="normal" font="default"> Fassahov,R.S.</style></author><author><style face="normal" font="default"> Mustafin,I.G.</style></author><author><style face="normal" font="default"> Shamsutdinov,A.F.</style></author><author><style face="normal" font="default"> Shilova,M.A.</style></author><author><style face="normal" font="default"> Rizvanov,A.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biochemistry and Clinical Laboratory Diagnostics, Medical State University, Butlerov Street 49, Kazan, Republic of Tatarstan, Russia</style></auth-address><titles><title><style face="normal" font="default">Cytokine Profile of Patients with Allergic Rhinitis Caused by Pollen, Mite, and Microbial Allergen Sensitization</style></title><secondary-title><style face="normal" font="default">J Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol Res</style></abbr-1></periodical><pages end="" start="3054217">3054217-</pages><volume><style face="normal" font="default">2017</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Allergic rhinitis (AR) is especially prevalent among the population of large cities. Immunologically, the airway epithelium is a region where the population of allergen-presenting cells concentrates. These cells actively express a group of receptors of the innate immune system. A specific cytokine profile is its representation. The study was aimed at evaluating the cytokine profile in patients with seasonal and perennial allergic rhinitis. The cytokine profile of nasal secretion and blood serum of 44 patients with AR was studied. 24 of them had seasonal allergic rhinitis (SAR), and 20 patients suffered from perennial allergic rhinitis (PAR). The patients' age ranged from 4 to 60 years. It was determined in our study that the activation of the GM-CSF production retained in patients with PAR sensitized to mite allergen components (Dermatophagoides pteronyssinus). There was a higher production profile of TNF-alpha and TSLP in nasal secretion in the patients with perennial allergic rhinitis and additional high sensitization to SEs. Sensitization to mold fungal allergen components significantly increases in patients with seasonal allergic rhinitis. They demonstrated high level of sensitization to the Aspergillus fumigatus component m3. Thus, along with other clinical trials, the study performed would clarify some aspects of molecular pathogenesis of human allergic rhinitis</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 2314-7156 (Electronic)IS - 2314-7156 (Linking)LA - engPT - Journal ArticleCO - Russia -</style></notes><work-type><style face="normal" font="default">10.1155/2017/3054217</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29109963">PM:29109963</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol Res\2017-2017-3054217.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol Res\2017-2017-3054217.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Tyurin YA</style></custom2><misc3><style face="normal" font="default">10.1155/2017/3054217</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86940</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hosakoppal,S.S.</style></author><author><style face="normal" font="default"> Bryce,P.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Allergy and Immunology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA</style></auth-address><titles><title><style face="normal" font="default">Transplant-acquired food allergy: current perspectives</style></title><secondary-title><style face="normal" font="default">J Asthma Allergy</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">J Asthma Allergy</style></full-title></periodical><pages end="315" start="307">307-315</pages><volume><style face="normal" font="default">10</style></volume><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Dietary Proteins</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Mechanisms that regulate the tolerance to dietary proteins or the loss of this and subsequent development of disease are poorly understood. In food allergy, there is growing awareness of the urgency in understanding these events to aid in the development of next-generation therapies and interventions. This review focuses on the accumulating evidence related to food allergy that develops after transplantation. This intriguing immunological phenomenon has been described in several different types of transplant settings and to variety of different foods. We outline these studies and the evidence from them that support transplant-acquired food allergy being a process regulated by both the donor allergic status and the recipient genetics and treatments. A number of key risk factors seem prevalent throughout transplant-acquired food allergy and include type of transplant, age and general health of the recipient, modality of immunosuppression and potentially the genetics of both donor and recipient. Importantly, these studies provide a window into better general understanding of food allergy, and facilitate clearer understanding of the critical immunological and epidemiological factors needed to allow the adoptive transfer of a food-specific allergic disease from one individual to another.</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.2147/JAA.S136319</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.2147/JAA.S136319</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Asthma Allergy\2017-10-307-15.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Asthma Allergy\2017-10-307-15.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Hosakoppal SS</style></custom2><misc3><style face="normal" font="default">10.2147/JAA.S136319</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86584</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nath,A.</style></author><author><style face="normal" font="default"> Szecsi,G.</style></author><author><style face="normal" font="default"> Csehi,B.</style></author><author><style face="normal" font="default"> Mednyanszky,Z.</style></author><author><style face="normal" font="default"> Kisko,G.</style></author><author><style face="normal" font="default"> Banyai,E.</style></author><author><style face="normal" font="default"> Dernovics,M.</style></author><author><style face="normal" font="default"> Koris,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Food Engineering, Faculty of Food Science, Szent Istvan University, Menesi st 44, HU-1118 Budapest, Hungary</style></auth-address><titles><title><style face="normal" font="default">Production of Hypoallergenic Antibacterial Peptides from Defatted Soybean Meal in Membrane Bioreactor: A Bioprocess Engineering Study with Comprehensive Product Characterization</style></title><secondary-title><style face="normal" font="default">Food Technol Biotechnol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Technol Biotechnol</style></abbr-1></periodical><pages end="324" start="308">308-324</pages><volume><style face="normal" font="default">55</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="9" Year="2017">2017/9</year></dates><abstract><style face="normal" font="default">Hypoallergenic antibacterial low-molecular-mass peptides were produced from defatted soybean meal in a membrane bioreactor. In the first step, soybean meal proteins were digested with trypsin in the bioreactor, operated in batch mode. For the tryptic digestion of soybean meal protein, optimum initial soybean meal concentration of 75 g/L, temperature of 40 degrees C and pH=9.0 were determined. After enzymatic digestion, low-molecular-mass peptides were purified with cross-flow flat sheet membrane (pore size 100 microm) and then with tubular ceramic ultrafiltration membrane (molecular mass cut-off 5 kDa). Effects of transmembrane pressure and the use of a static turbulence promoter to reduce the concentration polarization near the ultrafiltration membrane surface were examined and their positive effects were proven. For the filtration with ultrafiltration membrane, transmembrane pressure of 3.105 Pa with 3-stage discontinuous diafiltration was found optimal. The molecular mass distribution of purified peptides using ultrafiltration membrane was determined by a liquid chromatography-electrospray ionization quadrupole time-of-flight mass spectrometry setup. More than 96% of the peptides (calculated as relative frequency) from the ultrafiltration membrane permeate had the molecular mass M&lt;/=1.7 kDa and the highest molecular mass was found to be 3.1 kDa. The decrease of allergenic property due to the tryptic digestion and membrane filtration was determined by an enzyme-linked immunosorbent assay and it was found to exceed 99.9%. It was also found that the peptides purified in the ultrafiltration membrane promoted the growth of Pediococcus acidilactici HA6111-2 and they possessed antibacterial activity against Bacillus cereus</style></abstract><notes><style face="normal" font="default">DA - 20171101IS - 1330-9862 (Print)IS - 1330-9862 (Linking)LA - engPT - Journal ArticleCO - Hungary -</style></notes><work-type><style face="normal" font="default">10.17113/ftb.55.03.17.5040</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29089846">PM:29089846</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Technol Biotechnol\2017-55-308-24.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Technol Biotechnol\2017-55-308-24.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171101, Nath A</style></custom2><misc3><style face="normal" font="default">10.17113/ftb.55.03.17.5040</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86565</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Farne,H.A.</style></author><author><style face="normal" font="default"> Johnston,S.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Airway Disease Infection Section, National Heart and Lung Institute, Imperial College, London, UK</style></auth-address><titles><title><style face="normal" font="default">Immune mechanisms of respiratory viral infections in asthma</style></title><secondary-title><style face="normal" font="default">Curr Opin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Immunol</style></abbr-1></periodical><pages end="37" start="31">31-37</pages><volume><style face="normal" font="default">48</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="14" Month="8" Year="2017">2017/8/14</year></dates><abstract><style face="normal" font="default">The more severe pathology respiratory viral infections produce in asthma sufferers is a result of a dysregulated immune response. Excess type 2 inflammation is a well-described feature of virally induced asthma exacerbations, with growing evidence that production of antiviral interferons may also be impaired. However, the mechanisms underlying these are little understood. This review summarizes the current understanding and recent discoveries of the cellular and molecular events that follow viral infections in asthma. In particular, we discuss differences in viral sensing and intracellular signalling pathways upstream of interferon induction in asthma, and the role of epithelial-derived cytokines in orchestrating type 2 immunopathology, including type 2 innate lymhpoid cells (ILC2s)</style></abstract><notes><style face="normal" font="default">DA - 20170818IS - 1879-0372 (Electronic)IS - 0952-7915 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.coi.2017.07.017</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28818789">PM:28818789</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-31-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-31-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170818, Farne HA</style></custom2><misc3><style face="normal" font="default">10.1016/j.coi.2017.07.017</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87156</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Everstine,K.</style></author><author><style face="normal" font="default"> Abt,E.</style></author><author><style face="normal" font="default"> McColl,D.</style></author><author><style face="normal" font="default"> Popping,B.</style></author><author><style face="normal" font="default"> Morrison-Rowe,S.</style></author><author><style face="normal" font="default"> Lane,R.W.</style></author><author><style face="normal" font="default"> Scimeca,J.</style></author><author><style face="normal" font="default"> Winter,C.</style></author><author><style face="normal" font="default"> Ebert,A.</style></author><author><style face="normal" font="default"> Moore,J.C.</style></author><author><style face="normal" font="default"> Chin,H.B.</style></author></authors></contributors><auth-address><style face="normal" font="default">1 The U.S. Pharmacopeial Convention, 12601 Twinbrook Parkway, Rockville, Maryland 20852, USA</style></auth-address><titles><title><style face="normal" font="default">Development of a Hazard Classification Scheme for Substances Used in the Fraudulent Adulteration of Foods</style></title><secondary-title><style face="normal" font="default">J Food Prot</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Food Prot</style></abbr-1></periodical><pages end="36" start="31">31-36</pages><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="18" Month="12" Year="2017">2017/12/18</year></dates><abstract><style face="normal" font="default">Food fraud, the intentional misrepresentation of the true identity of a food product or ingredient for economic gain, is a threat to consumer confidence and public health and has received increased attention from both regulators and the food industry. Following updates to food safety certification standards and publication of new U.S. regulatory requirements, we undertook a project to (i) develop a scheme to classify food fraud-related adulterants based on their potential health hazard and (ii) apply this scheme to the adulterants in a database of 2,970 food fraud records. The classification scheme was developed by a panel of experts in food safety and toxicology from the food industry, academia, and the U.S. Food and Drug Administration. Categories and subcategories were created through an iterative process of proposal, review, and validation using a subset of substances known to be associated with the fraudulent adulteration of foods. Once developed, the scheme was applied to the adulterants in the database. The resulting scheme included three broad categories: 1, potentially hazardous adulterants; 2, adulterants that are unlikely to be hazardous; and 3, unclassifiable adulterants. Categories 1 and 2 consisted of seven subcategories intended to further define the range of hazard potential for adulterants. Application of the scheme to the 1,294 adulterants in the database resulted in 45% of adulterants classified in category 1 (potentially hazardous). Twenty-seven percent of the 1,294 adulterants had a history of causing consumer illness or death, were associated with safety-related regulatory action, or were classified as allergens. These results reinforce the importance of including a consideration of food fraud-related adulterants in food safety systems. This classification scheme supports food fraud mitigation efforts and hazard identification as required in the U.S. Food Safety Modernization Act Preventive Controls Rules</style></abstract><notes><style face="normal" font="default">IS - 1944-9097 (Electronic)IS - 0362-028X (Linking)LA - engPT - Journal ArticleCO - United States -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.4315/0362-028X.JFP-17-173</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29257723">PM:29257723</url></web-urls><related-urls><url ppv-ref="no">presto - 6 mesi</url></related-urls></urls><custom2><style face="normal" font="default">20171211, Everstine K</style></custom2><misc3><style face="normal" font="default">10.4315/0362-028X.JFP-17-173</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87403</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Namazova-Barahona,L.S.</style></author><author><style face="normal" font="default"> Snovskaya,M.A.</style></author><author><style face="normal" font="default"> Mitushin,I.L.</style></author><author><style face="normal" font="default"> Kozhevnikova,O.V.</style></author><author><style face="normal" font="default"> Batyrova,A.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Peculiarities of Allergy Diagnosis in Children</style></title><secondary-title><style face="normal" font="default">Vestn Ross Akad Med Nauk</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Vestn Ross Akad Med Nauk</style></abbr-1></periodical><pages end="41" start="33">33-41</pages><volume><style face="normal" font="default">72</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Components</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Allergic disease is a serious problem in practical healthcare. Over the last 40 years there has been exponential growth in the prevalence. According to the world health organization information, allergic diseases are at the 2nd place in prevalence the children, behind the viral infections. Their frequency and severity are increasing. In this regard, the relevance of timely and skilled diagnostic allergopathology is most important. In this study the current state of the question of allergy diagnostics is considered, the international experience is summarized and the approach to the allergy diagnosis based on use of step-by-step identification of a causal and significant factor of allergic reactions is offered. On the basis of the analysis of relevance and the importance for patients of one or the other allergens (taking into account a source of allergens and age of patients) use of a step-by-step allergy diagnostics algorithm is offered. The first step is definition of clinical implications of an allergy. It means direct contact of the phisition with the patient, clarification of its complaints, clinical symptoms, medical history disease. The second step is the confirmation of IgE-dependent mechanism. It involves the using of screening tests that are selected depending on the clinical symptoms and seasonality manifestations (the screening module). The third step is to identify the source of the allergens that are most meaningful for the patient with using test panels (modules). The panels include the most common and clinically relevant triggers of allergic reactions. The fourth step is the search for an individual significant allergens, which were not included in the diagnostic modules. On the fifth step, we plan to conduct component-divided diagnostics and detect the antibodies to unique components of significant allergens. The developed diagnostics algorithm, corresponds to needs of both the adult, and children's population and provides the personalized approach to the patients</style></abstract><notes><style face="normal" font="default">IS - 0869-6047 (Print)IS - 0869-6047 (Linking)LA - engPT - Journal ArticleCO - Russia -</style></notes><work-type><style face="normal" font="default">10.15690/vramn799</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29308841">PM:29308841</url></web-urls></urls><custom2><style face="normal" font="default">20171211, Namazova-Barahona LS</style></custom2><misc3><style face="normal" font="default">10.15690/vramn799</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87281</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tokodi,M.</style></author><author><style face="normal" font="default"> Csabi,E.</style></author><author><style face="normal" font="default"> Kiricsi,A.</style></author><author><style face="normal" font="default"> Kollar,E.</style></author><author><style face="normal" font="default"> Molnar,A.H.</style></author><author><style face="normal" font="default"> Rovo,L.</style></author><author><style face="normal" font="default"> Bella,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">1 Department of Oto-Rhino-Laryngology and Head-Neck Surgery, University of Szeged , Szeged, Hungary</style></auth-address><titles><title><style face="normal" font="default">The effect of nasal provocation with a single-dose allergen on the physical and cognitive performance of patients with ragweed allergy</style></title><secondary-title><style face="normal" font="default">Physiol Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Physiol Int</style></abbr-1></periodical><pages end="343" start="334">334-343</pages><volume><style face="normal" font="default">104</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="1" Month="12" Year="2017">2017/12/1</year></dates><abstract><style face="normal" font="default">Purpose This study aims to compare the impact of active allergic rhinitis on physical and cognitive abilities of trained allergic athletes to untrained allergic patients. Methods Cognitive, respiratory, and fitness functions were assessed before and after allergen exposure. Participants in both groups were provoked intranasally with ragweed allergen. Results The group of athletes revealed significantly higher average values in peak inspiratory flow and fitness index before and after provocation. In neuropsychological assessments, athletes performed significantly better after allergen provocation in complex working memory capacity. Due to single acute allergen exposure, the size of the nasal cavity and nasal inspiratory peak flow significantly decreased in both groups. The physical performance of both groups did not change after provocation. Executive functions and complex working memory capacity of athletes significantly improved resulting from provocation. Conclusions A single-shot allergen in high dose might cause an increase in mental concentration, which was more pronounced in the group of athletes. This study indicates that acute exposure to allergen cannot affect the physical performance and may result in increased mental focus in patients with allergy notwithstanding the declining respiratory functions</style></abstract><notes><style face="normal" font="default">IS - 2498-602X (Print)IS - 2498-602X (Linking)LA - engPT - Journal ArticleCO - Hungary -</style></notes><work-type><style face="normal" font="default">10.1556/2060.104.2017.4.6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29278026">PM:29278026</url></web-urls></urls><custom2><style face="normal" font="default">20171201, Tokodi M</style></custom2><misc3><style face="normal" font="default">10.1556/2060.104.2017.4.6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86795</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dos Santos,A.C.</style></author><author><style face="normal" font="default"> Land,M.G.P.</style></author><author><style face="normal" font="default"> Silva,N.P.D.</style></author><author><style face="normal" font="default"> Santos,K.O.</style></author><author><style face="normal" font="default"> Lima-Dellamora,E.D.C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ, Brazil.</style></auth-address><titles><title><style face="normal" font="default">Reactions related to asparaginase infusion in a 10-year retrospective cohort</style></title><secondary-title><style face="normal" font="default">Rev Bras Hematol Hemoter</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Bras Hematol Hemoter</style></abbr-1></periodical><pages end="342" start="337">337-342</pages><volume><style face="normal" font="default">39</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Asparaginase</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Although it is an essential component of the treatment of acute lymphoid leukemia in children, asparaginase causes adverse reactions that sometimes make it impossible to use it fully. Hypersensitivity reactions are the most frequent and may lead to early discontinuation of treatment. The present study aimed to investigate suspicions of adverse reactions during the infusion of asparaginase in a pediatric cohort. METHODS: A retrospective observational study was carried out at a university pediatric institute in the state of Rio de Janeiro. Information regarding clinical features and characteristics of adverse reactions was collected from hospital medical records. Suspicions of adverse reactions were classified regarding causality and severity. RESULTS: Seventy-three suspicions of adverse reactions were recorded during asparaginase infusion in 72 children in the study period. Allergic hypersensitivity reactions were suspected in 60.5% of the cases. Of these, 25% of the reactions occurred during induction and 61.1% in concomitant use with vincristine, findings that diverge from other studies. High-risk classification and younger age were considered risk factors for these reactions. A total of 72.4% of the reactions were classified as grade 1 or 2, which suggest that not all are related to antibody formation; this highlights the importance of differential diagnosis with other reactions, such as non-allergic hypersensitivity and hyperammonemia. CONCLUSION: The implementation of the differential diagnosis of reactions related to infusion of asparaginase with ammonia dosage and classification of the grade of reactions is crucial to facilitate the identification and proper management of each type of reaction</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1516-8484 (Print)IS - 1516-8484 (Linking)LA - engPT - Journal ArticleCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.bjhh.2017.08.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150106">PM:29150106</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Bras Hematol Hemoter\2017-39-337-42.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Bras Hematol Hemoter\2017-39-337-42.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Dos Santos AC</style></custom2><misc3><style face="normal" font="default">10.1016/j.bjhh.2017.08.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87031</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ding,S.</style></author><author><style face="normal" font="default"> Deng,Q.</style></author><author><style face="normal" font="default"> Xiang,Y.</style></author><author><style face="normal" font="default"> Chen,J.</style></author><author><style face="normal" font="default"> Huang,J.</style></author><author><style face="normal" font="default"> Lu,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Third Xiangya Hospital, Central South University, Changsha, China</style></auth-address><titles><title><style face="normal" font="default">Bullous pemphigoid associated with milia, increased serum IgE, autoantibodies against desmogleins, and refractory treatment in a young patient</style></title><secondary-title><style face="normal" font="default">An Bras Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">An Bras Dermatol</style></abbr-1></periodical><pages end="36" start="34">34-36</pages><volume><style face="normal" font="default">92</style></volume><number><style face="normal" font="default">5 Suppl 1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Bullous pemphigoid is a blistering autoimmune disease characterized by two hemidesmosomal proteins (anti-BP180 and 230). Pemphigus, by contrast, is characterized by two autoantibodies (anti-desmoglein 1 and 3). Coexistence of autoantibodies of bullous pemphigoid and pemphigus in a patient is rare. A 25-year-old male patient was admitted to our hospital, reporting a 3-month history of multiple papules, vesicles, and erosions over an extensive erythema on the entire body. Laboratory tests showed high levels of serum IgE, anti-BP180 antibodies, and anti-desmoglein 1 and 3. Histopathologic and immunopathologic features were characterized by bullous pemphigoid. No improvement was seen with systemic corticosteroid therapy, however, pulse corticosteriod therapy combined with methylprednisolone, immunosuppressants, immunomodulators, and plasmapheresis led to the recovery of his condition with numerous milia</style></abstract><notes><style face="normal" font="default">IS - 1806-4841 (Electronic)IS - 0365-0596 (Linking)LA - engPT - Case ReportsCO - China -</style></notes><work-type><style face="normal" font="default">10.1590/abd1806-4841.20176124</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29267440">PM:29267440</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\An Bras Dermatol\2017-92-S1-34-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\An Bras Dermatol\2017-92-S1-34-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171211, Ding S</style></custom2><misc3><style face="normal" font="default">10.1590/abd1806-4841.20176124</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86725</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Henry,E.K.</style></author><author><style face="normal" font="default"> Inclan-Rico,J.M.</style></author><author><style face="normal" font="default"> Siracusa,M.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Type 2 Cytokine Responses: Regulating Immunity to Helminth Parasites and Allergic Inflammation</style></title><secondary-title><style face="normal" font="default">Curr Pharmacol Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Pharmacol Rep</style></abbr-1></periodical><pages end="359" start="346">346-359</pages><volume><style face="normal" font="default">3</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2198-641X</style></isbn><abstract><style face="normal" font="default">It is well established that T helper type 2 (TH2) immune responses are necessary not only to provide protection against helminth parasites but also to promote the detrimental inflammation associated with allergies and asthma. Given the importance of type 2 immunity and inflammation, many studies have focused on better understanding the factors that regulate TH2 cell development and activation. As a result, significant progress has been made in understanding the signaling pathways and molecular events necessary to promote TH2 cell polarization. In addition to the adaptive compartment, emerging studies are better defining the innate immune pathways needed to promote TH2 cell responses. Given the recent and substantial growth of this field, the purpose of this review is to highlight recent studies defining the innate immune events that promote immunity to helminth parasites and allergic inflammation</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s40495-017-0114-1</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40495-017-0114-1</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Pharmacol Rep\2017-3-346-59.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Pharmacol Rep\2017-3-346-59.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Henry EK</style></custom2><misc3><style face="normal" font="default">10.1007/s40495-017-0114-1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86671</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chow,E.J.</style></author><author><style face="normal" font="default"> Sediva,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">Departments of Medicine and Pediatrics, Warren Alpert Medical School of Brown University; Rhode Island Hospital and Hasbro Children's Hospital, Providence, RIDepartment of Pediatrics, Warren Alpert Medical School of Brown University; Division of Pediatric Critical Care, Hasbro Children's Hospital, Providence, RI</style></auth-address><titles><title><style face="normal" font="default">Influenza A Infection and Anaphylaxis in a Pediatric Patient Hospitalized for Asthma Exacerbation</style></title><secondary-title><style face="normal" font="default">R I Med J (2013)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">R I Med J (2013)</style></abbr-1></periodical><pages end="36" start="35">35-36</pages><volume><style face="normal" font="default">100</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="11" Year="2017">2017/11/1</year></dates><abstract><style face="normal" font="default">Influenza infections can cause a variety of different systemic problems beyond respiratory symptoms. A 4-year-old boy with a history of atopy, infected with influenza A, presented to our hospital with an asthma exacerbation developed symptoms of anaphylaxis. He was treated with a full course of oseltamivir and symptoms resolved without recurrence of allergic reaction. Infections have been implicated as causes of anaphylaxis but this has mostly been limited to parasites. While viral infections have been documented as causes of urticarial rashes, anaphylaxis due to viral infection has only been reported once, in an adult patient. There have not been any reports of anaphylaxis related to influenza infections. Early recognition and treatment of patients with influenza may prevent progression of systemic allergic reactions. [Full article available at http://rimed.org/rimedicaljournal-2017-11.asp]</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 2327-2228 (Electronic)IS - 0363-7913 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29088573">PM:29088573</url></web-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171031, Chow EJ</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86492</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Egri Bosnyakne,H.</style></author><author><style face="normal" font="default"> Kerepesi,I.</style></author><author><style face="normal" font="default"> Keszthelyi,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Adverse effect of two-spotted spider mite (Tetranychus urticae Koch) on soybean protein composition</style></title><secondary-title><style face="normal" font="default">Acta Aliment</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Acta Aliment</style></full-title></periodical><pages end="360" start="355">355-360</pages><volume><style face="normal" font="default">46</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="8" Month="8" Year="2017">2017/8/8</year><pub-dates><date Day="14" Month="11" Year="2017">2017/11/14</date></pub-dates></dates><publisher><style face="normal" font="default">Akad+®miai Kiad+¦</style></publisher><isbn><style face="normal" font="default">0139-3006</style></isbn><abstract><style face="normal" font="default">Damage induced on soybean by Tetranychus urticae Koch (Acari: Tetranychidae) is easily recognizable. We were curious to know whether, in addition to this visual and quantitative damage, change occurs also in the nutritional value of the harvested product. The Weendei analysis showed that as compared to the healthy items, the protein content (P=0.048) of the miteinjured seeds as well as their composition (P=0.048) has changed. No significant changes in the raw fat content could be confirmed by the statistical results of the study (P=0.643). Concerning the contents of raw ash (P=0.069) and raw fibre (P=0.859), there were no significant differences. Three distinct changes in protein structure were confirmed by gel electrophoresis. Substantially less 69 kDa protein was detectable in the infested soybean, whereas no 48 kDa protein was present in the control sample; it only appeared in the infested ones. There was a higher amount of 30 kDa protein in the infested stock. In summary, alteration in the protein structure was caused by T. urticae, and changes were triggered in the protein content of the affected soybean plants. The protein structure-change in damaged soybean items caused further decline in the feed consuming capacity of farm animals</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Hungary -</style></notes><work-type><style face="normal" font="default">10.1556/066.2017.46.3.11</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1556/066.2017.46.3.11</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Aliment\2017-46-355-60.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Aliment\2017-46-355-60.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Egri Bosnyakne H</style></custom2><misc3><style face="normal" font="default">10.1556/066.2017.46.3.11</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87290</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Guo,H.</style></author><author><style face="normal" font="default"> Huang,S.</style></author><author><style face="normal" font="default"> Chen,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Environmental Science and Engineering, Fudan University, Shanghai 200032, China.</style></auth-address><titles><title><style face="normal" font="default">Air pollutants and asthma patient visits: Indication of source influence</style></title><secondary-title><style face="normal" font="default">Sci Total Environ</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Total Environ</style></abbr-1></periodical><pages end="362" start="355">355-362</pages><volume><style face="normal" font="default">625</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">BACKGROUND: Sources of air pollutants are significant factors for adverse health effect. Few current studies explored the linking of sources influence and ambient pollutants to asthma patient visits in Shanghai, China. OBJECTIVES: This study explored the associations between short-term exposures to ambient pollutants and asthma morbidity with terrestrial and marine source influence in Shanghai. METHODS: Generalized additive model (GAM) was used to explore the association of daily patient visits and ambient pollutants. These analyses were calculated in R statistical software in mgcv package. PSCF modeling was used to locate potential source areas contributing to the concentrations of pollutants. RESULTS: We found that per IQR of PM2.5, PM10, NO2, SO2, O3 and CO in terrestrial source were associated with an increase of 6.63% (95% CI: -0.27% to 14%), 6.48% (95% CI: 0.06% to 13.3%), 1.68% (95% CI: -2.68% to 6.24%), 2.81% (95% CI: -1.42% to 7.22%), -0.60% (95% CI: -5.94% to 5.04%) and 16.6% (95% CI: 8.68% to 25.2%), respectively in asthma patient visits. Per IQR of PM2.5, PM10, NO2, SO2, O3 and CO in marine source were associated with an increase of 5.34% (95% CI: 0.42% to 10.5%), 3.84% (95% CI: 0.08% to 7.74%), 3.21% (95% CI: -0.92% to 7.52%), 2.58% (95% CI: -1.02% to 6.30%), 1.42% (95% CI: -3.10% to 6.15%) and 8.81% (95% CI: 2.56% to 15.4%). The PSCF show all of the pollutants except O3 mainly come from terrestrial during observation. We also found that all of the pollutants except NO2 displayed the highest effect in the spring for relative risk of asthma morbidity. CONCLUSIONS: Ambient air pollutants that cause an increase in asthma patient visits, such as PM2.5, PM10, NO2, SO2 and CO are mainly produced from terrestrial sources, while O3 is primarily from marine sources. The association of ambient pollutants and asthma patient visits is closely related with seasons, especially with spring. PM2.5 and CO are major air pollutants increasing the relative risk of asthma patient visits in Shanghai</style></abstract><notes><style face="normal" font="default">IS - 1879-1026 (Electronic)IS - 0048-9697 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.scitotenv.2017.12.298</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29289783">PM:29289783</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Total Environ\2017-625-355-62.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Total Environ\2017-625-355-62.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Guo H</style></custom2><misc3><style face="normal" font="default">10.1016/j.scitotenv.2017.12.298</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86698</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pineda,F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Diater Laboratorios, Madrid, Spain.</style></auth-address><titles><title><style face="normal" font="default">The future of immunotherapy with individual allergens: Immunotherapy with fungi</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="38" start="36">36-38</pages><volume><style face="normal" font="default">45</style></volume><number><style face="normal" font="default">1S</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29129403">PM:29129403</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-36-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-36-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Pineda F</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87163</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Manso,L.</style></author><author><style face="normal" font="default"> Pineda,R.</style></author><author><style face="normal" font="default"> Huertas,B.</style></author><author><style face="normal" font="default"> Fernandez-Rivas,M.</style></author><author><style face="normal" font="default"> Dieguez,M.C.</style></author><author><style face="normal" font="default"> Cerecedo,I.</style></author><author><style face="normal" font="default"> Muriel,A.</style></author><author><style face="normal" font="default"> Fernandez,F.B.</style></author><author><style face="normal" font="default"> DunnGalvin,A.</style></author><author><style face="normal" font="default"> Antolin-Amerigo,D.</style></author><author><style face="normal" font="default"> De la Hoz,B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Seccion de Alergologia, Hospital Universitario del Sureste, Arganda del Rey (Madrid), Spain</style></auth-address><titles><title><style face="normal" font="default">Validation of the Spanish Version of the Food Allergy Quality of Life Questionnaire-Parent Form (S-FAQLQ-PF)</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="369" start="363">363-369</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: Food allergy is an emerging health problem. Several questionnaires can be used to establish health-related quality of life (HRQOL) in food allergy patients. Current questionnaires should be translated in such a way that they take account of the culture of the country in which they are to be used. Objective: To translate and perform a cross-sectional validation of the Food Allergy Quality of Life Questionnaire-Parent Form (FAQLQ-PF). METHODS: The parents of 54 children diagnosed with food allergy were recruited to assess the Spanish version of the FAQLQ-PF (S-FQLQ-PF). RESULTS: The S-FQLQ-PF was translated into Spanish according to WHO guidelines (including a forward-backward translation). The statistical analysis showed that feasibility, reliability, and internal consistency were very good for the global S-FAQLQ-PF score and for the different domains. Assessment of construct validity indicated that S-FAQLQ-PF has reduced capacity for measurement of HRQOL in younger children. Cross-sectional validation of the S-FAQLQ-PF demonstrated that HRQOL of a Spanish pediatric population was affected by patient age, severity of symptoms, and number of reactions. HRQOL was not affected by sex, food implicated, number of foods implicated, ingestion of the implicated food, or presence of anaphylaxis. CONCLUSIONS: Translation into Spanish and cultural validation of the FAQLQ-PF demonstrated the influence of factors, such as patient age, severity of symptoms, and number of reactions on the HRQOL of a pediatric Spanish population</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0182</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28656900">PM:28656900</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-363-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-363-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Manso L</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0182</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86966</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Abou-Hamdan,M.</style></author><author><style face="normal" font="default"> Gharib,B.</style></author><author><style face="normal" font="default"> Bajenoff,M.</style></author><author><style face="normal" font="default"> Julia,V.</style></author><author><style face="normal" font="default"> de Reggi,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">CNRS, NICN UMR 7259, Aix Marseille University, Marseille, France</style></auth-address><titles><title><style face="normal" font="default">Pantethine Down-Regulates Leukocyte Recruitment and Inflammatory Parameters in a Mouse Model of Allergic Airway Inflammation</style></title><secondary-title><style face="normal" font="default">Med Sci Monit Basic Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Med Sci Monit Basic Res</style></abbr-1></periodical><pages end="372" start="368">368-372</pages><volume><style face="normal" font="default">23</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="27" Month="11" Year="2017">2017/11/27</year></dates><abstract><style face="normal" font="default">BACKGROUND Migration of leukocytes into airways is the hallmark of allergic asthma. The aim of this study was to target the pathological process using pantethine, a pleiotropic natural compound which has been recently shown to down-regulate chemokine-driven T cell migration. MATERIAL AND METHODS Mice were sensitized to the Leishmania LACK antigen, then treated or not treated with pantethine and exposed to LACK or saline aerosol. After sacrifice of the animals, cells in the bronchoalveolar lavage were analyzed and inflammatory parameters were determined to evaluate inflammation seriousness. RESULTS As compared to untreated animals, pantethine-treated animals displayed a moderated response to the allergen, as documented by decreased infiltration of inflammatory cells (all types), in addition to reduced levels of lung Th2 cytokines and circulating LACK-specific IgE. CONCLUSIONS These data reveal the potential therapeutic importance of pantethine to moderate allergic asthma pathology. The compound has been previously shown to exert a broad range of protective activity in animals and in humans, with few or no adverse effects</style></abstract><notes><style face="normal" font="default">IS - 2325-4416 (Electronic)IS - 2325-4394 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.12659/MSMBR.904077</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29176546">PM:29176546</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Med Sci Monit Basic Res\2017-23-368-72.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Med Sci Monit Basic Res\2017-23-368-72.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171127, Abou-Hamdan M</style></custom2><misc3><style face="normal" font="default">10.12659/MSMBR.904077</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86495</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mocsai,R.T.</style></author><author><style face="normal" font="default"> Maczo,A.</style></author><author><style face="normal" font="default"> Grunwald-Gruber,C.</style></author><author><style face="normal" font="default"> Majer-Baranyi,K.</style></author><author><style face="normal" font="default"> Adanyi,N.</style></author><author><style face="normal" font="default"> Milotay,P.</style></author><author><style face="normal" font="default"> Czelecz,J.</style></author><author><style face="normal" font="default"> Tmoskozi-Farkas,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">Investigation of allergen proteins in five tomato cultivars</style></title><secondary-title><style face="normal" font="default">Acta Aliment</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Acta Aliment</style></full-title></periodical><pages end="377" start="369">369-377</pages><volume><style face="normal" font="default">46</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="8" Month="8" Year="2017">2017/8/8</year><pub-dates><date Day="14" Month="11" Year="2017">2017/11/14</date></pub-dates></dates><publisher><style face="normal" font="default">Akad+®miai Kiad+¦</style></publisher><isbn><style face="normal" font="default">0139-3006</style></isbn><abstract><style face="normal" font="default">Investigation of putative allergens from tomato berries is challenging as differences between human serum IgE specificity and reactivity as well as the non-specific binding of the primary and secondary antibodies often cause difficulties. In this study five tomato cultivars were investigated to evaluate their potential allergenicity in Hungarian tomato sensitive patients. The major allergens proved to be low molecular weight proteins, but several previously described allergens could be identified as well using IgE-Western blotting. IgE binding to cross-reactive carbohydrate determinants (CCDs) was ruled out through the use of CCD inhibitor, but non-specific binding of the secondary antibody remained an issue. IgE binding activity of a purified, immunoblot positive protein (band at 40 kDa), and non-specific binding of the secondary antibody to the same protein, was demonstrated with an Optical Waveguide Lightmode Spectroscopy (OWLS) based immunosensor. LC-ESI-MS/MS analysis showed this protein is an as-yet undescribed vicilin-type putative allergen</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Hungary -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.1556/066.2017.46.3.13</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1556/066.2017.46.3.13</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Acta Aliment\2017-46-369-77.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Acta Aliment\2017-46-369-77.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Mocsai RT</style></custom2><misc3><style face="normal" font="default">10.1556/066.2017.46.3.13</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87020</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zernotti,M.E.</style></author><author><style face="normal" font="default"> Pawankar,R.</style></author><author><style face="normal" font="default"> Ansotegui,I.</style></author><author><style face="normal" font="default"> Badellino,H.</style></author><author><style face="normal" font="default"> Croce,J.S.</style></author><author><style face="normal" font="default"> Hossny,E.</style></author><author><style face="normal" font="default"> Ebisawa,M.</style></author><author><style face="normal" font="default"> Rosario,N.</style></author><author><style face="normal" font="default"> Sanchez Borges,M.</style></author><author><style face="normal" font="default"> Zhang,Y.</style></author><author><style face="normal" font="default"> Zhang,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology, Catholic University of Cordoba, Cordoba, Argentina.</style></auth-address><titles><title><style face="normal" font="default">Otitis media with effusion and atopy: is there a causal relationship?</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="37">37-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Otitis Media with Effusion (OME) is an inflammatory condition of the middle ear cleft, acute or chronic, with collection of fluid in the middle ear with an intact tympanic membrane. It is a very common disease in childhood, the most frequent cause of hearing loss in childhood and often requiring surgery. OME is called chronic when the fluid in the middle ear persists for more than three months or when the episodes recur six or more times in one year. The current article covers various aspects of OME including definition, epidemiology. Pathomechanisms, risk factors, role of allergy in OME, impact of upper airway disease on OME, eosinophilic otitis media and management of OME</style></abstract><notes><style face="normal" font="default">IS - 1939-4551 (Print)IS - 1939-4551 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Argentina -CO - Egypt -CO - Japan -CO - Venezuela -CO - China -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0168-x</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29158869">PM:29158869</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\20171114-ZernottiME.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\20171114-ZernottiME.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Zernotti ME</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0168-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86571</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Singh,S.</style></author><author><style face="normal" font="default"> Bajaj,B.K.</style></author></authors></contributors><titles><title><style face="normal" font="default">Potential application spectrum of microbial proteases for clean and green industrial production</style></title><secondary-title><style face="normal" font="default">Energ Ecol Environ</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Energ Ecol Environ</style></full-title></periodical><pages end="386" start="370">370-386</pages><volume><style face="normal" font="default">2</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2363-8338</style></isbn><abstract><style face="normal" font="default">Enzymes are the cornerstones of metabolism and constitute the fundamental basis for existence of life. However, recently enzymes are being implicated in diverse industrial processes because of their specific and fast action for efficient bioconversion of substrate to product, and their capability to save raw materials, energy and chemicals for various manufacturing processes. Enzymes are considered as environment-friendly (green) chemicals that may potentially help replacing completely or reducing the usage of hazardous chemicals for industrial processes, thus promising sustainable production and manufacturing. Among various industrial enzymes microbial proteases dominate the world enzyme market due to their multifaceted application potential in varied bioindustries like food, pharmaceutical, textile, photographic, leather and detergent. Promising applications of proteases in agricultural sector for instance may include biocontrol of pests, degumming of silk, selective delignification of hemp and wool processing. However, for successful industrial applications the proteases must be robust enough to suit the process conditions which are generally hostile. Proteases intended for industrial applications must have activity and stability over wide range of temperature and pH extremes for prolonged time periods and even in the presence of various potential enzyme inhibitors. Of various microbial proteases those from Bacillus spp. have got special significance because the latter are known for their ability to produce sturdy enzymes that might have suitability for industrial process conditions. The current article presents an interpretive summary of the recent developments on application potential of proteases for various industries</style></abstract><notes><style face="normal" font="default">LA - ENGCO - India -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1007/s40974-017-0076-5</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40974-017-0076-5</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Energ Ecol Environ\2017-2-370-86.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Energ Ecol Environ\2017-2-370-86.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Singh S</style></custom2><misc3><style face="normal" font="default">10.1007/s40974-017-0076-5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86709</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Azar,A.</style></author><author><style face="normal" font="default"> Rank,M.A.</style></author><author><style face="normal" font="default"> Zarka,M.A.</style></author><author><style face="normal" font="default"> Chang,Y.H.</style></author><author><style face="normal" font="default"> Lal,D.</style></author></authors></contributors><titles><title><style face="normal" font="default">Gender-specific differences in serum immunoglobulin E levels and prevalence of fungus in sinonasal tissue noted in patients with chronic rhinosinusitis who underwent endoscopic sinus surgery</style></title><secondary-title><style face="normal" font="default">Am J Rhinol Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Rhinol Allergy</style></abbr-1></periodical><pages end="375" start="370">370-375</pages><volume><style face="normal" font="default">31</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="1" Month="11" Year="2017">2017/11/1</year></dates><abstract><style face="normal" font="default">BACKGROUND: We previously presented that women with chronic rhinosinusitis (CRS) who elected endoscopic sinus surgery (ESS) have a higher symptom burden than men. Causes of these gender-based differences warranted further study. OBJECTIVES: To study gender differences in another cohort of adult patients with CRS who underwent ESS and to compare key histopathologic and serologic features Methods: Patients with CRS who underwent ESS (from 2011 to 2014) with structured histopathology reports on surgical samples were studied. The 13-item structured histopathology report detailed key metrics of inflammation and the presence of fungal elements. Clinical, 22-item Sino-Nasal Outcome Test (SNOT-22) score, Lund-Mackay computed tomography (CT) score, serologic (immunoglobulin E [IgE] level, absolute eosinophil count) and histopathologic data were compared between male and female patients by using statistical software. RESULTS: We studied 130 eligible subjects (mean age, 54.7 years; 49.2% women). Compared with the men, the women had significantly higher preoperative SNOT-22 scores (women, 48.7; men 38.0 [p = 0.004]) but similar CT scores. Serum IgE levels were significantly higher among women versus men (peak, 433.3 versus 190.8 kU/L [p = 0.03]; closest to surgery, 435.0 versus 190.8 kU/L [p = 0.03]). Tissue fungal elements were significantly more prevalent in women versus men (19.0 versus 5.2%; p = 0.02). Up to this point, the analysis was agnostic of clinical details of the subjects. Further analysis was conducted regarding clinical features. Allergic fungal sinusitis (AFS) was found significantly more commonly in the female versus male patients (21.9 versus 9.1%; p = 0.04). Women versus men had a higher prevalence of migraine (19.4 versus 4.6%; p = 0.01) or any primary headache disorders (23.0 versus 6.2%; p = 0.007). CONCLUSION: Women who underwent ESS for CRS had higher SNOT-22 symptom burden. Worsened symptomatology may be secondary to a higher prevalence of primary headache disorders in women. However, surgeons should also be aware that female patients with CRS who seek ESS may have a higher prevalence of severe disease endotypes (more tissue fungal elements, elevated serum IgE levels) and phenotypes</style></abstract><notes><style face="normal" font="default">DA - 20171110IS - 1945-8932 (Electronic)IS - 1945-8932 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.2500/ajra.2017.31.4471</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29122081">PM:29122081</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto - MedLine</url></related-urls></urls><custom2><style face="normal" font="default">20171110, Azar A</style></custom2><misc3><style face="normal" font="default">10.2500/ajra.2017.31.4471</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87167</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Aeberhard,J.</style></author><author><style face="normal" font="default"> Haeberli,G.</style></author><author><style face="normal" font="default"> Muller,U.R.</style></author><author><style face="normal" font="default"> Helbling,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit Zieglerspital, Clinic of Internal Medicine, Spital Netz Bern AG, Bern, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Specific Immunotherapy in Hymenoptera Venom Allergy and Concomitant Malignancy: A Retrospective Follow-up Focusing on Effectiveness and Safety</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="377" start="370">370-377</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: Malignancies are often considered a contraindication for allergen-specific immunotherapy. Consequently, patients with severe Hymenoptera venom allergy and cancer require specific care. The aim of this retrospective study was to assess patients with Hymenoptera venom allergy and cancer undergoing venom immunotherapy (VIT). METHODS: The study population comprised all patients referred for evaluation of Hymenoptera venom allergy or for a routine check-up during VIT from January 1, 2004 to December 31, 2008. RESULTS: Of the patients assessed, 2% (51 of 2594) had a documented Hymenoptera venom allergy and cancer (25 female, 26 male; mean age 58 years). Of these, 42 patients received VIT (82%): 25 patients had a previously diagnosed malignancy, 16 were diagnosed with malignancy during VIT, and 1 patient was diagnosed with cancer after completion of VIT. The most frequent type of tumor was breast cancer in female patients (60%) and prostate cancer in male patients (39%). Systemic allergic reactions during VIT were recorded in 7% of patients. A total of 19 patients experienced a field sting or underwent a sting challenge test during VIT: 95% tolerated the sting well. VIT was halted definitively in 9 patients (new diagnosis of cancer in 7 patients, reactivation of cancer in 1, and progressive polyneuropathy in 1). CONCLUSIONS: The effectiveness and adverse effects of VIT in patients with Hymenoptera venom allergy and cancer in remission are comparable to those of patients without malignancy. Our findings show that patients with Hymenoptera venom allergy and cancer are eligible for VIT</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0184</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28675375">PM:28675375</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-370-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-370-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Aeberhard J</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0184</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87342</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mihos,F.</style></author><author><style face="normal" font="default"> Pereira,P.R.</style></author><author><style face="normal" font="default"> Matos de Almeida,A.B.</style></author><author><style face="normal" font="default"> Velloso Mergh,C.</style></author><author><style face="normal" font="default"> Queiroz da Cruz,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Study of protein profile and immunochemical reactivity for extracts of D. farinae, D. pteronyssinus and B. tropicalis mites in the city of Rio de Janeiro, Brazil</style></title><secondary-title><style face="normal" font="default">Braz J Allergy Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Braz J Allergy Immunol</style></full-title></periodical><pages end="386" start="379">379-386</pages><volume><style face="normal" font="default">1</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Mites</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Objective: In tropical countries like Brazil, the mapping of proteinconstituents of mite extracts becomes relevant in the contextof therapeutic evaluations of respiratory allergic diseases. Inaddition, this allows to set up an internal national database of thepopulation's sensitization profile. Extracts are complex mixturescontaining different proportions of biological materials, and thedetermination of their protein profile is necessary for an improvedperformance in diagnosis and therapy. Therefore, in this study, weused electrophoresis to characterize the protein constituents of B.tropicalis, D. farinae and D. pteronyssinus extracts, and evaluatedthe reactivity of specific immunoglobulins from atopic volunteersfrom the city of Rio de Janeiro, Brazil. Methods: Samples of theextracts were subjected to precipitation with acetone and appliedto polyacrylamide gel 12.5%. After the electrophoretic run, sampleswere transferred to a 0.45 µm nitrocellulose membrane, followedby incubation with the serum pool. Bands related to antigen-antibody reactivity were obtained by the colorimetric method,using peroxidase conjugated to secondary antibody. Results:The results obtained showed that protein precipitation favoredthe visualization of bands in the polyacrylamide gel; homogeneitywas evidenced by experiment reproducibility and low standarddeviation values. With regard to electrophoretic profile, the extractsshowed specific proteins in their composition, with positivereactivity to the immunochemical test. Conclusion: One mayinfer that mite extracts in Brazil present different allergens whencompared to extracts described in the American and Europeanliterature, warranting the development of new, specific criteria forextract standardization.</style></abstract><notes><style face="normal" font="default">LA - PORCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.5935/2526-5393.20170056</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5935/2526-5393.20170056</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Braz J Allergy Immunol\2017-1-379-86.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Braz J Allergy Immunol\2017-1-379-86.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Mihos F</style></custom2><misc3><style face="normal" font="default">10.5935/2526-5393.20170056</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86557</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Incorvaia,C.</style></author><author><style face="normal" font="default"> Fuiano,N.</style></author><author><style face="normal" font="default"> Martignago,I.</style></author><author><style face="normal" font="default"> Gritti,B.L.</style></author><author><style face="normal" font="default"> Ridolo,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Cardiac/Pulmonary Rehabilitation, ASST Pini/CTO, Milan, Italy</style></auth-address><titles><title><style face="normal" font="default">Local allergic rhinitis: evolution of concepts</style></title><secondary-title><style face="normal" font="default">Clin Transl Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Transl Allergy</style></abbr-1></periodical><pages end="" start="38">38-</pages><volume><style face="normal" font="default">7</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The discovery of an exclusive local production of IgE antibodies dates back to the 1970s, but only recently the pathophysiology of such phenomenon was deeply investigated, leading to the concept of local allergic rhinitis (LAR). Currently, LAR is defined by the occurrence, in patients with symptoms clearly suggesting allergic rhinitis but with negative results to common allergy testing, of allergen specific IgE in the nasal mucosa. Most studies investigating LAR were based on the development of rhinitis symptoms following nasal provocation test (NPT) with the suspected allergens, but such test may be performed by a number of options, none of them being as yet acknowledged and recommended in consensus document. On the other hand, also the mere detection of IgE in the nasal mucosa indicates, as for IgE measurement in blood or other tissues, allergic sensitization but cannot give the certainty of clinical allergy. Therefore, the combination of IgE detection in nasal mucosa and a positive result of NPT should be used to diagnose LAR. Recent data on the use for in vitro testing of molecular allergy diagnostics in place of whole allergen extracts suggest that this method could improve the sensitivity and specificity of laboratory tests, and an appraisal of the basophil activation test as a third level technique, to be implemented when the results of local IgE testing and NPT are uncertain, is currently ongoing</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 2045-7022 (Print)IS - 2045-7022 (Linking)LA - engPT - EditorialCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1186/s13601-017-0174-7</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29118971">PM:29118971</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-38.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-38.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Incorvaia C</style></custom2><misc3><style face="normal" font="default">10.1186/s13601-017-0174-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86949</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xiong,L.</style></author><author><style face="normal" font="default"> Wang,Y.</style></author><author><style face="normal" font="default"> Gong,X.</style></author><author><style face="normal" font="default"> Chen,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan II Road, Guangzhou, 510080, People's Republic of China</style></auth-address><titles><title><style face="normal" font="default">Prevalence of lactose intolerance in patients with diarrhea-predominant irritable bowel syndrome: data from a tertiary center in southern China</style></title><secondary-title><style face="normal" font="default">J Health Popul Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Health Popul Nutr</style></abbr-1></periodical><pages end="" start="38">38-</pages><volume><style face="normal" font="default">36</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">methods</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">BACKGROUND: Symptoms associated with lactose intolerance (LI) and diarrhea-predominant irritable bowel syndrome (IBS-D) are almost the same. These disease entities are difficult to differentiate clinically. In practice, differential diagnosis depends on self-reported patient milk intolerance. However, there is limited data on the prevalence of LI in China. The aim of this study was to investigate the prevalence of LI in IBS-D patients and asymptomatic healthy controls. METHODS: Lactose malabsorption (LM) was diagnosed by a lactose hydrogen breath test (HBT) and was defined by peak breath H2 excretion over the baseline level of >/= 20 ppm. LI-related symptoms were monitored for 8 h following lactose administration. LI was defined in LM patients with positive symptoms during the observation time. Patients with IBS-D were additionally asked if they were intolerant to milk. RESULTS: A total of 109 eligible IBS-D patients (Rome III criteria) and 50 healthy controls were enrolled in this study. Except for hydrogen non-producers, the prevalence of LM did not differ between IBS-D patients and the control group (85%, 82/96 vs 72%, 34/47; P = 0.061). There was, however, a higher LI prevalence in IBS patients than in healthy subjects (45%, 43/96 vs 17%, 8/47; P = 0.002). Sensitivity, specificity, and positive and negative predictive values of self-reported milk intolerance for detecting LI were 58, 58, 53, and 63%, respectively. CONCLUSIONS: Prevalence of LI is significantly higher in IBS-D patients than in healthy subjects. Self-reported milk intolerance is a poor diagnostic predictor of LI</style></abstract><notes><style face="normal" font="default">IS - 2072-1315 (Electronic)IS - 1606-0997 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1186/s41043-017-0113-1</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29157302">PM:29157302</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Health Popul Nutr\2017-36-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Health Popul Nutr\2017-36-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Xiong L</style></custom2><misc3><style face="normal" font="default">10.1186/s41043-017-0113-1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87164</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Akashi,M.</style></author><author><style face="normal" font="default"> Sato,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Saitama City Hospital, Saitama, Japan</style></auth-address><titles><title><style face="normal" font="default">Food Protein-Induced Enterocolitis Syndrome in Response to Quail's Egg in a Child Without Hen's Egg Allergy</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="382" start="381">381-382</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0190</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29199963">PM:29199963</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Akashi M</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0190</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87161</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nucera,E.</style></author><author><style face="normal" font="default"> Basta,F.</style></author><author><style face="normal" font="default"> Buonomo,A.</style></author><author><style face="normal" font="default"> Mezzacappa,S.</style></author><author><style face="normal" font="default"> Margiotta,D.P.</style></author><author><style face="normal" font="default"> Antonelli Incalzi,R.</style></author><author><style face="normal" font="default"> Schiavino,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Unit, Universita Cattolica del Sacro Cuore - Policlinico "A. Gemelli", Rome, Italy</style></auth-address><titles><title><style face="normal" font="default">A Case of Hypocomplementemic Urticarial Vasculitis Syndrome Successfully Treated With Omalizumab</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="384" start="382">382-384</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0191</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29199964">PM:29199964</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Nucera E</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0191</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86687</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,W.</style></author><author><style face="normal" font="default"> Yao,B.</style></author><author><style face="normal" font="default"> Cheng,H.M.</style></author><author><style face="normal" font="default"> Meng,F.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">The Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang 330006, China</style></auth-address><titles><title><style face="normal" font="default">[Study on Cellular Immunity Mechanisms of Suspended Moxibustion for Treating Neutrophilic Asthma in Rats]</style></title><secondary-title><style face="normal" font="default">Zhen Ci Yan Jiu</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Zhen Ci Yan Jiu</style></abbr-1></periodical><pages end="390" start="384">384-390</pages><volume><style face="normal" font="default">42</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="25" Month="10" Year="2017">2017/10/25</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To observe the influence of suspended moxibustion on neutrophilic asthma related signal factors in asthma rats. METHODS: Thirty-two SD rats were randomly divided into normal control, model, dexamethasone(DEX) and suspended moxibustion (MOX) groups, with 8 rats in each group. The neutrophil granulocyte asthma model was made by intranasal instillation of lipopolysaccharide (LPS), intraperitoneal injection of ovalbumin(OVA) and inhalation of OVA, once a day for 14 d. After modeling, rats of the DEX group received intraperitoneal injection of DEX (0.5 mg/kg), once daily for 14 d, and those of the MOX group treated by suspended MOX at "Danzhong" (CV 17), and bilateral "Feishu" (BL 13), "Pishu" (BL 20), and "Shen-shu" (BL 23) for 40 min, once a day, for 14 d. The total number of leukocytes and Wright's stain-displayed differential counts in the bronchoalveolar lavage fluid (BALF) were counted, and the content of IL-17 in the BALF was assayed by ELISA. The contents of T-helper 17 (Th 17) cells in the spleen and peripheral blood were detected using flow cytometry, and the expression of retinoic acid-related orphan receptor gamma t (ROR-gammat) mRNA and protein in the inferior lobe of the right lung were detected by quantitative real-time PCR, immunohistochemical stain and Western blot, respectively. RESULTS: Compared with the normal control group, the total number of leukocytes, the percentages of neutrophils, eosinophilis and lymphcytes and IL-17 content in the BALF, and Th 17 contents in the peripheral blood and spleen tissue were significantly increased in the model group (P&lt;0.01). After the treatment, the total numbers of leukocytes, the percentages of neutrophils, eosinophils and lymphocytes and IL-17 contents in the BALF, and Th 17 contents in the peripheral blood and spleen tissues were down-regulated considerably in both the DEX and MOX groups (P&lt;0.05, P&lt;0.01). Immunohistochemical stain, real-time PCR and Western blot measurements showed that the expression levels of ROR-gammat protein and mRNA in the lung tissues were notably higher in the model group than in the normal control group (P&lt;0.01), and significantly down-regulated in both DEX and MOX groups relevant to the model group (P&lt;0.05, P&lt;0.01). No significant differences were found between the DEX and MOX groups in all the aforementioned indexes (P&lt;0.05), except plasma Th 17 (P&lt;0.05). CONCLUSIONS: Suspended moxibustion, being comparable to DEX treatment, can reduce the inflammatory reactions of neutrophilic asthma rats by down-regulating the expression of ROR -gammat in the lung, and lowering IL-17 and neutrophils levels in the airway, and Th 17 in the peripheral blood and spleen</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1000-0607 (Print)IS - 1000-0607 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29105464">PM:29105464</url></web-urls></urls><custom2><style face="normal" font="default">20171106, Zhang W</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87160</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Alves,C.</style></author><author><style face="normal" font="default"> Afonso,I.</style></author><author><style face="normal" font="default"> Leiria-Pinto,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Dona Estefania Hospital, Immunoallergology department, Centro Hospitalar de Lisboa Central, Lisbon, PortugalDona Estefania Hospital, Pediatric Gastroenterology Department, Centro Hospitalar de Lisboa Central, Lisbon, PortugalCEDOC, Respiratory Research Group, Nova Medical School, Lisbon, Portugal</style></auth-address><titles><title><style face="normal" font="default">Is Saccharomyces boulardii Really Safe?</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="386" start="384">384-386</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Portugal -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0194</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29199965">PM:29199965</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Alves C</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0194</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87165</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Larco-Rojas,X.</style></author><author><style face="normal" font="default"> Gonzalez-Gutierrez,M.L.</style></author><author><style face="normal" font="default"> Vazquez-Cortes,S.</style></author><author><style face="normal" font="default"> Bartolome,B.</style></author><author><style face="normal" font="default"> Pastor-Vargas,C.</style></author><author><style face="normal" font="default"> Fernandez-Rivas,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Allergy Department, Hospital Clinico San Carlos, IdISSC, Madrid, SpainR+D Department, Roxall, Bilbao, SpainImmunology Department, IIS-Fundacion Jimenez Diaz, UAM, Madrid, SpainAllergy Department, Hospital Clinico San Carlos, IdISSC, Madrid, Spain</style></auth-address><titles><title><style face="normal" font="default">Occupational Asthma and Urticaria in a Fishmonger Due to Creatine Kinase, a Cross-Reactive Fish Allergen</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="388" start="386">386-388</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Fish allergen</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0195</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29199966">PM:29199966</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Larco-Rojas X</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0195</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87166</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sposato,B.</style></author><author><style face="normal" font="default"> Scalese,M.</style></author><author><style face="normal" font="default"> Milanese,M.</style></author><author><style face="normal" font="default"> Masieri,S.</style></author><author><style face="normal" font="default"> Cavaliere,C.</style></author><author><style face="normal" font="default"> Latorre,M.</style></author><author><style face="normal" font="default"> Scichilone,N.</style></author><author><style face="normal" font="default"> Matucci,A.</style></author><author><style face="normal" font="default"> Vultaggio,A.</style></author><author><style face="normal" font="default"> Ricci,A.</style></author><author><style face="normal" font="default"> Cresti,A.</style></author><author><style face="normal" font="default"> Paggiaro,P.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pneumology Department, Misericordia Hospital, Grosseto, Italy</style></auth-address><titles><title><style face="normal" font="default">Different Skin Prick Test Sensitization Patterns Do Not Influence the Response to Omalizumab in Severe Asthma</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="391" start="388">388-391</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0196</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29199967">PM:29199967</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Sposato B</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0196</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86694</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Juesas,C.R.</style></author><author><style face="normal" font="default"> Aguilar,C.M.</style></author><author><style face="normal" font="default"> Vieths,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Hospital de Sagunto, Valencia, Spain.</style></auth-address><titles><title><style face="normal" font="default">New routes of allergen immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="40" start="39">39-40</pages><volume><style face="normal" font="default">45</style></volume><number><style face="normal" font="default">1S</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Immunotherapy</style></keyword></keywords><dates><year Day="9" Month="11" Year="2017">2017/11/9</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" 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font="default"> Fiocchi,A.</style></author><author><style face="normal" font="default"> Pecora,V.</style></author><author><style face="normal" font="default"> Valentini,D.</style></author><author><style face="normal" font="default"> Mennini,M.</style></author><author><style face="normal" font="default"> Dahdah,L.</style></author><author><style face="normal" font="default"> Mazzina,O.</style></author><author><style face="normal" font="default"> Santamaria,F.</style></author><author><style face="normal" font="default"> Valluzzi,R.</style></author><author><style face="normal" font="default"> Mukherjee,A.</style></author><author><style face="normal" font="default"> Kandhare,A.</style></author><author><style face="normal" font="default"> Bodhankar,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Proceedings of the 2017 WAO Symposium on Hot Topics in Allergy: Pediatric &amp; Regulatory Aspects</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="39">39-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">S2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENG</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0170-3</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0170-3</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10S2-39.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10S2-39.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Traina G</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0170-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87162</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ceballos,M.</style></author><author><style face="normal" font="default"> De Castro,C.</style></author><author><style face="normal" font="default"> Fonseca,G.M.</style></author><author><style face="normal" font="default"> Postigo,I.</style></author><author><style face="normal" font="default"> Martinez,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immunology, Microbiology and Parasitology, Faculty of Pharmacy and Laboratory of Parasitology and Allergy, LascarayAllergy Department, ADESLAS Medical Center, Cordoba, SpainDepartment of Immunology, Microbiology and Parasitology, Faculty of Pharmacy and Laboratory of Parasitology and Allergy, LascarayDepartment of Immunology, Microbiology and Parasitology, Faculty of Pharmacy and Laboratory of Parasitology and Allergy, Lascaray</style></auth-address><titles><title><style face="normal" font="default">IgE-Binding Aldolases From Artemia and Mysis Species Causing Respiratory Allergy to Aquarium Fish Food</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="393" start="391">391-393</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0198</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29199968">PM:29199968</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-378-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Ceballos M</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0198</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87396</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bartuzi,Z.</style></author><author><style face="normal" font="default"> Kaczmarski,M.</style></author><author><style face="normal" font="default"> Czerwionka-Szaflarska,M.</style></author><author><style face="normal" font="default"> Malaczynska,T.</style></author><author><style face="normal" font="default"> Krogulska,A.</style></author></authors></contributors><titles><title><style face="normal" font="default">The diagnosis and management of food allergies. Position paper of the Food Allergy Section the Polish Society of Allergology</style></title><secondary-title><style face="normal" font="default">Postepy Dermatol Alergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Postepy Dermatol Alergol</style></abbr-1></periodical><pages end="404" start="391">391-404</pages><volume><style face="normal" font="default">34</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1642-395X</style></isbn><abstract><style face="normal" font="default">The paper concerns the current position of the Polish Society of Allergology Food Allergy Section on the diagnosis and management of food allergies. The aim of this position is to provide evidence-based recommendations on the diagnosis and management of patients with allergic hypersensitivity to foods. This position statement includes a systematic review of studies in three areas, namely, the epidemiology, diagnosis and management of food allergies. While taking into account the specific Polish setting, in this publication we also used the current European Academy of Allergy and Clinical Immunology (EAACI) position paper and other current position statements, including those of the United States National Institute of Allergy and Infectious Diseases (NIAID)</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.5114/ada.2017.71104</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5114/ada.2017.71104</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-391-404.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-391-404.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171021, Bartuzi Z</style></custom2><misc3><style face="normal" font="default">10.5114/ada.2017.71104</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87159</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liccardi,G.</style></author><author><style face="normal" font="default"> Calzetta,L.</style></author><author><style face="normal" font="default"> Salzillo,A.</style></author><author><style face="normal" font="default"> Apicella,G.</style></author><author><style face="normal" font="default"> Di Maro,E.</style></author><author><style face="normal" font="default"> Rogliani,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pulmonology, Haematology and Oncology, Division of Pneumology and Allergology, High Speciality "A.Cardarelli" Hospital, Naples, Italy</style></auth-address><titles><title><style face="normal" font="default">What Could the Role of Can f 5 Allergen Be in Dog-Sensitized Patients in "Real Life"?</style></title><secondary-title><style face="normal" font="default">J Investig Allergol Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Investig Allergol Clin Immunol</style></abbr-1></periodical><pages end="398" start="397">397-398</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1018-9068 (Print)IS - 1018-9068 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.18176/jiaci.0189</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29199970">PM:29199970</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-397-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Investig Allergol Clin Immunol\2017-27-397-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Liccardi G</style></custom2><misc3><style face="normal" font="default">10.18176/jiaci.0189</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86559</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Romberg,N.</style></author><author><style face="normal" font="default"> Vogel,T.P.</style></author><author><style face="normal" font="default"> Canna,S.W.</style></author></authors></contributors><auth-address><style face="normal" font="default">aDivision of Immunology and Allergy, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania bDivison of Immunology, Allergy and Rheumatology, Department of Pediatrics, Baylor College of Medicine and Center for Human Immunobiology, Texas Children's Hospital, Houston, Texas cRK Mellon Institute for Pediatric Research/Pediatric Rheumatology, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, USA</style></auth-address><titles><title><style face="normal" font="default">NLRC4 inflammasomopathies</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="404" start="398">398-404</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: The purpose of the review is to highlight developments in autoinflammatory diseases associated with gain-of-function mutations in the gene encoding NLR-family CARD-containing protein 4 (NLRC4), the NLRC4-inflammasomopathies. RECENT FINDINGS: Three years since the identification of the first autoinflammation with infantile enterocolitis (AIFEC) patients, there is an improved understanding of how the NLRC4 inflammasome and interleukin 18 (IL-18) contribute to gut inflammation in myeloid and also intestinal epithelial cells. This information has opened new therapeutic avenues to treat AIFEC patients with targeted agents like recombinant IL-18 binding protein and antiinterferon-gamma antibodies. Additional phenotypes traditionally associated with NLRP3 mutations like familial cold autoinflammatory syndrome and neonatal onset multisystem inflammatory disease (NOMID), have now also been associated with gain-of-function NLRC4 mutations. Finally, NLRC4 somatic mosaicism has now been identified in a NOMID and an AIFEC patient, a finding emphasizing nontraditional modes of inheritance in autoinflammatory diseases. SUMMARY: The NLRC4 inflammasomopathies constitute a growing autoinflammatory disease category that spans a broad clinical spectrum from cold urticaria to NOMID and the often fatal disease AIFEC. Rapid case identification with biomarkers like elevated serum IL-18 concentrations and early intervention with targeted immunomodulatory therapies are key strategies to improving outcomes for AIFEC patients</style></abstract><notes><style face="normal" font="default">DA - 20170928IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000396</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28957823">PM:28957823</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-398-404.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-398-404.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170928, Romberg N</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000396</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86697</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zimmer,J.</style></author><author><style face="normal" font="default"> Bonertz,A.</style></author><author><style face="normal" font="default"> Vieths,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Paul-Ehrlich-Institut, Paul-Ehrlich-Str. 51-59, Langen, Germany</style></auth-address><titles><title><style face="normal" font="default">Quality requirements for allergen extracts and allergoids for allergen immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="11" start="4">4-11</pages><volume><style face="normal" font="default">45</style></volume><number><style face="normal" font="default">1S</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="8" Month="11" Year="2017">2017/11/8</year></dates><abstract><style face="normal" font="default">All allergen products for allergen immunotherapy currently marketed in the European Union are pharmaceutical preparations derived from allergen-containing source materials like pollens, mites and moulds. Especially this natural origin results in particular demands for the regulatory requirements governing allergen products. Furthermore, the development of regulatory requirements is complicated by the so far missing universal link between certain quality parameters, in particular biological potency, on the one hand and clinical efficacy on the other hand. As a consequence, each allergen product for specific immunotherapy has to be assessed individually for its quality, safety and efficacy. At the same time, biological potency of allergen products is most commonly determined using IgE inhibition assays based on human sera relative to product-specific in house references, ruling out full comparability of products from different manufacturers. This review article aims to summarize the current quality requirements for allergen products including the special requirements implemented for control of chemically modified allergen extracts (allergoids)</style></abstract><notes><style face="normal" font="default">DA - 20171112IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29128092">PM:29128092</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-4-11.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-4-11.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171112, Zimmer J</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86686</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gagete,E.</style></author><author><style face="normal" font="default"> Delazari dos Santos,L.</style></author><author><style face="normal" font="default"> Gomes de Pontes,L.</style></author><author><style face="normal" font="default"> Morato Castro,F..</style></author></authors></contributors><titles><title><style face="normal" font="default">Who has anaphylaxis in Brazil? Validation of a questionnaire for population studies</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="40">40-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">The incidence of anaphylaxis is increasing in several parts of the world; thus, determining the prevalence of the disease in a given region is important to understand the factors involved and to promote measures to avoid this type of allergic reaction. Aiming this objective, we validated an instrument for a population-basedstudy that assesses the prevalence of anaphylaxis in the Brazilian population</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0171-2</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0171-2</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-40.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-40.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Gagete E</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0171-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87181</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shi,M.</style></author><author><style face="normal" font="default"> Cen,Y.</style></author><author><style face="normal" font="default"> Sohail,M.</style></author><author><style face="normal" font="default"> Xu,G.</style></author><author><style face="normal" font="default"> Wei,F.</style></author><author><style face="normal" font="default"> Ma,Y.</style></author><author><style face="normal" font="default"> Xu,X.</style></author><author><style face="normal" font="default"> Ma,Y.</style></author><author><style face="normal" font="default"> Song,Y.</style></author><author><style face="normal" font="default"> Hu,Q.</style></author></authors></contributors><titles><title><style face="normal" font="default">Aptamer based fluorometric +¦-lactoglobulin assay based on the use of magnetic nanoparticles and carbon dots</style></title><secondary-title><style face="normal" font="default">Microchimica Acta</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Microchimica Acta</style></abbr-1></periodical><pages end="" start="40">40-</pages><volume><style face="normal" font="default">185</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1436-5073</style></isbn><abstract><style face="normal" font="default">The authors describe a fluorometric aptamer based assay for detecting +¦-lactoglobulin by using carbon dots (C-dots) as a signal indicator. The aptamer was immoblized on magnetite (Fe3O4) nanoparticles (MNPs), and the C-dots served as a label for the complementary oligonucleotide (cDNA). The assay is based on the hybridization that takes place between aptamer and cDNA. In the presence of +¦-lactoglobulin (+¦-LG), the aptamer preferentially binds to +¦-LG, and this leads to a partial release of the C-dots-cDNA into the solution. After magnetic separation, the supernatant of the solution contains the released C-dots-cDNA which are quantified by fluorometry, best under excitation/emission wavelengths of 354/447-ánm. Under the optimal conditions, the fluorescence intensity is proportional to the logarithm of the +¦-LG concentration in the 0.25 to 50-áng mL</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">êÆ1 range, with a 37-ápg mL</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">êÆ1 detection limit. The method was successfully applied to the determination of +¦-LG in hypoallergenic formulations, and the results demonstrated that this assay is a promising tool in food quality control. Conceivably, it also provides the opportunity for detection of other analytes</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1007/s00604-017-2569-5</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s00604-017-2569-5</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Microchimica Acta\2017-185-40.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Microchimica Acta\2017-185-40.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Shi M</style></custom2><misc3><style face="normal" font="default">10.1007/s00604-017-2569-5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87094</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jin,H.</style></author><author><style face="normal" font="default"> Wang,L.</style></author><author><style face="normal" font="default"> Li,B.</style></author><author><style face="normal" font="default"> Cai,C.</style></author><author><style face="normal" font="default"> Ye,J.</style></author><author><style face="normal" font="default"> Xia,J.</style></author><author><style face="normal" font="default"> Ma,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Diseases, Hangzhou First People's Hospital, The Fourth Clinical College of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, China</style></auth-address><titles><title><style face="normal" font="default">Astragaloside IV Ameliorates Airway Inflammation in an Established Murine Model of Asthma by Inhibiting the mTORC1 Signaling Pathway</style></title><secondary-title><style face="normal" font="default">Evid Based Complement Alternat Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Evid Based Complement Alternat Med</style></abbr-1></periodical><pages end="" start="4037086">4037086-</pages><volume><style face="normal" font="default">2017</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Astragaloside IV (AS-IV), a main active constituent of Astragalus membranaceus, has been confirmed to have antiasthmatic effects. However, it remained unclear whether the beneficial effects of AS-IV on asthma were attributed to the mTOR inhibition; this issue was the focus of the present work. BALB/c mice were sensitized and challenged with ovalbumin followed with 3 weeks of rest/recovery and then reexposure to ovalbumin. AS-IV was administrated during the time of rest and reexposure. The characteristic features of allergic asthma, including airway hyperreactivity, histopathology, cytokines (IL-4, IL-5, IL-13, IL-17, and INF-gamma), and CD4(+)CD25(+)Foxp3(+)Treg cells in bronchoalveolar lavage fluid (BALF), and downstream proteins of mTORC1/2 signaling were examined. AS-IV markedly suppressed airway hyperresponsiveness and reduced IL-4, IL-5, and IL-17 levels and increased INF-gamma levels in the BALF. Histological studies showed that AS-IV markedly decreased inflammatory infiltration in the lung tissues. Notably, AS-IV inhibited mTORC1 activity, whereas it had limited effects on mTORC2, as assessed by phosphorylation of mTORC1 and mTORC2 substrates S6 ribosomal protein, p70 S6 Kinase, and Akt, respectively. CD4(+)CD25(+)Foxp3(+)Treg cells in BALF were not significantly changed by AS-IV. Together, these results suggest that the antiasthmatic effects of AS-IV were at least partially from inhibiting the mTORC1 signaling pathway</style></abstract><notes><style face="normal" font="default">IS - 1741-427X (Print)IS - 1741-427X (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1155/2017/4037086</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29234390">PM:29234390</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Evid Based Complement Alternat Med\2017-2017-4037086.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Evid Based Complement Alternat Med\2017-2017-4037086.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171214, Jin H</style></custom2><misc3><style face="normal" font="default">10.1155/2017/4037086</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86594</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,D.H.</style></author><author><style face="normal" font="default"> Kim,S.W.</style></author><author><style face="normal" font="default"> Kim,S.W.</style></author><author><style face="normal" font="default"> Kang,J.M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Interleukin-37 Relieves Allergic Inflammation in a House Dust Mite Allergic Rhinitis Murine Model</style></title><secondary-title><style face="normal" font="default">Iran J Allergy Asthma Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Iran J Allergy Asthma Immunol</style></full-title></periodical><pages end="417" start="404">404-417</pages><volume><style face="normal" font="default">16</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy,Dermatophagoides farinae,Mice,Rhinitis,Regulatory,T Lymphocytes</style></keyword></keywords><dates><year Day="28" Month="10" Year="2017">2017/10/28</year></dates><abstract><style face="normal" font="default">The purpose of this study was to investigate the effects of interleukin-37 (IL-37) on a Dermatophagoides farinae ( Der f )-induced murine model of allergic rhinitis (AR). BALB/c mice, except the control groups, were sensitized intraperitoneally and challenged intranasally with Der f ( Der f group). The IL-37 and IL-37+anti-CD25 groups were administered IL-37 intranasally. The IL-37+anti-CD25 groups were administered anti-CD25 monoclonal antibody intraperitoneally before challenge. Allergic symptoms and the average eosinophil number were counted. The levels of cytokines and transcription factors in the nasal mucosa were measured by Real-Time polymerase chain reaction (PCR) and western blotting. The levels of Der f -specific immunoglobulin E (IgE) were measured. The CD4 + CD25 + Foxp3 + T cells among splenic mononuclear cells were analyzed by flow cytometry. The allergic symptom scores and Der f -specific IgE levels were lower in the IL-37 group compared to the Der f group. Additionally, the levels of the transcription factor GATA-3 and ROR-+¦t and those of the cytokines IL-4, IL-5, IL-13, and IL-17, representing both T helper (Th)2 and Th17 responses, were lower in the IL-37 group in comparison with the Der f group. However, the Th1 responsewas not suppressed after administration of IL-37. IL-37 increased the IL-10 level; however, Real-Time PCR, western blotting, and flow cytometry results showed the limited action of IL-37 on CD4 + CD25 + Foxp3 + T cells. This study demonstrates that intranasal IL-37 can suppress Th2 and Th17 responses in an AR murine model. Furthermore, these data suggest that IL-10 is increased, but CD4 + CD25 + Foxp3 + T cells are not correlated with the IL-37-induced mechanism. -á</style></abstract><notes><style face="normal" font="default">LA - ENGCO - South Korea -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://ijaai.tums.ac.ir/index.php/ijaai/article/view/1104</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Iran J Allergy Asthma Immunol\2017-16-404-17.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Iran J Allergy Asthma Immunol\2017-16-404-17.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Kim DH</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>85231</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yang,J.</style></author><author><style face="normal" font="default"> Zhao,Y.</style></author><author><style face="normal" font="default"> Li,S.</style></author><author><style face="normal" font="default"> Han,J.</style></author><author><style face="normal" font="default"> Yu,Y.</style></author><author><style face="normal" font="default"> Fan,Z.</style></author><author><style face="normal" font="default"> Liu,H.</style></author><author><style face="normal" font="default"> Cui,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">College of TCM, North China University of Science and Technology, Tangshan 063000, Hebei Pro-vince, China</style></auth-address><titles><title><style face="normal" font="default">[Regulation of acupuncture on expression of AKT protein in lung tissues of asthma rats]</style></title><secondary-title><style face="normal" font="default">Zhongguo Zhen Jiu</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Zhongguo Zhen Jiu</style></abbr-1></periodical><pages end="410" start="406">406-410</pages><volume><style face="normal" font="default">37</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword></keywords><dates><year Day="12" Month="4" Year="2017">2017/4/12</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To explore the effects of acupuncture on the expression of protein kinase B (PKB/AKT) in lung tissues of asthma rats. METHODS: Forty SPF male SD rats were randomly divided into a blank group, a model group, an acupuncture group and a blocker group, 10 rats in each one. The rat model of asthma was established by egg albumin stimulation in the model group, acupuncture group and blocker group. Since the establishment of rat model, the rats in the acupuncture group were treated with acupuncture at "Dazhui" (GV 14), "Feishu" (BL 13) and "Fengmen" (BL 12) before atomization; the rats in the blocker group were treated with intervention of blocker LY294002, once every two days, for 7 times. There was no treatment in the blank group and model group. HE staining was applied to observe the morphologic changes of lung tissues; the immunohistochemical method was applied to test the protein expression of AKT in lung tissue. RESULTS: HE staining indicated the infiltration and aggregation of a variety of inflammatory cells around airways, as well as bronchial smooth muscle spasm and confined lumen in the model group; in the acupuncture group and blocker group the inflammatory cells were less and confined lumen was relieved. Compared with the blank group, the protein expression of AKT was higher in the model group (P&lt;0.05); compared with the model group, the protein expression of AKT in the acupuncture group and blocker group was reduced (both P&lt;0.05); the differences between the acupuncture group and blank group, blocker group were not significant (both P>0.05). CONCLUSIONS: Acupuncture could reduce the protein expression of AKT in lung tissue in asthma rats, leading to relieved inflammation reaction and airway remodeling</style></abstract><notes><style face="normal" font="default">IS - 0255-2930 (Print)IS - 0255-2930 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.13703/j.0255-2930.2017.04.015</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29231594">PM:29231594</url></web-urls></urls><custom2><style face="normal" font="default">20171214, Yang J</style></custom2><misc3><style face="normal" font="default">10.13703/j.0255-2930.2017.04.015</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86713</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nagasaki,T.</style></author><author><style face="normal" font="default"> Matsumoto,H.</style></author><author><style face="normal" font="default"> Oguma,T.</style></author><author><style face="normal" font="default"> Ito,I.</style></author><author><style face="normal" font="default"> Inoue,H.</style></author><author><style face="normal" font="default"> Iwata,T.</style></author><author><style face="normal" font="default"> Tajiri,T.</style></author><author><style face="normal" font="default"> Kanemitsu,Y.</style></author><author><style face="normal" font="default"> Izuhara,Y.</style></author><author><style face="normal" font="default"> Morimoto,C.</style></author><author><style face="normal" font="default"> Ishiyama,Y.</style></author><author><style face="normal" font="default"> Sunadome,H.</style></author><author><style face="normal" font="default"> Niimi,A.</style></author><author><style face="normal" font="default"> Hirai,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan</style></auth-address><titles><title><style face="normal" font="default">Sensitization to Staphylococcus aureus enterotoxins in smokers with asthma</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="414" start="408">408-414</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Sensitization to Staphylococcus aureus enterotoxins (SEs) augments eosinophilic inflammation in asthma. Recent epidemiologic studies demonstrate that sensitization to SEs is increased in healthy smokers; however, there is no evidence on the association between sensitization to SEs and eosinophilic inflammation in smokers with asthma. OBJECTIVE: To clarify the role of SEs on clinical indexes, including eosinophilic inflammation and lung function in smokers with asthma. METHODS: The frequency of atopic sensitization to SEs was examined in adult patients with asthma. In current or ex-smokers with asthma, the association of sensitization to SEs with eosinophilic inflammation, airflow limitation, or treatment steps was determined. Clinical indexes were examined at the first visit, and treatment steps were assessed 6 months after enrollment. RESULTS: Overall, 23 current smokers, 40 ex-smokers, and 118 never smokers with asthma were enrolled. The frequency of sensitization to SEs, but not to other aeroallergens, was significantly higher in current, ex-, and never smokers, in decreasing order. In current or ex-smokers with asthma, patients with sensitization to SEs exhibited higher serum levels of total and specific IgE to aeroallergens, higher blood eosinophil counts, greater airflow limitation, and more severe disease 6 months later than those without sensitization to SE. A longer smoking abstinence period was associated with serum specific IgE levels to SEs, and 3 years was the best cutoff of abstinence period to predict the absence of sensitization to SEs. CONCLUSION: Sensitization to SEs is increased in smokers with asthma, and it may be a marker of eosinophilic inflammation and severe asthma in smokers with asthma. TRIAL REGISTRATION: umin.ac.jp Identifier: UMIN000007818</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150068">PM:29150068</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-408-14.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-408-14.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Nagasaki T</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86852</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,Y.</style></author><author><style face="normal" font="default"> Peng,J.</style></author><author><style face="normal" font="default"> Zhou,Y.</style></author><author><style face="normal" font="default"> Cui,Y.</style></author></authors></contributors><titles><title><style face="normal" font="default">Comparison of atopy patch testing to skin prick testing for diagnosing mite-induced atopic dermatitis: a systematic review and meta-analysis</style></title><secondary-title><style face="normal" font="default">Clin Transl Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Transl Allergy</style></abbr-1></periodical><pages end="" start="41">41-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2045-7022</style></isbn><abstract><style face="normal" font="default">Atopic dermatitis (AD) can occur after contact with aeroallergens like house dust mites, pollen, and animal dander. Despite its controversial diagnostic value, the atopy patch test (APT) has been used as an important tool in the diagnosis of AD caused by house dust mites. Here, we present a meta-analysis comparing APT to the common skin prick test (SPT) in the diagnosis of mite-induced AD</style></abstract><notes><style face="normal" font="default">LA - ENGCO - China -</style></notes><work-type><style face="normal" font="default">10.1186/s13601-017-0178-3</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s13601-017-0178-3</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-41.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-41.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Liu Y</style></custom2><misc3><style face="normal" font="default">10.1186/s13601-017-0178-3</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>61438</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Heine,R.G.</style></author><author><style face="normal" font="default"> AlRefaee,F.</style></author><author><style face="normal" font="default"> Bachina,P.</style></author><author><style face="normal" font="default"> De Leon,J.C.</style></author><author><style face="normal" font="default"> Geng,L.</style></author><author><style face="normal" font="default"> Gong,S.</style></author><author><style face="normal" font="default"> Madrazo,J.A.</style></author><author><style face="normal" font="default"> Ngamphaiboon,J.</style></author><author><style face="normal" font="default"> Ong,C.</style></author><author><style face="normal" font="default"> Rogacion,J.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Murdoch Childrens Research Institute, Melbourne, Australia.</style></auth-address><titles><title><style face="normal" font="default">Lactose intolerance and gastrointestinal cow's milk allergy in infants and children - common misconceptions revisited</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="41">41-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Hydrolysis</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Lactose is the main carbohydrate in human and mammalian milk. Lactose requires enzymatic hydrolysis by lactase into D-glucose and D-galactose before it can be absorbed. Term infants express sufficient lactase to digest about one liter of breast milk daily. Physiological lactose malabsorption in infancy confers beneficial prebiotic effects, including the establishment of Bifidobacterium-rich fecal microbiota. In many populations, lactase levels decline after weaning (lactase non-persistence; LNP). LNP affects about 70% of the world's population and is the physiological basis for primary lactose intolerance (LI). Persistence of lactase beyond infancy is linked to several single nucleotide polymorphisms in the lactase gene promoter region on chromosome 2. Primary LI generally does not manifest clinically before 5 years of age. LI in young children is typically caused by underlying gut conditions, such as viral gastroenteritis, giardiasis, cow's milk enteropathy, celiac disease or Crohn's disease. Therefore, LI in childhood is mostly transient and improves with resolution of the underlying pathology. There is ongoing confusion between LI and cow's milk allergy (CMA) which still leads to misdiagnosis and inappropriate dietary management. In addition, perceived LI may cause unnecessary milk restriction and adverse nutritional outcomes. The treatment of LI involves the reduction, but not complete elimination, of lactose-containing foods. By contrast, breastfed infants with suspected CMA should undergo a trial of a strict cow's milk protein-free maternal elimination diet. If the infant is not breastfed, an extensively hydrolyzed or amino acid-based formula and strict cow's milk avoidance are the standard treatment for CMA. The majority of infants with CMA can tolerate lactose, except when an enteropathy with secondary lactase deficiency is present</style></abstract><notes><style face="normal" font="default">IS - 1939-4551 (Print)IS - 1939-4551 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Australia -CO - Kuwait -CO - India -CO - Philippines -CO - China -CO - Thailand -CO - Singapore -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0173-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29270244">PM:29270244</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-41.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-41.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Heine RG</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0173-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86712</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Barrett,M.A.</style></author><author><style face="normal" font="default"> Humblet,O.</style></author><author><style face="normal" font="default"> Marcus,J.E.</style></author><author><style face="normal" font="default"> Henderson,K.</style></author><author><style face="normal" font="default"> Smith,T.</style></author><author><style face="normal" font="default"> Eid,N.</style></author><author><style face="normal" font="default"> Sublett,J.W.</style></author><author><style face="normal" font="default"> Renda,A.</style></author><author><style face="normal" font="default"> Nesbitt,L.</style></author><author><style face="normal" font="default"> Van Sickle,D.</style></author><author><style face="normal" font="default"> Stempel,D.</style></author><author><style face="normal" font="default"> Sublett,J.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Propeller Health, San Francisco, California.</style></auth-address><titles><title><style face="normal" font="default">Effect of a mobile health, sensor-driven asthma management platform on asthma control</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="421" start="415">415-421</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Asthma inflicts a significant health and economic burden in the United States. Self-management approaches to monitoring and treatment can be burdensome for patients. OBJECTIVE: To assess the effect of a digital health management program on asthma outcomes. METHODS: Residents of Louisville, Kentucky, with asthma were enrolled in a single-arm pilot study. Participants received electronic inhaler sensors that tracked the time, frequency, and location of short-acting beta-agonist (SABA) use. After a 30-day baseline period during which reference medication use was recorded by the sensors, participants received access to a digital health intervention designed to enhance self-management. Changes in outcomes, including mean daily SABA use, symptom-free days, and asthma control status, were compared among the initial 30-day baseline period and all subsequent months of the intervention using mixed-model logistic regressions and chi2 tests. RESULTS: The mean number of SABA events per participant per day was 0.44 during the control period and 0.27 after the first month of the intervention, a 39% reduction. The percentage of symptom-free days was 77% during the baseline period and 86% after the first month, a 12% improvement. Improvement was observed throughout the study; each intervention month demonstrated significantly lower SABA use and higher symptom-free days than the baseline month (P &lt; .001). Sixty-nine percent had well-controlled asthma during the baseline period, 67% during the first month of the intervention. Each intervention month demonstrated significantly higher percentages than the baseline month (P &lt; .001), except for month 1 (P = .80). CONCLUSION: A digital health asthma management intervention demonstrated significant reductions in SABA use, increased number of symptom-free days, and improvements in asthma control. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02162576</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150069">PM:29150069</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-415-21.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-415-21.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Barrett MA</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87394</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Owczarek,W.</style></author><author><style face="normal" font="default"> Slowinska,M.</style></author><author><style face="normal" font="default"> Lesiak,A.</style></author><author><style face="normal" font="default"> Ciazinska,M.</style></author><author><style face="normal" font="default"> Maciag,A.</style></author><author><style face="normal" font="default"> Paluchowska,E.</style></author><author><style face="normal" font="default"> Marek-Jozefowicz,L.</style></author><author><style face="normal" font="default"> Czajkowski,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">The incidence and management of cutaneous adverse events of the epidermal growth factor receptor inhibitors</style></title><secondary-title><style face="normal" font="default">Postepy Dermatol Alergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Postepy Dermatol Alergol</style></abbr-1></periodical><pages end="428" start="418">418-428</pages><volume><style face="normal" font="default">34</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1642-395X</style></isbn><abstract><style face="normal" font="default">Overexpression of the epidermal growth factor receptor (EGFR) is found in many cancers, including those of the head and neck area, non-small-cell lung cancer, and colorectal, cervical, prostate, breast, ovary, stomach, and pancreatic cancer. The EGFR inhibitors are used at present in the treatment of such cancers. Skin lesions that develop during and after cancer treatment may be due to specific cytostatics, molecular-targeted drugs, radiation therapy, complementary therapy, or the cancer itself, and hence knowledge is essential to distinguish between them. The mechanism through which skin toxicity arises during treatment with EGFR inhibitors is not well known, but seems to be due to the modification of the RAS/RAF/MEK/ERK signal path associated with its activation, which results in the similarity between the adverse effects of EGFR inhibitors and the treatment of melanoma with BRAF and MEK inhibitors. The most common side effects are pruritus, xerosis, papulopustular rash, hand-foot skin reaction, alopecia and dystrophy of the hair, and paronychia. This work presents options for prevention and suggestions for managing these adverse events, which are of importance in the care of patients undergoing oncological treatment</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.5114/ada.2017.71106</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5114/ada.2017.71106</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-418-28.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-418-28.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171021, Owczarek W</style></custom2><misc3><style face="normal" font="default">10.5114/ada.2017.71106</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>76749</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Li,H.Z.</style></author><author><style face="normal" font="default"> Gao,Z.Y.</style></author><author><style face="normal" font="default"> Huang,W.</style></author><author><style face="normal" font="default"> Ren,G.P.</style></author><author><style face="normal" font="default"> Xu,H.N.</style></author><author><style face="normal" font="default"> Zhang,X.</style></author><author><style face="normal" font="default"> Fu,H.</style></author><author><style face="normal" font="default"> Zhang,Y.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Mudanjiang Medical University, Mudanjiang 157011, China</style></auth-address><titles><title><style face="normal" font="default">[Effects of Fritillariae Cirrhosae Bulbus on MMP-2,MMP-9 and TIMP-1 in murine asthma model]</style></title><secondary-title><style face="normal" font="default">Zhongguo Zhong Yao Za Zhi</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Zhongguo Zhong Yao Za Zhi</style></full-title></periodical><pages end="4186" start="4180">4180-4186</pages><volume><style face="normal" font="default">42</style></volume><number><style face="normal" font="default">21</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">To investigate the effects of Fritillariae Cirrhosae Bulbus on airway remodeling and matrix metalloproteinase-2(MMP-2), matrix metalloproteinase-9(MMP-9), tissue inhibitor-1 of metalloproteinase(TIMP-1) of a murine asthma model, and explore its mechanism in treatment of asthma. BALB/C murines were randomly divided into the normal group, model group, high dose group, low dose group, and positive control group. Except for the normal group, all the other groups received ovalbumin(OVA) to establish murine asthma model. After successful modeling, the murines in high dose group and low dose group were orally administered with Fritillariae Cirrhosae Bulbus powder at the dose of 18.0 mg*kg(-)(1) and 9.0 mg*kg(-)(1), respectively; the murines in positive control group were injected intraperitoneally with dexamethasone at the dose of 0.5 mg*kg(-)(1); while the murines in normal group and the model group were orally administered with the same volume of normal saline. All the drugs were given to murines per day for 28 d. The variations of airway responsiveness, variations of the total cell count and leukocyte differential count in bronchoalveolar lavage fluid(BALF), and the variations of thicknesses of bronchial wall and airway smooth muscle of each group were observed. The levels of MMP-2, MMP-9 and TIMP-1 were measured by ELISA; and the expression levels of MMP-2, MMP-9 and TIMP-1 mRNA were detected by RT-PCR. The results showed that as compared with the normal group, the airway responsiveness, the count of total cells, neutrophils, macrophage, lymphocytes, eosinophils in BALF, and the thicknesses of bronchial wall and airway smooth muscle were increased significantly in the model group(P&lt;0.01); as compared with the model group, the above indicators were decreased significantly in the high dose group, low dose group and positive control group (P&lt;0.05 or P&lt;0.01). As compared with the normal group, the levels and expressions of MMP-2, MMP-9 and TIMP-1 mRNA were increased significantly in the model group(P&lt;0.01); while as compared with the model group, these levels were decreased significantly in the high dose group, low dose group and positive control group(P&lt;0.01). In conclusion, Fritillariae Cirrhosae Bulbus can improve airway remodeling in a murine asthma model, and its mechanisms may be related to down-regulating MMP-2, MMP-9 and TIMP-1 levels</style></abstract><notes><style face="normal" font="default">IS - 1001-5302 (Print)IS - 1001-5302 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.19540/j.cnki.cjcmm.20170928.018</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29271158">PM:29271158</url></web-urls></urls><custom2><style face="normal" font="default">20171215, Li HZ</style></custom2><misc3><style face="normal" font="default">10.19540/j.cnki.cjcmm.20170928.018</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86854</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Blankestijn,M.A.</style></author><author><style face="normal" font="default"> Knulst,A.C.</style></author><author><style face="normal" font="default"> Knol,E.F.</style></author><author><style face="normal" font="default"> Le,T.M.</style></author><author><style face="normal" font="default"> Rockmann,H.</style></author><author><style face="normal" font="default"> Otten,H.G.</style></author><author><style face="normal" font="default"> Klemans,R.J.B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Allergology, University Medical Center Utrecht, Utrecht University, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">Sensitization to PR-10 proteins is indicative of distinctive sensitization patterns in adults with a suspected food allergy</style></title><secondary-title><style face="normal" font="default">Clin Transl Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Transl Allergy</style></abbr-1></periodical><pages end="" start="42">42-</pages><volume><style face="normal" font="default">7</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: The extent of co-sensitization within and between food protein families in an adult population is largely unknown. This study aimed to identify the most frequently recognized components in the PR-10 and storage protein family, as well as patterns in (co-)sensitization, in a birch-endemic area. Methods: Results of ImmunoCAP ISAC, performed during routine care in Dutch adult outpatients suspected of food allergy, were collected. Results: A total of 305 patients were selected, aged 16-79 years (median 32 years). Sensitization to one or more PR-10 proteins was most frequent (74% of all subjects), followed by 35% to storage protein and 15% to nsLTPs. Within the PR-10 family, subjects were most often sensitized to Bet v 1 (73% of 305), Cor a 1.04 (72%) and Mal d 1 (68%). Sensitization to PR-10s from soy, celery and kiwi occurred distinctively less often (&lt; 55% of Bet v 1 sensitized subjects) compared to other food PR-10s (all > 70%). Subjects sensitized to these 'less common PR-10 proteins' were sensitized to more food and inhalant components on the ISAC, compared to subjects sensitized to 'common PR-10 proteins' (median 22 vs 13 out of 112, p &lt; 0.0001). Seven subjects demonstrated sensitization to food PR-10 proteins, without concomitant sensitization to pollen PR-10s. Within the storage proteins, sensitization to multiple peanut allergens was most common (on average 3 out of 4). Conclusions: Sensitization to PR-10 food proteins could occur without concomitant sensitization to common PR-10 from pollen in a subset of subjects. Less commonly recognized PR-10 proteins appear to be an indication of polysensitization</style></abstract><notes><style face="normal" font="default">IS - 2045-7022 (Print)IS - 2045-7022 (Linking)LA - engPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1186/s13601-017-0177-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29201345">PM:29201345</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-42.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-42.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171123, Blankestijn MA</style></custom2><misc3><style face="normal" font="default">10.1186/s13601-017-0177-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87299</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Herrmann,I.</style></author><author><style face="normal" font="default"> Einhorn,L.</style></author><author><style face="normal" font="default"> Panakova,L.</style></author></authors></contributors><titles><title><style face="normal" font="default">Gender aspects in allergies of pets </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô A secondary publication and update</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="42">42-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">Allergies need not-áonly affect humans; this multifactorial and complex disease can also affect animals. Comparative allergology investigates the many similarities between the pathogenesis, clinics, diagnosis, and therapy of the disorders in humans and pet animals. In contrast to human allergy research, the veterinary field lacks access to a central database, which means there are no cohort studies published. This limits not only the research on breed and regional differences in allergies, but also further studies on the impact of gender in allergies of domestic animals. Moreover, domestic cats, dogs and male horses are castrated in most cases, which neutralises any effects of sexual hormones. In this review article a-áfew interesting findings regarding gender aspects in companion animals were extracted from current literature. In summary, there is a lack of data on gender effects on allergies in cats, dogs or horses</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0172-1</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0172-1</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-42.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-42.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Herrmann I</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0172-1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86558</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bucciol,G.</style></author><author><style face="normal" font="default"> Van Nieuwenhove,E.</style></author><author><style face="normal" font="default"> Moens,L.</style></author><author><style face="normal" font="default"> Itan,Y.</style></author><author><style face="normal" font="default"> Meyts,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">aChildhood Immunology, Department of Microbiology and Immunology, KU Leuven, Belgium</style></auth-address><titles><title><style face="normal" font="default">Whole exome sequencing in inborn errors of immunity: use the power but mind the limits</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="430" start="421">421-430</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: Next-generation sequencing, especially whole exome sequencing (WES), has revolutionized the molecular diagnosis of inborn errors of immunity. This review summarizes the generation and analysis of next-generation sequencing data. RECENT FINDINGS: The focus is on prioritizing strategies for unveiling the potential disease-causing variant. We also highlighted oversights and imperfections of WES and targeted panel sequencing, as well as the need for functional validation. SUMMARY: The information is crucial for a judicious use of WES by researchers, but even more so by the clinical immunologist</style></abstract><notes><style face="normal" font="default">DA - 20170922IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - Belgium -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000398</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28938278">PM:28938278</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-421-30.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-421-30.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170922, Bucciol G</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000398</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86780</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wills-Karp,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Histamine-releasing factor: a promising therapeutic target for food allergy</style></title><secondary-title><style face="normal" font="default">J Clin Invest</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Clin Invest</style></abbr-1></periodical><pages end="4241" start="4238">4238-4241</pages><volume><style face="normal" font="default">127</style></volume><number><style face="normal" font="default">12</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="13" Month="11" Year="2017">2017/11/13</year></dates><abstract><style face="normal" font="default">The prevalence of food allergies has been increasing at an alarming rate over the last few decades. Despite the dramatic increase in disease prevalence, the development of effective therapies has not kept pace. In this issue of the JCI, Ando et al. provide a causal link between histamine-releasing factor (HRF) interactions with IgE and food allergy in a murine model. Successful oral immunotherapy of both egg-allergic human patients and food-allergic mice was associated with sustained suppression of HRF-reactive IgE levels. These results support a role for HRF-IgE interactions in the amplification of intestinal inflammation and suggest HRF as a therapeutic target in food allergy</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1558-8238 (Electronic)IS - 0021-9738 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1172/JCI98297</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130933">PM:29130933</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls><related-urls><url ppv-ref="no">presto -</url></related-urls></urls><custom2><style face="normal" font="default">20171113, Wills-Karp M</style></custom2><misc3><style face="normal" font="default">10.1172/JCI98297</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86856</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Romita,P.</style></author><author><style face="normal" font="default"> Fuso,C.</style></author><author><style face="normal" font="default"> Ettorre,G.</style></author><author><style face="normal" font="default"> Bonamonte,D.</style></author><author><style face="normal" font="default"> Foti,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biomedical Science and Human Oncology, Dermatological Clinic, University of Bari, 70124 Bari, Italy</style></auth-address><titles><title><style face="normal" font="default">Contact urticaria caused by a silk bed quilt in a young atopic female</style></title><secondary-title><style face="normal" font="default">Contact Dermatitis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Contact Dermatitis</style></abbr-1></periodical><pages end="426" start="425">425-426</pages><volume><style face="normal" font="default">77</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1600-0536 (Electronic)IS - 0105-1873 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1111/cod.12858</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29164700">PM:29164700</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Contact Dermatitis\2017-77-425-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Contact Dermatitis\2017-77-425-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171111, Romita P</style></custom2><misc3><style face="normal" font="default">10.1111/cod.12858</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87343</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fernandes,A.</style></author><author><style face="normal" font="default"> Madureira,C.</style></author><author><style face="normal" font="default"> Jacob,S.</style></author><author><style face="normal" font="default"> Lopes,S.</style></author><author><style face="normal" font="default"> Carvalho,F.</style></author></authors></contributors><titles><title><style face="normal" font="default"> A case of allergy to pomegranate and walnut: what is the role of lipid transfer protein Pru p 3?</style></title><secondary-title><style face="normal" font="default">Braz J Allergy Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Braz J Allergy Immunol</style></full-title></periodical><pages end="430" start="427">427-430</pages><volume><style face="normal" font="default">1</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Peach</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Lipid transfer proteins (LTPs) are pan-allergens that are responsiblefor cross-reactivity between fruits, vegetables, and pollen. Pru p 3,the LTP present in the peach, is recognized as a marker of severityin food allergy. Pomegranate and walnut have been reported tobe involved in allergic reactions due to the existence of LTPs. Wereport the case of a teenager admitted with rash and swollen lipsafter the ingestion of pomegranate, and reporting a similar reactionin the past after ingesting walnut. Skin tests showed positive resultsfor commercial extracts of walnut and pomegranate pulp, and werenegative for grass and peach. The total immunoglobulin E (IgE)was 87.2 IU/mL and specific IgE (sIgE) testing for walnut andhazelnut was positive. sIgE determination using the ISAC method(immuno-solid-phase allergen chip) was positive for hazelnut (CorA 8), peach (Pru p 3) and walnut (Jug r3). There was no historyof allergic reaction after the ingestion of peach. The present casequestions the relevance of Pru p 3 in patients who are not allergicto peach, and whether this is the only cross-reactive marker withpomegranate.</style></abstract><notes><style face="normal" font="default">LA - PORCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.5935/2526-5393.20170063</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5935/2526-5393.20170063</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Braz J Allergy Immunol\2017-1-427-30.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Braz J Allergy Immunol\2017-1-427-30.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170120, Fernandes A</style></custom2><misc3><style face="normal" font="default">10.5935/2526-5393.20170063</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87497</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Morsy,K.</style></author><author><style face="normal" font="default"> Badr,A.M.</style></author><author><style face="normal" font="default"> Abdel-Ghaffar,F.</style></author><author><style face="normal" font="default"> El Deeb,S.</style></author><author><style face="normal" font="default"> Ebead,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Biology Department, College of Science, King Khalid University, Abha, Saudi Arabia</style></auth-address><titles><title><style face="normal" font="default">Pathogenic Potential of Fresh, Frozen, and Thermally Treated Anisakis spp. Type II (L3) (Nematoda: Anisakidae) after Oral Inoculation into Wistar Rats: A Histopathological Study</style></title><secondary-title><style face="normal" font="default">J Nematol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Nematol</style></abbr-1></periodical><pages end="436" start="427">427-436</pages><volume><style face="normal" font="default">49</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anisakidae</style></keyword><keyword><style face="normal" font="default"> Anisakidosis</style></keyword><keyword><style face="normal" font="default"> Anisakis</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword><keyword><style face="normal" font="default"> Zoonotic nematodes</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">The third-stage (L3) larvae of Anisakis are the etiological agents of human anisakiasis caused by consumption of raw or undercooked seafood infected with anisakid nematodes. Infection with these worms is associated with abdominal pain, nausea, and diarrhea and can lead to massive infiltration of eosinophils and the formation of granulomas in the gastrointestinal tract if the larvae are not removed. Food allergy affects populations worldwide, and despite several reports on the presence of the potentially zoonotic nematodes among edible fishes in Egypt, there are few immunological and molecular studies investigating the epidemiology of these parasites. Anisakidosis, a human infection with nematodes of the family Anisakidae, is caused most commonly by Anisakis spp. In the present study, seventy specimens of the European seabass Dicentrarchus labrax commercialized in Alexandria city along the Mediterranean Sea were acquired during the period from July to December, 2015. Fish were necropsied and dissected to investigate the presence of nematode larvae. Thirty fish (42.9%) of the total were parasitized by nematode larvae which were morphologically identified as Anisakis spp. Type II (L3) according to light and scanning electron microscopy. The pathogenic potential of oral inoculation of fresh, frozen, and thermally treated larvae into Wistar rats was elucidated by histological examination of their thymus and spleen. Results obtained indicated that neither cooling nor freezing of the parasite could destroy their allergenic capacity. So, it is important to create a wider awareness of this potential risk to human health. It is becoming increasingly likely that the impact of Anisakis spp. on human health has been underestimated, and it is perhaps time to consider more sweeping measures than those currently enforced to protect the public health</style></abstract><notes><style face="normal" font="default">IS - 0022-300X (Print)IS - 0022-300X (Linking)LA - engPT - Journal ArticleCO - Saudi Arabia -CO - Egypt -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29353932">PM:29353932</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Nematol\2017-49-427-36.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Nematol\2017-49-427-36.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20180113, Morsy K</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87080</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kocaturk,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Role of Biologics and Future Perspectives in the Treatment of Urticaria</style></title><secondary-title><style face="normal" font="default">Curr Treat Options Allergy</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Treat Options Allergy</style></full-title></periodical><pages end="437" start="428">428-437</pages><volume><style face="normal" font="default">4</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Omalizumab</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2196-3053</style></isbn><abstract><style face="normal" font="default">Purpose of review The management of chronic urticaria has substantially changed with the introduction of omalizumab to the treatment. Omalizumab did not only provide marked improvement in the treatment of the disease but also opened new horizons for the understanding of the pathways involved in the pathogenesis. But because of its requirement of hospital visits, cost, and only providing symptomatic relief, novel therapeutic targets are needed. Anti-IgE has gained a special interest given the high efficacy of omalizumab</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Turkey -</style></notes><work-type><style face="normal" font="default">10.1007/s40521-017-0145-1</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40521-017-0145-1</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Treat Options Allergy\2017-4-428-37.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Treat Options Allergy\2017-4-428-37.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Kocaturk E</style></custom2><misc3><style face="normal" font="default">10.1007/s40521-017-0145-1</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86853</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bozek,A.</style></author><author><style face="normal" font="default"> Kolodziejczyk,K.</style></author><author><style face="normal" font="default"> Kozlowska,R.</style></author><author><style face="normal" font="default"> Canonica,G.W.</style></author></authors></contributors><titles><title><style face="normal" font="default">Evidence of the efficacy and safety of house dust mite subcutaneous immunotherapy in elderly allergic rhinitis patients: a randomized, double-blind placebo-controlled trial</style></title><secondary-title><style face="normal" font="default">Clin Transl Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Transl Allergy</style></abbr-1></periodical><pages end="" start="43">43-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2045-7022</style></isbn><abstract><style face="normal" font="default">Allergen specific immunotherapy (AIT) in elderly patients is controversial, and there is still little evidence supporting the safety and efficacy of this treatment in this population. The study objective was to evaluate the safety and efficacy of AIT for house dust mite allergens in patients over 65-áyears of age with allergic rhinitis (AR) and a documented allergy to house dust mites. The primary endpoint was the change from baseline in the mean average adjusted symptom score (AAdSS) and the total combined rhinitis score (TCRS) difference in the least square means for the label compared to placebo</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -CO - Italy -</style></notes><work-type><style face="normal" font="default">10.1186/s13601-017-0180-9</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s13601-017-0180-9</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-43.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-43.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Bozek A</style></custom2><misc3><style face="normal" font="default">10.1186/s13601-017-0180-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87300</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Afify,S.M.</style></author><author><style face="normal" font="default"> Pali-Scholl,I.</style></author></authors></contributors><titles><title><style face="normal" font="default">Adverse reactions to food: the female dominance </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô A secondary publication and update</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="43">43-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">Gender-specific differences are evident in food intolerance and allergy. In this review, we will highlight and summarize the dissimilarities in prevalence of adverse food reactions, focusing on IgE-mediated food allergies and intolerances regarding frequency of symptoms and predisposing factors. After puberty, females suffer more frequently from food-related symptoms than males. Several factors may be responsible for this observation, for example hormonal effects, gender-specific behavior, perception of risk, or intake of medications. In this context, concrete studies related to adverse food reactions are still lacking</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0174-z</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0174-z</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-43.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-43.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Afify SM</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0174-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86855</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Alcaraz-Mor,R.</style></author><author><style face="normal" font="default"> Lehucher-Michel,M.P.</style></author></authors></contributors><auth-address><style face="normal" font="default">AP-HM, Service de Medecine et Sante au Travail, 13005 Marseille, FranceAix-Marseille Universite - EA 3279, 13385 Marseille cedex 5, FranceAP-HM, Service de Medecine et Sante au Travail, 13005 Marseille, FranceAix-Marseille Universite - EA 3279, 13385 Marseille cedex 5, France</style></auth-address><titles><title><style face="normal" font="default">Re: Protein contact dermatitis caused by lime in a pastry chef (Contact Dermatitis 2015: 73: 54-56)</style></title><secondary-title><style face="normal" font="default">Contact Dermatitis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Contact Dermatitis</style></abbr-1></periodical><pages end="431" start="430">430-431</pages><volume><style face="normal" font="default">77</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1600-0536 (Electronic)IS - 0105-1873 (Linking)LA - engPT - LetterCO - France -</style></notes><work-type><style face="normal" font="default">10.1111/cod.12887</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29164699">PM:29164699</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Contact Dermatitis\2017-77-430-1.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Contact Dermatitis\2017-77-430-1.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Alcaraz-Mor R</style></custom2><misc3><style face="normal" font="default">10.1111/cod.12887</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87013</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Galera,M.D.</style></author><author><style face="normal" font="default"> Elvira-Rendueles,B.</style></author><author><style face="normal" font="default"> Moreno,J.M.</style></author><author><style face="normal" font="default"> Negral,L.</style></author><author><style face="normal" font="default"> Ruiz-Abellon,M.C.</style></author><author><style face="normal" font="default"> Garcia-Sanchez,A.</style></author><author><style face="normal" font="default"> Moreno-Grau,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Applied Mathematics and Statistics, Technical University of Cartagena, Dr. Fleming sn, 30202, Cartagena, Spain.</style></auth-address><titles><title><style face="normal" font="default">Analysis of airborne Olea pollen in Cartagena (Spain)</style></title><secondary-title><style face="normal" font="default">Sci Total Environ</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Total Environ</style></abbr-1></periodical><pages end="445" start="436">436-445</pages><volume><style face="normal" font="default">622-623</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="5" Month="12" Year="2017">2017/12/5</year></dates><abstract><style face="normal" font="default">Olive cultivation is of great importance in Southern Europe but olive pollen is the leading cause of allergy in many regions where it is grown. The best preventive measure for allergic patients is to avoid exposure. Thus, aerobiological monitoring networks must supply realistic pollen classes for the different types of allergic pollen. Even though those pollen classes are defined, they do not necessarily fit local data. Altogether, they should use predictive models to assess flowering intensity in advance. In this study, the Olea pollen degree of exposure classes (OPDEC) are defined based on percentiles and a predictive model is suggested for Cartagena, Spain. 24year (1993-2016) Olea pollen counts series was used to characterize the Main Pollen Season (MPS). The aerobiological samples were processed following the methodology proposed by Hirst and developed by the Spanish Aerobiology Network. The aerobiological database was completed with the meteorological data supplied by AEMET (Spanish State Meteorological Agency). MPS evolution over time, and its relation with temperature and rainfall, has been analysed. The study showed an increase in MPS duration and the amount of Olea pollen grains collected both in MPS and the peak day. The OPDEC should fit local data to improve preventive measures. Based on the 24year series, the proposed OPDEC for Cartagena are: Low (&lt;/=10grains/m(3)), Medium (between 10 and 50grains/m(3)), High (between 51 and 100grains/m(3)) and Very High (>/=100grains/m(3)). Olea pollen estimations in the MPS and in the peak day were obtained by means of three Regression Methods and climatic factors. The analysis reveals that the Bagging for Regression Trees (BRT) method is a good predictive alternative and stablishes the importance for each meteorological variable</style></abstract><notes><style face="normal" font="default">IS - 1879-1026 (Electronic)IS - 0048-9697 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.scitotenv.2017.11.349</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29220768">PM:29220768</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Total Environ\2017-622_623-436-45.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Total Environ\2017-622_623-436-45.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Galera MD</style></custom2><misc3><style face="normal" font="default">10.1016/j.scitotenv.2017.11.349</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87079</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Happel,C.S.</style></author><author><style face="normal" font="default"> Saini,S.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Biomarkers to Diagnose, Assess and Treat Chronic Spontaneous Urticaria: Not There Yet</style></title><secondary-title><style face="normal" font="default">Curr Treat Options Allergy</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Treat Options Allergy</style></full-title></periodical><pages end="449" start="438">438-449</pages><volume><style face="normal" font="default">4</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2196-3053</style></isbn><abstract><style face="normal" font="default">Purpose of Review Biomarkers to identify patients with chronic spontaneous urticaria (CSU), to grade clinical severity of CSU, and to guide therapy selection in patients with CSU have not yet been validated in any large CSU patient population. As such, there is insufficient evidence to recommend routine use of any particular biomarker. This review will summarize ongoing research in the field of biomarker development and how it could 1-áday benefit diagnosis, severity grading, and treatment decisions in CSU</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s40521-017-0147-z</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40521-017-0147-z</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Treat Options Allergy\2017-4-438-49.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Treat Options Allergy\2017-4-438-49.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Happel CS</style></custom2><misc3><style face="normal" font="default">10.1007/s40521-017-0147-z</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86574</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chen,H.</style></author><author><style face="normal" font="default"> Xu,X.</style></author><author><style face="normal" font="default"> Cheng,S.</style></author><author><style face="normal" font="default"> Xu,Y.</style></author><author><style face="normal" font="default"> Xuefei,Q.</style></author><author><style face="normal" font="default"> Cao,Y.</style></author><author><style face="normal" font="default"> Xie,J.</style></author><author><style face="normal" font="default"> Wang,C.Y.</style></author><author><style face="normal" font="default"> Xu,Y.</style></author><author><style face="normal" font="default"> Xiong,W.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China</style></auth-address><titles><title><style face="normal" font="default">Small interfering RNA directed against microRNA-155 delivered by a lentiviral vector attenuates asthmatic features in a mouse model of allergic asthma</style></title><secondary-title><style face="normal" font="default">Exp Ther Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Exp Ther Med</style></abbr-1></periodical><pages end="4396" start="4391">4391-4396</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">Asthma is a chronic T helper type 2 (Th2) cell-mediated inflammatory disease characterized by airway hyperresponsiveness (AHR) and airway inflammation. Although the majority of patients with asthma can achieve a good level of control with existing treatments, asthma runs a chronic course and the effectiveness of current treatment is not satisfactory for certain patients. MicroRNAs (miRNAs) are short noncoding RNAs that suppress gene expression at the post-transcriptional level; their role in regulating allergic inflammation remains largely unknown. The present study aimed to explore the role of miRNA-155 in the pathogenesis of asthma and its potential as a target for treatment. The expression of miRNA-155 increased in ovalbumin-sensitized and challenged mice compared with control mice, and lentiviral vector-delivered small interfering (si)RNA targeting miRNA-155 resulted in reduced AHR, airway inflammation and Th2 cytokine production. The data from the present study indicate that miRNA-155 serves an important role in the pathogenesis of asthma, and that lentiviral vector-delivered siRNA targeting miRNA-155 may serve as a novel approach for the treatment of allergic asthma</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1792-0981 (Print)IS - 1792-0981 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3892/etm.2017.5093</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29104649">PM:29104649</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Exp Ther Med\2017-14-4391-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Exp Ther Med\2017-14-4391-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Chen H</style></custom2><misc3><style face="normal" font="default">10.3892/etm.2017.5093</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87070</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Frohlich,M.</style></author><author><style face="normal" font="default"> Pinart,M.</style></author><author><style face="normal" font="default"> Keller,T.</style></author><author><style face="normal" font="default"> Reich,A.</style></author><author><style face="normal" font="default"> Cabieses,B.</style></author><author><style face="normal" font="default"> Hohmann,C.</style></author><author><style face="normal" font="default"> Postma,D.S.</style></author><author><style face="normal" font="default"> Bousquet,J.</style></author><author><style face="normal" font="default"> Anto,J.M.</style></author><author><style face="normal" font="default"> Keil,T.</style></author><author><style face="normal" font="default"> Roll,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Social Medicine, Epidemiology and Health Economics, Charite - Universitatsmedizin Berlin, Berlin, Germany.</style></auth-address><titles><title><style face="normal" font="default">Is there a sex-shift in prevalence of allergic rhinitis and comorbid asthma from childhood to adulthood? A meta-analysis</style></title><secondary-title><style face="normal" font="default">Clin Transl Allergy</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Transl Allergy</style></abbr-1></periodical><pages end="" start="44">44-</pages><volume><style face="normal" font="default">7</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Adult</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: Allergic rhinitis and asthma as single entities affect more boys than girls in childhood but more females in adulthood. However, it is unclear if this prevalence sex-shift also occurs in allergic rhinitis and concurrent asthma. Thus, our aim was to compare sex-specific differences in the prevalence of coexisting allergic rhinitis and asthma in childhood, adolescence and adulthood. Methods: Post-hoc analysis of systematic review with meta-analysis concerning sex-specific prevalence of allergic rhinitis. Using random-effects meta-analysis, we assessed male-female ratios for coexisting allergic rhinitis and asthma in children (0-10 years), adolescents (11-17) and adults (> 17). Electronic searches were performed using MEDLINE and EMBASE for the time period 2000-2014. We included population-based observational studies, reporting coexisting allergic rhinitis and asthma as outcome stratified by sex. We excluded non-original or non-population-based studies, studies with only male or female participants or selective patient collectives. Results: From a total of 6539 citations, 10 studies with a total of 93,483 participants met the inclusion criteria. The male-female ratios (95% CI) for coexisting allergic rhinitis and asthma were 1.65 (1.52; 1.78) in children (N = 6 studies), 0.61 (0.51; 0.72) in adolescents (N = 2) and 1.03 (0.79; 1.35) in adults (N = 2). Male-female ratios for allergic rhinitis only were 1.25 (1.19; 1.32, N = 5) in children, 0.80 (0.71; 0.89, N = 2) in adolescents and 0.98 (0.74; 1.30, N = 2) in adults, respectively. Conclusions: The prevalence of coexisting allergic rhinitis and asthma shows a clear male predominance in childhood and seems to switch to a female predominance in adolescents. This switch was less pronounced for allergic rhinitis only</style></abstract><notes><style face="normal" font="default">IS - 2045-7022 (Print)IS - 2045-7022 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Germany -CO - Spain -CO - Chile -CO - Netherlands -CO - France -</style></notes><work-type><style face="normal" font="default">10.1186/s13601-017-0176-5</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29225773">PM:29225773</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-44.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Transl Allergy\2017-7-44.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Frohlich M</style></custom2><misc3><style face="normal" font="default">10.1186/s13601-017-0176-5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87294</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Raulf,M.</style></author><author><style face="normal" font="default"> Bruning,T.</style></author><author><style face="normal" font="default"> Jensen-Jarolim,E.</style></author><author><style face="normal" font="default"> van Kampen,V.</style></author></authors></contributors><titles><title><style face="normal" font="default">Gender-related aspects in occupational allergies </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô Secondary publication and update</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="44">44-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">For years occupational allergies have been among the most frequently recorded occupational diseases, and both the skin as well as the respiratory tract may be affected. An estimated 9 to 15% of adult asthma is (partially) caused by work-related exposure. Gender-specific differences in exposure cause different risks in the workplace which affect the health of employees. This also applies to exposure and working conditions when handling sensitizing working substances. The presented gender-specific analysis of the German documentation of confirmed occupational respiratory allergic diseases and occupational skin diseases reveals clear differences between men and women in the number of diseases and also in exposure conditions and working areas</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Austria -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0175-y</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0175-y</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-44.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-44.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Raulf M</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0175-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86561</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wahn,U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Charite, Berlin, Germany</style></auth-address><titles><title><style face="normal" font="default">Preventing new sensitization and asthma onset by allergen immunotherapy: the current evidence</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="446" start="443">443-446</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: Specific allergen immunotherapy is considered a key candidate for a successful preventive intervention in atopic diseases. The strong association of atopic manifestations such as rhinitis and asthma with atopic sensitizations (specific serum IgE) provide a rationale for early intervention in childhood and adolescence. RECENT FINDINGS: Currently, the documentation of the disease-modifying intervention effects is limited to the secondary prevention of asthma symptoms in children with allergic rhinoconjunctivitis. These effects appear to be rather allergen specific than nonspecific. SUMMARY: Documentation on disease modification including a reduction of asthma symptoms in children, particularly with grass pollen tablets has become quite robust. It is not clear up to now, if the new onset of allergic sensitizations can be modified. So far data on primary prevention are not conclusive</style></abstract><notes><style face="normal" font="default">DA - 20171002IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000399</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28968272">PM:28968272</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-443-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-443-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171002, Wahn U</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000399</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86562</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">van de Veen,W.</style></author></authors></contributors><auth-address><style face="normal" font="default">aSwiss Institute of Allergy and Asthma Research, University of Zurich, Davos bChristine Kuhne-Center for Allergy Research and Education (CK-CARE), Davos, Switzerland</style></auth-address><titles><title><style face="normal" font="default">The role of regulatory B cells in allergen immunotherapy</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="452" start="447">447-452</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: Allergen immunotherapy (AIT) is currently the only curative treatment available for allergic diseases, and has been used in clinical practice for over a century. Induction and maintenance of immune tolerance to nonhazardous environmental and self-antigens is essential to maintain homeostasis and prevent chronic inflammation. Regulatory B (BREG) cells are immunoregulatory cells that protect against chronic inflammatory responses primarily through production of anti-inflammatory cytokines such as IL-10, transforming growth factor-beta, and IL-35. The importance of BREG cells has been extensively demonstrated in the context of autoimmune diseases. Data showing their role in the regulation of allergic responses are slowly accumulating. This review summarizes recent findings relevant to the topic of BREG cells and their potential role in AIT. RECENT FINDINGS: BREG cells support AIT in models of allergic airway inflammation and intestinal inflammation through induction of regulatory T (TREG) cells. In humans BREG frequency increases during venom immunotherapy while the phenotype of allergen-specific B cells changes. Mechanisms of BREG-mediated tolerance to allergens include IL-10-mediated suppression of effector T cell, including TH2 responses, induction of TREG cells, IL-10-mediated inhibition of Dendritic cell maturation, modulation of T follicular helper responses, and production of anti-inflammatory IgG4 antibodies. SUMMARY: Current evidence supports a potential role for BREG cells in induction and maintenance of allergen tolerance during AIT. A better understanding of the role of B cells and BREG cells in AIT could open potential new windows for developing targeted therapies specifically focused on promoting BREG responses during AIT</style></abstract><notes><style face="normal" font="default">DA - 20170928IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000400</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28957824">PM:28957824</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-447-52.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-447-52.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170928, van de Veen W</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000400</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86519</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pouliquen,I.J.</style></author><author><style face="normal" font="default"> Howarth,P.</style></author><author><style face="normal" font="default"> Austin,D.</style></author><author><style face="normal" font="default"> Gunn,G.</style></author><author><style face="normal" font="default"> Meyer,E.</style></author><author><style face="normal" font="default"> Price,R.G.</style></author><author><style face="normal" font="default"> Bradford,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical Pharmacology Modelling &amp; Simulation, GlaxoSmithKline, Uxbridge, UK</style></auth-address><titles><title><style face="normal" font="default">Response to case report: Airway autoimmune responses in severe eosinophilic asthma following low-dose Mepolizumab therapy</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Clin Immunol</style></abbr-1></periodical><pages end="" start="45">45-</pages><volume><style face="normal" font="default">13</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171109IS - 1710-1484 (Print)IS - 1710-1484 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1186/s13223-017-0217-6</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29118815">PM:29118815</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-45.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-45.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171109, Pouliquen IJ</style></custom2><misc3><style face="normal" font="default">10.1186/s13223-017-0217-6</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86980</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Meldrum,K.</style></author><author><style face="normal" font="default"> Guo,C.</style></author><author><style face="normal" font="default"> Marczylo,E.L.</style></author><author><style face="normal" font="default"> Gant,T.W.</style></author><author><style face="normal" font="default"> Smith,R.</style></author><author><style face="normal" font="default"> Leonard,M.O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Toxicology Department, Centre for Radiation, Chemical and Environmental Hazards, Public Health England, Chilton, Harwell Campus, OX11 0RQ, UK</style></auth-address><titles><title><style face="normal" font="default">Mechanistic insight into the impact of nanomaterials on asthma and allergic airway disease</style></title><secondary-title><style face="normal" font="default">Part Fibre Toxicol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Part Fibre Toxicol</style></abbr-1></periodical><pages end="" start="45">45-</pages><volume><style face="normal" font="default">14</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="21" Month="11" Year="2017">2017/11/21</year></dates><abstract><style face="normal" font="default">Asthma is a chronic respiratory disease known for its high susceptibility to environmental exposure. Inadvertent inhalation of engineered or incidental nanomaterials is a concern for human health, particularly for those with underlying disease susceptibility. In this review we provide a comprehensive analysis of those studies focussed on safety assessment of different nanomaterials and their unique characteristics on asthma and allergic airway disease. These include in vivo and in vitro approaches as well as human and population studies. The weight of evidence presented supports a modifying role for nanomaterial exposure on established asthma as well as the development of the condition. Due to the variability in modelling approaches, nanomaterial characterisation and endpoints used for assessment in these studies, there is insufficient information for how one may assign relative hazard potential to individual nanoscale properties. New developments including the adoption of standardised models and focussed in vitro and in silico approaches have the potential to more reliably identify properties of concern through comparative analysis across robust and select testing systems. Importantly, key to refinement and choice of the most appropriate testing systems is a more complete understanding of how these materials may influence disease at the cellular and molecular level. Detailed mechanistic insight also brings with it opportunities to build important population and exposure susceptibilities into models. Ultimately, such approaches have the potential to more clearly extrapolate relevant toxicological information, which can be used to improve nanomaterial safety assessment for human disease susceptibility</style></abstract><notes><style face="normal" font="default">IS - 1743-8977 (Electronic)IS - 1743-8977 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1186/s12989-017-0228-y</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29157272">PM:29157272</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Part Fibre Toxicol\2017-14-45.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Part Fibre Toxicol\2017-14-45.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171121, Meldrum K</style></custom2><misc3><style face="normal" font="default">10.1186/s12989-017-0228-y</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87298</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Untersmayr,E.</style></author><author><style face="normal" font="default"> Jensen,A.N.</style></author><author><style face="normal" font="default"> Walch,K.</style></author></authors></contributors><titles><title><style face="normal" font="default">Sex hormone allergy: clinical aspects, causes and therapeutic strategies </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô Update and secondary publication</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="45">45-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">Sex hormone allergy as a clinical syndrome has been known for almost a century. Due to the diversity of clinical presentation regarding symptoms and disease patterns, the optimal patient care represents an enormous interdisciplinary challenge. Frequently, hypersensitivity reactions affect more than one sex hormone and double positive tests for estrogen and progesterone have been described. Since the menstrual cycle dependent symptoms range from skin afflictions, gynecological problems to non-specific reactions, different pathophysiological mechanisms seem likely</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0176-x</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0176-x</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-45.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-45.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Untersmayr E</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0176-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87402</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ghazali,H.</style></author><author><style face="normal" font="default"> Gammoudi,M.</style></author><author><style face="normal" font="default"> Yahmadi,A.</style></author><author><style face="normal" font="default"> Chaaebeni,G.</style></author><author><style face="normal" font="default"> Souyah,A.</style></author><author><style face="normal" font="default"> Souissi,S.</style></author></authors></contributors><titles><title><style face="normal" font="default">Anaphylaxis in an emergency department: Epidemiology, clinical features and management</style></title><secondary-title><style face="normal" font="default">Tunis Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Tunis Med</style></abbr-1></periodical><pages end="52" start="45">45-52</pages><volume><style face="normal" font="default">95</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Tunisia</style></keyword></keywords><dates><year Day="0" Month="1" Year="2017">2017/1</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Studies report that anaphylaxis was under-diagnosed in emergency department (ED) and emergency management was often in disagreement with international recommendations. AIM OF THE STUDY: The aim of this study was to describe the epidemiology, clinical features, management and outcome of patients with anaphylaxis presenting to an ED. METHODS: Prospective, observational study over four years (June 2010 to May 2014). INCLUSION CRITERIA: patients (> 14 years of age) presenting consecutively to the ED with the diagnosis of anaphylaxis. Collection of epidemiological, clinical and therapeutic parameters Results: During the study, 239 patients were enrolled. Mean age = 40+/-15 years. Sex-ratio=0.8. History of anaphylaxis was reported in 40% of cases. Clinical features n (%): cutaneous features 229 (96), cardiovascular features 124 (52), respiratory features 127 (53), gastrointestinal features 48 (20) and neurologic features 4 (10). Most common allergens: drugs 62%, food 24% and insects 4%. No causes were apparent in 8% of cases. An anaphylactic shock was recorded in 73 patients (31%). Adrenaline was used in 83%of patients, intravenously in 31%. Corticosteroids and histamine H1 antagonist were prescribed in 98 and 51% respectively. Biphasic reactions were reported in three patients. There was no death cases registered. CONCLUSION: Our results showed that the prevalence of anaphylaxis was low.This demonstrates that anaphylaxis is a situation which remains underestimated. It is therefore imperative to conduct prospective multicenter studies in emergency services for better determination of its impact and its risk factors</style></abstract><notes><style face="normal" font="default">IS - 0041-4131 (Print)IS - 0041-4131 (Linking)LA - engPT - Journal ArticleCO - Tunisia -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29327768">PM:29327768</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Tunis Med\2017-95-45-52.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Tunis Med\2017-95-45-52.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171224, Ghazali H</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86560</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Asero,R.</style></author><author><style face="normal" font="default"> Canonica,G.W.</style></author><author><style face="normal" font="default"> Cristaudo,A.</style></author><author><style face="normal" font="default"> Fierro,M.T.</style></author><author><style face="normal" font="default"> Girolomoni,G.</style></author><author><style face="normal" font="default"> Marzano,A.V.</style></author><author><style face="normal" font="default"> Nettis,E.</style></author><author><style face="normal" font="default"> Pepe,P.</style></author><author><style face="normal" font="default"> Pigatto,P.</style></author><author><style face="normal" font="default"> Rossi,O.</style></author></authors></contributors><auth-address><style face="normal" font="default">aAmbulatorio di Allergologia, Clinica San Carlo, Paderno Dugnan</style></auth-address><titles><title><style face="normal" font="default">Critical appraisal of the unmet needs in the treatment of chronic spontaneous urticaria with omalizumab: an Italian perspective</style></title><secondary-title><style face="normal" font="default">Curr Opin Allergy Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Allergy Clin Immunol</style></abbr-1></periodical><pages end="459" start="453">453-459</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: The humanized anti-IgE antibody omalizumab has been available for patients with chronic spontaneous urticaria (CSU) in Italy since 2015. This review summarizes the unresolved issues and unmet therapeutic needs associated with omalizumab and discusses practical recommendations for its use in the management of CSU. RECENT FINDINGS: Although modern second-generation H1-antihistamines are the standard of care for patients with CSU, adjunctive treatments (including omalizumab) may be required for effective control of symptoms in many patients. Evidence from clinical trials and experience from daily clinical practice suggest that the use of omalizumab in patients with CSU who have inadequate response to H1-antihistamines remains challenging. SUMMARY: Based on current international guidelines, omalizumab labelling information and our experience in clinical practice, we provide treatment recommendations regarding the use of omalizumab in patients with CSU. These include: optimal treatment duration, the use of concomitant antihistamine therapy, the definition and management of disease relapse after treatment, and the management of patients with late or no response to treatment</style></abstract><notes><style face="normal" font="default">DA - 20171002IS - 1473-6322 (Electronic)IS - 1473-6322 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1097/ACI.0000000000000404</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28968274">PM:28968274</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-453-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Allergy Clin Immunol\2017-17-453-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171002, Asero R</style></custom2><misc3><style face="normal" font="default">10.1097/ACI.0000000000000404</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86779</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ando,T.</style></author><author><style face="normal" font="default"> Kashiwakura,J.I.</style></author><author><style face="normal" font="default"> Itoh-Nagato,N.</style></author><author><style face="normal" font="default"> Yamashita,H.</style></author><author><style face="normal" font="default"> Baba,M.</style></author><author><style face="normal" font="default"> Kawakami,Y.</style></author><author><style face="normal" font="default"> Tsai,S.H.</style></author><author><style face="normal" font="default"> Inagaki,N.</style></author><author><style face="normal" font="default"> Takeda,K.</style></author><author><style face="normal" font="default"> Iwata,T.</style></author><author><style face="normal" font="default"> Shimojo,N.</style></author><author><style face="normal" font="default"> Fujisawa,T.</style></author><author><style face="normal" font="default"> Nagao,M.</style></author><author><style face="normal" font="default"> Matsumoto,K.</style></author><author><style face="normal" font="default"> Kawakami,Y.</style></author><author><style face="normal" font="default"> Kawakami,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Laboratory for Cytokine Regulation, RIKEN Center for Integrative Medical Sciences (RIKEN IMS), Yokohama, Japan</style></auth-address><titles><title><style face="normal" font="default">Histamine-releasing factor enhances food allergy</style></title><secondary-title><style face="normal" font="default">J Clin Invest</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Clin Invest</style></abbr-1></periodical><pages end="4553" start="4541">4541-4553</pages><volume><style face="normal" font="default">127</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Mastocytosis</style></keyword></keywords><dates><year Day="13" Month="11" Year="2017">2017/11/13</year></dates><abstract><style face="normal" font="default">Food allergy occurs due to IgE- and mast cell-dependent intestinal inflammation. Previously, we showed that histamine-releasing factor (HRF), a multifunctional protein secreted during allergy, interacts with a subset of IgE molecules and that the HRF dimer activates mast cells in an HRF-reactive IgE-dependent manner. In this study, we investigated whether HRF plays any role in food allergy. Specifically, we determined that prophylactic and therapeutic administration of HRF inhibitors that block HRF-IgE interactions reduces the incidence of diarrhea and mastocytosis in a murine model of food allergy. Food allergy-associated intestinal inflammation was accompanied by increased secretion of the HRF dimer into the intestine in response to proinflammatory, Th2, and epithelial-derived cytokines and HRF-reactive IgE levels at the elicitation phase. Consistent with these data, patients with egg allergy had higher blood levels of HRF-reactive IgE compared with individuals that were not hypersensitive. Successful oral immunotherapy in egg-allergy patients and food-allergic mice reduced HRF-reactive IgE levels, thereby suggesting a pathological role for HRF in food allergy. Together, these results suggest that antigen and HRF dimer amplify intestinal inflammation by synergistically activating mast cells and indicate that HRF has potential as a therapeutic target in food allergy</style></abstract><notes><style face="normal" font="default">DA - 20171113IS - 1558-8238 (Electronic)IS - 0021-9738 (Linking)LA - engPT - Journal ArticleCO - Japan -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1172/JCI96525</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29130935">PM:29130935</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Clin Invest\20171113-AndoT.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Clin Invest\20171113-AndoT.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Ando T</style></custom2><misc3><style face="normal" font="default">10.1172/JCI96525</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86573</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ferrer,M.</style></author><author><style face="normal" font="default"> Boccon-Gibod,I.</style></author><author><style face="normal" font="default"> Goncalo,M.</style></author><author><style face="normal" font="default"> Inaloz,H.S.</style></author><author><style face="normal" font="default"> Knulst,A.</style></author><author><style face="normal" font="default"> Lapeere,H.</style></author><author><style face="normal" font="default"> Parthasaradhi,A.</style></author><author><style face="normal" font="default"> Stingl,G.</style></author><author><style face="normal" font="default"> Tagka,A.</style></author><author><style face="normal" font="default"> Valenzuela,F.</style></author><author><style face="normal" font="default"> Yeung,J.</style></author><author><style face="normal" font="default"> Thomsen,S.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Allergy and Clinical Immunology, Clinica Universidad de Navarra, Pamplona, Spain</style></auth-address><titles><title><style face="normal" font="default">Expert opinion: defining response to omalizumab in patients with chronic spontaneous urticaria</style></title><secondary-title><style face="normal" font="default">Eur J Dermatol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Eur J Dermatol</style></abbr-1></periodical><pages end="463" start="455">455-463</pages><volume><style face="normal" font="default">27</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="10" Year="2017">2017/10/1</year></dates><abstract><style face="normal" font="default">Omalizumab (a recombinant, humanized anti-immunoglobulin-E antibody) has been shown in three pivotal Phase III trials (ASTERIA I, II and GLACIAL) and real-world studies to be effective and well-tolerated for the treatment of chronic spontaneous urticaria (CSU), and is the only licensed third-line treatment for CSU. However, the definition of response to omalizumab treatment often differs between clinical trials, real-world studies, and daily practice of individual physicians globally. As such, a consensus definition of "complete", "partial" and "non-response" to omalizumab is required in order to harmonize treatment management and compare data. Here, it is proposed that a disease measurement tool, for example, the 7-Day Urticaria Activity Score (UAS7) or Urticaria Control Test (UCT) is required for defining response. The addition of quality of life measurements is helpful to gain insight into a patient's disease burden and its changes during treatment. A potential omalizumab treatment approach based on speed and pattern of response at 1-3 and 3-6 months is suggested. In cases where there is no response during the first 1-3 months, physicians should consider reassessing the original CSU diagnosis. Moreover, in patients showing partial response at 12 weeks, treatment with omalizumab should be continued in order to maximize the possibility of achieving symptom control. If patients have a UAS7>6 and/or UCT&lt;12, then continued treatment is advised, dependent on physician judgement and patient expectations. In treatment responders, omalizumab treatment can be resumed at a later stage after discontinuation with the same degree of symptom control</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1952-4013 (Electronic)IS - 1167-1122 (Linking)LA - engPT - Journal ArticleCO - Spain -CO - France -CO - Portugal -CO - Turkey -CO - Netherlands -CO - Belgium -CO - India -CO - Austria -CO - Greece -CO - Chile -CO - Canada -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1684/ejd.2017.3085</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29084635">PM:29084635</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Eur J Dermatol\2017-27-455-63.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Eur J Dermatol\2017-27-455-63.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Ferrer M</style></custom2><misc3><style face="normal" font="default">10.1684/ejd.2017.3085</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87081</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Arasi,S.</style></author><author><style face="normal" font="default"> Pajno,G.B.</style></author></authors></contributors><titles><title><style face="normal" font="default">Evidence Gaps in Oral Immunotherapy for Food Allergy</style></title><secondary-title><style face="normal" font="default">Curr Treat Options Allergy</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Curr Treat Options Allergy</style></full-title></periodical><pages end="467" start="458">458-467</pages><volume><style face="normal" font="default">4</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2196-3053</style></isbn><abstract><style face="normal" font="default">Purpose of review IgE-mediated food allergy (FA) is a potentially life-threatening condition with negative impact on the quality of life of patients and their family. It has been emerging as a public health priority in westernized countries in the recent two decades. The current standard approach to FA consists of the strict avoidance of the triggering food and keeping rescue medication readily available in the event an allergic reaction occurs. However, an elimination diet may be difficult and frustrating, above all for those foods (e.g., milk and egg) that are pivotal in the common diet</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Italy -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s40521-017-0146-0</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1007/s40521-017-0146-0</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Treat Options Allergy\2017-4-458-67.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Treat Options Allergy\2017-4-458-67.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Arasi S</style></custom2><misc3><style face="normal" font="default">10.1007/s40521-017-0146-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87297</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Koper,I.</style></author><author><style face="normal" font="default"> Hufnagl,K.</style></author><author><style face="normal" font="default"> Ehmann,R.</style></author></authors></contributors><titles><title><style face="normal" font="default">Gender aspects and influence of hormones on bronchial asthma </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô Secondary publication and update</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="46">46-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">There is good evidence for gender-specific differences in asthma regarding all affected areas, from intra- to extra-cellular mediators to the whole organ structure und functioning of the lung. These result from complex, in parts synergistic, in other parts opposing, effects-á</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çö especially of female sex hormones, and rather protective effects of male hormones-áagainst asthma, which include effects on the cellular immune system. Additionally, there are gender differences of sociocultural origin, regarding presentation, doctor</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖs diagnosis and treatment of asthma symptoms, as well as the undertaken coping strategies concerning the female or male patient</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖs complaints. Taking into account gender-specific differences in asthma would contribute to improved individual diagnosis and therapies</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Germany -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0177-9</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0177-9</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-46.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-46.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Koper I</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0177-9</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86975</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kim,Y.H.</style></author><author><style face="normal" font="default"> Choi,Y.J.</style></author><author><style face="normal" font="default"> Lee,E.J.</style></author><author><style face="normal" font="default"> Kang,M.K.</style></author><author><style face="normal" font="default"> Park,S.H.</style></author><author><style face="normal" font="default"> Kim,D.Y.</style></author><author><style face="normal" font="default"> Oh,H.</style></author><author><style face="normal" font="default"> Park,S.J.</style></author><author><style face="normal" font="default"> Kang,Y.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Food and Nutrition, Hallym University, 1, Hallymdaehak-gil, Chuncheon, Gangwon 24252, Korea</style></auth-address><titles><title><style face="normal" font="default">Novel glutathione-containing dry-yeast extracts inhibit eosinophilia and mucus overproduction in a murine model of asthma</style></title><secondary-title><style face="normal" font="default">Nutr Res Pract</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nutr Res Pract</style></abbr-1></periodical><pages end="469" start="461">461-469</pages><volume><style face="normal" font="default">11</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">BACKGROUND/OBSECTIVE: Airway inflammation by eosinophils, neutrophils and alveolar macrophages is a characteristic feature of asthma that leads to pathological subepithelial thickening and remodeling. Our previous study showed that oxidative stress in airways resulted in eosinophilia and epithelial apoptosis. The current study investigated whether glutathione-containing dry yeast extract (dry-YE) ameliorated eosinophilia, goblet cell hyperplasia and mucus overproduction. MATERIALS/METHOD: This study employed 2 microg/mL lipopolysaccharide (LPS)- or 20 ng/mL eotaxin-1-exposed human bronchial epithelial cells and ovalbumin (OVA)-challenged mice. Dry-YE employed in this study contained a significant amount of glutathione (140 mg in 100 g dry yeast). RESULTS: Human bronchial epithelial cell eotaxin-1 and mucin 5AC (MUC5AC) were markedly induced by the endotoxin LPS, which was dose-dependently attenuated by nontoxic dry-YE at 10-50 microg/mL. Moreover, dry-YE inhibited the MUC5AC induction enhanced by eotaxin-1, indicating that eotaxin-1-mediated eosinophilia may prompt the MUC5AC induction. Oral supplementation with 10-100 mg/kg dry-YE inhibited inflammatory cell accumulation in airway subepithelial regions with a reduction of lung tissue level of intracellular adhesion molecule-1. In addition, >/= 50 mg/kg dry-YE diminished the lung tissue levels of eotaxin-1, eosinophil major basic protein and MUC5AC in OVA-exposed mice. Alcian blue/periodic acid schiff staining revealed that the dry-YE supplementation inhibited goblet cell hyperplasia and mucus overproduction in the trachea and bronchiolar airways of OVA-challenged mice. CONCLUSIONS: Oxidative stress may be involved in the induction of eotaxin-1 and MUC5AC by endotoxin episode and OVA challenge. Dry-YE effectively ameliorated oxidative stress-responsive epithelial eosinophilia and mucus-secreting goblet cell hyperplasia in cellular and murine models of asthma</style></abstract><notes><style face="normal" font="default">IS - 1976-1457 (Print)IS - 1976-1457 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.4162/nrp.2017.11.6.461</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29209456">PM:29209456</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nutr Res Pract\2017-11-461-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nutr Res Pract\2017-11-461-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171206, Kim YH</style></custom2><misc3><style face="normal" font="default">10.4162/nrp.2017.11.6.461</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86714</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fang,S.</style></author><author><style face="normal" font="default"> Bajoghli,A.</style></author><author><style face="normal" font="default"> Bajoghli,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Utah School of Medicine, Salt Lake City, Utah.</style></auth-address><titles><title><style face="normal" font="default">Shiitake mushroom-induced flagellate dermatitis</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="463" start="462">462-463</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.007</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150072">PM:29150072</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-462-3.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-462-3.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Fang S</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.007</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86782</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tanticharoenwiwat,P.</style></author><author><style face="normal" font="default"> Kulalert,P.</style></author><author><style face="normal" font="default"> Dechatiwongse Na Ayudhya,T.</style></author><author><style face="normal" font="default"> Koontongkaew,S.</style></author><author><style face="normal" font="default"> Jiratchariyakul,W.</style></author><author><style face="normal" font="default"> Soawakontha,R.</style></author><author><style face="normal" font="default"> Booncong,P.</style></author><author><style face="normal" font="default"> Poachanukoon,O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Center of Excellence for Allergy, Asthma and Pulmonary Disease, Thammasat University Hospital, Pathumthani 12120, Thailand</style></auth-address><titles><title><style face="normal" font="default">Inhibitory effect of Phlai capsules on skin test responses among allergic rhinitis patients: a randomized, three-way crossover study</style></title><secondary-title><style face="normal" font="default">J Integr Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Integr Med</style></abbr-1></periodical><pages end="468" start="462">462-468</pages><volume><style face="normal" font="default">15</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">BACKGROUND: Zingiber cassumunar Roxb., commonly known as Phlai in Thai, has been used as a traditional medicine in Thailand for the treatment of various diseases, including inflammation and chronic airway disease. OBJECTIVE: The purpose of this study was to assess the antihistaminic effect of Phlai on skin testing. DESIGN, SETTING, PARTICIPANTS AND INTERVENTION: This was a randomized, open-label, three-way crossover study. Twenty allergic rhinitis (AR) patients were enrolled. In randomized sequence, patients received a single dose of Phlai capsules (100 or 200 mg) or loratadine (10 mg) with a washout period of 1 week between each treatment. MAIN OUTCOME MEASURES: Skin prick testing for histamine and common aeroallergen (house dust mite) were performed before treatment and after 1, 2, 3, 4, 6, 8, 12 and 24 hours of treatment. The main treatment outcomes were the mean wheal and flare responses to the skin prick test after treatment. RESULTS: Both 100 mg and 200 mg Phlai doses suppressed wheal and flare responses to house dust mite allergen, but only 200 mg of Phlai capsules significantly suppressed wheal and flare responses to histamine. Repeated measures analysis of variance showed that loratadine caused more wheal and flare suppression than Phlai capsules in responses to the histamine skin prick test. However, there were no significant differences among the effects of 100 mg Phlai capsules, 200 mg Phlai capsules and loratadine in suppression of wheal and flare induced by the mite skin prick test. Both doses of Phlai were well-tolerated with no adverse events. CONCLUSION: Both 100 mg (compound D 4 mg) and 200 mg (compound D 8 mg) Phlai capsules, when taken as a single therapeutic dose, inhibited skin reactivity to histamine and mite skin prick tests in AR patients. TRIAL REGISTRATION: Thai clinical trial registry (TCTR20160510001)</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 2095-4964 (Print)LA - engPT - Journal ArticleCO - Thailand -</style></notes><work-type><style face="normal" font="default">10.1016/S2095-4964(17)60353-4</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29103416">PM:29103416</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171106, Tanticharoenwiwat P</style></custom2><misc3><style face="normal" font="default">10.1016/S2095-4964(17)60353-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86715</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Brooks,C.</style></author><author><style face="normal" font="default"> Coffman,A.</style></author><author><style face="normal" font="default"> Erwin,E.</style></author><author><style face="normal" font="default"> Mikhail,I.</style></author></authors></contributors><auth-address><style face="normal" font="default">The Ohio State University College of Medicine, Columbus, Ohio</style></auth-address><titles><title><style face="normal" font="default">Diagnosis and treatment of food allergic reactions in pediatric emergency settings</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="468" start="467">467-468</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.287</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150075">PM:29150075</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-467-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-467-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Brooks C</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.287</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86711</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Yamasaki,A.</style></author><author><style face="normal" font="default"> Hoehle,L.P.</style></author><author><style face="normal" font="default"> Phillips,K.M.</style></author><author><style face="normal" font="default"> Campbell,A.P.</style></author><author><style face="normal" font="default"> Caradonna,D.S.</style></author><author><style face="normal" font="default"> Gray,S.T.</style></author><author><style face="normal" font="default"> Sedaghat,A.R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otolaryngology, Harvard Medical School, Boston, Massachusetts; Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts</style></auth-address><titles><title><style face="normal" font="default">Cockroach hypersensitivity is associated with greater severity of chronic rhinosinusitis</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="470" start="469">469-470</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171118IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29150076">PM:29150076</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-469-70.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-469-70.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Yamasaki A</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87018</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Homann,A.</style></author><author><style face="normal" font="default"> Rockendorf,N.</style></author><author><style face="normal" font="default"> Kromminga,A.</style></author><author><style face="normal" font="default"> Frey,A.</style></author><author><style face="normal" font="default"> Platts-Mills,T.A.</style></author><author><style face="normal" font="default"> Jappe,U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Clinical and Molecular Allergology, Priority Research Area Asthma &amp; Allergy, Airway Research Center North (ARCN), German Center for Lung Research (DZL), Research Center Borstel, Borstel, Germany</style></auth-address><titles><title><style face="normal" font="default">Glycan and Peptide IgE Epitopes of the TNF-alpha Blockers Infliximab and Adalimumab - Precision Diagnostics by Cross-Reactivity Immune Profiling of Patient Sera</style></title><secondary-title><style face="normal" font="default">Theranostics</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Theranostics</style></abbr-1></periodical><pages end="4709" start="4699">4699-4709</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">19</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Biological drugs like therapeutic antibodies are widely used for the treatment of various diseases like inflammatory disorders and cancer. A drawback of these novel treatments is the substantial proportion of patients experiencing adverse reactions such as loss-of-drug effect or hypersensitivity reactions. These reactions are associated with pre-existing and/or developing anti-drug antibodies. Especially IgE development is a risk factor for life-threatening systemic anaphylaxis. METHODS: In order to characterize the individual drug-specific serum IgE, an IgE cross-reactivity immune profiling (ICRIP) assay was developed. Individual IgG epitopes of anti-drug antibodies against adalimumab were identified by epitope mapping via peptide microarray. RESULTS: ICRIP analyses of sera from patients treated with the therapeutic antibodies adalimumab (ADL) and infliximab (IFX) reveal individual, distinct IgE binding patterns. IgG epitopes were identified mostly located in the variable region of ADL. CONCLUSIONS: Using ICRIP and peptide microarrays for pharmacovigilance of the TNF-alpha blockers IFX and ADL, risk factors and biomarkers before and during therapy shall be identified. These diagnostic systems provide the basis for a safe and efficacious therapy decision for each patient in cases of adverse drug reactions mediated by different types of anti-drug antibodies</style></abstract><notes><style face="normal" font="default">IS - 1838-7640 (Electronic)IS - 1838-7640 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - United States -</style></notes><work-type><style face="normal" font="default">10.7150/thno.20654</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29187897">PM:29187897</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Theranostics\2017-7-4699-709.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Theranostics\2017-7-4699-709.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171017, Homann A</style></custom2><misc3><style face="normal" font="default">10.7150/thno.20654</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87296</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jensen-Jarolim,E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Gender effects in allergology </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô Secondary publications and update</style></title><secondary-title><style face="normal" font="default">World Allergy Organ J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">World Allergy Organ J</style></abbr-1></periodical><pages end="" start="47">47-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1939-4551</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Austria -</style></notes><work-type><style face="normal" font="default">10.1186/s40413-017-0178-8</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s40413-017-0178-8</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-47.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\World Allergy Organ J\2017-10-47.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Jensen-Jarolim E</style></custom2><misc3><style face="normal" font="default">10.1186/s40413-017-0178-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86864</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Numminen,J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Duodecim</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Duodecim</style></abbr-1></periodical><pages end="478" start="473">473-478</pages><volume><style face="normal" font="default">133</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">There have been no major changes in the pharmacological treatment of allergic rhinitis in recent years. Treatment is symptomatic and tailored individually, taking into account the type and severity of symptoms. Few new products have entered the market, and treatment is still largely based on antihistamines and nasally administered glucocorticoids. However, the general strategies for treating allergic rhinitis have developed over the last decade due to the introduction of the Finnish National Allergy Program. The treatment should aim at improving tolerance. Avoiding allergens is not necessary but it may help in controlling the symptoms. Hyposensitization, the only disease-modifying therapy, is a recommended, effective and safe form of treatment. New, practical sublingual hyposensitization products have facilitated treatment implementation and moved it from outpatient clinics into homes, which is a more patient-oriented approach and also cost-effective in the long term. However, the unit costs of treatment are relatively high for the patients</style></abstract><notes><style face="normal" font="default">IS - 0012-7183 (Print)IS - 0012-7183 (Linking)LA - engPT - Journal ArticleCO - Finland -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29205994">PM:29205994</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Duodecim\2017-133-473-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Duodecim\2017-133-473-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Numminen J</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87037</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Oppenheimer,J.J.</style></author><author><style face="normal" font="default"> Greenberger,P.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">UMDNJ-NJ Medical School, Cedar Knolls, New Jersey. Electronic address: nallopp22@gmail.comNorthwestern University, Chicago, Illinois</style></auth-address><titles><title><style face="normal" font="default">Baseline asthma burden, comorbidities, and biomarkers in omalizumab-treated patients in PROSPERO</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="475" start="474">474-475</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - EditorialCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.021</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29223296">PM:29223296</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-474-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-474-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Oppenheimer JJ</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.021</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87038</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Stier,M.T.</style></author><author><style face="normal" font="default"> Peebles,R.S.,Jr.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.</style></auth-address><titles><title><style face="normal" font="default">Innate lymphoid cells and allergic disease</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="488" start="480">480-488</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">immunology</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.08.290</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29223298">PM:29223298</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-480-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-480-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Stier MT</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.08.290</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87254</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nabavi,M.</style></author><author><style face="normal" font="default"> Lavavpour,M.</style></author><author><style face="normal" font="default"> Arshi,S.</style></author><author><style face="normal" font="default"> Bemanian,M.H.</style></author><author><style face="normal" font="default"> Esmaeilzadeh,H.</style></author><author><style face="normal" font="default"> Molatefi,R.</style></author><author><style face="normal" font="default"> Rekabi,M.</style></author><author><style face="normal" font="default"> Ahmadian,J.</style></author><author><style face="normal" font="default"> Eslami,N.</style></author><author><style face="normal" font="default"> Shokri,S.</style></author><author><style face="normal" font="default"> Darabi,K.</style></author><author><style face="normal" font="default"> Sedighi,G.R.</style></author><author><style face="normal" font="default"> Fallahpour,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">Characteristics, Etiology and Treatment of Pediatric and Adult Anaphylaxis in Iran</style></title><secondary-title><style face="normal" font="default">Iran J Allergy Asthma Immunol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Iran J Allergy Asthma Immunol</style></full-title></periodical><pages end="487" start="480">480-487</pages><volume><style face="normal" font="default">16</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Adult anaphylaxis,Anaphylaxis registry,Anaphylaxis etiology,Anaphylaxis treatment,Children anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> etiology</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="23" Month="12" Year="2017">2017/12/23</year></dates><abstract><style face="normal" font="default">Despite the increasing prevalence of anaphylaxis, there is little information about the characteristics and practice of healthcare providers in treating anaphylaxis, so this study was conducted to record the characteristics and therapeutic approaches of anaphylaxis from May 2012 until April 2015, the data of all patients diagnosed with anaphylaxis in the Allergy department of three referral university hospitals in Tehran, Iran were recorded. Thereafter, the demographics, clinical features, triggers and therapeutic approach were evaluated. This study investigated 136 individuals, 64 males (47%) between 6 months and 68 years old, as well as 72 others (52.94%) under 18 years of age (pediatric). The following were the most common organs involved: Skin 86.02% (pediatric 91.66% vs adult 79.68%), respiratory tract 51.47% (pediatric 43.05% vs adult 60.93%), cardiovascular 50.73% (pediatric 54.16% vs adult 46.87%), gastrointestinal 20.58% (pediatric 27.7% vs adult 12.5% ) and neurologic system 5.88% (only in adults). The following were the most identified causing foods 69 (50.37%)[42 pediatric (children) and 27 adults], drugs 34( 25%)[14 pediatric and 20 adults], idiopathic 16( 11.77%)[3 pediatric and 13 adults], insect sting 7( 5.15%)[3 pediatric and 4 adults] , exercise 6( 4.42%) [1 pediatric and 5 adults]. Milk, egg and wheat were the most common causative foods in pediatric cases but sesame, as well as egg and milk were the most common causes in adults. Epinephrine injection, auto injector epinephrine prescription as a discharging plan and referral to an allergist were: 10.78, 1.96 and 7.8 %, respectively. In this case series we found that, cutaneous, respiratory, cardiovascular and gastrointestinal complains were the most common manifestations and food, drug and idiopathic were the most common causes.In this study, the diagnosis of anaphylaxis, epinephrine subscription and referral to an allergist were significantly lower in comparison to other studies</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Iran -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url ppv-ref="no">http://ijaai.tums.ac.ir/index.php/ijaai/article/view/1452</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Iran J Allergy Asthma Immunol\2017-16-480-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Iran J Allergy Asthma Immunol\2017-16-480-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Nabavi M</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87201</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Cid Del Prado-Izquierdo,M.L.</style></author><author><style face="normal" font="default"> Zarco-Cid Del Prado,O.</style></author><author><style face="normal" font="default"> Visoso-Salgado,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Medica Bosques, Clinica de Asma, Alergia e Inmunologia, Toluca, Estado de Mexico, Mexico. lucy_14delprado@hotmail.com</style></auth-address><titles><title><style face="normal" font="default">[Severe atopic dermatitis and hiper-IgE]</style></title><secondary-title><style face="normal" font="default">Rev Alerg Mex</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Rev Alerg Mex</style></abbr-1></periodical><pages end="492" start="487">487-492</pages><volume><style face="normal" font="default">64</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">BACKGROUND: Atopic dermatitis (AD) is a chronic inflammatory and complex skin disease, typically occurring in individuals with a personal or family history of atopy. It is characterized by lesions of dermatitis, pruritus and dry skin (xerosis) that evolve with chronic course and intermittent outbreaks alternating with remission phases. AD appears from 5-15 % of the general population, 10-20 % of the pediatric population, and 1-3 % of the adult population. CLINICAL REPORT: A 19-year-old male patient with a severe AD (SCORAD of 84.3), and hyper-IgE (34 400 UI/mL), who was treated with deflazacort, Healing creams and emollients, as well as detergent-free gel. With which did not progress favorably, so a combinated therapy with deflazacort, methotrexate, tacrolimus, and transfer factor was prescribed, obtaining excellent results. CONCLUSION: There are many algorithms reported in the literature for the treatment of AD, but the evolution of the disease is the only one that will give us the guidelines for the treatment to be followed</style></abstract><notes><style face="normal" font="default">IS - 0002-5151 (Print)IS - 0002-5151 (Linking)LA - spaPT - English AbstractPT - Journal ArticleCO - Mexico -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29249110">PM:29249110</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Alerg Mex\2017-64-487-92.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Alerg Mex\2017-64-487-92.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Cid Del Prado-Izquierdo ML</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87395</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Asawa,Y.</style></author><author><style face="normal" font="default"> Asawa,N.</style></author></authors></contributors><titles><title><style face="normal" font="default">Influence of lifestyle factors and stress on the radioallergosorbent test scores: two case reports</style></title><secondary-title><style face="normal" font="default">Postepy Dermatol Alergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Postepy Dermatol Alergol</style></abbr-1></periodical><pages end="500" start="499">499-500</pages><volume><style face="normal" font="default">34</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Stress</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1642-395X</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Japan -</style></notes><work-type><style face="normal" font="default">10.5114/ada.2017.71120</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5114/ada.2017.71120</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-499-500.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-499-500.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171021, Asawa Y</style></custom2><misc3><style face="normal" font="default">10.5114/ada.2017.71120</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86692</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Rivas-Juesas,C.</style></author><author><style face="normal" font="default"> Tomas,Bartra J.</style></author><author><style face="normal" font="default"> Purroy Tabar,A.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Hospital de Sagunto, Valencia, Spain.</style></auth-address><titles><title><style face="normal" font="default">Requirements of a new allergen regulation</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="6" start="5">5-6</pages><volume><style face="normal" font="default">45</style></volume><number><style face="normal" font="default">1S</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="10" Month="11" Year="2017">2017/11/10</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171114IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - Journal ArticleCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.09.004</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29132811">PM:29132811</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-5-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-5-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Rivas-Juesas C</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.09.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87427</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tse,R.</style></author><author><style face="normal" font="default"> Wong,C.X.</style></author><author><style face="normal" font="default"> Kesha,K.</style></author><author><style face="normal" font="default"> Garland,J.</style></author><author><style face="normal" font="default"> Tran,Y.</style></author><author><style face="normal" font="default"> Anne,S.</style></author><author><style face="normal" font="default"> Elstub,H.</style></author><author><style face="normal" font="default"> Cala,A.D.</style></author><author><style face="normal" font="default"> Palmiere,C.</style></author><author><style face="normal" font="default"> Patchett,K.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Forensic Pathology, LabPLUS, Auckland City Hospital, Auckland 1148, New Zealand.</style></auth-address><titles><title><style face="normal" font="default">Post mortem tryptase cut-off level for anaphylactic death</style></title><secondary-title><style face="normal" font="default">Forensic Sci Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Forensic Sci Int</style></abbr-1></periodical><pages end="8" start="5">5-8</pages><volume><style face="normal" font="default">284</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Multivariate Analysis</style></keyword><keyword><style face="normal" font="default"> New Zealand</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">Serum mast cell tryptase is used to support the diagnosis of anaphylaxis. The recommended clinical cut-off for total tryptase (&lt;11.4mug/L) appears unsuitable in the post mortem setting due to largely unknown processes which result in significantly elevated levels in these samples. Consequently there is no widely accepted tryptase cut-off level for diagnosing an anaphylactic death. This 5-year retrospective study compared total tryptase levels in post mortem femoral blood in anaphylactic deaths and control. Univariate and multivariate analysis was used to assess the relative contribution of other factors (age, gender, post mortem interval, and presence of resuscitation) on post mortem tryptase levels. Nine anaphylactic deaths and 45 controls were identified. Receiver-operating characteristic (ROC) curve analysis identified an optimal cut-off of 53.8mug/L, with sensitivity of 89%, and specificity of 93%, for total post mortem tryptase in femoral blood to diagnosis anaphylaxis. No other factors showed any statistical significant contribution to post mortem tryptase elevation. Femoral total post mortem tryptase level of 53.8mug/L and above is a useful ancillary test in diagnosing an anaphylactic death</style></abstract><notes><style face="normal" font="default">IS - 1872-6283 (Electronic)IS - 0379-0738 (Linking)LA - engPT - Journal ArticleCO - New Zealand -CO - Australia -CO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1016/j.forsciint.2017.12.035</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29331682">PM:29331682</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Forensic Sci Int\2017-284-5-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Forensic Sci Int\2017-284-5-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, Tse R</style></custom2><misc3><style face="normal" font="default">10.1016/j.forsciint.2017.12.035</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86823</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Coattrenec,Y.</style></author><author><style face="normal" font="default"> Jaques,D.</style></author><author><style face="normal" font="default"> Jandus,P.</style></author><author><style face="normal" font="default"> Harr,T.</style></author><author><style face="normal" font="default"> Spoerl,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Immunology and Allergology, Department of Medical Specialties, University Hospital and Medical Faculty, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva, Switzerland</style></auth-address><titles><title><style face="normal" font="default">Anaphylactic shock following castor bean contact: a case report</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Clin Immunol</style></abbr-1></periodical><pages end="" start="50">50-</pages><volume><style face="normal" font="default">13</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: The castor bean plant, Ricinus communis, is known to have allergenic and toxic properties. Castor bean allergy has been described mainly as an occupational inhalation allergy in laboratory workers, in persons working in oil processing mills or in agricultural industry. So far, only one case of anaphylactic reaction due to castor bean sensitization confirmed by specific IgE has been described in literature. Case presentation: A 30-year-old woman presented to the emergency room with severe angioedema followed by urticaria, hypotension and tachycardia. She recovered after treatment with antihistamines, corticosteroids, nebulized adrenaline and intravenous fluids. Food induced anaphylaxis was excluded by allergological investigations. After repeated thorough history, the patient mentioned having bitten into a castor bean just before the reaction. Cutaneous test (prick-to-prick) and specific IgE for castor bean were highly positive. Conclusions: We report the second case of a severe anaphylactic reaction to castor beans, confirmed by IgE testing, reported in the literature. It underlines the importance of a meticulous history in allergology and highlights the fact, that castor beans may cause potentially fatal anaphylaxis</style></abstract><notes><style face="normal" font="default">IS - 1710-1484 (Print)IS - 1710-1484 (Linking)LA - engPT - Journal ArticleCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1186/s13223-017-0221-x</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29201066">PM:29201066</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-50.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-50.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Coattrenec Y</style></custom2><misc3><style face="normal" font="default">10.1186/s13223-017-0221-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86566</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ober,C.</style></author><author><style face="normal" font="default"> Sperling,A.I.</style></author><author><style face="normal" font="default"> von Mutius,E.</style></author><author><style face="normal" font="default"> Vercelli,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA.</style></auth-address><titles><title><style face="normal" font="default">Immune development and environment: lessons from Amish and Hutterite children</style></title><secondary-title><style face="normal" font="default">Curr Opin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Immunol</style></abbr-1></periodical><pages end="60" start="51">51-60</pages><volume><style face="normal" font="default">48</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="24" Month="8" Year="2017">2017/8/24</year></dates><abstract><style face="normal" font="default">Children who grow up in traditional farm environments are protected from developing asthma and allergy. This 'farm effect' can be largely explained by the child's early life contact with farm animals, in particular cows, and their microbes. Our studies in Amish and Hutterite school children living on farms in the U.S. have further demonstrated that this protection is mediated through innate immune pathways. Although very similar with respect to ancestry and many lifestyle factors that are associated with asthma risk, Amish and Hutterites follow farming practices that are associated with profound differences in the levels of house dust endotoxin, in the prevalence of asthma and atopy among school children, and in the proportions, phenotypes, and functions of immune cells from these children. In this review, we will consider our studies in Amish and Hutterites children in the context of the many previous studies in European farm children and discuss how these studies have advanced our understanding of the asthma-protective 'farm effect'</style></abstract><notes><style face="normal" font="default">DA - 20170827IS - 1879-0372 (Electronic)IS - 0952-7915 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -CO - Germany -</style></notes><work-type><style face="normal" font="default">10.1016/j.coi.2017.08.003</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28843541">PM:28843541</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-51-60.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-51-60.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170827, Ober C</style></custom2><misc3><style face="normal" font="default">10.1016/j.coi.2017.08.003</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87029</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Andorf,S.</style></author><author><style face="normal" font="default"> Manohar,M.</style></author><author><style face="normal" font="default"> Dominguez,T.</style></author><author><style face="normal" font="default"> Block,W.</style></author><author><style face="normal" font="default"> Tupa,D.</style></author><author><style face="normal" font="default"> Kshirsagar,R.A.</style></author><author><style face="normal" font="default"> Sampath,V.</style></author><author><style face="normal" font="default"> Chinthrajah,R.S.</style></author><author><style face="normal" font="default"> Nadeau,K.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Observational long-term follow-up study of rapid food oral immunotherapy with omalizumab</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Clin Immunol</style></abbr-1></periodical><pages end="" start="51">51-</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Omalizumab</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1710-1492</style></isbn><abstract><style face="normal" font="default">A number of clinical studies focused on treating a single food allergy through oral immunotherapy (OIT) with adjunctive omalizumab treatment have been published. We previously demonstrated safety and tolerability of a rapid OIT protocol using omalizumab in a phase 1 study to achieve desensitization to multiple (up to 5) food allergens in parallel, rapidly (7</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô36-áweeks; median-á=-á18-áweeks). In the current long-term, observational study, we followed 34 food allergic participants for over 5-áyears, who had originally undergone the phase 1 rapid OIT protocol</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1186/s13223-017-0223-8</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s13223-017-0223-8</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-51.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-51.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Andorf S</style></custom2><misc3><style face="normal" font="default">10.1186/s13223-017-0223-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86696</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tortajada-Girbes,M.</style></author><author><style face="normal" font="default"> Torres-Borrego,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Allergology and Pneumology Unit, Dr. Peset University Hospital, Valencia, Spain</style></auth-address><titles><title><style face="normal" font="default">The influence of microorganisms in allergic diseases</style></title><secondary-title><style face="normal" font="default">Allergol Immunopathol (Madr)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergol Immunopathol (Madr)</style></abbr-1></periodical><pages end="520" start="519">519-520</pages><volume><style face="normal" font="default">45</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergic diseases</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 1578-1267 (Electronic)IS - 0301-0546 (Linking)LA - engPT - EditorialCO - Spain -</style></notes><work-type><style face="normal" font="default">10.1016/j.aller.2017.10.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29110881">PM:29110881</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-519-20.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergol Immunopathol (Madr)\2017-45-519-20.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Tortajada-Girbes M</style></custom2><misc3><style face="normal" font="default">10.1016/j.aller.2017.10.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87028</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Andorf,S.</style></author><author><style face="normal" font="default"> Manohar,M.</style></author><author><style face="normal" font="default"> Dominguez,T.</style></author><author><style face="normal" font="default"> Block,W.</style></author><author><style face="normal" font="default"> Tupa,D.</style></author><author><style face="normal" font="default"> Kshirsagar,R.A.</style></author><author><style face="normal" font="default"> Sampath,V.</style></author><author><style face="normal" font="default"> Chinthrajah,R.S.</style></author><author><style face="normal" font="default"> Nadeau,K.C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Feasibility of sustained response through long-term dosing in food allergy immunotherapy</style></title><secondary-title><style face="normal" font="default">Allergy Asthma Clin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Allergy Asthma Clin Immunol</style></abbr-1></periodical><pages end="" start="52">52-</pages><volume><style face="normal" font="default">13</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1710-1492</style></isbn><abstract><style face="normal" font="default">Clinical trials using oral immunotherapy (OIT) for the treatment of food allergies have shown promising results. We previously demonstrated the feasibility of desensitization for up to 5 food allergens simultaneously through OIT. In this observational study, we report the findings of long-term follow-up (LTFU) of the participants treated through a single site OIT phase 1 trial</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United States -</style></notes><work-type><style face="normal" font="default">10.1186/s13223-017-0224-7</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1186/s13223-017-0224-7</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-52.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Allergy Asthma Clin Immunol\2017-13-52.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171211, Andorf S</style></custom2><misc3><style face="normal" font="default">10.1186/s13223-017-0224-7</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87197</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nayyar,B.G.</style></author><author><style face="normal" font="default"> Woodward,S.</style></author><author><style face="normal" font="default"> Mur,L.A.J.</style></author><author><style face="normal" font="default"> Akram,A.</style></author><author><style face="normal" font="default"> Arshad,M.</style></author><author><style face="normal" font="default"> Saqlan Naqvi,S.M.</style></author><author><style face="normal" font="default"> Akhund,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Botany, Pir Mehr Ali Shah Arid Agriculture University, Rawalpindi 46300, Pakistan</style></auth-address><titles><title><style face="normal" font="default">The Incidence of Alternaria Species Associated with Infected Sesamum indicum L. Seeds from Fields of the Punjab, Pakistan</style></title><secondary-title><style face="normal" font="default">Plant Pathol J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Plant Pathol J</style></abbr-1></periodical><pages end="553" start="543">543-553</pages><volume><style face="normal" font="default">33</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Alternaria</style></keyword><keyword><style face="normal" font="default"> ASIA</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">Sesame (Sesamum indicum) is an important oil seed crop of Asia. Yields can be negatively impacted by various factors, including disease, particularly those caused by fungi which create problems in both production and storage. Foliar diseases of sesame such as Alternaria leaf blight may cause significant yield losses, with reductions in plant health and seed quality. The work reported here determined the incidence of Alternaria species infecting sesame seeds grown in the Punjab, Pakistan. A total of 428 Alternaria isolates were obtained from 105 seed samples and grouped into 36 distinct taxonomic groups based on growth pattern and morphological characters. Isolation frequency and relative density of surface sterilized and non-surface sterilized seeds showed that three isolates (A13, A47 and A215) were the most common morphological groups present. These isolates were further identified using sequencing of the Internal Transcribed Spacer (ITS) region of ribosomal DNA (rDNA) and the Alternaria major allergen gene (Alt a 1). Whilst ITS of rDNA did not resolve the isolates into Alternaria species, the Alt a 1 sequences exhibited > 99% homology with Alternaria alternata (KP123850.1) in GenBank accessions. The pathogenicity and virulence of these isolates of Alternaria alternata was confirmed in inoculations of sesame plants resulting in typical symptoms of leaf blight disease. This work confirms the identity of a major source of sesame leaf blight in Pakistan which will aid in formulating effective disease management strategies</style></abstract><notes><style face="normal" font="default">IS - 1598-2254 (Print)IS - 1598-2254 (Linking)LA - engPT - Journal ArticleCO - Pakistan -CO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.5423/PPJ.OA.04.2017.0081</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29238277">PM:29238277</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Plant Pathol J\2017-33-543-53.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Plant Pathol J\2017-33-543-53.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Nayyar BG</style></custom2><misc3><style face="normal" font="default">10.5423/PPJ.OA.04.2017.0081</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87200</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mokhtari-Zaer,A.</style></author><author><style face="normal" font="default"> Hosseini,M.</style></author><author><style face="normal" font="default"> Boskabady,M.H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</style></auth-address><titles><title><style face="normal" font="default">The effects of exercise on depressive- and anxiety-like behaviors as well as lung and hippocampus oxidative stress in ovalbumin-sensitized juvenile rats</style></title><secondary-title><style face="normal" font="default">Respir Physiol Neurobiol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Physiol Neurobiol</style></abbr-1></periodical><pages end="62" start="55">55-62</pages><volume><style face="normal" font="default">248</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Exercise</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword><keyword><style face="normal" font="default"> Stress</style></keyword></keywords><dates><year Day="7" Month="12" Year="2017">2017/12/7</year></dates><abstract><style face="normal" font="default">Allergic asthma during early life period has been reported to be associated with neurochemical and behavioral disorders, including anxiety and depression. We aimed to determine the effects of exercise on depressive- and anxiety-like behaviors as well as lung and hippocampus oxidative stress in ovalbumin (OVA)-sensitized juvenile rats. Animals were divided into 4 groups including control (non-exercised and non-sensitized), Exe (exercise and non-sensitized); OVA (non-exercised and OVA-sensitized); and OVA+Exe (exercised and OVA-sensitized). The rats were subjected to chronic OVA sensitization followed by 4 weeks of treadmill exercise training. Compared to the control group, the OVA group had an increase in anxiety- and depressive-like behavior, lung inflammation, and oxidative stress index in the lung and hippocampus. Compared to the OVA group, the OVA+Exe group had a decline in anxiety- and depressive-like behavior, lung inflammation, and oxidative stress index in the lung and hippocampus. No significant difference in terms of the above-mentioned parameters, were found between the control group and the Exe group. Exercise decreased depressive- and anxiety-like behaviors in OVA-sensitized juvenile rats; this effect might have been mainly mediated by improvement in antioxidant system</style></abstract><notes><style face="normal" font="default">IS - 1878-1519 (Electronic)IS - 1569-9048 (Linking)LA - engPT - Journal ArticleCO - Iran -</style></notes><work-type><style face="normal" font="default">10.1016/j.resp.2017.12.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29224851">PM:29224851</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Physiol Neurobiol\2017-248-55-62.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Physiol Neurobiol\2017-248-55-62.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Mokhtari-Zaer A</style></custom2><misc3><style face="normal" font="default">10.1016/j.resp.2017.12.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87397</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bozek,A.</style></author><author><style face="normal" font="default"> Krupa-Borek,I.</style></author><author><style face="normal" font="default"> Jarzab,J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Twenty years</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇÖ observation of subcutaneous pollen allergoid immunotherapy efficacy in adults</style></title><secondary-title><style face="normal" font="default">Postepy Dermatol Alergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Postepy Dermatol Alergol</style></abbr-1></periodical><pages end="565" start="561">561-565</pages><volume><style face="normal" font="default">34</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1642-395X</style></isbn><abstract><style face="normal" font="default">Introduction : It is valuable to determine the long-term efficacy of allergen-specific immunotherapy (SIT) and whether it can cure allergy. Aim : For this study, patients were prospectively observed for 20 years after completion of SIT to determine its effectiveness. Material and methods : A total of 1006 patients who underwent SIT for pollen allergy were observed for 20 years to assess the efficacy of SIT. The rhinitis symptom score (RSS) and asthma symptom score (ASS) were measured after SIT completion. The possibility of allergy cure was estimated based on three sets of criteria: group A </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô neither symptoms nor intake of medication during the analysis period, group B </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô no symptoms during the analysis period (but possible medication intake), and group C </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô at most one mild symptom during the analysis period. Results : After SIT, approximately 25% of patients showed complete relief of allergy symptoms and had no need for symptomatic drug treatment during the pollen season. The level of effectiveness of SIT was similar throughout the treatment period. During the observation period after SIT, RSS ranged from 1.51 to 1.82, and ASS ranged from 1.22 to 1.29. The treatment effect at 10 and 20 years after SIT was comparable, regardless of whether criterion A or B was used. However, the effect of SIT using criterion C was lower than those using criteria A and B for the analyzed time points. Conclusions : For this study cohort, SIT had a long-term effect that did not depend significantly on the duration of immunotherapy against pollen</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.5114/ada.2017.72462</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5114/ada.2017.72462</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-561-5.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-561-5.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Bozek A</style></custom2><misc3><style face="normal" font="default">10.5114/ada.2017.72462</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87392</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Czarnecka-Operacz,M.</style></author><author><style face="normal" font="default"> Sadowska-Przytocka,A.</style></author><author><style face="normal" font="default"> Jenerowicz,D.</style></author><author><style face="normal" font="default"> Szeliga,A.</style></author><author><style face="normal" font="default"> Adamski,Z.</style></author><author><style face="normal" font="default"> Lacka,K.</style></author></authors></contributors><titles><title><style face="normal" font="default">Thyroid function and thyroid autoantibodies in patients with chronic spontaneous urticaria</style></title><secondary-title><style face="normal" font="default">Postepy Dermatol Alergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Postepy Dermatol Alergol</style></abbr-1></periodical><pages end="572" start="566">566-572</pages><volume><style face="normal" font="default">34</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> autoimmune diseases</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1642-395X</style></isbn><abstract><style face="normal" font="default">Introduction : Chronic urticaria (CU) is a skin disease caused by autoantibodies against high affinity immunoglobulin E (IgE) receptor and against IgE. It is characterized by hives, erythematous wheals and redness present minimum twice a week for at least 6 weeks. It is observed that there is a strong association between CU and autoimmune diseases, such as autoimmune thyroiditis (AT). Aim : To verify the frequency of AT in patients suffering from chronic spontaneous urticaria (CSU) and to confirm the coexistence of CU and AT in the Polish population. Material and methods : One hundred and forty-eight patients with CSU were included to the study. The presence of anti-thyroperoxydase antibodies (anti-TPO) and anti-thyroglobulin antibodies (anti-Tg) was checked and thyrotropin (TSH), free thyroxine (fT4) and free triiodothyronine (fT3) concentration was measured. Results were compared with outcomes in a group of 35 patients with no history of skin disease. Results : Thirty-three patients were diagnosed with AT. Frequency of elevated anti-TPO (p = 0.0045) and anti-Tg (p = 0.013) levels was much higher in patients with CU. A comparison of the current study and previous ones was conducted. In a group with CU, there was a higher risk of elevated anti-TPO (OR = 6.69) and anti-Tg (OR = 6.01) levels. Conclusions : There is a statistically significant difference in the presence of AT between the patients with CU and the whole population. Doctors should consider examining patients with CU for AT. Adequate therapy and guidance for patients could be implemented at an early stage of thyroid disease and help induce remission of skin disorders</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.5114/ada.2017.72464</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5114/ada.2017.72464</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-566-72.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-566-72.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Czarnecka-Operacz M</style></custom2><misc3><style face="normal" font="default">10.5114/ada.2017.72464</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87040</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Ogundipe,F.</style></author><author><style face="normal" font="default"> Hennis,E.C.A.</style></author><author><style face="normal" font="default"> Mehari,A.</style></author><author><style face="normal" font="default"> Gillum,R.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Internal Medicine, Howard University College of Medicine, Washington, DC</style></auth-address><titles><title><style face="normal" font="default">Toxocara species exposure, symptoms of asthma, and fractional exhaled nitric oxide in the US population</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="570" start="569">569-570</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.09.063</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29223300">PM:29223300</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-569-70.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-569-70.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Oguundipe F</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.09.063</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87039</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Silvers,W.S.</style></author><author><style face="normal" font="default"> Bernard,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Greenwood Village, Colorado. Electronic address: skiersnoz@silversmd.comGreenwood Village, Colorado</style></auth-address><titles><title><style face="normal" font="default">Spectrum and prevalence of reactions to marijuana in a Colorado allergy practice</style></title><secondary-title><style face="normal" font="default">Ann Allergy Asthma Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Allergy Asthma Immunol</style></abbr-1></periodical><pages end="571" start="570">570-571</pages><volume><style face="normal" font="default">119</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1534-4436 (Electronic)IS - 1081-1206 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.anai.2017.10.028</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29223301">PM:29223301</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-570-1.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Allergy Asthma Immunol\2017-119-570-1.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171118, Silvers WS</style></custom2><misc3><style face="normal" font="default">10.1016/j.anai.2017.10.028</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87393</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jahnz-Rozyk,K.</style></author><author><style face="normal" font="default"> Raciborski,F.</style></author><author><style face="normal" font="default"> Sliwczynski,A.M.</style></author><author><style face="normal" font="default"> Klak,A.</style></author><author><style face="normal" font="default"> Pinkas,J.</style></author></authors></contributors><titles><title><style face="normal" font="default">Anaphylaxis in Poland: the epidemiology and direct costs</style></title><secondary-title><style face="normal" font="default">Postepy Dermatol Alergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Postepy Dermatol Alergol</style></abbr-1></periodical><pages end="579" start="573">573-579</pages><volume><style face="normal" font="default">34</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Registries</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1642-395X</style></isbn><abstract><style face="normal" font="default">Introduction : Epidemiological data on anaphylaxis have been underestimated both in Poland and worldwide. Aim : To evaluate the prevalence of anaphylaxis in Poland, including a classification by gender, age and residential region. Material and methods : The data used in the analysis were derived from two sources, the National Health Fund records of healthcare services for 2008</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô2015 (official statistics) and a questionnaire-based survey conducted in 2015 on a sample of 305 allergists practicing in different regions of Poland. Results : In 2015, 3144 people received treatment for anaphylactic shock (T78.0, T78.2, T80.5, T88.6) with an estimated prevalence rate of anaphylaxis of 8.2 per 100,000 (8.4 for females and 7.9 for males). The highest prevalence rate was found for women aged 50</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô54 years (14.5 per 100,000). There was a very large difference in the prevalence of anaphylaxis between rural and urban areas (13.1 vs. 0.8 per 100,000). In 2015, the Polish NHF spent PLN 3.5 million (EUR 835,000) on the management of anaphylaxis. Of the allergists surveyed, 73% had been currently managing patients who had experienced anaphylactic shock. The most common causes of anaphylaxis included insect venom (41.4%), food (29.8%) and drugs (17.4%). Conclusions : A central anaphylaxis registry should be established in Poland. This is the only approach that would allow collecting a wide range of reliable information on the cases, management and consequences of anaphylaxis. Ongoing management of patients who have experienced anaphylactic shock should be improved</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.5114/pdia.2017.70361</style></work-type><urls><web-urls><url ppv-ref="no">http://dx.doi.org/10.5114/pdia.2017.70361</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-573-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Postepy Dermatol Alergol\2017-34-573-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171223, Jahnz-Rozyk K</style></custom2><misc3><style face="normal" font="default">10.5114/pdia.2017.70361</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86535</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Barbariol,S.</style></author><author><style face="normal" font="default"> Eymann,A.</style></author><author><style face="normal" font="default"> Llera,J.</style></author><author><style face="normal" font="default"> Parisi,C.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Seccion de Alergia del Servicio de Clinica Pediatrica del Hospital Italiano de Buenos Aires, Buenos Aires, Argentina</style></auth-address><titles><title><style face="normal" font="default">Strategies for compliance with the internship program among three pediatric interns with latex allergy</style></title><secondary-title><style face="normal" font="default">Arch Argent Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Arch Argent Pediatr</style></abbr-1></periodical><pages end="587" start="583">583-587</pages><volume><style face="normal" font="default">115</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="12" Year="2017">2017/12/1</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Latex allergy is common in the hospital setting. OBJETIVE: To describe the clinical situation of three pediatric interns with latex allergy and the prevention strategies implemented during clinical clerkships in pediatric and neonatal intensive care units. PATIENTS, METHODS, AND OUTCOMES: The three interns referred symptom exacerbation during their internship program. Diagnosis was confirmed based on a compatible history and positive specific immunoglobulin E. A semi-structured interview was done to describe perceptions about prevention strategies, the personnel were trained, and nitrile gloves were provided for carrying out procedures. Interns completed their clinical clerkships without having allergic reactions. Positive aspects referred by interns were that they felt cared for and experienced an improved quality of life; negative aspects were a bad predisposition and resistance against change among some other interns. Strategies designed to this end permitted interns to continue their internship program</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1668-3501 (Electronic)IS - 0325-0075 (Linking)LA - engLA - spaPT - Journal ArticleCO - Argentina -</style></notes><work-type><style face="normal" font="default">10.5546/aap.2017.eng.583</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29087119">PM:29087119</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Arch Argent Pediatr\2017-115-583-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Arch Argent Pediatr\2017-115-583-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Barbariol S</style></custom2><misc3><style face="normal" font="default">10.5546/aap.2017.eng.583</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86582</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liang,J.</style></author><author><style face="normal" font="default"> Tan,C.C.</style></author><author><style face="normal" font="default"> Taylor,S.L.</style></author><author><style face="normal" font="default"> Baumert,J.L.</style></author><author><style face="normal" font="default"> Lopata,A.L.</style></author><author><style face="normal" font="default"> Lee,N.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">ARC Training Centre for Advanced Technologies in Food Manufacture, School of Chemical Engineering, University of New South Wales, New South Wales, Australia</style></auth-address><titles><title><style face="normal" font="default">Quantitative analysis of species specificity of two anti-parvalbumin antibodies for detecting southern hemisphere fish species demonstrating strong phylogenetic association</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="596" start="588">588-596</pages><volume><style face="normal" font="default">237</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Antibodies,Monoclonal</style></keyword><keyword><style face="normal" font="default"> Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style face="normal" font="default"> Parvalbumins</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Phylogeny</style></keyword><keyword><style face="normal" font="default"> Species Specificity</style></keyword></keywords><dates><year Day="15" Month="12" Year="2017">2017/12/15</year></dates><abstract><style face="normal" font="default">This study aimed to develop a novel approach to determine the correlation between the parvalbumin (PAV) contents and their corresponding immunoreactivity (detectability) in southern hemisphere fish species. The immuno-detected PAV contents of the test fish species were estimated by a quantitative SDS-PAGE. A quantitative Enzyme-Linked ImmunoSorbent Assay (ELISA) was formatted to assess relative immunoreactivity of PAV. Sixteen species (forty-three percent) displayed a positive correlation with the anti-cod PAV polyclonal antibody, but no correlation with the anti-carp PAV monoclonal antibody. There was a strong phylogenetic association of the PAV immunoreactivity. Species from the order of Perciformes showed strong binding with both antibodies; whereas species from Salmoniformes, Ophidiiformes, Scombriformes, Scorpaeniformes, and Tetraodontiformes showed weak or no binding. This approach showed for the first time a statistical correlation between the PAV content and the immunoreactivity and allowed to rank the relative species/order specificity of the two antibodies for the southern hemisphere fish PAV</style></abstract><notes><style face="normal" font="default">DA - 20170802IS - 0308-8146 (Print)IS - 0308-8146 (Linking)LA - engPT - Journal ArticleRN - 0 (Allergens)RN - 0 (Antibodies, Monoclonal)RN - 0 (Parvalbumins)SB - IMCO - Australia -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2017.05.153</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28764040">PM:28764040</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\2017-237-588-96.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\2017-237-588-96.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170802, Liang J</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2017.05.153</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87003</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gloaguen,A.</style></author><author><style face="normal" font="default"> Cesareo,E.</style></author><author><style face="normal" font="default"> Vaux,J.</style></author><author><style face="normal" font="default"> Valdenaire,G.</style></author><author><style face="normal" font="default"> Ganansia,O.</style></author><author><style face="normal" font="default"> Renolleau,S.</style></author><author><style face="normal" font="default"> Pouessel,G.</style></author><author><style face="normal" font="default"> Beaudouin,E.</style></author><author><style face="normal" font="default"> Lefort,H.</style></author><author><style face="normal" font="default"> Meininger,C.</style></author></authors></contributors><titles><title><style face="normal" font="default">Management of anaphylaxis in emergency medicine. French Society of Emergency Medicine (SFMU) Guidelines with the Contribution of French Allergology Society (SFA) and the French Speaking Group in Pediatric Intensive Care and Emergency (GFRUP), and the support of the French Pediatric Pneumology and Allergology Society (SP2A)</style></title><secondary-title><style face="normal" font="default">Rev Fr Allergol</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Rev Fr Allergol</style></full-title></periodical><pages end="614" start="595">595-614</pages><volume><style face="normal" font="default">57</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Emergency medicine</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">1877-0320</style></isbn><abstract><style face="normal" font="default">These formalized expert guidelines were written by the French Society of Emergency Medicine (SFMU), in partnership with the French Allergology Society (SFA) and the French Speaking Group in Pediatric Intensive Care and Emergency (GFRUP), and the support of the French Pediatric Pneumology and Allergology Society (SP2A). Their goal is to educate emergency physicians to early diagnosis of this potentially fatal reaction of severe hypersensitivity, the specific features associated with age, and risk factors identification. Anaphylaxis diagnosis is clinical and used Sampson's clinical criteria. The authors offer helps sheets for emergency medical services dispatch and triage criteria for emergency department nurses. As underlined by the international guidelines, the main treatment is early administration of intramuscular epinephrine. If an epinephrine auto-injector is available, the emergency medical services dispatch center on-call physician (112-call) should encourage its immediate use. The second line of treatment is based on the eviction of the triggering factor, the appropriate waiting position, oxygen therapy, and depending on the symptoms, fluid therapy, bronchodilator and epinephrine nebulization. The severity of the prognosis and the unpredictability of developments justify the deployment of a mobile intensive care unit. A minimum six-hour hospital observation is indicated. Tryptase kinetics evaluation contributes to a posteriori diagnosis. At emergency department discharge, the patient must have a prescription of an emergency kit (containing two epinephrine auto-injectors and +¦2-agonists), written instructions and a detailed written hospital report. A specialized consultation with an allergologist is essential after the emergency department discharge</style></abstract><notes><style face="normal" font="default">LA - FRECO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.reval.2017.10.004</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.reval.2017.10.004</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Rev Fr Allergol\2017-57-595-614.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Rev Fr Allergol\2017-57-595-614.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Gloaguen A</style></custom2><misc3><style face="normal" font="default">10.1016/j.reval.2017.10.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87429</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">MacGiobuin,S.</style></author><author><style face="normal" font="default"> Stitt,V.</style></author><author><style face="normal" font="default"> Philbin,D.</style></author><author><style face="normal" font="default"> Higgins,B.</style></author><author><style face="normal" font="default"> McGuire,G.</style></author><author><style face="normal" font="default"> O'Regan,A.M.</style></author><author><style face="normal" font="default"> Kelly,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Western Training Programme in General Practice, The Nurses Home, University College Hospital, Galway</style></auth-address><titles><title><style face="normal" font="default">Food Allergy Emergencies in Children - To what extent are Early Years Services Prepared? A cross-sectional survey</style></title><secondary-title><style face="normal" font="default">Ir Med J</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ir Med J</style></abbr-1></periodical><pages end="" start="600">600-</pages><volume><style face="normal" font="default">110</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Child</style></keyword><keyword><style face="normal" font="default"> Children</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword></keywords><dates><year Day="8" Month="8" Year="2017">2017/8/8</year></dates><abstract><style face="normal" font="default">Food allergies are common in preschool children. This study's aims are to establish prevalence, to clarify management practices, levels of preparedness and the perceived role of General Practitioners amongst Early Years Services providers. This study is an anonymous, quantitative, cross sectional study. An online questionnaire was distributed to 282 Early Years Service providers. Data were analysed using SPSS. Response rate was 35% (n=98). Prevalence of food allergy was 3% (n=119). Allergic reactions to food had occurred on site in 16% (n=15). Written emergency action plans were available in 47% of facilities (n=46). Medications were not kept on site in 63% (n=62) of facilities. General practitioners were felt to have an important role in the management of food allergies by 76% of respondents (n=61). This study identifies significant areas for improvement in the management of food allergic child in Early Years Services</style></abstract><notes><style face="normal" font="default">IS - 0332-3102 (Print)IS - 0332-3102 (Linking)LA - engPT - Journal ArticleCO - Ireland -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29341512">PM:29341512</url></web-urls></urls><custom2><style face="normal" font="default">20170808, MacGiobuin S</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86568</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nagy,E.</style></author><author><style face="normal" font="default"> Hegedus,G.</style></author><author><style face="normal" font="default"> Taller,J.</style></author><author><style face="normal" font="default"> Kutasy,B.</style></author><author><style face="normal" font="default"> Virag,E.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Pannonia, Georgikon Faculty, Department of Plant Science and Biotechnology, Keszthely, Hungary</style></auth-address><titles><title><style face="normal" font="default">Illumina sequencing of the chloroplast genome of common ragweed (Ambrosia artemisiifolia L.)</style></title><secondary-title><style face="normal" font="default">Data Brief</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Data Brief</style></abbr-1></periodical><pages end="611" start="606">606-611</pages><volume><style face="normal" font="default">15</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">Common ragweed (Ambrosia artemisiifolia L.) is the most widespread weed and the most dangerous pollen allergenic plant in large areas of the temperate zone. Since herbicides like PSI and PSII inhibitors have their target genes in the chloroplast genome, understanding the chloroplast genome may indirectly support the exploration of herbicide resistance and development of novel control methods. The aim of the present study was to sequence and reconstruct for the chloroplast genome of A. artemisiifolia and establish a molecular dataset. We used an Illumina MiSeq protocol to sequence the chloroplast genome of isolated intact organelles of ragweed plants grown in our experimental garden. The assembled chloroplast genome was found to be 152,215 bp (GC: 37.6%) in a quadripartite structure, where 80 protein coding genes, 30 tRNA and 4 rRNA genes were annotated in total. We also report the complete sequence of 114 genes encoded in A. artemisiifolia chloroplast genome supported by both MIRA and Velvet de novo assemblers and ordered to Helianthus annuus L. using the Geneious software</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 2352-3409 (Print)IS - 2352-3409 (Linking)LA - engPT - Journal ArticleCO - Hungary -</style></notes><work-type><style face="normal" font="default">10.1016/j.dib.2017.10.009</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29085876">PM:29085876</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Data Brief\2017-15-606-11.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Data Brief\2017-15-606-11.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Nagy E</style></custom2><misc3><style face="normal" font="default">10.1016/j.dib.2017.10.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86831</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fu,T.</style></author><author><style face="normal" font="default"> Wang,L.</style></author><author><style face="normal" font="default"> Zeng,Q.</style></author><author><style face="normal" font="default"> Zhang,Y.</style></author><author><style face="normal" font="default"> Sheng,B.</style></author><author><style face="normal" font="default"> Han,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Respiration, the 1st People's Hospital of Jining, Jining, China</style></auth-address><titles><title><style face="normal" font="default">Ghrelin Ameliorates Asthma by Inhibiting Endoplasmic Reticulum Stress</style></title><secondary-title><style face="normal" font="default">Am J Med Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Med Sci</style></abbr-1></periodical><pages end="625" start="617">617-625</pages><volume><style face="normal" font="default">354</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="12/14/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">analysis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Glucose</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">BACKGROUND: This study aimed to confirm the ameliorative effect of ghrelin on asthma and investigate its mechanism. MATERIALS AND METHODS: The murine model of asthma was induced by ovalbumin (OVA) treatment and assessed by histological pathology and airway responsiveness to methacholine. The total and differential leukocytes were counted. Tumor necrosis factor alpha, interferon gamma, interleukin-5 and interleukin-13 levels in bronchoalveolar lavage fluid were quantified by commercial kits. The protein levels in pulmonary tissues were measured by Western blot analysis. RESULTS: Ghrelin ameliorated the histological pathology and airway hyperresponsiveness in the OVA-induced asthmatic mouse model. Consistently, OVA-increased total and differential leukocytes and levels of tumor necrosis factor alpha, interferon gamma, interleukin-5 and interleukin-13 in bronchoalveolar lavage fluid were significantly attenuated by ghrelin. Ghrelin prevented the increased protein levels of the endoplasmic reticulum stress markers glucose regulated protein 78 and CCAAT/enhancer binding protein homologous protein and reversed the reduced levels of p-Akt in asthmatic mice. CONCLUSIONS: Ghrelin might prevent endoplasmic reticulum stress activation by stimulating the Akt signaling pathway, which attenuated inflammation and ameliorated asthma in mice. Ghrelin might be a new target for asthma therapy</style></abstract><notes><style face="normal" font="default">IS - 1538-2990 (Electronic)IS - 0002-9629 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.amjms.2017.08.022</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29208260">PM:29208260</url></web-urls><pdf-urls><url ppv-ref="no">hanlp_jnhospital@163.com</url></pdf-urls><text-urls><url ppv-ref="no">researchgate</url></text-urls></urls><custom2><style face="normal" font="default">20171203, Fu T</style></custom2><misc3><style face="normal" font="default">10.1016/j.amjms.2017.08.022</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87000</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Saraya,T.</style></author><author><style face="normal" font="default"> Ohkuma,K.</style></author><author><style face="normal" font="default"> Fujiwara,M.</style></author><author><style face="normal" font="default"> Miyaoka,C.</style></author><author><style face="normal" font="default"> Wada,S.</style></author><author><style face="normal" font="default"> Watanabe,T.</style></author><author><style face="normal" font="default"> Mikura,S.</style></author><author><style face="normal" font="default"> Inoue,M.</style></author><author><style face="normal" font="default"> Oda,M.</style></author><author><style face="normal" font="default"> Sada,M.</style></author><author><style face="normal" font="default"> Ogawa,Y.</style></author><author><style face="normal" font="default"> Honda,K.</style></author><author><style face="normal" font="default"> Tamura,M.</style></author><author><style face="normal" font="default"> Yokoyama,T.</style></author><author><style face="normal" font="default"> Kurai,D.</style></author><author><style face="normal" font="default"> Ishii,H.</style></author><author><style face="normal" font="default"> Takizawa,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Clinical characterization of 52 patients with immunoglobulin G4-related disease in a single tertiary center in Japan: Special reference to lung disease in thoracic high-resolution computed tomography</style></title><secondary-title><style face="normal" font="default">Respir Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Med</style></abbr-1></periodical><pages end="67" start="62">62-67</pages><volume><style face="normal" font="default">132</style></volume><number><style face="normal" font="default">Supplement C</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">High-resolution computed tomography</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin G4-related disease</style></keyword><keyword><style face="normal" font="default"> Lung involvement</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">0954-6111</style></isbn><abstract><style face="normal" font="default">Immunoglobulin G4-related disease (IgG4-RD) is a rare multi-organ disorder. Physicians rarely encounter patients with IgG4-RD and its range of symptoms. To elucidate the clinical characterization of IgG4-RD, along with the clinical significance of lung involvement, we retrospectively reviewed the medical records of patients who satisfied the comprehensive diagnostic criteria for IgG4-RD. We identified 52 patients with IgG4-RD. Of these, 32 patients underwent tissue biopsies, resulting in categorization as definite (n-á=-á23) or possible (n-á=-á9) IgG4-RD cases. Among the 23 definite IgG4-RD cases, those with positive lung involvement (n-á=-á8) had significantly higher values of serum LDH (median 220 IU/L, interquartile range (IQR) 175</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô378 vs. median 184, IQR 136</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô249, p-á=-á0.039), IgG (median 2769-ámg/dL, IQR 2028</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô7807 vs. median 2048, IQR 1168</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô4376, p-á=-á0.009), and soluble interleukin-2 receptors (median 1620 U/mL, IQR 871</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô2250 vs. median 733, IQR 271</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô1600, p-á=-á0.003) than those with negative lung involvement (n-á=-á15). Similarly, a significant number of patients with positive lung involvement were positive for rheumatoid factor (71.4% vs. 23.1%, p-á=-á0.041) or hypocomplementemia (50% vs. 0%, p-á=-á0.036). Sixteen patients also showed lung involvement (definite n-á=-á8, possible n-á=-á8); thoracic computed tomography (CT) of these patients revealed mediastinal lymphadenopathies (n-á=-á14, 87.5%), ground glass opacity (n-á=-á11, 68.8%), consolidation (n-á=-á8, 50%), thickening of the bronchovascular bundles (n-á=-á7, 43.8%), small nodules (n-á=-á5, 31.3%), bronchiectasis (n-á=-á4, 25%), and reticular shadows (n-á=-á4, 25%), and pulmonary function tests, using a standard technique involving a single breath, revealed decreased diffusion capacity for carbon monoxide. IgG4-RD is associated with diverse thoracic CT findings and a decreased diffusion capacity, and careful multidisciplinary assessment is needed to enable differentiation of IgG4-RD from lymphoproliferative disorders</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.rmed.2017.09.006</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.rmed.2017.09.006</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Med\2017-132SC-62-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Med\2017-132SC-62-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171120, Saraya T</style></custom2><misc3><style face="normal" font="default">10.1016/j.rmed.2017.09.006</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86832</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Johnson,J.R.</style></author><author><style face="normal" font="default"> Harker,J.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">1 School of Life and Health Sciences Aston University Birmingham, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Allergic Airway Disease: More than Meets the IgE?</style></title><secondary-title><style face="normal" font="default">Am J Respir Cell Mol Biol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Am J Respir Cell Mol Biol</style></abbr-1></periodical><pages end="632" start="631">631-632</pages><volume><style face="normal" font="default">57</style></volume><number><style face="normal" font="default">6</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1535-4989 (Electronic)IS - 1044-1549 (Linking)LA - engPT - Journal ArticleCO - United KIngdom -</style></notes><work-type><style face="normal" font="default">10.1165/rcmb.2017-0271ED</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29192831">PM:29192831</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171202, Johnson JR</style></custom2><misc3><style face="normal" font="default">10.1165/rcmb.2017-0271ED</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86791</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kaul,S.</style></author><author><style face="normal" font="default"> Zimmer,J.</style></author><author><style face="normal" font="default"> Dehus,O.</style></author><author><style face="normal" font="default"> Constanzo,A.</style></author><author><style face="normal" font="default"> DaasConstanzo,A.</style></author><author><style face="normal" font="default"> Buchheit,K.H.</style></author><author><style face="normal" font="default"> Asturias,J.</style></author><author><style face="normal" font="default"> Arilla,M.C.</style></author><author><style face="normal" font="default"> Barber,D.</style></author><author><style face="normal" font="default"> Bertocchi,A.</style></author><author><style face="normal" font="default"> Brunetto,B.</style></author><author><style face="normal" font="default"> Carnes,J.A.</style></author><author><style face="normal" font="default"> Chapman,M.</style></author><author><style face="normal" font="default"> Chaudemanche,G.</style></author><author><style face="normal" font="default"> Dayan-Kenigsberg,J.</style></author><author><style face="normal" font="default"> Doring,S.</style></author><author><style face="normal" font="default"> Fuhrer,F.</style></author><author><style face="normal" font="default"> Gallego,M.T.</style></author><author><style face="normal" font="default"> Iacovacci,P.</style></author><author><style face="normal" font="default"> Hanschmann,K.M.</style></author><author><style face="normal" font="default"> Holzhauser,T.</style></author><author><style face="normal" font="default"> Hrabina,M.</style></author><author><style face="normal" font="default"> Ledesma,A.</style></author><author><style face="normal" font="default"> Moingeon,P.</style></author><author><style face="normal" font="default"> Nony,E.</style></author><author><style face="normal" font="default"> Pini,C.</style></author><author><style face="normal" font="default"> Plunkett,G.</style></author><author><style face="normal" font="default"> Raulf,M.</style></author><author><style face="normal" font="default"> Reese,G.</style></author><author><style face="normal" font="default"> Sandberg,E.</style></author><author><style face="normal" font="default"> Sander,I.</style></author><author><style face="normal" font="default"> Smith,B.</style></author><author><style face="normal" font="default"> Strecker,D.</style></author><author><style face="normal" font="default"> Valerio,C.</style></author><author><style face="normal" font="default"> van Ree,R.</style></author><author><style face="normal" font="default"> Weber,B.</style></author><author><style face="normal" font="default"> Vieths,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Paul-Ehrlich-Institut, Paul-Ehrlich-Str. 51-59, D-63225 Langen, Germany</style></auth-address><titles><title><style face="normal" font="default">Validation of ELISA methods for quantification of the major birch allergen Bet v 1 (BSP090)</style></title><secondary-title><style face="normal" font="default">Pharmeur Bio Sci Notes</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pharmeur Bio Sci Notes</style></abbr-1></periodical><pages end="87" start="69">69-87</pages><volume><style face="normal" font="default">2017</style></volume><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">To date, the potency of allergen products in Europe is expressed in manufacturer-specific units relative to a product-specific in-house reference. Consequently, cross-product comparability of allergen products from different manufacturers with respect to strength and efficacy is impossible. The Biological Standardisation Programme (BSP) project BSP090 addresses this issue via the establishment of reference standards in conjunction with ELISA methods for the quantification of major allergens in allergen products. Since the initiation of BSP090, the recombinant major allergen Bet v 1 has been adopted by the European Pharmacopoeia Commission as a Chemical Reference Substance (CRS). In parallel, two sandwich ELISA systems for quantification of Bet v 1 were found suitable in preliminary phases of BSP090 to be validated in a large collaborative study. In this study, the candidate ELISA systems were compared with respect to accuracy, precision and variability. Thirteen participating laboratories tested model samples containing the CRS as well as spiked and unspiked birch pollen extracts. Both in pre-testing and in the collaborative study, the 2 candidate ELISA systems confirmed their suitability to quantify recombinant and native Bet v 1. As no clear-cut decision for one of the ELISA systems could be made based on the results of the collaborative study, a post-study testing was performed. Bet v 1 content of 30 birch pollen allergen products was determined in parallel in both ELISA systems. Consequently, 1 candidate ELISA system was selected to be proposed as the future European Pharmacopoeia standard method for Bet v 1 quantification</style></abstract><notes><style face="normal" font="default">DA - 20171116IS - 2075-2504 (Electronic)IS - 2075-2164 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - France -CO - Spain -CO - Italy -CO - United States -CO - France -CO - Denmark -CO - Netherlands -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29143737">PM:29143737</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20171116, Kaul S</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87083</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Hong,Q.</style></author><author><style face="normal" font="default"> Zhou,S.</style></author><author><style face="normal" font="default"> Zhao,H.</style></author><author><style face="normal" font="default"> Peng,J.</style></author><author><style face="normal" font="default"> Li,Y.</style></author><author><style face="normal" font="default"> Shang,Y.</style></author><author><style face="normal" font="default"> Wu,M.</style></author><author><style face="normal" font="default"> Zhang,W.</style></author><author><style face="normal" font="default"> Lu,S.</style></author><author><style face="normal" font="default"> Li,S.</style></author><author><style face="normal" font="default"> Yu,S.</style></author><author><style face="normal" font="default"> Wang,W.</style></author><author><style face="normal" font="default"> Wang,Q.</style></author></authors></contributors><auth-address><style face="normal" font="default">School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China</style></auth-address><titles><title><style face="normal" font="default">Allergenicity of recombinant Humulus japonicus pollen allergen 1 after combined exposure to ozone and nitrogen dioxide</style></title><secondary-title><style face="normal" font="default">Environ Pollut</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Environ Pollut</style></abbr-1></periodical><pages end="715" start="707">707-715</pages><volume><style face="normal" font="default">234</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> Allergenicity</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> ASIA</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> IgE-binding</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword></keywords><dates><year Day="11" Month="12" Year="2017">2017/12/11</year></dates><abstract><style face="normal" font="default">Ozone (O3) and nitrogen dioxide (NO2) are thought to play primary roles in aggravating air pollution-induced health problems. However, the effects of joint O3/NO2 on the allergenicity of pollen allergens are unclear. Humulus japonicus pollen allergen 1 (Hum j1) is a profilin protein that causes widespread pollinosis in eastern Asia. In order to study the effects of combined O3/NO2 on the allergenicity of Hum j1, tandem six-histidine peptide tag (His6)-fused recombinant Hum j1 (rHum j1) was expressed in a prokaryotic system and purified through His6 affinity chromatography. The purified rHum j1 was used to immunize SD rats. Rat sera with high titers of IgG and IgE antibodies against rHum j1 were used for allergenicity quantification. The rHum j1 was exposed to O3/NO2, and changes in allergenicity of the exposed rHum j1 were assayed using the immunized rat antibodies. Tandem LC-MS/LC (liquid chromatography-mass spectrometer/liquid chromatography spectrometer) chromatography and UV and circular dichroism (CD) spectroscopy were used to study the structural changes in rHum j1. Our data demonstrated that a novel disulfide bond between the sulfhydryl groups of two neighboring cysteine molecules was formed after the rHum j1 exposure to joint O3/NO2, and therefore IgE-binding affinity was increased and the allergenicity was reinforced. Our results provided clues to elucidate the mechanism behind air pollution-induced increase in pollinosis prevalence</style></abstract><notes><style face="normal" font="default">IS - 1873-6424 (Electronic)IS - 0269-7491 (Linking)LA - engPT - Journal ArticleCO - Japan -CO - China -</style></notes><work-type><style face="normal" font="default">10.1016/j.envpol.2017.11.078</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29241157">PM:29241157</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Environ Pollut\2017-234-707-15.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Environ Pollut\2017-234-707-15.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171215, Hong Q</style></custom2><misc3><style face="normal" font="default">10.1016/j.envpol.2017.11.078</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87222</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Spiewak,R.</style></author><author><style face="normal" font="default"> Gora-Florek,A.</style></author><author><style face="normal" font="default"> Horoch,A.</style></author><author><style face="normal" font="default"> Jarosz,M.J.</style></author><author><style face="normal" font="default"> Dorynska,A.</style></author><author><style face="normal" font="default"> Golec,M.</style></author><author><style face="normal" font="default"> Dutkiewicz,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Experimental Dermatology and Cosmetology, Jagiellonian University Medical College, Krakow, Poland.</style></auth-address><titles><title><style face="normal" font="default">Risk factors for work-related eczema and urticaria among vocational students of agriculture</style></title><secondary-title><style face="normal" font="default">Ann Agric Environ Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ann Agric Environ Med</style></abbr-1></periodical><pages end="721" start="716">716-721</pages><volume><style face="normal" font="default">24</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aged</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Atopy</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rhinitis</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="23" Month="12" Year="2017">2017/12/23</year></dates><abstract><style face="normal" font="default">INTRODUCTION AND OBJECTIVE: Farmers are at high risk of occupational skin diseases which may start already during vocational training. This study was aimed at identification of risk factors for work-related skin diseases among vocational students of agriculture. MATERIAL AND METHODS: The study involved 440 students (245 males, 195 females aged 17-21 years) in 11 vocational schools which were at least 100 km from each other. The protocol included a physician-managed questionnaire and medical examination, skin prick tests, patch tests, total IgE and Phadiatop. Logistic regression model was used for the identification of relevant risk factors. RESULTS: Work-related dermatoses were diagnosed in 29 study participants (6.6%, 95%CI: 4.3-8.9%): eczema in 22, urticaria in 14, and co-existence of both in 7 students. Significant risk factors for work-related eczema were: history of respiratory allergy (OR=10.10; p&lt;0.001), history of eczema (itchy rash) provoked by wet work and detergents before entering the school (OR=5.85; p&lt;0.001), as well as history of contact dermatitis to metals, rubber or cosmetics prior to inscription (OR=2.84; p=0.016), and family history of any skin disease (OR=2.99; p=0.013). Significant risk factors for work-related urticaria were: history of allergic rhinitis and asthma prior to inscription (OR=7.29; p=0.006), positive skin prick tests to work place allergens (OR=4.65; p=0.002) and to environmental allergens (OR=3.79; p=0.009), and positive Phadiatop test (OR=3.61; p=0.013). CONCLUSIONS: Work-related skin diseases are common among vocational students of agriculture. Atopy, past history of asthma, allergic rhinitis, and eczema (either atopic, allergic or irritant) are relevant risk factors for work-related eczema and urticaria in young farmers, along with family history of any skin disease. Positive skin prick tests seem relevant, especially in the case of urticaria. Asking simple, aimed questions during health checks while enrolling students into agricultural schools would suffice to identify students at risk for work-related eczema and urticaria, giving them the chance for selecting a safer profession, and hopefully avoiding an occupational disease in the future</style></abstract><notes><style face="normal" font="default">IS - 1898-2263 (Electronic)IS - 1232-1966 (Linking)LA - engPT - Journal ArticleCO - Poland -</style></notes><work-type><style face="normal" font="default">10.26444/aaem/81002</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29284253">PM:29284253</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Ann Agric Environ Med\2017-24-716-21.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Ann Agric Environ Med\2017-24-716-21.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Spiewak R</style></custom2><misc3><style face="normal" font="default">10.26444/aaem/81002</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86863</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Min,J.Y.</style></author><author><style face="normal" font="default"> Min,K.B.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Republic of Korea</style></auth-address><titles><title><style face="normal" font="default">Marijuana use is associated with hypersensitivity to multiple allergens in US adults</style></title><secondary-title><style face="normal" font="default">Drug Alcohol Depend</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Drug Alcohol Depend</style></abbr-1></periodical><pages end="77" start="74">74-77</pages><volume><style face="normal" font="default">182</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Alternaria</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="20" Month="11" Year="2017">2017/11/20</year></dates><abstract><style face="normal" font="default">BACKGROUND: The recent legalization of marijuana use for both medical and recreational purposes in several states of the United Sates is expected to further increase the already high prevalence of marijuana use. Although allergic reactions are uncommon, the potential of marijuana use and cultivation to cause allergy should be considered. We aimed to investigate whether marijuana use is associated with the prevalence of sensitization to specific allergens. METHODS: A total of 2671 adults (aged 20-59 years) who participated in the 2005-2006 National Health and Nutrition Examination Survey were included. Participants completed a questionnaire on marijuana use and underwent sensitization tests to 19 specific allergens. Those who reported marijuana use for at least 1 day in the past 30 days were considered marijuana users. RESULTS: No difference was found in the history of allergy between marijuana users and non-users. Compared with marijuana non-users as a reference group, the adjusted odds ratio (AOR) of sensitization to a specific allergen among marijuana users was significantly greater for antibodies against the following: Alternaria alternata (AOR=1.67; 95% confidence interval (CI), 1.04-2.70), D. farinae (AOR=1.68; 95% CI, 1.27-2.22), D. pteronyssin (AOR=1.65; 95% CI, 1.32-2.06), ragweed (AOR=1.84; 95% CI, 1.30-2.59), rye grass (AOR=1.49; 95% CI, 1.12-1.97), Bermuda grass (AOR=1.55; 95% CI, 1.03-2.33), oak (AOR=1.76; 95% CI, 1.14-2.70), birch (AOR=2.09; 95% CI, 1.23-3.55), peanut (AOR=1.91; 95% CI, 1.25-2.92), and cat dander (AOR=1.51; 95% CI=1.13-2.03). CONCLUSIONS: We provide preliminary findings to suggest that marijuana use is associated with sensitization to specific allergens, including molds, dust mites, plants, and cat dander</style></abstract><notes><style face="normal" font="default">IS - 1879-0046 (Electronic)IS - 0376-8716 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.1016/j.drugalcdep.2017.09.039</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29172121">PM:29172121</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Drug Alcohol Depend\2017-182-74-7.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Drug Alcohol Depend\2017-182-74-7.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171210, Min JY</style></custom2><misc3><style face="normal" font="default">10.1016/j.drugalcdep.2017.09.039</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>81584</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Han,J.</style></author><author><style face="normal" font="default"> Li,S.</style></author><author><style face="normal" font="default"> Zhao,Y.</style></author><author><style face="normal" font="default"> Yang,J.</style></author><author><style face="normal" font="default"> Yu,Y.</style></author><author><style face="normal" font="default"> Sun,N.</style></author><author><style face="normal" font="default"> Cui,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">TCM College, North China University of Science and Technology, Tangshan 063000, Hebei Province, China</style></auth-address><titles><title><style face="normal" font="default">[Acupuncture for TGF-beta1 expression in lung tissues of asthma rats]</style></title><secondary-title><style face="normal" font="default">Zhongguo Zhen Jiu</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Zhongguo Zhen Jiu</style></abbr-1></periodical><pages end="746" start="741">741-746</pages><volume><style face="normal" font="default">37</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword></keywords><dates><year Day="12" Month="7" Year="2017">2017/7/12</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To explore the regulation of acupuncture for transforming growth factor beta1 (TGF-beta1) expression in the lung tissues of bronchial asthmatic rats. METHODS: Forty SPF male SD rats were randomly divided into a blank group, a model group, an acupuncture group and a shallow fast acupuncture group, 10 rats in each group. Asthma model was established in the model, acupuncture, and shallow fast acupuncture groups, and no intervention was applied in the blank and model groups. Before atomization excitation, 20 min acupuncture was applied at "Dazhui" (GV 14) "Feishu" (BL 13) "Fengmen" (BL 12) in the acupuncture group. Acupuncture only into skin without needle retained at the above acupoints was used in the shallow fast acupuncture group before atomization excitation from the day of model established. All the treatment was given 7 times, once the other day. The pathological lunge tissues of rats were observed by HE staining; the protein expression of TGF-beta1 in the lung tissues was examined by immunohistochemical staining and immunofluorescence staining. The TGF-beta1 expressions in bronchoalveolar lavage fluid (BALF) and serum were showed by ELISA. RESULTS: There were changes in the lung tissues in the model group, including mucus plug in the bronchial lumen, irregular bronchial epithelium, thick airway smooth muscle, local break, narrow lumen, a large number of inflammatory cell infiltration. The phenomena in the acupuncture group were improved and those in the shallow fast acupuncture group were not apparently changed compared with those in the model group. The IOD value of TGF-beta1 expression in the model group increased compared with that in the blank group (P&lt;0.05); the positive expression in the acupuncture group was lower than those in the model and shallow fast acupuncture groups (both P&lt;0.05). The contents of TGF-beta1 in BALF and serum of the acupuncture group were lower than those in the model and shallow fast acupuncture groups (all P&lt;0.05). CONCLUSIONS: Acupuncture may improve airway inflammatory response and remolding of asthma by inhibiting TGF-beta1 expression</style></abstract><notes><style face="normal" font="default">IS - 0255-2930 (Print)IS - 0255-2930 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.13703/j.0255-2930.2017.07.016</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29231548">PM:29231548</url></web-urls></urls><custom2><style face="normal" font="default">20171214, Han J</style></custom2><misc3><style face="normal" font="default">10.13703/j.0255-2930.2017.07.016</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86657</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Latifi-Pupovci,H.</style></author><author><style face="normal" font="default"> Lokaj-Berisha,V.</style></author><author><style face="normal" font="default"> Lumezi,B.</style></author></authors></contributors><auth-address><style face="normal" font="default">University of Prishtina, Medical Faculty, Department of Physiology &amp; Immunology, Prishtina, Kosovo</style></auth-address><titles><title><style face="normal" font="default">Relationship of Cord Blood Immunoglobulin E and Maternal Immunoglobulin E with Birth Order and Maternal History of Allergy in Albanian Mother/Neonate Pairs</style></title><secondary-title><style face="normal" font="default">Open Access Maced J Med Sci</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Open Access Maced J Med Sci</style></abbr-1></periodical><pages end="756" start="751">751-756</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">6</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="15" Month="10" Year="2017">2017/10/15</year></dates><abstract><style face="normal" font="default">BACKGROUND: Previous studies reported that familial factors such as birth order and mothers atopy might influence cord blood levels and development of allergies. AIM: The aim of the study was to evaluate the relationship of cord blood IgE and maternal IgE with birth order and mothers history of allergy in Albanian mother/neonate pairs. MATERIAL AND METHODS: Study population represented 291 mother-infant pairs. Mothers were interviewed with a questionnaire for personal history of allergy and pregnancy history whereas serum IgE levels were determined using sandwich IRMA assay. RESULTS: The mean level of cIgE in neonates with detectable levels was 1.59 (n = 78). No significant difference in means of cIgE was found between first born and later born neonates (p = 0.232) and between neonates of mothers with a negative and positive history of allergy (p = 0.125). Also, no significant difference was found between means of mIgE by birth order, whereas there was a significant difference of mIgE between mothers with and without a history of allergy (p = 0.01). In a group of neonates with detectable cIgE levels, maternal IgE levels were moderately correlated with cIgE levels. CONCLUSION: Cord blood IgE is not affected by birth order and mothers history of allergy, whereas mothers IgE are affected by the history of allergy but not by birth order</style></abstract><notes><style face="normal" font="default">DA - 20171106IS - 1857-9655 (Print)IS - 1857-9655 (Linking)LA - engPT - Journal ArticleCO - Kosovo -</style></notes><work-type><style face="normal" font="default">10.3889/oamjms.2017.150</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29104683">PM:29104683</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Open Access Maced J Med Sci\2017-5-751-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Open Access Maced J Med Sci\2017-5-751-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171106, Latifi-Pupovci H</style></custom2><misc3><style face="normal" font="default">10.3889/oamjms.2017.150</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87191</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Christiansen,E.S.</style></author><author><style face="normal" font="default"> Kjaer,H.F.</style></author><author><style face="normal" font="default"> Eller,E.</style></author><author><style face="normal" font="default"> Bindslev-Jensen,C.</style></author><author><style face="normal" font="default"> Host,A.</style></author><author><style face="normal" font="default"> Mortz,C.G.</style></author><author><style face="normal" font="default"> Halken,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology and Allergy Center, Odense Research Centre for Anaphylaxis (ORCA), Odense University Hospital, University of Southern Denmark, Odense, Denmark</style></auth-address><titles><title><style face="normal" font="default">Early-life sensitization to hen's egg predicts asthma and rhinoconjunctivitis at 14 years of age</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="783" start="776">776-783</pages><volume><style face="normal" font="default">28</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">BACKGROUND: Sensitization to both inhalant and food allergens has been shown to be risk factors for development of asthma and rhinoconjunctivitis (RC). However, few studies have addressed the role of transient or persistent IgE sensitization to specific allergens in early life for later development of allergic diseases. The aim of this study was to explore the association between transient and persistent sensitization in early life and the development of asthma and RC at 6 and 14 years. METHODS: The Danish Allergy Research Center (DARC) cohort is a prospective non-interventional birth cohort study comprising 562 children. For the purpose of this study, we examined a subgroup of the original cohort with specific IgE measured at, at least 3 of 4 follow-ups between 3 and 18 months of age (n = 366). Multiple logistic regression models were used to investigate the association between transient and persistent early-life sensitization to groups of and to individual allergens and asthma and RC at 6 and 14 years compared to a reference group with no sensitization. RESULTS: Both transient early-life sensitization and persistent early-life sensitization to cow's milk or hen's egg proteins were associated with asthma (aOR 3.99[1.41-11.32] and 5.95[1.78-19.92]) and RC (aOR 2.94[1.19-7.28] and 6.18[1.86-20.53]) at 14 years, this association being driven mainly by sensitization to hen's egg. Transient early-life sensitization to house dust mite (HDM) had increased risk of asthma (aOR 3.80[1.17-12.41]) at 14 years. CONCLUSIONS: Early transient IgE sensitization and persistent IgE sensitization to hen's egg were associated with asthma and RC at 14 years. Furthermore, sensitization to HDM was associated with asthma at 14 years</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12815</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28981985">PM:28981985</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\2017-28-776-83.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\2017-28-776-83.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Christiansen ES</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12815</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86887</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kounis,N.G.</style></author><author><style face="normal" font="default"> Koniari,I.</style></author><author><style face="normal" font="default"> Soufras,G.</style></author><author><style face="normal" font="default"> Koutsogiannis,N.</style></author><author><style face="normal" font="default"> Hahalis,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Cardiology University of Patras Medical School, Rion, Patras, Achaia, Greece.</style></auth-address><titles><title><style face="normal" font="default">Specific IgE levels in pericardial and cerebrospinal fluids in forensic casework: The presence of additional molecules for sudden cardiac death diagnosis</style></title><secondary-title><style face="normal" font="default">Forensic Sci Int</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Forensic Sci Int</style></abbr-1></periodical><pages end="" start="79">79-</pages><volume><style face="normal" font="default">282</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">IgE</style></keyword></keywords><dates><year Day="6" Month="11" Year="2017">2017/11/6</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1872-6283 (Electronic)IS - 0379-0738 (Linking)LA - engPT - LetterCO - Greece -</style></notes><work-type><style face="normal" font="default">10.1016/j.forsciint.2017.11.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29172173">PM:29172173</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Forensic Sci Int\2017-282-79.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Forensic Sci Int\2017-282-79.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171208, Kounis NG</style></custom2><misc3><style face="normal" font="default">10.1016/j.forsciint.2017.11.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87250</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Segal,N.</style></author><author><style face="normal" font="default"> Stauber,T.</style></author><author><style face="normal" font="default"> Rosenblum,R.</style></author><author><style face="normal" font="default"> Levy,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Kipper Institute of immunology, Schneider Children's Medical Center of Israel, Petach Tikva</style></auth-address><titles><title><style face="normal" font="default">[THE SERUM LEVELS OF MILK AND PEANUT-SPECIFIC IGE: ROLE IN THE EVALUATION OF THE RISK FOR ALLERGIC REACTION IN CHILDREN IN ISRAEL]</style></title><secondary-title><style face="normal" font="default">Harefuah</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Harefuah</style></abbr-1></periodical><pages end="795" start="791">791-795</pages><volume><style face="normal" font="default">156</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">BACKGROUND: The performance characteristics of the ImmunoCAP assay for detecting specific IgE antibodies in the evaluation of milk and peanut allergy have been established. However, the results are not comparable to the IMMULITE 2000, another FDA-approved assay available in Israel, owing to differences in the extracts used, technical method, and population studied. OBJECTIVES: To establish the performance characteristics and predictive values for the IMMULITE 2000 assay in Israel. METHODS: The database of the Allergy Clinic at Schneider Children's Medical Center in Israel was searched for all patients referred for evaluation of allergies in 2006-2009. The results of the milk- and peanut-specific IgE antibody tests were collected and correlated with the clinical diagnoses of milk and peanut allergy or tolerance. Sensitivity, specificity and positive and negative predictive values were calculated as well as receiver operating characteristic (ROC) plots. RESULTS: The prevalence of milk allergy was 30% (111/369 patients), and peanut allergy, 6% (31/505 patients). The area under the ROC curve was 0.954 for milk allergy and 0.956 for peanut allergy. The levels with a positive predictive value of >/=95% were 10 kU/L and 3 kU/L, respectively. The level of peanut-specific IgE antibodies with a >/=95% positive predictive value was lower than found for the ImmunoCAP in the USA and Europe. CONCLUSIONS: These findings indicate that the decision points used for predicting the risk of future allergic reactions must be calculated separately for different assay methods and different populations. Our findings may assist the allergists in Israel to decide whether to perform a supervised oral challenge in order to verify if the patient has developed tolerance to milk or peanuts</style></abstract><notes><style face="normal" font="default">IS - 0017-7768 (Print)IS - 0017-7768 (Linking)LA - hebPT - English AbstractPT - Journal ArticleCO - Israel -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29292620">PM:29292620</url></web-urls></urls><custom2><style face="normal" font="default">20171227, Segal N</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86732</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Klimek,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Zentrum fur Rhinologie und Allergologie, An den Quellen 10, 65183, Wiesbaden, Deutschland.</style></auth-address><titles><title><style face="normal" font="default">[Surf the allergy Tsunami : Future chances for ENT]</style></title><secondary-title><style face="normal" font="default">HNO</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">HNO</style></abbr-1></periodical><pages end="800" start="797">797-800</pages><volume><style face="normal" font="default">65</style></volume><number><style face="normal" font="default">10</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1433-0458 (Electronic)IS - 0017-6192 (Linking)LA - gerPT - EditorialCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1007/s00106-017-0412-2</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29149353">PM:29149353</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\HNO\2017-65-797-800.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\HNO\2017-65-797-800.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Klimek L</style></custom2><misc3><style face="normal" font="default">10.1007/s00106-017-0412-2</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86953</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Laino,J.</style></author><author><style face="normal" font="default"> Wangorsch,A.</style></author><author><style face="normal" font="default"> Blanco,F.</style></author><author><style face="normal" font="default"> Wolfheimer,S.</style></author><author><style face="normal" font="default"> Krause,M.</style></author><author><style face="normal" font="default"> Flaczyk,A.</style></author><author><style face="normal" font="default"> Moller,T.M.</style></author><author><style face="normal" font="default"> Tsai,M.</style></author><author><style face="normal" font="default"> Galli,S.</style></author><author><style face="normal" font="default"> Vieths,S.</style></author><author><style face="normal" font="default"> Toda,M.</style></author><author><style face="normal" font="default"> Scheurer,S.</style></author><author><style face="normal" font="default"> Schulke,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Vice President's Research Group 1: Molecular Allergology, Paul-Ehrlich-Institut, Langen, Germany</style></auth-address><titles><title><style face="normal" font="default">Targeting of Immune Cells by Dual TLR2/7 Ligands Suppresses Features of Allergic Th2 Immune Responses in Mice</style></title><secondary-title><style face="normal" font="default">J Immunol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Immunol Res</style></abbr-1></periodical><pages end="" start="7983217">7983217-</pages><volume><style face="normal" font="default">2017</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Background: TLR ligands can promote Th1-biased immune responses, mimicking potent stimuli of viruses and bacteria. Aim: To investigate the adjuvant properties of dual TLR2/7 ligands compared to those of the mixture of both single ligands. Methods: Dual TLR2/7 ligands: CL401, CL413, and CL531, including CL264 (TLR7-ligand) and Pam2CysK4 (TLR2-ligand), were used. Immune-modulatory capacity of the dual ligands with the individual ligands alone or as a mixture in mouse BMmDCs, BMmDC:TC cocultures, or BMCMCs was compared and assessed in naive mice and in a mouse model of OVA-induced intestinal allergy. Results: CL413 and CL531 induced BMmDC-derived IL-10 secretion, suppressed rOVA-induced IL-5 secretion from OVA-specific DO11.10 CD4(+) TCs, and induced proinflammatory cytokine secretion in vivo. In contrast, CL401 induced considerably less IL-10 secretion and led to IL-17A production in BMmDC:TC cocultures, but not BMCMC IL-6 secretion, or IL-6 or TNF-alpha production in vivo. No immune-modulating effects were observed with single ligands. All dual TLR2/7 ligands suppressed DNP-induced IgE-and-Ag-specific mast cell degranulation. Compared to vaccination with OVA, vaccination with the mixture CL531 and OVA, significantly suppressed OVA-specific IgE production in the intestinal allergy model. Conclusions: Based on beneficial immune-modulating properties, CL413 and CL531 may have utility as potential adjuvants for allergy treatment</style></abstract><notes><style face="normal" font="default">IS - 2314-7156 (Electronic)IS - 2314-7156 (Linking)LA - engPT - Journal ArticleCO - Germany -CO - United States -</style></notes><work-type><style face="normal" font="default">10.1155/2017/7983217</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29204451">PM:29204451</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Immunol Res\2017-2017-7983217.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Immunol Res\2017-2017-7983217.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Laino J</style></custom2><misc3><style face="normal" font="default">10.1155/2017/7983217</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87249</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Levy,Y.</style></author></authors></contributors><auth-address><style face="normal" font="default">Kipper Institute of Immunology, Schneider Children's Medical Center of Israel, Petach Tikva, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv</style></auth-address><titles><title><style face="normal" font="default">[ALLERGIC REACTIONS TO CHILDHOOD VACCINATIONS]</style></title><secondary-title><style face="normal" font="default">Harefuah</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Harefuah</style></abbr-1></periodical><pages end="803" start="799">799-803</pages><volume><style face="normal" font="default">156</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">INTRODUCTION: Childhood vaccinations are one of the greatest achievements of modern medicine, having significantly reduced the morbidity and mortality of many infectious diseases all over the world. Anaphylactic reaction to vaccinations is rare and is estimated to occur at a rate of 1 per million doses. Allergic reaction to vaccinations can be induced by the microbial antigens, toxoids, and also by residual proteins which are derived from cultures media and stabilizers, such as ovalbumine, gelatin and yeasts. Other adverse events include large local reactions at the injection site, delayed rashes or hypotonic-hyporesponsive episodes. Parents of children who have experienced adverse reactions to vaccines, might unnecessarily be advised to avoid subsequent vaccinations. Therefore, it is important to evaluate these children in order to decide on the nature of the adverse event, whether there is a contraindication to subsequent vaccinations, and to assess the risk for future allergic reactions. If needed, skin tests with the relevant vaccines and administration of vaccines in graded doses under supervision and preparation for treatment of the anaphylactic reaction in the Allergy clinic, can ensure the effective completion of childhood immunizations. In this article, we will review the data on allergic reactions to childhood vaccinations, and the protocols suggested for the evaluation and management of children with food allergies and children who have experienced allergic reactions to vaccinations</style></abstract><notes><style face="normal" font="default">IS - 0017-7768 (Print)IS - 0017-7768 (Linking)LA - hebPT - English AbstractPT - Journal ArticlePT - ReviewCO - Israel -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29292622">PM:29292622</url></web-urls></urls><custom2><style face="normal" font="default">20171227, Levy Y</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86800</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Shen,Y.</style></author><author><style face="normal" font="default"> Hong,S.L.</style></author><author><style face="normal" font="default"> Zhang,M.</style></author><author><style face="normal" font="default"> Ke,X.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China</style></auth-address><titles><title><style face="normal" font="default">Observation of systemic adverse reactions by specific immunotherapy and analysis of risk factors in allergic rhinitis</style></title><secondary-title><style face="normal" font="default">Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi</style></abbr-1></periodical><pages end="805" start="801">801-805</pages><volume><style face="normal" font="default">52</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword></keywords><dates><year Day="7" Month="11" Year="2017">2017/11/7</year></dates><abstract><style face="normal" font="default">Objective: To investigate the systemic adverse effects of specific subcutaneous immunotherapy (SCIT) in patients with allergic rhinitis (AR) and explore the possible risk factors. Methods: A retrospective study was conducted on AR patients who underwent SCIT from January 2014 to January 2017 in Department of Otorhinolaryngology, the First Affiliated Hospital of Chongqing Medical University. For patients with adverse reactions, the detailed medical history during treatment was reviewed. Results: A total of 1608 injections were performed on 102 patients, there were 12 cases / 21 times systemic adverse events, including systemic urticaria, angioedema and Grade systemic adverse reactions. There were 3 cases of grade adverse reactions. Systemic adverse reaction was prone to an initial treatment phase where the dose and concentration of the injection were increasing. Meanwhile, it was more common in young patients aged 20-40 years old and easy to occur in May and June. About the possible risk factors, the most common one was obvious local adverse reactions (17/21), followed by prolonged injection interval (9/21), the recent exposure to a large number of allergens (7/21) and strong positive skin prick results (7/21). Conclusions: The systemic adverse effects, which were induced by SCIT, mainly included systemic urticaria, angioedema and Grade systemic adverse reactions. Systemic adverse reaction was prone to an initial treatment phase where the dose and concentration of the injection were increasing</style></abstract><notes><style face="normal" font="default">DA - 20171116IS - 1673-0860 (Print)IS - 1673-0860 (Linking)LA - chiPT - English AbstractPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3760/cma.j.issn.1673-0860.2017.11.001</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29141287">PM:29141287</url></web-urls></urls><custom2><style face="normal" font="default">20171116, Shen Y</style></custom2><misc3><style face="normal" font="default">10.3760/cma.j.issn.1673-0860.2017.11.001</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86723</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Gonzalez,T.</style></author><author><style face="normal" font="default"> Biagini Myers,J.M.</style></author><author><style face="normal" font="default"> Herr,A.B.</style></author><author><style face="normal" font="default"> Khurana Hershey,G.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunology Graduate Program, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA</style></auth-address><titles><title><style face="normal" font="default">Staphylococcal Biofilms in Atopic Dermatitis</style></title><secondary-title><style face="normal" font="default">Curr Allergy Asthma Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Allergy Asthma Rep</style></abbr-1></periodical><pages end="" start="81">81-</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="23" Month="10" Year="2017">2017/10/23</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder that is a major public health burden worldwide. AD lesions are often colonized by Staphylococcus aureus and Staphylococcus epidermidis. An important aspect of Staphylococcus spp. is their propensity to form biofilms, adhesive surface-attached colonies that become highly resistant to antibiotics and immune responses, and recent studies have found that clinical isolates colonizing AD skin are often biofilm-positive. Biofilm formation results in complex bacterial communities that have unique effects on keratinocytes and host immunity. This review will summarize recent studies exploring the role of staphyloccocal biofilms in atopic dermatitis and the implications for treatment. RECENT FINDINGS: Recent studies suggest an important role for biofilms in the pathogenesis of numerous dermatologic diseases including AD. S. aureus biofilms have been found to colonize the eccrine ducts of AD skin, and these biofilms influence secretion of keratinocyte cytokines and trigger differentiation and apoptosis of keratinocytes. These activities may act to disrupt barrier function and promote disease pathogenesis as well as allergen sensitization. Formation of biofilm is a successful strategy that protects the bacteria from environmental danger, antibiotics, and phagocytosis, enabling chronic persistence in the host. An increasing number of S. aureus skin isolates are resistant to conventional antibiotics, and staphylococcal biofilm communities are prevalent on the skin of individuals with AD. Staphylococcal colonization of the skin impacts skin barrier function and plays multiple important roles in AD pathogenesis</style></abstract><notes><style face="normal" font="default">DA - 20171024IS - 1534-6315 (Electronic)IS - 1529-7322 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s11882-017-0750-x</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29063212">PM:29063212</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Asthma Rep\2017-17-81.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Asthma Rep\2017-17-81.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171024, Gonzalez T</style></custom2><misc3><style face="normal" font="default">10.1007/s11882-017-0750-x</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87190</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mastrorilli,C.</style></author><author><style face="normal" font="default"> Caffarelli,C.</style></author><author><style face="normal" font="default"> Hoffmann-Sommergruber,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Pediatric Clinic, Department of Medicine and Surgery, University of Parma, Parma, Italy</style></auth-address><titles><title><style face="normal" font="default">Food allergy and atopic dermatitis: Prediction, progression, and prevention</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="840" start="831">831-840</pages><volume><style face="normal" font="default">28</style></volume><number><style face="normal" font="default">8</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergen</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> infections</style></keyword><keyword><style face="normal" font="default"> Management of food allergy</style></keyword><keyword><style face="normal" font="default"> Prediction</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">The rising burden of allergic diseases in childhood requires a compelling need to identify individuals at risk for atopy very early in life or even predict the onset of food allergy and atopic dermatitis since pregnancy. The development and clinical phenotypes of atopic diseases in childhood depend on a complex interaction between genetic and environmental factors, such as allergen exposure, air pollution, and infections. Preventive strategies may include avoidance measures, diet supplements, and early complementary food introduction. Overall, the management of allergic diseases has been improving to date toward a patient's tailored approach. This review will cover the current understanding of risk factors, prediction, and management of food allergy and atopic dermatitis in childhood and discuss how these may contribute to the modification of the natural history of food allergy and atopic dermatitis</style></abstract><notes><style face="normal" font="default">IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Italy -CO - Austria -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12831</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29117431">PM:29117431</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\2017-28-831-40.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\2017-28-831-40.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171220, Mastrorilli C</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12831</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86903</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Aliu,H.</style></author><author><style face="normal" font="default"> Rask,C.</style></author><author><style face="normal" font="default"> Brimnes,J.</style></author><author><style face="normal" font="default"> Andresen,T.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Immunology Department, In vivo Biology Team, ALK Abello A/S, Horsholm</style></auth-address><titles><title><style face="normal" font="default">Enhanced efficacy of sublingual immunotherapy by liposome-mediated delivery of allergen</style></title><secondary-title><style face="normal" font="default">Int J Nanomedicine</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Int J Nanomedicine</style></full-title></periodical><pages end="8388" start="8377">8377-8388</pages><volume><style face="normal" font="default">12</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">allergens</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> Subcutaneous immunotherapy</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Immunotherapy by sublingual administration of allergens provides high patient compliance and has emerged as an alternative to subcutaneous immunotherapy for the treatment of IgE-associated allergic diseases. However, sublingual immunotherapy (SLIT) can cause adverse events. Development of allergen delivery systems enabling more efficient delivery and hence lower allergen load might reduce the adverse events. In the present study, we have investigated neutral and cationic liposomes as delivery systems of ovalbumin (OVA), as a model allergen, in an OVA-induced allergic airway inflammation model. We investigated the liposome carriers' ability to improve tolerance induction of antigens compared to the corresponding dose of free OVA. Mice were treated sublingually over 2 weeks with free or liposome encapsulated OVA followed by intraperitoneal injections and intranasal challenge. Mice sublingually treated with OVA-liposomes showed a significant reduction of airway eosinophilia and splenocyte proliferation in comparison to free OVA. A similar nonsignificant pattern was seen for OVA-specific IgE antibodies. In addition, reduced levels of interferon-gamma and interleukin-5 were observed in spleen cell culture supernatants from OVA-liposome-treated mice compared to the sham-treated group. In conclusion, in vivo efficacy data showed that prophylactic SLIT with OVA-liposomes is significantly more effective in preventing allergic inflammation than the corresponding dose of free OVA</style></abstract><notes><style face="normal" font="default">IS - 1178-2013 (Electronic)IS - 1176-9114 (Linking)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.2147/IJN.S137033</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29200850">PM:29200850</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Int J Nanomedicine\2017-12-8377-88.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Int J Nanomedicine\2017-12-8377-88.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171122, Aliu H</style></custom2><misc3><style face="normal" font="default">10.2147/IJN.S137033</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86790</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">He,R.</style></author><author><style face="normal" font="default"> Shen,N.</style></author><author><style face="normal" font="default"> Zhang,H.</style></author><author><style face="normal" font="default"> Ren,Y.</style></author><author><style face="normal" font="default"> He,M.</style></author><author><style face="normal" font="default"> Xu,J.</style></author><author><style face="normal" font="default"> Guo,C.</style></author><author><style face="normal" font="default"> Xie,Y.</style></author><author><style face="normal" font="default"> Gu,X.</style></author><author><style face="normal" font="default"> Lai,W.</style></author><author><style face="normal" font="default"> Peng,X.</style></author><author><style face="normal" font="default"> Yang,G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Parasitology, College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, China</style></auth-address><titles><title><style face="normal" font="default">Molecular characteristics and serodiagnostic potential of chitinase-like protein from Sarcoptes scabiei</style></title><secondary-title><style face="normal" font="default">Oncotarget</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Oncotarget</style></abbr-1></periodical><pages end="84005" start="83995">83995-84005</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">48</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="13" Month="10" Year="2017">2017/10/13</year></dates><abstract><style face="normal" font="default">Scabies, caused by the mite Sarcoptes scabiei, is an allergic skin disease that affects millions of people and other mammals worldwide. This highly contagious parasitic disease is among the top 50 epidemic disease and is regarded as a neglected tropical disease. Diagnosis of scabies is difficult in the early stage, and the pathogenesis of scabies is not currently clear. Here, we expressed, identified and located the chitinase-like protein of S. scabiei (SsCLP), and evaluated its potential as an early-stage diagnostic antigen for rabbit scabies. Indirect ELISA using recombinant SsCLP (rSsCLP) exhibited diagnostic sensitivity of 94.4% (17/18) and specificity of 86.7% (26/30). Early diagnostic test after artificial infection of rabbits with S. scabiei for 1 week showed a positive detection rate of 96.7% (29/30). Immunolocalization assays showed that fluorescence signals were localized on the surface of mites and, in infected rabbits, were observed in keratinized skin and embedded mites. Intradermal skin tests of rabbits by injecting rSsCLP showed a wheal, flare and erythema reaction. These results suggest that S. scabiei chitinase-like protein is conducive to host invasion, participates in inducing the allergic response of the host, and is an effective antigen for the diagnosis of S. scabiei</style></abstract><notes><style face="normal" font="default">DA - 20171115IS - 1949-2553 (Electronic)IS - 1949-2553 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.18632/oncotarget.21056</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29137399">PM:29137399</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Oncotarget\2017-8-83995-4005.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Oncotarget\2017-8-83995-4005.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171115, He R</style></custom2><misc3><style face="normal" font="default">10.18632/oncotarget.21056</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86668</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kupczyk,M.</style></author><author><style face="normal" font="default"> Malewska,K.</style></author><author><style face="normal" font="default"> Pyziak,A.</style></author><author><style face="normal" font="default"> Szostakowska,A.</style></author><author><style face="normal" font="default"> Kuna,P.</style></author></authors></contributors><titles><title><style face="normal" font="default">Nasal allergen challenge in clinical practice </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô A real life study</style></title><secondary-title><style face="normal" font="default">Pol J Allergol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pol J Allergol</style></abbr-1></periodical><pages end="88" start="84">84-88</pages><volume><style face="normal" font="default">4</style></volume><number><style face="normal" font="default">3</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Nasal allergen challenge</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Symptoms score</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Alternaria</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><isbn><style face="normal" font="default">2353-3854</style></isbn><abstract><style face="normal" font="default">Nasal allergen challenge represents, together with skin tests and specific IgE, one of the basic diagnostic tools used in allergology. The goals of the study were to evaluate types of allergens used, the clinical picture of the challenge, and its safety in our daily clinical practice. In total 136 challenges in 109 patients were analyzed. The study group included 60 women and 49 men, with an average age of 34 years. In 15 patients (13.8% of the study group), apart from allergic rhinitis, bronchial asthma was also diagnosed. Eighty-two patients (75.23%) were challenged with 1, and 27 subjects (24.77%) with 2 allergens. The majority of challenges were performed with house dust mites (58 challenges, 42.6%), followed by Alternaria, mugwort, grasses, birch, hazel, and alder. The clinical picture mimicked the symptoms reported after the natural exposure to the specific allergen. The mean score after the allergen challenge in the group with the positive result was 154.95 points (p&lt;0.05 vs control solution), and in those with negative challenge 36.67 points. Side effects after the challenge, including itchy throat, cough, dyspnea and facial pruritus, were reported by 21 patients. None of side effects was serious or required any medical intervention. Among evaluated factors only female sex (OR 3.59, 95% CI 1.33</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çô9.68, p=0.012), but not diagnosis of asthma, 2 challenges per day or the type of allergen used, was associated with a higher risk of adverse events. In conclusions, nasal allergen challenge represents safe and valuable diagnostic tool in our clinical practice</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Poland -</style></notes><work-type><style face="normal" font="default">10.1016/j.alergo.2017.06.004</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.alergo.2017.06.004</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pol J Allergol\2017-4-84-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pol J Allergol\2017-4-84-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Kupczyk M</style></custom2><misc3><style face="normal" font="default">10.1016/j.alergo.2017.06.004</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86724</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Leonard,S.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pediatric Allergy &amp; Immunology, Rady Children's Hospital San Diego, University of California, 3020 Children's Way, MC 5114, San Diego, CA, 92123, USA.</style></auth-address><titles><title><style face="normal" font="default">Non-IgE-mediated Adverse Food Reactions</style></title><secondary-title><style face="normal" font="default">Curr Allergy Asthma Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Allergy Asthma Rep</style></abbr-1></periodical><pages end="" start="84">84-</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="14" Month="11" Year="2017">2017/11/14</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: The purpose of this review is to update what is currently known about the major non-IgE-mediated food allergies: food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP), and food protein-induced enteropathy (FPE). These conditions are similar in that symptoms are regulated to the gastrointestinal tract; therefore understanding their specific features is important for diagnosis and management. RECENT FINDINGS: The most progress has been made in understanding FPIES with several recent large cohorts being described. The first international consensus guidelines for FPIES were published in 2017 and propose specific diagnostic criteria for acute FPIES as well as guidance for diagnosing chronic FPIES. Recent studies in FPIAP have challenged our thinking about the recommended duration of food avoidance and that cow's milk avoidance is the primary management with reports of self-resolution without dietary management. FPE continues to appear to be on the decline. FPIES, FPIAP, and FPE are distinguished from one another by their main clinical features: delayed repetitive vomiting in FPIES, benign blood in stool in FPIAP, and chronic diarrhea in FPE. Due to the risk of nutritional deficiencies with food avoidance in both infant and maternal diets if breastfeeding, confirmation of diagnosis with challenges is encouraged. Additional studies are needed for these conditions to elucidate pathophysiology, search for diagnostic markers, and understand natural history</style></abstract><notes><style face="normal" font="default">DA - 20171115IS - 1534-6315 (Electronic)IS - 1529-7322 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s11882-017-0744-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29138990">PM:29138990</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Allergy Asthma Rep\2017-17-84.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Allergy Asthma Rep\2017-17-84.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171115, Leonard SA</style></custom2><misc3><style face="normal" font="default">10.1007/s11882-017-0744-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87100</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Magno Pereira,V.</style></author><author><style face="normal" font="default"> Andrade,C.</style></author><author><style face="normal" font="default"> Figueira,R.</style></author><author><style face="normal" font="default"> Faria,G.</style></author><author><style face="normal" font="default"> Jasmins,L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Gastroenterology, Funchal, Portugal</style></auth-address><titles><title><style face="normal" font="default">Infliximab-Induced Lupus: A Case Report</style></title><secondary-title><style face="normal" font="default">G E Port J Gastroenterol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">G E Port J Gastroenterol</style></abbr-1></periodical><pages end="88" start="84">84-88</pages><volume><style face="normal" font="default">24</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword></keywords><dates><year Day="0" Month="3" Year="2017">2017/3</year></dates><abstract><style face="normal" font="default">We report the case of a 48-year-old, leukodermic female diagnosed with ulcerative proctitis for 4 years and latent tuberculosis. She was allergic to salicylates and had a minor allergic reaction to infliximab (rash, vertigo, and headache). Thereafter, she started azathioprine (2.5 mg/kg/day). She maintained intravenous infliximab, together with prophylaxis with clemastine and hydrocortisone, due to the steroid-dependent proctitis. The therapy was continued every 8 weeks with anti-tumor necrosis factor for about 3 years. The analytical evaluation when she was diagnosed with ulcerative proctitis (February 2011) showed negative antinuclear antibodies (ANA), double-stranded-DNA antibodies (anti-dsDNA), antineutrophil cytoplasmic antibodies and anti-Saccharomyces cerevisiae antibodies, and a positive outer membrane protein antibody. About 2 years and 6 months after starting infliximab (November 2013), the patient complained of inflammatory symmetrical polyarthralgia (knee, shoulder, elbow, and wrist) without synovitis, which started every week before the administration of infliximab. Resolution of symptoms was observed after each infliximab infusion. In July 2014, the autoantibody re-evaluation showed positive ANA with a homogeneous pattern with a titer of 1:640, weak positive anti-dsDNA (30.2), and positive anti-histone with C3 decreased (80.3). She was then diagnosed with lupus induced by infliximab and initiated hydroxychloroquine 400 mg. Infliximab was suspended. On re-evaluation, the erythrocyte sedimentation rate was 25 mm/h (1st hour), C-reactive protein 0.5 mg/dL (previously erythrocyte sedimentation rate 15 mm/h and C-reactive protein 1.2 mg/dL), and endoscopically, the mucosa was scarred, with some atrophy and scarce mucus in the lower rectum. About 10 months after discontinuation of infliximab, repeated autoantibodies proved all negative, keeping only low C3 (87). The patient also reported complete resolution of the arthralgia</style></abstract><notes><style face="normal" font="default">IS - 2341-4545 (Print)IS - 2387-1954 (Linking)LA - engPT - Journal ArticleCO - Portugal -</style></notes><work-type><style face="normal" font="default">10.1159/000450877</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29255743">PM:29255743</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\G E Port J Gastroenterol\2017-24-84-8.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\G E Port J Gastroenterol\2017-24-84-8.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171213, Magno Pereira V</style></custom2><misc3><style face="normal" font="default">10.1159/000450877</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86996</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wu,Z.</style></author><author><style face="normal" font="default"> Li,K.</style></author><author><style face="normal" font="default"> Zhan,S.</style></author><author><style face="normal" font="default"> Tong,P.</style></author><author><style face="normal" font="default"> Li,X.</style></author><author><style face="normal" font="default"> Yang,A.</style></author><author><style face="normal" font="default"> Chen,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">a State Key Laboratory of Food Science and Technology , Nanchang University , Nanchang , China</style></auth-address><titles><title><style face="normal" font="default">Purification of antibody against Ara h 2 by a homemade immunoaffinity chromatography column</style></title><secondary-title><style face="normal" font="default">Prep Biochem Biotechnol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Prep Biochem Biotechnol</style></abbr-1></periodical><pages end="846" start="841">841-846</pages><volume><style face="normal" font="default">47</style></volume><number><style face="normal" font="default">8</style></number><reprint-status date="12/24/2017" status="on-request"/><keywords><keyword><style face="normal" font="default">2S Albumins,Plant</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Antibodies</style></keyword><keyword><style face="normal" font="default"> Antigens,Plant</style></keyword><keyword><style face="normal" font="default"> Arachis</style></keyword><keyword><style face="normal" font="default"> Chromatography,Affinity</style></keyword><keyword><style face="normal" font="default"> Glycoproteins</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> isolation &amp; purification</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Rabbits</style></keyword></keywords><dates><year Day="14" Month="9" Year="2017">2017/9/14</year></dates><abstract><style face="normal" font="default">Antibodies are used extensively in numerous applications both in vivo and in vitro. To purify anti-Ara h 2 polyclonal antibody, a homemade immunoaffinity chromatography (IAC) column method was established. The properties of homemade column were compared with those of the mAb affinity protein G (MPG) agarose high flow, a commercially available column successfully used in capturing polyclonal antibodies. During antibody purification from rabbits' antiserum against Ara h 2, the column capacity, recovery, and purification factor were characterized for IAC and MPG. The homemade IAC could separate the corresponding antibody with higher specificity and lower cost but with lower recovery and column capacity than those of MPG. Thus, the homemade IAC is a specific, inexpensive, and suitable method that can be used for various laboratory purifications</style></abstract><notes><style face="normal" font="default">IS - 1532-2297 (Electronic)IS - 1082-6068 (Linking)LA - engPT - Journal ArticleRN - 0 (2S Albumins, Plant)RN - 0 (Antibodies)RN - 0 (Antigens, Plant)RN - 0 (Ara h 2 allergen, Arachis hypogaea)RN - 0 (Glycoproteins)SB - IMCO - China -</style></notes><work-type><style face="normal" font="default">10.1080/10826068.2017.1342265</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28635559">PM:28635559</url></web-urls><pdf-urls><url ppv-ref="no">researchgate</url></pdf-urls></urls><custom2><style face="normal" font="default">20170914, Wu Z</style></custom2><misc3><style face="normal" font="default">10.1080/10826068.2017.1342265</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86998</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Talini,D.</style></author><author><style face="normal" font="default"> Ciberti,A.</style></author><author><style face="normal" font="default"> Bartoli,D.</style></author><author><style face="normal" font="default"> Del Guerra,P.</style></author><author><style face="normal" font="default"> Iaia,T.E.</style></author><author><style face="normal" font="default"> Lemmi,M.</style></author><author><style face="normal" font="default"> Innocenti,A.</style></author><author><style face="normal" font="default"> Di Pede,F.</style></author><author><style face="normal" font="default"> Latorre,M.</style></author><author><style face="normal" font="default"> Carrozzi,L.</style></author><author><style face="normal" font="default"> Paggiaro,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">CeRIMP, Regione Toscana, Pisa, Italy.</style></auth-address><titles><title><style face="normal" font="default">Work-related asthma in a sample of subjects with established asthma</style></title><secondary-title><style face="normal" font="default">Respir Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Respir Med</style></abbr-1></periodical><pages end="91" start="85">85-91</pages><volume><style face="normal" font="default">130</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="0" Month="9" Year="2017">2017/9</year></dates><abstract><style face="normal" font="default">OBJECTIVE: To assess the impact of occupational exposure to irritants or sensitizers on the occurrence, recrudescence and worsening of asthma and to identify unrecognized cases of work related asthma (WRA) including Work-Exacerbated Asthma (WEA) and Occupational Asthma (OA), in a general asthma clinic population sample. SETTING, DESIGN AND PARTICIPANTS: The study was a population-based cross sectional survey. 1289 asthmatic subjects (from 15 to 46 yrs old) living in a vast district of Tuscany (Italy) were identified from the Medical Reimbursement Register of the National Health System. 893 subjects agreed to take part in the study. Subjects who were currently working or had worked in past were classified in different categories of occupational risk exposure (No, Low or High) according to the italian standard classification for industries and job titles, associated with the judgment of occupational hygiene experts. RESULTS: 41% of subjects worked in industries and in job titles at risk for exposure to airway irritants and/or sensitizers, 48.6% reported an occupational exposure to gases, dust and fumes, more males than females. Prevalence of WEA and OA was higher in subjects who worked at higher risk exposure; these subjects reported a higher prevalence of markers of asthma severity (asthma control, level of treatment, FEV1) than subjects without WRA. Risk of WEA was significantly associated to female gender, older age, and self-reported exposure, while risk of OA was associated to job title with higher exposure risk to occupational asthmogens. CONCLUSIONS: Our study shows a high prevalence of WRA (especially WEA) associated with employment in industries and job titles at risk for airways sensitizers and/or irritants; data also support a role for occupational exposure in determining a poor asthma control and a higher level of asthma severity</style></abstract><notes><style face="normal" font="default">IS - 1532-3064 (Electronic)IS - 0954-6111 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1016/j.rmed.2017.07.008</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29206638">PM:29206638</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Respir Med\2017-130-85-91.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Respir Med\2017-130-85-91.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170912, Talini D</style></custom2><misc3><style face="normal" font="default">10.1016/j.rmed.2017.07.008</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87363</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Roviezzo,F.</style></author><author><style face="normal" font="default"> Rossi,A.</style></author><author><style face="normal" font="default"> Caiazzo,E.</style></author><author><style face="normal" font="default"> Orlando,P.</style></author><author><style face="normal" font="default"> Riemma,M.A.</style></author><author><style face="normal" font="default"> Iacono,V.M.</style></author><author><style face="normal" font="default"> Guarino,A.</style></author><author><style face="normal" font="default"> Ialenti,A.</style></author><author><style face="normal" font="default"> Cicala,C.</style></author><author><style face="normal" font="default"> Peritore,A.</style></author><author><style face="normal" font="default"> Capasso,R.</style></author><author><style face="normal" font="default"> Di Marzo,V.</style></author><author><style face="normal" font="default"> Izzo,A.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pharmacy, School of Medicine, University of Naples Federico II, Naples, Italy</style></auth-address><titles><title><style face="normal" font="default">Palmitoylethanolamide Supplementation during Sensitization Prevents Airway Allergic Symptoms in the Mouse</style></title><secondary-title><style face="normal" font="default">Front Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Front Pharmacol</style></abbr-1></periodical><pages end="" start="857">857-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> Sensitization</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">One important risk factor for the development of asthma is allergen sensitization. Recent increasing evidence suggests a prominent role of mast cells in asthma pathophysiology. Since Palmitoylethanolamide (PEA), an endogenous lipid mediator chemically related to - and co-released with- the endocannabinoid anandamide, behaves as a local autacoid down-regulator of mast cell activation and inflammation, we explored the possible contribution of PEA in allergic sensitization, by using ovalbumin (OVA) as sensitizing agent in the mouse. PEA levels were dramatically reduced in the bronchi of OVA-treated animals. This effect was coupled to a significant up-regulation of CB2 and GPR55 receptors, two of the proposed molecular PEA targets, in bronchi harvested from allergen-sensitized mice. PEA supplementation (10 mg/kg, 15 min before each allergen exposure) prevented OVA-induced bronchial hyperreactivity, but it did not affect IgE plasma increase. On the other hand, PEA abrogated allergen-induced cell recruitment as well as pulmonary inflammation. Evaluation of pulmonary sections evidenced a significant inhibitory action of PEA on pulmonary mast cell recruitment and degranulation, an effect coupled to a reduction of leukotriene C4 production. These findings demonstrate that allergen sensitization negatively affects PEA bronchial levels and suggest that its supplementation has the potential to prevent the development of asthma-like features</style></abstract><notes><style face="normal" font="default">IS - 1663-9812 (Print)IS - 1663-9812 (Linking)LA - engPT - Journal ArticleCO - Italy -</style></notes><work-type><style face="normal" font="default">10.3389/fphar.2017.00857</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29311913">PM:29311913</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Pharmacol\2018-8-857.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Pharmacol\2018-8-857.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171212, Roviezzo F</style></custom2><misc3><style face="normal" font="default">10.3389/fphar.2017.00857</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86546</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Juel,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Plastic Surgery, Aalborg University Hospital, Aalborg, Denmark</style></auth-address><titles><title><style face="normal" font="default">Debut of Gastroesophageal Reflux Concomitant with Administration of Sublingual Immunotherapy</style></title><secondary-title><style face="normal" font="default">Case Rep Gastrointest Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Case Rep Gastrointest Med</style></abbr-1></periodical><pages end="" start="8905372">8905372-</pages><volume><style face="normal" font="default">2017</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Gastroesophageal reflux disease (GORD) is an often debilitating condition characterised by retrograde flow of content from stomach into the oesophagus, where the low pH of the stomach acid irritates the mucosa of the oesophagus. The most dominant symptoms in GORD are pyrosis, regurgitation, and dysphagia. Sublingual immunotherapy (SLIT) was first described in 1986. Following this description, the use has greatly increased in the treatment of allergic rhinitis, as an alternative to subcutaneously administered immunotherapy. Side effects are commonly of oropharyngeal and gastrointestinal nature, for example, swelling, itching, irritation, ulceration of the oropharynx and nausea, abdominal pain, vomiting, and diarrhoea. More serious side effects are dominated by respiratory tract and systemic manifestations. A 30-year-old male experienced refractory, relentless, and debilitation GORD subsequent to administration of sublingual immunotherapy for house dust mite in allergic rhinitis. The patient had to stop the SLIT after two weeks of administration due to GORD. The cessation resulted in rapid resolution of symptoms</style></abstract><notes><style face="normal" font="default">DA - 20171107IS - 2090-6528 (Print)LA - engPT - Journal ArticleCO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1155/2017/8905372</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29109876">PM:29109876</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Case Rep Gastrointest Med\2017-2017-8905372.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Case Rep Gastrointest Med\2017-2017-8905372.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171107, Juel J</style></custom2><misc3><style face="normal" font="default">10.1155/2017/8905372</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86977</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wang,Y.J.</style></author><author><style face="normal" font="default"> Li,L.</style></author><author><style face="normal" font="default"> Song,W.J.</style></author><author><style face="normal" font="default"> Zhou,Y.J.</style></author><author><style face="normal" font="default"> Cao,M.D.</style></author><author><style face="normal" font="default"> Zuo,X.R.</style></author><author><style face="normal" font="default"> Wei,J.F.</style></author></authors></contributors><auth-address><style face="normal" font="default">Research Division of Clinical Pharmacology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China</style></auth-address><titles><title><style face="normal" font="default">Canis familiaris allergen Can f 6: expression, purification and analysis of B-cell epitopes in Chinese dog allergic children</style></title><secondary-title><style face="normal" font="default">Oncotarget</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Oncotarget</style></abbr-1></periodical><pages end="90807" start="90796">90796-90807</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">53</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergenicity</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="31" Month="10" Year="2017">2017/10/31</year></dates><abstract><style face="normal" font="default">Dog allergy is common worldwide. However, the allergenicity of dog allergy is still unclear in China as well as in special group, such as children. In this study, we chose Can f 6, a major dog allergen which belongs to the lipocalin to study its allergenicity in Chinese dog allergic children. Can f 6 gene was subcloned into pET-28a vector and transformed into E. coli BL21 (DE3) cells for expression. The recombinant Can f 6 was purified by nickel affinity chromatography, identified by SDS-PAGE, and tested for its allergenicity by Western blot with sera and basophil activation test. Secondary structures, B cell epitopes and homology modeling of Can f 6 were predicted by using a series of bioinformatical approaches. And the verification of B cell epitopes was detected by ELISA. The recombinant allergen showed an explicit band with the molecular weight of 20 kDa by SDS-PAGE. Sera from 56.3 % (18/32) of dog-allergic children patients reacted with Can f 6. The induction of the expression of CD63 and CCR3 of dog allergic children in passively sensitized basophils was up to approximately 5.0 times higher than healthy subjects. The secondary structure of Can f 6 contains 3 alpha-helices, 9 beta-sheets and random coils. Five B cell epitopes of Can f 6 were predicted and were confirmed successfully by ELISA. The results showed Can f 6 is a major allergen in Chinese children, which provides a basis for further study of Can f 6 in diagnosis and treatment of symptoms in children in China. The structural information of Can f 6 will help to form a foundation for the future design of vaccines and therapies for Can f 6 related allergies</style></abstract><notes><style face="normal" font="default">IS - 1949-2553 (Electronic)IS - 1949-2553 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.18632/oncotarget.21822</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29207604">PM:29207604</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Oncotarget\2017-8-90796-807.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Oncotarget\2017-8-90796-807.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Wang YJ</style></custom2><misc3><style face="normal" font="default">10.18632/oncotarget.21822</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86785</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Feuille,E.</style></author><author><style face="normal" font="default"> Lawrence,C.</style></author><author><style face="normal" font="default"> Volel,C.</style></author><author><style face="normal" font="default"> Sicherer,S.H.</style></author><author><style face="normal" font="default"> Wang,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pediatric Allergy and Immunology, Jaffe Food Allergy Institute, Icahn School of Medicine at Mount Sinai, New York, NY</style></auth-address><titles><title><style face="normal" font="default">Time Trends in Food Allergy Diagnoses, Epinephrine Orders, and Epinephrine Administrations in New York City Schools</style></title><secondary-title><style face="normal" font="default">J Pediatr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pediatr</style></abbr-1></periodical><pages end="99" start="93">93-99</pages><volume><style face="normal" font="default">190</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">OBJECTIVES: To assess time trends in food allergy diagnoses, epinephrine autoinjector (EAI) prescriptions, and EAI administrations in the school setting. STUDY DESIGN: In this retrospective study, deidentified student data from the New York City Department of Health and Mental Hygiene, which oversees >1 million students in 1800 schools, were provided to investigators. Data from school years 2007-2008 to 2012-2013 pertaining to diagnoses of food allergy, student-specific EAI orders, and EAI administrations among students in New York City were analyzed for trends over time, via the use of ORs and chi2 calculation. RESULTS: The prevalences of providing physician documentation of food allergy and EAI orders, and the incidence of EAI administrations, all increased approximately 3-fold over the years of the study. Of 337 EAI administrations, more than one-half used stock EAI, and three-quarters were for students without a student-specific order preceding the incident. CONCLUSIONS: The rise in food allergy diagnoses, EAI prescriptions, and EAI administrations suggest either a true increase in allergic disease, increased reporting, and/or, in the case of EAI administrations, increased appropriate use. As the majority of EAI administrations used stock supply, availability of nonstudent-specific stock EAI appears vital to management of anaphylaxis in schools. Collaboration between physicians, families, and schools is needed to identify students at risk for severe allergic reactions and to ensure preparedness and availability of EAI in the event of anaphylaxis</style></abstract><notes><style face="normal" font="default">DA - 20171116IS - 1097-6833 (Electronic)IS - 0022-3476 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/j.jpeds.2017.07.038</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29144278">PM:29144278</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pediatr\2017-190-93-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pediatr\2017-190-93-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171116, Feuille E</style></custom2><misc3><style face="normal" font="default">10.1016/j.jpeds.2017.07.038</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86783</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Fishman,J.</style></author><author><style face="normal" font="default"> Youngs,R.</style></author><author><style face="normal" font="default"> Fisher,E.</style></author><author><style face="normal" font="default"> Hussain,M.</style></author></authors></contributors><titles><title><style face="normal" font="default">All change...transcanal endoscopic ear surgery and house dust mite immunotherapy for allergic rhinitis</style></title><secondary-title><style face="normal" font="default">J Laryngol Otol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Laryngol Otol</style></abbr-1></periodical><pages end="" start="939">939-</pages><volume><style face="normal" font="default">131</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergic rhinitis</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword></keywords><dates><year Day="0" Month="11" Year="2017">2017/11</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">DA - 20171117IS - 1748-5460 (Electronic)IS - 0022-2151 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1017/S0022215117002274</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29148358">PM:29148358</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Laryngol Otol\2017-131-939.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Laryngol Otol\2017-131-939.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171117, Fishman J</style></custom2><misc3><style face="normal" font="default">10.1017/S0022215117002274</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87362</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Liu,X.</style></author><author><style face="normal" font="default"> Shen,J.</style></author><author><style face="normal" font="default"> Fan,D.</style></author><author><style face="normal" font="default"> Qiu,X.</style></author><author><style face="normal" font="default"> Guo,Q.</style></author><author><style face="normal" font="default"> Zheng,K.</style></author><author><style face="normal" font="default"> Luo,H.</style></author><author><style face="normal" font="default"> Shu,J.</style></author><author><style face="normal" font="default"> Lu,C.</style></author><author><style face="normal" font="default"> Zhang,G.</style></author><author><style face="normal" font="default"> Lu,A.</style></author><author><style face="normal" font="default"> Ma,C.</style></author><author><style face="normal" font="default"> He,X.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing, China</style></auth-address><titles><title><style face="normal" font="default">Yupingfeng San Inhibits NLRP3 Inflammasome to Attenuate the Inflammatory Response in Asthma Mice</style></title><secondary-title><style face="normal" font="default">Front Pharmacol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Front Pharmacol</style></abbr-1></periodical><pages end="" start="944">944-</pages><volume><style face="normal" font="default">8</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Yupingfeng San (YPFS) is a representative Traditional Chinese Medicine (TCM) formula with accepted therapeutic effect on Asthma. However, its action mechanism is still obscure. In this study, we used network pharmacology to explore potential mechanism of YPFS on asthma. Nucleotide-binding oligomerization domain (NOD)-like receptor pathway was shown to be the top one shared signaling pathway associated with both YPFS and asthma. In addition, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome was treated as target protein in the process of YPFS regulating asthma. Further, experimental validation was done by using LPS-stimulated U937 cells and ovalbumin (OVA)-sensitized BALB/c mice model. In vitro experiments showed that YPFS significantly decreased the production of TNF-alpha and IL-6, as well as both mRNA and protein levels of IL-1beta, NLRP3, Caspase-1 and ASC in LPS-stimulated U937 cells. In vivo experiment indicated that YPFS treatment not only attenuated the clinical symptoms, but also reduced inflammatory cell infiltration, mucus secretion and MUC5AC production in lung tissue of asthmatic mice. Moreover, YPFS treatment remarkably decreased the mRNA and protein levels of IL-1beta, NLRP3, Caspase-1 and ASC in lung tissue of asthmatic mice. In conclusion, these results demonstrated that YPFS could inhibit NLRP3 inflammasome components to attenuate the inflammatory response in asthma</style></abstract><notes><style face="normal" font="default">IS - 1663-9812 (Print)IS - 1663-9812 (Linking)LA - engPT - Journal ArticleCO - China -CO - Hong Kong -</style></notes><work-type><style face="normal" font="default">10.3389/fphar.2017.00944</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29311942">PM:29311942</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Front Pharmacol\2018-8-944.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Front Pharmacol\2018-8-944.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171222, Liu X</style></custom2><misc3><style face="normal" font="default">10.3389/fphar.2017.00944</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87187</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Movassagh,H.</style></author><author><style face="normal" font="default"> Shan,L.</style></author><author><style face="normal" font="default"> Duke-Cohan,J.S.</style></author><author><style face="normal" font="default"> Chakir,J.</style></author><author><style face="normal" font="default"> Halayko,A.J.</style></author><author><style face="normal" font="default"> Koussih,L.</style></author><author><style face="normal" font="default"> Gounni,A.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB, Canada</style></auth-address><titles><title><style face="normal" font="default">Downregulation of semaphorin 3E promotes hallmarks of experimental chronic allergic asthma</style></title><secondary-title><style face="normal" font="default">Oncotarget</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Oncotarget</style></abbr-1></periodical><pages end="98963" start="98953">98953-98963</pages><volume><style face="normal" font="default">8</style></volume><number><style face="normal" font="default">58</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> Allergic asthma</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword></keywords><dates><year Day="17" Month="11" Year="2017">2017/11/17</year></dates><abstract><style face="normal" font="default">Guidance cues such as semaphorins are attractive novel therapeutic targets for allergic disorders. We have previously described an inhibitory effect of semaphorin 3E (Sema3E) on human airway smooth muscle cell function. We have further addressed a canonical role for Sema3E in acute model of allergic asthma in vivo. Considering the chronic nature of the disease, the potential implication of Sema3E to alleviate long-lasting deficits should be investigated. Expression of Sema3E in a chronic model of allergic asthma was assessed after exposure to house dust mite (HDM) as a clinically relevant allergen. Chronic features of allergic asthma including airway hyper-responsiveness (AHR), inflammation, and remodeling were studied in Sema3E-deficient mice. Additionally, the effect of exogenous Sema3E treatment was evaluated in prophylactic and therapeutic experimental models. We have demonstrated that expression of Sema3E is robustly suppressed in the airways upon chronic HDM exposure. Chronic allergic airway disease was significantly augmented in Sema3E-deficient mouse model which was associated with an increased AHR, remodeling, and Th2/Th17 inflammation. Intranasal Sema3E administration restored chronic deficits of allergic asthma in mice. Data from this study unveil a key regulatory role of Sema3E in chronic course of asthma via orchestration of impaired inflammatory and remodeling responses</style></abstract><notes><style face="normal" font="default">IS - 1949-2553 (Electronic)IS - 1949-2553 (Linking)LA - engPT - Journal ArticleCO - Canada -CO - United States -</style></notes><work-type><style face="normal" font="default">10.18632/oncotarget.22144</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29228740">PM:29228740</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Oncotarget\2017-8-98953-63.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Oncotarget\2017-8-98953-63.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171207, Movassagh H</style></custom2><misc3><style face="normal" font="default">10.18632/oncotarget.22144</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86563</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kabashima,K.</style></author><author><style face="normal" font="default"> Nomura,T.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawahara, Sakyoku, Kyoto 606-8507, Japan</style></auth-address><titles><title><style face="normal" font="default">Revisiting murine models for atopic dermatitis and psoriasis with multipolar cytokine axes</style></title><secondary-title><style face="normal" font="default">Curr Opin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Immunol</style></abbr-1></periodical><pages end="107" start="99">99-107</pages><volume><style face="normal" font="default">48</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="12" Month="9" Year="2017">2017/9/12</year></dates><abstract><style face="normal" font="default">Atopic dermatitis (AD) and psoriasis are one of the common skin diseases. Animal models are a powerful tool to analyze these diseases, which are complicated by multiple cytokine pathways. However, many discrepancies between the human diseases and murine models have been noticed. Therefore, investigators should be aware of the differences between the murine AD models and human AD when translating murine data to human skin diseases. This review highlights the differences between the inflammatory profiles between murine models and human diseases focusing on AD and psoriasis</style></abstract><notes><style face="normal" font="default">DA - 20170915IS - 1879-0372 (Electronic)IS - 0952-7915 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Singapore -CO - Japan -</style></notes><work-type><style face="normal" font="default">10.1016/j.coi.2017.08.010</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="28915378">PM:28915378</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-99-107.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-99-107.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170915, Kabashima K</style></custom2><misc3><style face="normal" font="default">10.1016/j.coi.2017.08.010</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86567</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Quigley,J.</style></author><author><style face="normal" font="default"> Sanders,G.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Psychiatry, University of Michigan, Rachel Upjohn Building, 4250 Plymouth Rd, Ann Arbor, MI, 48109-2700, USA</style></auth-address><titles><title><style face="normal" font="default">Food Allergy in Patients Seeking Mental Health Care: What the Practicing Psychiatrist Should Know</style></title><secondary-title><style face="normal" font="default">Curr Psychiatry Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Psychiatry Rep</style></abbr-1></periodical><pages end="" start="99">99-</pages><volume><style face="normal" font="default">19</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="30" Month="10" Year="2017">2017/10/30</year></dates><abstract><style face="normal" font="default">PURPOSE OF REVIEW: This review provides an overview of food allergy among children and adolescents in the context of its impact on psychosocial functioning, and quality of life (QoL). RECENT FINDINGS: The prevalence of food allergy is increasing. The burden of day to day management of food allergy is significant and can have a negative impact on QoL for both parents of those with food allergy, and the children themselves. This can impact social functioning, academic functioning, and mental health. Children with food allergy experience more bullying than peers. Greater internalizing of symptoms has been identified in adolescents with food allergy. Typical developmental considerations in the transition from adolescence to adulthood can be impacted significantly. Those caring for children with food allergy should consider the impact of food allergy on the individual and family level within the context of social and emotional development</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1535-1645 (Electronic)IS - 1523-3812 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - United States -</style></notes><work-type><style face="normal" font="default">10.1007/s11920-017-0849-8</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29086043">PM:29086043</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Psychiatry Rep\2017-19-99.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Psychiatry Rep\2017-19-99.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Quigley J</style></custom2><misc3><style face="normal" font="default">10.1007/s11920-017-0849-8</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86862</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kadam,K.</style></author><author><style face="normal" font="default"> Karbhal,R.</style></author><author><style face="normal" font="default"> Jayaraman,V.K.</style></author><author><style face="normal" font="default"> Sawant,S.</style></author><author><style face="normal" font="default"> Kulkarni-Kale,U.</style></author></authors></contributors><auth-address><style face="normal" font="default">Bioinformatics CentreBioinformatics CentreCentre for Modeling and Simulation, Savitribai Phule Pune University, Pune 411007, IndiaShiv Nadar University, Gautam Buddha Nagar, Uttar Pradesh 201314, IndiaBioinformatics CentreBioinformatics Centre</style></auth-address><titles><title><style face="normal" font="default">AllerBase: a comprehensive allergen knowledgebase</style></title><secondary-title><style face="normal" font="default">Database (Oxford)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Database (Oxford)</style></abbr-1></periodical><pages end="" start="bax066">bax066-</pages><volume><style face="normal" font="default">2017</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="1" Month="1" Year="2017">2017/1/1</year></dates><abstract><style face="normal" font="default">Database URL: http://bioinfo.net.in/AllerBase/Home.html</style></abstract><notes><style face="normal" font="default">IS - 1758-0463 (Electronic)IS - 1758-0463 (Linking)LA - engPT - Journal ArticleCO - India -</style></notes><work-type><style face="normal" font="default">10.1093/database/bax066</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29220458">PM:29220458</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Database (Oxford)\2017-2017-bax066.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Database (Oxford)\2017-2017-bax066.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171201, Hadam K</style></custom2><misc3><style face="normal" font="default">10.1093/database/bax066</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86974</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Geersing,T.H.</style></author><author><style face="normal" font="default"> Hilgersom,W.J.A.</style></author><author><style face="normal" font="default"> Tempels-Pavlica,Z.</style></author><author><style face="normal" font="default"> Rumke,H.C.</style></author><author><style face="normal" font="default"> de Koning,L.C.M.J.</style></author><author><style face="normal" font="default"> Borgsteede,S.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Stichting Health Base, afd. Medicatiebewaking, Houten</style></auth-address><titles><title><style face="normal" font="default">[Hypersensitivity reactions and vaccines]</style></title><secondary-title><style face="normal" font="default">Ned Tijdschr Geneeskd</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Ned Tijdschr Geneeskd</style></abbr-1></periodical><pages end="" start="D1491">D1491-</pages><volume><style face="normal" font="default">161</style></volume><number><style face="normal" font="default">0</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Safety</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">A lot of questions are being asked in the Netherlands about the safety of vaccination. More knowledge among care providers helps with regard to good medical practice and information.- Severe hypersensitivity reactions to vaccines are rare. Chicken-egg protein, gelatine and thiomersal are the most important vaccine components that may provoke severe reactions.- Acute treatment of patients with severe hypersensitivity reactions consists of intramuscular adrenaline.- In case of a severe reaction to a vaccine or a vaccine component, the subsequent course of action is determined by the physician referred to: the allergist or paediatric allergist. For most patients, vaccination or revaccination is possible in a setting where acute treatment is possible.- Slight side effects and delayed hypersensitivity reactions are not good reasons for additional measures with respect to vaccination.- It is important to record hypersensitivity reactions completely and unambiguously in the patient file</style></abstract><notes><style face="normal" font="default">IS - 1876-8784 (Electronic)IS - 0028-2162 (Linking)LA - dutPT - English AbstractPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29219793">PM:29219793</url></web-urls></urls><custom2><style face="normal" font="default">20171202, Geersing TH</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87232</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">van de Griendt,E.J.</style></author><author><style face="normal" font="default"> Tuut,M.K.</style></author><author><style face="normal" font="default"> de Groot,H.</style></author><author><style face="normal" font="default"> Brand,P.L.P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Paediatrics, De Kinderkliniek, Almere, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">Applicability of evidence from previous systematic reviews on immunotherapy in current practice of childhood asthma treatment: a GRADE (Grading of Recommendations Assessment, Development and Evaluation) systematic review</style></title><secondary-title><style face="normal" font="default">BMJ Open</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">BMJ Open</style></abbr-1></periodical><pages end="" start="e016326">e016326-</pages><volume><style face="normal" font="default">7</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Sublingual immunotherapy</style></keyword></keywords><dates><year Day="28" Month="12" Year="2017">2017/12/28</year></dates><abstract><style face="normal" font="default">OBJECTIVE: Because most children with asthma now use inhaled corticosteroids (ICS), the added benefit of immunotherapy in asthmatic children needs to be examined. We re-assessed the effectiveness of subcutaneous (SCIT) and sublingual immunotherapy (SLIT) in childhood asthma treatment focusing on studies with patient-relevant outcome measures and children using ICS. METHODS: We used the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach to systematically search and appraise the evidence using predefined critical patient-relevant outcomes (asthma symptoms, asthma control and exacerbations). We searched to retrieve systematic reviews and randomised controlled trials on immunotherapy for asthma in children (1960-2017). We assessed the quality of the body of evidence with GRADE criteria. RESULTS: The quality of the evidence for SCIT was very low due to a large risk of bias and indirectness (dated studies in children not using ICS). No effect of SCIT was found for asthma symptoms; no studies reported on asthma control. For asthma exacerbations, studies favoured SCIT. We have little confidence in this effect estimate, due to the very low quality of evidence. For SLIT, quality of the evidence was very low due to a large risk of bias, indirectness and imprecision. The outcome 'asthma symptoms' could not be calculated due to lack of standardisation and large clinical heterogeneity. Other predefined outcomes were not reported. CONCLUSION: The beneficial effects of immunotherapy in childhood asthma found in earlier reviews are no longer considered applicable, because of indirectness (studies performed in children not being treated according to current asthma guidelines with ICS). There was absence of evidence to properly determine the effectiveness or lack thereof of immunotherapy in asthma treatment in children with ICS</style></abstract><notes><style face="normal" font="default">IS - 2044-6055 (Electronic)IS - 2044-6055 (Linking)LA - engPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1136/bmjopen-2017-016326</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29288175">PM:29288175</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMJ Open\2017-7-e016326.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMJ Open\2017-7-e016326.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171228, van de Griendt EJ</style></custom2><misc3><style face="normal" font="default">10.1136/bmjopen-2017-016326</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86667</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pazhoohan,S.</style></author><author><style face="normal" font="default"> Raoufy,M.R.</style></author><author><style face="normal" font="default"> Javan,M.</style></author><author><style face="normal" font="default"> Hajizadeh,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</style></auth-address><titles><title><style face="normal" font="default">Effect of Rho-kinase inhibition on complexity of breathing pattern in a guinea pig model of asthma</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0187249">e0187249-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">10</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Asthma represents an episodic and fluctuating behavior characterized with decreased complexity of respiratory dynamics. Several evidence indicate that asthma severity or control is associated with alteration in variability of lung function. The pathophysiological basis of alteration in complexity of breathing pattern in asthma has remained poorly understood. Regarding the point that Rho-kinase is involved in pathophysiology of asthma, in present study we investigated the effect of Rho-kinase inhibition on complexity of respiratory dynamics in a guinea pig model of asthma. Male Dunkin Hartley guinea pigs were exposed to 12 series of inhalations with ovalbumin or saline. Animals were treated by the Rho-kinase inhibitor Y-27632 (1mM aerosols) prior to each allergen challenge. We recorded respiration of conscious animals using whole-body plethysmography. Exposure to ovalbumin induced lung inflammation, airway hyperresponsiveness and remodeling including goblet cell hyperplasia, increase in the thickness of airways smooth muscles and subepithelial collagen deposition. Complexity analysis of respiratory dynamics revealed a dramatic decrease in irregularity of respiratory rhythm representing less complexity in asthmatic guinea pigs. Inhibition of Rho-kinase reduced the airway remodeling and hyperreponsiveness, but had no significant effect on lung inflammation and complexity of respiratory dynamics in asthmatic animals. It seems that airway hyperresponsiveness and remodeling do not significantly affect the complexity of respiratory dynamics. Our results suggest that inflammation might be the probable cause of shift in the respiratory dynamics away from the normal fluctuation in asthma</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Iran -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0187249</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29088265">PM:29088265</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0187249.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0187249.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Pazhoohan S</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0187249</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86666</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Tranquet,O.</style></author><author><style face="normal" font="default"> Gaudin,J.C.</style></author><author><style face="normal" font="default"> Patil,S.</style></author><author><style face="normal" font="default"> Steinbrecher,J.</style></author><author><style face="normal" font="default"> Matsunaga,K.</style></author><author><style face="normal" font="default"> Teshima,R.</style></author><author><style face="normal" font="default"> Sakai,S.</style></author><author><style face="normal" font="default"> Larre,C.</style></author><author><style face="normal" font="default"> Denery-Papini,S.</style></author></authors></contributors><auth-address><style face="normal" font="default">UR 1268 Biopolymers Interactions Assemblies, INRA, Nantes, France</style></auth-address><titles><title><style face="normal" font="default">A chimeric IgE that mimics IgE from patients allergic to acid-hydrolyzed wheat proteins is a novel tool for in vitro allergenicity assessment of functionalized glutens</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0187415">e0187415-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: Acid-hydrolyzed wheat proteins (acid-HWPs) have been shown to provoke severe allergic reactions in Europe and Japan that are distinct from classical wheat allergies. Acid-HWPs were shown to contain neo-epitopes induced by the deamidation of gluten proteins. However, products with variable rates of deamidation can be found. OBJECTIVES: In this work, we studied the effect of the extent of wheat proteins deamidation on its allergenicity. A recombinant chimeric IgE was produced and compared to patients' IgE for its capacity to assess the IgE-mediated triggering potential of acid-HWPs. METHODS: Sera from acid-HWP allergic patients were analyzed via ELISA and a functional basophil assay for their IgE reactivity to wheat proteins with different deamidation levels. A chimeric mouse/human IgE (chIgE-DG1) specific for the main neo-epitope, QPEEPFPE, involved in allergy to acid-HWPs was characterized with respect to its functionality and its reactivity compared to that of patients' IgE. RESULTS: Acid-HWPs with medium (30%) and high (50-60%) deamidation levels displayed a markedly stronger IgE binding and capacity to activate basophils than those of samples with weak (15%) deamidation levels. The monoclonal chIgE-DG1 allowed basophil degranulation in the presence of deamidated wheat proteins. ChIgE-DG1 was found to mimic patients' IgE reactivity and displayed the same ability to rank acid-HWP products in a degranulation assay. CONCLUSION: Increasing the deamidation level of products from 15% to 60% resulted in an approximately 2-fold increase in their antigenicity and a 100-fold increase in their eliciting potential. The chimeric ChIgE-DG1 may be a useful tool to evaluate functionalized glutens for their allergenic potential. By mimicking patient sera reactivity, chIgE-DG1 also provided data on the patients' IgE repertoire and on the functionality of certain repeated epitopes in gluten proteins</style></abstract><notes><style face="normal" font="default">DA - 20171108IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - France -CO - United States -CO - Japan -CO - France -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0187415</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29117222">PM:29117222</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0187415.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0187415.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171108, Tranquet O</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0187415</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86990</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Elbert,N.J.</style></author><author><style face="normal" font="default"> Kiefte-de Jong,J.C.</style></author><author><style face="normal" font="default"> Voortman,T.</style></author><author><style face="normal" font="default"> Nijsten,T.E.C.</style></author><author><style face="normal" font="default"> de Jong,N.W.</style></author><author><style face="normal" font="default"> Jaddoe,V.W.V.</style></author><author><style face="normal" font="default"> de Jongste,J.C.</style></author><author><style face="normal" font="default"> Gerth van Wijk,R.</style></author><author><style face="normal" font="default"> Duijts,L.</style></author><author><style face="normal" font="default"> Pasmans,S.G.M.A.</style></author></authors></contributors><auth-address><style face="normal" font="default">The Generation R Study Group, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands</style></auth-address><titles><title><style face="normal" font="default">Allergenic food introduction and risk of childhood atopic diseases</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0187999">e0187999-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: The role of timing and diversity of allergenic food introduction in the development of childhood allergic sensitization and atopic diseases is controversial. OBJECTIVE: To examine whether timing and diversity of allergenic food introduction are associated with allergic sensitization, allergy and eczema in children until age 10 years. MATERIALS AND METHODS: This study among 5,202 children was performed in a population-based prospective cohort. Timing (age &lt;/=6 months vs. >6 months) and diversity (0, 1, 2 and >/=3 foods) of allergenic food (cow's milk, hen's egg, peanut, tree nuts, soy and gluten) introduction were assessed by questionnaires at ages 6 and 12 months. At age 10 years, inhalant and food allergic sensitization were measured by skin prick tests, and physician-diagnosed inhalant and food allergy by questionnaire. Data on parental-reported physician-diagnosed eczema were obtained from birth until age 10 years. RESULTS: Children introduced to gluten at age &lt;/=6 months had a decreased risk of eczema (aOR (95% CI): 0.84 (0.72, 0.99)), compared with children introduced to gluten at age >6 months. However, timing of allergenic food introduction was not associated with allergic sensitization or physician-diagnosed allergy. Children introduced to >/=3 allergenic foods at age &lt;/=6 months had a decreased risk of physician-diagnosed inhalant allergy (0.64 (0.42, 0.98)), compared with children not introduced to any allergenic food at age &lt;/=6 months. However, diversity of allergenic food introduction was not associated with allergic sensitization, physician-diagnosed food allergy or eczema. CONCLUSION: Neither timing nor diversity of allergenic food introduction was consistently associated with childhood allergic sensitization, allergy or eczema</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0187999</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29176842">PM:29176842</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0187999.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0187999.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171127, Elbert NJ</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0187999</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86994</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">McKnight,C.G.</style></author><author><style face="normal" font="default"> Morris,S.C.</style></author><author><style face="normal" font="default"> Perkins,C.</style></author><author><style face="normal" font="default"> Zhu,Z.</style></author><author><style face="normal" font="default"> Hildeman,D.A.</style></author><author><style face="normal" font="default"> Bendelac,A.</style></author><author><style face="normal" font="default"> Finkelman,F.D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Immunology, Allergy and Rheumatology, Department of Medicine, College of Medicine, University of Cincinnati, Cincinnati, Ohio, United States of America</style></auth-address><titles><title><style face="normal" font="default">NKT cells contribute to basal IL-4 production but are not required to induce experimental asthma</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0188221">e0188221-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">CD1d-deficiency results in a selective deletion of NKT cells in mice that is reported to prevent murine allergic airway disease (AAD). Because we find 2-3 fold lower basal IL-4 production in CD1d- mice than in wild-type (WT) mice, we hypothesized that the contribution made by NKT cells to AAD would depend on the strength of the stimulus used to induce the disease. Consequently, we compared CD1d-deficient mice to WT mice in the development of AAD, using several models of disease induction that differed in the type and dose of allergen, the site of sensitization and the duration of immunization. Surprisingly we found equivalent allergic inflammation and airway disease in WT and CD1d- mice in all models investigated. Consistent with this, NKT cells constituted only ~2% of CD4+ T cells in the lungs of mice with AAD, and IL-4-transcribing NKT cells did not expand with disease induction. Concerned that the congenital absence of NKT cells might have caused a compensatory shift within the immune response, we administered an anti-CD1d monoclonal Ab (mAb) to block NKT function before airway treatments, before or after systemic sensitization to antigen. Such Ab treatment did not affect disease severity. We suggest that the differences reported in the literature regarding the significance of NKT cells in the induction of allergic airway disease may have less to do with the methods used to study the disease and more to do with the animals themselves and/or the facilities used to house them</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0188221</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29182669">PM:29182669</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0188221.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0188221.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171128, McKnight CG</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0188221</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87198</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Thomas,R.G.</style></author><author><style face="normal" font="default"> Rivera Reyes,B.M.</style></author><author><style face="normal" font="default"> Gaston,B.M.</style></author><author><style face="normal" font="default"> Rivera Acosta,N.B.</style></author><author><style face="normal" font="default"> Bederman,I.R.</style></author><author><style face="normal" font="default"> Smith,L.A.</style></author><author><style face="normal" font="default"> Sutton,M.T.</style></author><author><style face="normal" font="default"> Wang,B.</style></author><author><style face="normal" font="default"> Hunt,J.F.</style></author><author><style face="normal" font="default"> Bonfield,T.L.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Pediatrics, Division of Pulmonology, University Hospitals Cleveland Medical Center, Rainbow Babies and Children's Hospital, Cleveland, Ohio, United States of America</style></auth-address><titles><title><style face="normal" font="default">Conjugation of nitrated acetaminophen to Der p1 amplifies peripheral blood monocyte response to Der p1</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0188614">e0188614-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergen</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> Pediatrics</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">BACKGROUND: An association of acetaminophen use and asthma was observed in the International Study of Asthma and Allergies in Childhood study. However there are no clear mechanisms to explain an association between acetaminophen use and immunologic pathology. In acidic conditions like those in the stomach and inflamed airway, tyrosine residues are nitrated by nitrous and peroxynitrous acids. The resulting nitrotyrosine is structurally similar to 2,4-dinitrophenol and 2,4-dinitrochlorobenzene, known haptens that enhance immune responses by covalently binding proteins. Nitrated acetaminophen shares similar molecular structure. OBJECTIVE: We hypothesized the acetaminophen phenol ring undergoes nitration under acidic conditions, producing 3-nitro-acetaminophen which augments allergic responses by acting as a hapten for environmental allergens. METHODS: 3-nitro-acetaminophen was formed from acetaminophen in the presence of acidified nitrite, purified by high performance liquid chromatography, and assayed by gas-chromatography mass spectrometry. Purified 3-nitro-acetaminophen was reacted with Dermatophagoides pteronyssinus (Der p1) and analyzed by mass spectrometry to identify the modification site. Human peripheral blood mononuclear cells proliferation response was measured in response to 3-nitro-acetaminophen and to 3-nitro-acetaminophen-modified Der p1. RESULTS: Acetaminophen was modified by nitrous acid forming 3-nitro-acetaminophen over a range of different acidic conditions consistent with airway inflammation and stomach acidity. The Der p1 protein-hapten adduct creation was confirmed by liquid chromatography-mass spectrometry proteomics modifying cysteine 132. Peripheral blood mononuclear cells exposed to 3-nitro-acetaminophen-modified Der p1 had increased proliferation and cytokine production compared to acetaminophen and Der p1 alone (n = 7; p &lt; 0.05). CONCLUSION: These data suggests 3-nitro-acetaminophen formation and reaction with Der p1 provides a mechanism by which stomach acid or infection-induced low airway pH in patients could enhance the allergic response to proteins such as Der p1</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0188614</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29228007">PM:29228007</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0188614.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0188614.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171211, Thomas RG</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0188614</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86995</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Chaisri,U.</style></author><author><style face="normal" font="default"> Tungtrongchitr,A.</style></author><author><style face="normal" font="default"> Indrawattana,N.</style></author><author><style face="normal" font="default"> Meechan,P.</style></author><author><style face="normal" font="default"> Phurttikul,W.</style></author><author><style face="normal" font="default"> Tasaniyananda,N.</style></author><author><style face="normal" font="default"> Saelim,N.</style></author><author><style face="normal" font="default"> Chaicumpa,W.</style></author><author><style face="normal" font="default"> Sookrung,N.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Tropical Pathology, Faculty of Tropical Medicine, Bangkok, Thailand</style></auth-address><titles><title><style face="normal" font="default">Immunotherapeutic efficacy of liposome-encapsulated refined allergen vaccines against Dermatophagoides pteronyssinus allergy</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0188627">e0188627-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">adverse effects</style></keyword><keyword><style face="normal" font="default"> allergens</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Immunotherapy</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> Vaccines</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Allergen specific immunotherapy (AIT) can modulate the allergic response causing a long-term symptom subsidence/abolishment which leads to reduced drug use and prevention of new sensitization. AIT of house dust mite allergy (HDM) using the mite crude extract (CE) as the therapeutic agent is not only less effective than the AIT for many other allergens, but also frequently causes adverse effects during the treatment course. In this study, mouse model of Dermatophagoides pteronyssinus (Dp) allergy was invented for testing therapeutic efficacies of intranasally administered liposome (L) encapsulated vaccines made of single Dp major allergens (L-Der p 1, L-Der p 2), combined allergens (L-Der p 1 and Der p 2), and crude Dp extract (L-CE). The allergen sparing intranasal route was chosen as it is known that the effective cells induced at the nasal-associated lymphoid tissue can exert their activities at the lower respiratory tissue due to the common mucosal traffic. Liposome was chosen as the vaccine delivery vehicle and adjuvant as the micelles could reduce toxicity of the entrapped cargo. The Dp-CE allergic mice received eight doses of individual vaccines/placebo on alternate days. All vaccine formulations caused reduction of the Th2 response of the Dp allergic mice. However, only the vaccines made of single refined allergens induced expressions of immunosuppressive cytokines (TGF-beta, IL-35 and/or IL-10) which are the imperative signatures of successful AIT. The data emphasize the superior therapeutic efficacy of single refined major allergen vaccines than the crude allergenic extract vaccine</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Thailand -</style></notes><work-type><style face="normal" font="default">    10.1371/journal.pone.0188627</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29182623">PM:29182623</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0188627.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0188627.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171128, Chaisri U</style></custom2><misc3><style face="normal" font="default">    10.1371/journal.pone.0188627</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86991</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kuecuekbalaban,P.</style></author><author><style face="normal" font="default"> Schmidt,S.</style></author><author><style face="normal" font="default"> Beutel,M.</style></author><author><style face="normal" font="default"> Weidner,K.</style></author><author><style face="normal" font="default"> de Zwaan,M.</style></author><author><style face="normal" font="default"> Braehler,E.</style></author><author><style face="normal" font="default"> Muehlan,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department Health and Prevention, Ernst-Moritz-Arndt-University Greifswald, Greifswald, Germany</style></auth-address><titles><title><style face="normal" font="default">Socio-demographic, health-related, and individual correlates of diagnostic self-testing by lay people: Results from a representative survey in Germany</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0188653">e0188653-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">INTRODUCTION: A broad range of self-tests (testing for e.g. HIV, cancer, hepatitis B/C) have become available and can be conducted by lay consumers without the help of a health professional. The aims of this study were to (a) investigate the prevalence of self-testing, (b) identify the most frequently used self-tests, and (c) explore the associations between socio-demographic, health-related and individual factors with self-testing. METHODS: A face-to-face plus paper-pencil cross-sectional survey was conducted. The sample consisted of 2.527 respondents who were representative of the German population in terms of the age, sex, and residence. Basic descriptive statistics and univariate logistic regression analyses were performed. RESULTS: 8.5% of the participants reported having used one or more self-tests in the past, totalling 363 self-tests, with a mean of 1.7 (min. = 1, max. = 6). The three self-tests most frequently indicated were for detecting diabetes, bowel cancer, and allergies. Self-testers were older (Nagelkerke R2 = .006, p &lt; .01), had a higher BMI (Nagelkerke R2 = .013, p &lt; .001) and displayed more physical and mental fatigue (Nagelkerke R2 = .031, p &lt; .001) than non-testers. Self-testers also reported higher global life satisfaction values (Nagelkerke R2 = .008, p &lt; .01) and a higher educational level (Nagelkerke R2 = .015, p &lt; .01). CONCLUSIONS: Self-testing is fairly prevalent in Germany Given the current shortage of physicians in Germany, especially in rural areas, and recent studies on the use of self-medication, the topic of self-testing has a great practical and socio-political relevance. Future studies should investigate further predictors of self-testing (e.g. contextual, situational and individual factors) as well as the emotional consequences of testing as a layperson without the attendance of a health professional</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Germany -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0188653</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29190726">PM:29190726</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0188653.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0188653.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS ONE\2017-12-e0188653.SAV</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS ONE\2017-12-e0188653.SAV</url></image-urls></urls><custom2><style face="normal" font="default">20171130, Kuecuekbalaban P</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0188653</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86992</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bao,A.</style></author><author><style face="normal" font="default"> Che,K.F.</style></author><author><style face="normal" font="default"> Bozinovski,S.</style></author><author><style face="normal" font="default"> Ji,J.</style></author><author><style face="normal" font="default"> Gregory,J.A.</style></author><author><style face="normal" font="default"> Kumlien,G.S.</style></author><author><style face="normal" font="default"> Adner,M.</style></author><author><style face="normal" font="default"> Cardell,L.O.</style></author><author><style face="normal" font="default"> Linden,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Unit for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden</style></auth-address><titles><title><style face="normal" font="default">Recombinant human IL-26 facilitates the innate immune response to endotoxin in the bronchoalveolar space of mice in vivo</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0188909">e0188909-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Humans</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Interleukin (IL)-26 is released in response to bacterial endotoxin (LPS) in the bronchoalveolar space of humans in vivo and it may potentiate neutrophil chemotaxis by enhanced IL-26 receptor stimulation. However, the effects of extracellular IL-26 protein on the innate immune response in the lungs in vivo remain unknown. Here, we characterized these effects of IL-26 on a wide range of aspects of the innate immune response to LPS in different compartments of the lungs in vivo over time. We administrated recombinant human (rh) IL-26 protein in the bronchoalveolar space using intranasal instillation in a mouse in vivo model, with and without prior instillation of LPS. We verified gene expression of the IL-26 receptor complex in mouse lungs and observed that, after instillation of LPS, rhIL-26 increases the phosphorylation of STAT3, a signaling molecule of the IL-26 receptor complex. We also observed that rhIL-26 exerted additional stimulatory and inhibitory actions that are compartment- and time-dependent, resulting in alterations of cytokines, proteinases, tissue inflammation and the accumulation of innate effector cells. Without the prior instillation of LPS, rhIL-26 exerted time-dependent effects on total gelatinase activity but few other effects. Most important, after instillation of LPS, rhIL-26 cleared inflammatory cells from local tissue and increased the accumulation of innate effector cells in the bronchoalveolar space. Tentatively, rhIL-26 may facilitate the innate immune response towards the bronchoalveolar space in vivo and represents a potential target for therapy in lung disorders involving the innate immune response</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Sweden -CO - China -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0188909</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29206862">PM:29206862</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0188909.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0188909.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171205, Bao A</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0188909</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86993</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Spierenburg,E.A.J.</style></author><author><style face="normal" font="default"> Smit,L.A.M.</style></author><author><style face="normal" font="default"> Krop,E.J.M.</style></author><author><style face="normal" font="default"> Heederik,D.</style></author><author><style face="normal" font="default"> Hylkema,M.N.</style></author><author><style face="normal" font="default"> Wouters,I.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute for Risk Assessment Sciences, Division of Environmental Epidemiology, Utrecht University, Utrecht, the Netherlands</style></auth-address><titles><title><style face="normal" font="default">Occupational endotoxin exposure in association with atopic sensitization and respiratory health in adults: Results of a 5-year follow-up</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0189097">e0189097-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="in-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Lung function</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">The objective of the present longitudinal study was to investigate the effects of occupational endotoxin exposure on respiratory health and atopic sensitization in adults. Health outcomes and personal endotoxin exposure estimates were determined for 234 farmers and agricultural workers both at baseline and 5 years later. A questionnaire was used to assess respiratory symptoms, spirometry tests were performed and total and specific IgE levels were measured in serum. A twofold increase in personal endotoxin exposure was associated with less hay fever (OR 0.68, 95%CI 0.54-0.87) and grass IgE positivity (OR 0.81, 95%CI 0.68-0.97) at both time points ("persistent" versus "never"). Although not statistically significant, a consistent protective pattern was observed for an increased loss of hay fever symptoms (OR 2.19, 95%CI 0.96-4.99) and grass IgE positivity (OR 1.24, 95%CI 0.76-2.02), and for less new-onset of hay fever (OR 0.87, 95%CI 0.65-1.17), grass IgE positivity (OR 0.83, 95%CI 0.61-1.12) and atopic sensitization (OR 0.75, 95%CI 0.55-1.02). Endotoxin exposure was not associated with changes in lung function. We showed that occupational endotoxin exposure is associated with a long-term protective effect on hay fever and grass IgE positivity. Results on longitudinal changes in hay fever, atopy and grass IgE positivity in adulthood were consistent with a protective effect of endotoxin exposure, but results need to be confirmed in larger cohorts. An effect of endotoxin exposure on lung function decline was not found</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticleCO - Netherlands -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0189097</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29211772">PM:29211772</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0189097.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0189097.pdf</url></text-urls><related-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS ONE\2017-12-e0189097.xlsx</url></related-urls><image-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS ONE\2017-12-e0189097.xlsx</url></image-urls></urls><custom2><style face="normal" font="default">20171206, Spierenburg EA</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0189097</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87199</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pineiro-Hermida,S.</style></author><author><style face="normal" font="default"> Alfaro-Arnedo,E.</style></author><author><style face="normal" font="default"> Gregory,J.A.</style></author><author><style face="normal" font="default"> Torrens,R.</style></author><author><style face="normal" font="default"> Ruiz-Martinez,C.</style></author><author><style face="normal" font="default"> Adner,M.</style></author><author><style face="normal" font="default"> Lopez,I.P.</style></author><author><style face="normal" font="default"> Pichel,J.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Lung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, SpainLung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, SpainUnit of Experimental Asthma and Allergy Research, Karolinska Institutet, Institute of Environmental Medicine (IMM), Stockholm, SwedenLung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, SpainPneumology Service, Hospital San Pedro, Logrono, SpainUnit of Experimental Asthma and Allergy Research, Karolinska Institutet, Institute of Environmental Medicine (IMM), Stockholm, SwedenLung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, SpainLung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, Spain</style></auth-address><titles><title><style face="normal" font="default">Characterization of the acute inflammatory profile and resolution of airway inflammation after Igf1r-gene targeting in a murine model of HDM-induced asthma</style></title><secondary-title><style face="normal" font="default">PLoS One</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">PLoS One</style></abbr-1></periodical><pages end="" start="e0190159">e0190159-</pages><volume><style face="normal" font="default">12</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword></keywords><dates><year Day="0" Month="0" Year="2017">2017</year></dates><abstract><style face="normal" font="default">Asthma is a chronic inflammatory disease characterized by bronchial hyperresponsiveness, mucus overproduction and airway remodeling. Notably, we have recently demonstrated that insulin-like growth factor 1 receptor (IGF1R) deficiency in mice attenuates airway hyperresponsiveness and mucus secretion after chronic house dust mite (HDM) exposure. On this basis, inbred C57BL/6 and Igf1r-deficient mice were given HDM extract to study the acute inflammatory profile and implication of Igf1r in acute asthma pathobiology. Additionally, Igf1r-deficiency was therapeutically induced in mice to evaluate the resolution of HDM-induced inflammation. Acute HDM exposure in inbred C57BL/6 mice led to a progressive increase in inflammation, airway remodeling and associated molecular indicators. Preventively-induced Igf1r-deficiency showed reduced neutrophil and eosinophil numbers in BALF and bone marrow, a significant reduction of airway remodeling and decreased levels of related markers. In addition, therapeutic targeting of Igf1r promoted the resolution of HDM-induced-inflammation. Our results demonstrate for the first time that Igf1r is important in acute asthma pathobiology and resolution of HDM-induced inflammation. Thus, IGF1R is suggested to be a promising candidate for future therapeutic approaches for the treatment and prevention of asthma</style></abstract><notes><style face="normal" font="default">IS - 1932-6203 (Electronic)IS - 1932-6203 (Linking)LA - engPT - Journal ArticlePT - Research Support, Non-U.S. Gov'tCO - Spain -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1371/journal.pone.0190159</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29272313">PM:29272313</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\PLoS One\2017-12-e0190159.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\PLoS One\2017-12-e0190159.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171211, Pineiro-Hermida S</style></custom2><misc3><style face="normal" font="default">10.1371/journal.pone.0190159</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86789</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Jung,S.Y.</style></author><author><style face="normal" font="default"> Lee,S.Y.</style></author><author><style face="normal" font="default"> Choi,D.W.</style></author><author><style face="normal" font="default"> See,H.J.</style></author><author><style face="normal" font="default"> Kwon,D.A.</style></author><author><style face="normal" font="default"> Do,J.R.</style></author><author><style face="normal" font="default"> Shon,D.H.</style></author><author><style face="normal" font="default"> Shin,H.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Food Biotechnology Program, Korea University of Science and Technology, Daejeon 34113, Korea.</style></auth-address><titles><title><style face="normal" font="default">Skullcap (Scutellaria Baicalensis) Hexane Fraction Inhibits the Permeation of Ovalbumin and Regulates Th1/2 Immune Responses</style></title><secondary-title><style face="normal" font="default">Nutrients</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nutrients</style></abbr-1></periodical><pages end="" start="E1184">E1184-</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Water</style></keyword></keywords><dates><year Day="28" Month="10" Year="2017">2017/10/28</year></dates><abstract><style face="normal" font="default">Skullcap (Scutellaria baicalensis) is well known for its anti-inflammatory and anti-allergic effects. In our previous study, we found that skullcap could inhibit allergen permeation and regulate Th1/2 immune balance. To reveal the key fractions and components of skullcap, we fractionated skullcap extract into five fractions: hexane, chloroform, ethyl acetate, butanol, and water fraction. Among these fractions, the hexane fraction significantly suppressed the production of Th2-mediated cytokines (Interleukin (IL)-4, 5, 10 and 13) and increased Th1-mediated cytokines (Interferon (IFN)-gamma and IL-12). Furthermore, the hexane fraction inhibited the permeation of ovalbumin (OVA), used as an allergen, across the intestinal epithelial cell monolayer. To confirm the active compounds in the hexane fraction, fatty acids were analyzed. Linoleic acid (LA, C18:2 (>59.7%)) was identified as the most important fatty acid in the skullcap hexane fraction. LA significantly suppressed IL-4 production and increased IFN-gamma secretion, as well as inhibiting OVA permeation. Thus, LA significantly diminished the permeation of allergen by enhancing intestinal barrier function and regulated allergic responses to maintain Th1/Th2 immune balance</style></abstract><notes><style face="normal" font="default">DA - 20171116IS - 2072-6643 (Electronic)IS - 2072-6643 (Linking)LA - engPT - Journal ArticleCO - South Korea -</style></notes><work-type><style face="normal" font="default">10.3390/nu9111184</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29143798">PM:29143798</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nutrients\2017-9-E1184.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nutrients\2017-9-E1184.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171116, Jung SY</style></custom2><misc3><style face="normal" font="default">10.3390/nu9111184</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86656</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Leccioli,V.</style></author><author><style face="normal" font="default"> Oliveri,M.</style></author><author><style face="normal" font="default"> Romeo,M.</style></author><author><style face="normal" font="default"> Berretta,M.</style></author><author><style face="normal" font="default"> Rossi,P.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, via Ferrata 1, 27100 Pavia, Italy.</style></auth-address><titles><title><style face="normal" font="default">A New Proposal for the Pathogenic Mechanism of Non-Coeliac/Non-Allergic Gluten/Wheat Sensitivity: Piecing Together the Puzzle of Recent Scientific Evidence</style></title><secondary-title><style face="normal" font="default">Nutrients</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Nutrients</style></abbr-1></periodical><pages end="" start="E1203">E1203-</pages><volume><style face="normal" font="default">9</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">Non-coeliac/non-allergic gluten/wheat sensitivity (NCG/WS) is a gluten-related disorder, the pathogenesis of which remains unclear. Recently, the involvement of an increased intestinal permeability has been recognized in the onset of this clinical condition. However, mechanisms through which it takes place are still unclear. In this review, we attempt to uncover these mechanisms by providing, for the first time, an integrated vision of recent scientific literature, resulting in a new hypothesis about the pathogenic mechanisms involved in NCG/WS. According to this, the root cause of NCG/WS is a particular dysbiotic profile characterized by decreased butyrate-producing-Firmicutes and/or Bifidobacteria, leading to low levels of intestinal butyrate. Beyond a critical threshold of the latter, a chain reaction of events and vicious circles occurs, involving other protagonists such as microbial lipopolysaccharide (LPS), intestinal alkaline phosphatase (IAP) and wheat alpha-amylase trypsin inhibitors (ATIs). NCG/WS is likely to be a multi-factor-onset disorder, probably transient and preventable, related to quality and balance of the diet, and not to the presence of gluten in itself. If future studies confirm our proposal, this would have important implications both for the definition of the disease, as well as for the prevention and therapeutic-nutritional management of individuals with NCG/WS</style></abstract><notes><style face="normal" font="default">DA - 20171103IS - 2072-6643 (Electronic)IS - 2072-6643 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Italy -CO - Malta -</style></notes><work-type><style face="normal" font="default">10.3390/nu9111203</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29099090">PM:29099090</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Nutrients\2017-9-E1203.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Nutrients\2017-9-E1203.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171103, Leccioli V</style></custom2><misc3><style face="normal" font="default">10.3390/nu9111203</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87195</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wicher,S.A.</style></author><author><style face="normal" font="default"> Lawson,K.L.</style></author><author><style face="normal" font="default"> Jacoby,D.B.</style></author><author><style face="normal" font="default"> Fryer,A.D.</style></author><author><style face="normal" font="default"> Drake,M.G.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Physiology and Pharmacology, Oregon Health &amp; Sciences University, Portland, Oregon</style></auth-address><titles><title><style face="normal" font="default">Ozone-induced eosinophil recruitment to airways is altered by antigen sensitization and tumor necrosis factor-alpha blockade</style></title><secondary-title><style face="normal" font="default">Physiol Rep</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Physiol Rep</style></abbr-1></periodical><pages end="" start="e13538">e13538-</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">24</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">airway</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Eosinophil</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><abstract><style face="normal" font="default">Ozone is an atmospheric pollutant that causes lung inflammation and airway hyperresponsiveness. Ozone's effects occur in two distinct phases that are mediated by different populations of eosinophils. In the acute phase 1 day after exposure, mature airway-resident eosinophils alter parasympathetic nerve function that results in airway hyperresponsiveness. At this time point, the severity of hyperresponsiveness correlates with the number of eosinophils in close proximity to airway nerves, but not with eosinophils in bronchoalveolar lavage. Three days later, newly divided eosinophils are recruited to airways by a tumor necrosis factor-alpha-dependent mechanism. These new eosinophils paradoxically attenuate ozone-induced airway hyperresponsiveness. Ozone's effects on airway tissue eosinophils and nerve-associated eosinophils 3 days after exposure are unknown. Thus, we tested ozone's effects on eosinophils in airway subepithelium and around airway nerves 1 and 3 days after ozone in nonsensitized and ovalbumin-sensitized guinea pigs with or without the tumor necrosis factor-alpha antagonist, etanercept, and compared changes in eosinophils with ozone-induced airway hyperresponsiveness. More eosinophils were present in small, noncartilaginous airways and along small airway nerves compared to large cartilaginous airways in all treatment groups. The number of airway and nerve-associated eosinophils were unaffected 1 day after ozone exposure, whereas significantly fewer airway eosinophils were present 3 days later. Airway and nerve-associated eosinophils were also decreased in small airways 3 days after ozone in sensitized animals. These changes were blocked by etanercept. Airway eosinophils, but not nerve-associated or bronchoalveolar lavage eosinophils correlated with airway hyperresponsiveness 3 days after ozone. Our findings indicate ozone causes persistent alterations in airway eosinophils and reinforce the importance of characterizing eosinophils' effects within distinct airway compartments</style></abstract><notes><style face="normal" font="default">IS - 2051-817X (Electronic)IS - 2051-817X (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.14814/phy2.13538</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29242307">PM:29242307</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Physiol Rep\2017-5-E13538.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Physiol Rep\2017-5-E13538.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171209, Wicher SA</style></custom2><misc3><style face="normal" font="default">10.14814/phy2.13538</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87291</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Apostolico,J.S.</style></author><author><style face="normal" font="default"> Oliveira Filho,J.N.</style></author><author><style face="normal" font="default"> Fernandes,E.R.</style></author><author><style face="normal" font="default"> Silva,F.R.</style></author><author><style face="normal" font="default"> Andersen,M.L.</style></author><author><style face="normal" font="default"> Keller,A.C.</style></author><author><style face="normal" font="default"> Rosa,D.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">REM-sleep deprivation predisposes neutrophilic lung inflammation in allergic mice</style></title><secondary-title><style face="normal" font="default">Sleep Med</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">Sleep Med</style></full-title></periodical><pages end="" start="e16">e16-</pages><volume><style face="normal" font="default">40, Supplement 1</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><isbn><style face="normal" font="default">1389-9457</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Brazil -</style></notes><work-type><style face="normal" font="default">10.1016/j.sleep.2017.11.040</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.sleep.2017.11.040</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sleep Med\2017-40S1-e16.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sleep Med\2017-40S1-e16.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171230, Apostolico JS</style></custom2><misc3><style face="normal" font="default">10.1016/j.sleep.2017.11.040</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86639</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kahl,C.G.</style></author><author><style face="normal" font="default"> Deas,C.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Flight Medicine, 42nd Medical Group, Maxwell Air Force Base, Montgomery, AL 36113Department of Pharmacy Practice, Samford University McWhorter School of Pharmacy, 800 Lakeshore Drive, Birmingham, AL 35229</style></auth-address><titles><title><style face="normal" font="default">Exercise-Induced Anaphylaxis in an Air Force Aviator Taking a HMG-CoA Reductase Inhibitor: A Case Report and Review of the Presentation, Diagnoses, and Treatment</style></title><secondary-title><style face="normal" font="default">Mil Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mil Med</style></abbr-1></periodical><pages end="e1819" start="e1816">e1816-e1819</pages><volume><style face="normal" font="default">182</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="5" Year="2017">2017/5</year></dates><abstract><style face="normal" font="default">BACKGROUND: A 46-year-old healthy male Air Force pilot presented to the emergency department (ED) experiencing symptoms of exercise-induced anaphylaxis (EIAn), during a vigorous outdoor run. The patient recovered in the ED and was seen, subsequently, by a civilian allergist; eventually a diagnosis consistent with EIAn was made. EIAn is a rare but potentially life-threatening syndrome believed to involve IgE mediated release of histamine and other immunoactive compounds, during or after exercise. The diagnosis is determined by a strong clinical suspicion along with careful exclusion of other potential diagnoses. Interestingly, this particular patient was also found to have a possible correlation between the introduction of 3-hydroxy-3-methylglutaryl-coenzyme A, for hyperlipidemia, shortly before his first episode of EIAn, and remission of the condition since discontinuing the statin medication. METHODS: A detailed review of the clinical notes, ED presentation, and all subspecialty consultation notes were include in the compilation of this case report, in conjunction with a careful review of all current literature pertaining to drug exacerbated, exercise-induced EIAn. The review of literature was also conducted to review potential mechanisms of this particular hypersensitivity reaction, and to give a thorough discussion of the history and presentation of this disorder. RESULTS: The patient described in this case was successfully treated over a 2-year period, with exercise modifications and a daily second generation antihistamine. Nearly a year after his initial diagnoses, in an acute visit to the flight medicine clinic for muscle soreness and elevated creatine kinase isoenzymes, the patient's medication profile was reviewed and his statin medication was discontinued. The clinical notes revealed that the statin was started a few months before his first onset of EIAn, and following its discontinuation, the patient has been asymptomatic for over a year, exercising regularly, and completed a successful forward deployment to an austere desert environment. DISCUSSION: To our knowledge, this is the first reported case of possible statin exacerbated, EIAn. Data concerning the incidence of drug-induced hypersensitivity to statins are limited as is any discussion on prevalence of EIAn in adult populations. There have been, however, case reports documenting statin immunological effects on serum IgE levels, which may offer a potential mechanism of statin-exacerbated EIAn. However, the role of IgE antibodies in drug-induced anaphylactic reactions remains unclear. In this patient's case, there was no measure of statin-specific immune reactivity performed; however, the timing of statin initiation of monotherapy in relation to presentation of EIAn strongly supports the diagnosis of statin-exacerbated EIAn. Although the mechanisms involving statin-induced EIAn remain elusive, this case report illustrates the need for military providers to recognize this condition and cofactors that may contribute to its genesis. Moreover, this case also illustrates the need for increased research and surveillance of this condition in civilian and military populations</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1930-613X (Electronic)IS - 0026-4075 (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.7205/MILMED-D-16-00247</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29087932">PM:29087932</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mil Med\2017-182-e1816-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mil Med\2017-182-e1816-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Kahl CG</style></custom2><misc3><style face="normal" font="default">10.7205/MILMED-D-16-00247</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86651</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xu,J.</style></author><author><style face="normal" font="default"> Chen,Z.</style></author><author><style face="normal" font="default"> Han,D.</style></author><author><style face="normal" font="default"> Li,Y.</style></author><author><style face="normal" font="default"> Sun,X.</style></author><author><style face="normal" font="default"> Wang,Z.</style></author><author><style face="normal" font="default"> Jin,H.</style></author></authors></contributors><auth-address><style face="normal" font="default">College of Science, Northeast Agricultural University, Harbin 150030, Heilongjiang, China</style></auth-address><titles><title><style face="normal" font="default">Structural and Functional Properties Changes of beta-Conglycinin Exposed to Hydroxyl Radical-Generating Systems</style></title><secondary-title><style face="normal" font="default">Molecules</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Molecules</style></abbr-1></periodical><pages end="" start="E1893">E1893-</pages><volume><style face="normal" font="default">22</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="3" Month="11" Year="2017">2017/11/3</year></dates><abstract><style face="normal" font="default">The objective of the present study was to examine the structural and functional changes of beta-conglycinin exposed to oxidizing radicals produced by FeCl(3)/H(2)O(2)/ascorbic acid hydroxyl radical-generating system (HRGS) for 3 h at room temperature. Increasing H(2)O(2) concentrations resulted in a loss of histidine residues, lysine residues, and available lysine, which was accompanied by the formation of protein carbonyls and disulphide bonds (p &lt; 0.05). Changes in secondary structure, surface hydrophobicity, and intrinsic fluorescence indicated that hydroxyl radicals had induced protein unfolding and conformational alterations. Results from SDS-PAGE implied that a small amount of protein cross-linkages produced by oxidative incubation. The emulsifying properties of beta-conglycinin were gradually improved with the increasing extent of oxidation. The structural changes above contributed to the reduction of potential allergenicity of beta-conglycinin, as verified by specific ELISA analysis. These results suggest that moderate oxidation could partially improve the protein functional properties and reduced the potential allergy of protein, providing guidance for effective use of moderately oxidized soy protein in the industry</style></abstract><notes><style face="normal" font="default">DA - 20171103IS - 1420-3049 (Electronic)IS - 1420-3049 (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.3390/molecules22111893</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29099771">PM:29099771</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Molecules\2017-22-E1893.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Molecules\2017-22-E1893.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171103, Xu J</style></custom2><misc3><style face="normal" font="default">10.3390/molecules22111893</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86682</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Irifuku,R.</style></author><author><style face="normal" font="default"> Yanase,Y.</style></author><author><style face="normal" font="default"> Kawaguchi,T.</style></author><author><style face="normal" font="default"> Ishii,K.</style></author><author><style face="normal" font="default"> Takahagi,S.</style></author><author><style face="normal" font="default"> Hide,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Dermatology, Graduate School of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.</style></auth-address><titles><title><style face="normal" font="default">Impedance-Based Living Cell Analysis for Clinical Diagnosis of Type I Allergy</style></title><secondary-title><style face="normal" font="default">Sensors (Basel)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sensors (Basel)</style></abbr-1></periodical><pages end="" start="E2503">E2503-</pages><volume><style face="normal" font="default">17</style></volume><number><style face="normal" font="default">11</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="31" Month="10" Year="2017">2017/10/31</year></dates><abstract><style face="normal" font="default">Non-invasive real time evaluation of living cell conditions and functions are increasingly desired in the field of clinical diagnosis. For diagnosis of type I allergy, the identification of antigens that induces activation of mast cells and basophils is crucial to avoid symptoms of allergic diseases. However, conventional tests, such as detection of antigen-specific IgE antibody and skin tests, are either of low reliability or are invasive. To overcome such problems, we hereby applied an impedance sensor for label-free and real-time monitoring of mast cell reactions in response to stimuli. When IgE-sensitized RBL-2H3 cells cultured on the electrodes were stimulated with various concentrations of antigens, dose-dependent cell index (CI) increases were detected. Moreover, we confirmed that the impedance sensor detected morphological changes rather than degranulation as the indicator of cell activation. Furthermore, the CI of human IgE receptor-expressing cells (RBL-48 cells) treated with serum of a sweat allergy-positive patient, but not with serum from a sweat allergy-negative patient, significantly increased in response to purified human sweat antigen. We thus developed a technique to detect the activation of living cells in response to stimuli without any labeling using the impedance sensor. This system may represent a high reliable tool for the diagnosis of type I allergy</style></abstract><notes><style face="normal" font="default">DA - 20171031IS - 1424-8220 (Electronic)IS - 1424-8220 (Linking)LA - engPT - Journal ArticleCO - Japan -</style></notes><work-type><style face="normal" font="default">10.3390/s17112503</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29088110">PM:29088110</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sensors (Basel)\2017-17-E2503.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sensors (Basel)\2017-17-E2503.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171031, Irifuku R</style></custom2><misc3><style face="normal" font="default">10.3390/s17112503</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87179</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Majeed,H.</style></author><author><style face="normal" font="default"> Majeed,H.</style></author></authors></contributors><titles><title><style face="normal" font="default">Acknowledging the environmental allergy epidemic in children in the UK</style></title><secondary-title><style face="normal" font="default">Lancet Planet Health</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Lancet Planet Health</style></abbr-1></periodical><pages end="e350" start="e349">e349-e350</pages><volume><style face="normal" font="default">1</style></volume><number><style face="normal" font="default">9</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword></keywords><dates><year Day="0" Month="12" Year="2017">2017/12</year></dates><isbn><style face="normal" font="default">2542-5196</style></isbn><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Canada -</style></notes><work-type><style face="normal" font="default">10.1016/S2542-5196(17)30161-4</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/S2542-5196(17)30161-4</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Lancet Planet Health\2017-1-e349-50.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Lancet Planet Health\2017-1-e349-50.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171202, Majeed H</style></custom2><misc3><style face="normal" font="default">10.1016/S2542-5196(17)30161-4</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86846</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Zhang,J.H.</style></author><author><style face="normal" font="default"> Chen,Y.P.</style></author><author><style face="normal" font="default"> Yang,X.</style></author><author><style face="normal" font="default"> Li,C.Q.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Emergency, the First Affiliated Hospital of Guangxi Medical University, The Guangxi Talent Highland for Emergency and Rescue Medicine, Guangxi Colleges and Universities Key Laboratory of Emergency Medicine Research, Nanning, Guangxi, China</style></auth-address><titles><title><style face="normal" font="default">Vitamin D3 levels and NLRP3 expression in murine models of obese asthma: association with asthma outcomes</style></title><secondary-title><style face="normal" font="default">Braz J Med Biol Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Braz J Med Biol Res</style></abbr-1></periodical><pages end="" start="e6841">e6841-</pages><volume><style face="normal" font="default">51</style></volume><number><style face="normal" font="default">1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword></keywords><dates><year Day="13" Month="11" Year="2017">2017/11/13</year></dates><abstract><style face="normal" font="default">Vitamin D (25(OH)D3) is an essential nutrient that plays a role in the immune system. Serum 25(OH)D3 is found to be associated with asthma. However, the role of vitamin D in obese asthma remains unclear. Therefore, we investigated the association between vitamin D levels and asthma outcomes in a murine model of obese asthma. We also evaluated NLRP3 inflammasome activity in the pathogenesis of obese asthma. We divided 20 male Balb/c mice (3-4 weeks old) into 4 groups: normal control, asthma, obese, and obese asthma and developed an obese asthma mouse model. Airway hyperreactivity, cytokine concentrations, 25(OH)D3 levels, NLRP3 mRNA and IL-1beta mRNA expressions were measured. Lung histology and bronchoalveolar lavage fluid (BALF) cell count were also determined. Obese asthma mice showed a significant increase in airway hyper-responsiveness, airway inflammation, pro-inflammatory cytokine levels and NLRP3 mRNA, IL-1beta mRNA expression. Both asthma and obese groups had lower 25(OH)D3 levels. Vitamin D levels in obese asthma were the lowest among all groups. Vitamin D levels correlated negatively with body weight, lung resistance levels at 25 mg/mL of methacholine, total inflammatory cells, and IL-1beta and IL-17 concentrations in BALF. These data demonstrated an association between serum vitamin D levels and outcomes of obese asthma, and indicated that NLRP3 inflammasome may play a role in this disorder</style></abstract><notes><style face="normal" font="default">IS - 1414-431X (Electronic)IS - 0100-879X (Linking)LA - engPT - Journal ArticleCO - China -</style></notes><work-type><style face="normal" font="default">10.1590/1414-431X20176841</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29160418">PM:29160418</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Braz J Med Biol Res\2017-51-e6841.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Braz J Med Biol Res\2017-51-e6841.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171113, Zhang JH</style></custom2><misc3><style face="normal" font="default">10.1590/1414-431X20176841</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87463</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Loste,A.</style></author><author><style face="normal" font="default"> Clement,M.</style></author><author><style face="normal" font="default"> Delbosc,S.</style></author><author><style face="normal" font="default"> Gaston,A.T.</style></author><author><style face="normal" font="default"> Morvan,M.</style></author><author><style face="normal" font="default"> Even,G.</style></author><author><style face="normal" font="default"> Andreata,F.</style></author><author><style face="normal" font="default"> Deschamps,L.</style></author><author><style face="normal" font="default"> Deschildre,C.</style></author><author><style face="normal" font="default"> Louedec,L.</style></author><author><style face="normal" font="default"> Arock,M.</style></author><author><style face="normal" font="default"> Caligiuri,G.</style></author><author><style face="normal" font="default"> Nicoletti,A.</style></author><author><style face="normal" font="default"> Le Borgne,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">LVTS INSERM U1148, Universite Paris Diderot, Sorbonne Paris Cite, DHU Fire, Paris, France</style></auth-address><titles><title><style face="normal" font="default">Role of IgE antibodies and mast cells in atherosclerosis</style></title><secondary-title><style face="normal" font="default">Atherosclerosis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Atherosclerosis</style></abbr-1></periodical><pages end="" start="e9">e9-</pages><volume><style face="normal" font="default">263</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Antibodies</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword></keywords><dates><year Day="0" Month="8" Year="2017">2017/8</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1879-1484 (Electronic)IS - 0021-9150 (Linking)LA - engPT - Journal ArticleCO - France -</style></notes><work-type><style face="normal" font="default">10.1016/j.atherosclerosis.2017.06.056</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29366265">PM:29366265</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Atherosclerosis\2017-263-e9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Atherosclerosis\2017-263-e9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170812, Loste A</style></custom2><misc3><style face="normal" font="default">10.1016/j.atherosclerosis.2017.06.056</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86636</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Nolin,J.D.</style></author><author><style face="normal" font="default"> Lai,Y.</style></author><author><style face="normal" font="default"> Ogden,H.L.</style></author><author><style face="normal" font="default"> Manicone,A.M.</style></author><author><style face="normal" font="default"> Murphy,R.C.</style></author><author><style face="normal" font="default"> An,D.</style></author><author><style face="normal" font="default"> Frevert,C.W.</style></author><author><style face="normal" font="default"> Ghomashchi,F.</style></author><author><style face="normal" font="default"> Naika,G.S.</style></author><author><style face="normal" font="default"> Gelb,M.H.</style></author><author><style face="normal" font="default"> Gauvreau,G.M.</style></author><author><style face="normal" font="default"> Piliponsky,A.M.</style></author><author><style face="normal" font="default"> Altemeier,W.A.</style></author><author><style face="normal" font="default"> Hallstrand,T.S.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Medicine, Division of Pulmonary and Critical Care</style></auth-address><titles><title><style face="normal" font="default">Secreted PLA2 group X orchestrates innate and adaptive immune responses to inhaled allergen</style></title><secondary-title><style face="normal" font="default">JCI Insight</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">JCI Insight</style></abbr-1></periodical><pages end="" start="e94929">e94929-</pages><volume><style face="normal" font="default">2</style></volume><number><style face="normal" font="default">21</style></number><reprint-status status="no-file"/><keywords/><dates><year Day="2" Month="11" Year="2017">2017/11/2</year></dates><abstract><style face="normal" font="default">Phospholipase A2 (PLA2) enzymes regulate the formation of eicosanoids and lysophospholipids that contribute to allergic airway inflammation. Secreted PLA2 group X (sPLA2-X) was recently found to be increased in the airways of asthmatics and is highly expressed in airway epithelial cells and macrophages. In the current study, we show that allergen exposure increases sPLA2-X in humans and in mice, and that global deletion of Pla2g10 results in a marked reduction in airway hyperresponsiveness (AHR), eosinophil and T cell trafficking to the airways, airway occlusion, generation of type-2 cytokines by antigen-stimulated leukocytes, and antigen-specific immunoglobulins. Further, we found that Pla2g10-/- mice had reduced IL-33 levels in BALF, fewer type-2 innate lymphoid cells (ILC2s) in the lung, less IL-33-induced IL-13 expression in mast cells, and a marked reduction in both the number of newly recruited macrophages and the M2 polarization of these macrophages in the lung. These results indicate that sPLA2-X serves as a central regulator of both innate and adaptive immune response to proteolytic allergen</style></abstract><notes><style face="normal" font="default">DA - 20171102IS - 2379-3708 (Electronic)IS - 2379-3708 (Linking)LA - engPT - Journal ArticleCO - United States -CO - Canada -</style></notes><work-type><style face="normal" font="default">10.1172/jci.insight.94929</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29093264">PM:29093264</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\JCI Insight\2017-2-e94929.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\JCI Insight\2017-2-e94929.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171102, Nolin JD</style></custom2><misc3><style face="normal" font="default">10.1172/jci.insight.94929</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87194</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kalkman,H.O.</style></author><author><style face="normal" font="default"> Feuerbach,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">Gansbuhlgartenweg 7, CH4132 Muttenz, Switzerland.</style></auth-address><titles><title><style face="normal" font="default">Microglia M2A Polarization as Potential Link between Food Allergy and Autism Spectrum Disorders</style></title><secondary-title><style face="normal" font="default">Pharmaceuticals (Basel)</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pharmaceuticals (Basel)</style></abbr-1></periodical><pages end="" start="E95">E95-</pages><volume><style face="normal" font="default">10</style></volume><number><style face="normal" font="default">4</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Mast cells</style></keyword><keyword><style face="normal" font="default"> Neurons</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="9" Month="12" Year="2017">2017/12/9</year></dates><abstract><style face="normal" font="default">Atopic diseases are frequently co-morbid with autism spectrum disorders (ASD). Allergic responses are associated with an activation of mast cells, innate lymphoid cells, and Th2 cells. These cells produce type-2 cytokines (IL4 and IL13), which stimulate microglia and macrophages to adopt a phenotype referred to as 'alternative activation' or 'M2A'. M2A-polarized macrophages and microglia play a physiological role in tissue repair by secreting growth factors such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1. In ASD there is evidence for increased type-2 cytokines, microglia activation, M2A polarization, and increased levels of growth factors. In neurons, these growth factors drive a signal transduction pathway that leads to activation of the enzyme mammalian Target of Rapamycin (mTOR), and thereby to the inhibition of autophagy. Activation of mTOR is an effect that is also common to several of the genetic forms of autism. In the central nervous system, redundant synapses are removed via an autophagic process. Activation of mTOR would diminish the pruning of redundant synapses, which in the context of ASD is likely to be undesired. Based on this line of reasoning, atopic diseases like food allergy, eczema or asthma would represent risk factors for autism spectrum disorders</style></abstract><notes><style face="normal" font="default">IS - 1424-8247 (Print)IS - 1424-8247 (Linking)LA - engPT - Journal ArticlePT - ReviewCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.3390/ph10040095</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29232822">PM:29232822</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pharmaceuticals (Basel)\2017-10-E95.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pharmaceuticals (Basel)\2017-10-E95.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171209, Kalkman HO</style></custom2><misc3><style face="normal" font="default">10.3390/ph10040095</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86564</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Sokolowska,M.</style></author><author><style face="normal" font="default"> Akdis,C.A.</style></author></authors></contributors><titles><title><style face="normal" font="default">Highlights in immune response, microbiome and precision medicine in allergic disease and asthma</style></title><secondary-title><style face="normal" font="default">Curr Opin Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Curr Opin Immunol</style></abbr-1></periodical><pages end="ix" start="iv">iv-ix</pages><volume><style face="normal" font="default">48</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">immunology</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Atopic dermatitis</style></keyword></keywords><dates><year Day="0" Month="10" Year="2017">2017/10</year></dates><isbn><style face="normal" font="default">0952-7915</style></isbn><abstract><style face="normal" font="default">Several recent key findings in immunology of allergic diseases that have led to a need of reassessment of our current thinking are reviewed in this issue of the journal. Recently developed strong evidence on the role of hygiene hypothesis in protection from allergic disease and its immune mechanisms is reviewed by Ober et al. The authors pointed out immunologic mechanisms of lower prevalence of asthma and allergic sensitization observed among Amish children living on traditional farms with higher endotoxin levels as compared to Hutterite children living on industrialized farms. Barcik et al. reviewed that biologically active histamine in humans is produced by certain bacteria in the gut in addition to several cells, and has broad immunoregulatory functions. Turcanu et al. reviewed immune mechanisms of a revolutionary change to protect from food allergy. The immunologic window of opportunity in the infants can be used to enable oral tolerance in severe allergy predisposed children. Accordingly, van de Veen et al. reviewed general mechanisms of allergen tolerance highlighting recent findings. Extensive usage of precision medicine due to emerging biologics is knocking the doors of allergic diseases and asthma. Boyd et al. reviewed the existing and future </style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Ç£immune monitoring</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">ÇØ approaches in the multiple omics perspective with the hope of identifying better correlates of disease status, predictors of therapeutic outcomes, and potential side-effects of treatment. Paul et al. reviewed newly uncovered innate and adaptive immunologic mechanisms that contribute to the pathogenesis of eosinophilic esophagitis. Further highlighting newly developing disease subgroups and precision medicine, Guttman-Yassky &amp;amp; Kruger reviewed clinical subtypes of atopic dermatitis and psoriasis, which may potentially benefit from newly developing highly efficient biologicals. Complementing this paper, Kabashima &amp;amp; Nomura reviewed similarities and distinctions in mouse models of atopic dermatitis and psoriasis</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Switzerland -</style></notes><work-type><style face="normal" font="default">10.1016/j.coi.2017.10.009</style></work-type><urls><web-urls><url ppv-ref="no">https://doi.org/10.1016/j.coi.2017.10.009</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-iv-ix.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Curr Opin Immunol\2017-48-iv-ix.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Sokolowska M</style></custom2><misc3><style face="normal" font="default">10.1016/j.coi.2017.10.009</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86843</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wise,J.</style></author></authors></contributors><auth-address><style face="normal" font="default">London</style></auth-address><titles><title><style face="normal" font="default">New test for asthma will save NHS millions, says NICE</style></title><secondary-title><style face="normal" font="default">BMJ</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">BMJ</style></full-title></periodical><pages end="" start="j5540">j5540-</pages><volume><style face="normal" font="default">359</style></volume><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Asthma</style></keyword></keywords><dates><year Day="28" Month="11" Year="2017">2017/11/28</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 1756-1833 (Electronic)IS - 0959-535X (Linking)LA - engPT - Journal ArticleCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1136/bmj.j5540</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29183986">PM:29183986</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\BMJ\2017-359-j5540.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\BMJ\2017-359-j5540.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171124, Wise J</style></custom2><misc3><style face="normal" font="default">10.1136/bmj.j5540</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87237</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Griese,S.E.</style></author><author><style face="normal" font="default"> Kisselburgh,H.M.</style></author><author><style face="normal" font="default"> Bartenfeld,M.T.</style></author><author><style face="normal" font="default"> Thomas,E.</style></author><author><style face="normal" font="default"> Rao,A.K.</style></author><author><style face="normal" font="default"> Sobel,J.</style></author><author><style face="normal" font="default"> Dziuban,E.J.</style></author></authors></contributors><auth-address><style face="normal" font="default">Office of Science and Public Health Practice, Office of Public Health Preparedness and Response, Centers for Disease Control and Prevention, Atlanta, Georgia</style></auth-address><titles><title><style face="normal" font="default">Pediatric Botulism and Use of Equine Botulinum Antitoxin in Children: A Systematic Review</style></title><secondary-title><style face="normal" font="default">Clin Infect Dis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Infect Dis</style></abbr-1></periodical><pages end="S29" start="S17">S17-S29</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">suppl_1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adult</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="27" Month="12" Year="2017">2017/12/27</year></dates><abstract><style face="normal" font="default">Background: Botulism manifests with cranial nerve palsies and flaccid paralysis in children and adults. Botulism must be rapidly identified and treated; however, clinical presentation and treatment outcomes of noninfant botulism in children are not well described. Methods: We searched 12 databases for peer-reviewed and non-peer-reviewed reports with primary data on botulism in children (persons &lt;18 years of age) or botulinum antitoxin administration to children. Reports underwent title and abstract screening and full text review. For each case, patient demographic, clinical, and outcome data were abstracted. Results: Of 7065 reports identified, 184 met inclusion criteria and described 360 pediatric botulism cases (79% confirmed, 21% probable) that occurred during 1929-2015 in 34 countries. Fifty-three percent were male; age ranged from 4 months to 17 years (median, 10 years). The most commonly reported signs and symptoms were dysphagia (53%), dysarthria (39%), and generalized weakness (37%). Inpatient length of stay ranged from 1 to 425 days (median, 24 days); 14% of cases required intensive care unit admission; 25% reported mechanical ventilation. Eighty-three (23%) children died. Median interval from illness onset to death was 1 day (range, 0-260 days). Among patients who received antitoxin (n = 193), 23 (12%) reported an adverse event, including rash, fever, serum sickness, and anaphylaxis. Relative risk of death among patients treated with antitoxin compared with patients not treated with antitoxin was 0.24 (95% confidence interval, .14-.40; P &lt; .0001). Conclusions: Dysphagia and dysarthria were the most commonly reported cranial nerve symptoms in children with botulism; generalized weakness was described more than paralysis. Children who received antitoxin had better survival; serious adverse events were rare. Most deaths occurred early in the clinical course; therefore, botulism in children should be identified and treated rapidly</style></abstract><notes><style face="normal" font="default">IS - 1537-6591 (Electronic)IS - 1058-4838 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1093/cid/cix812</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29293924">PM:29293924</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Infect Dis\2017-66S1-17-29.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Infect Dis\2017-66S1-17-29.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Griese SE</style></custom2><misc3><style face="normal" font="default">10.1093/cid/cix812</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87236</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Schussler,E.</style></author><author><style face="normal" font="default"> Sobel,J.</style></author><author><style face="normal" font="default"> Hsu,J.</style></author><author><style face="normal" font="default"> Yu,P.</style></author><author><style face="normal" font="default"> Meaney-Delman,D.</style></author><author><style face="normal" font="default"> Grammer,L.C.,III</style></author><author><style face="normal" font="default"> Nowak-Wegrzyn,A.</style></author></authors></contributors><auth-address><style face="normal" font="default">Division of Pulmonology, Allergy and Immunology, Weill Cornell Medicine, New York, New York</style></auth-address><titles><title><style face="normal" font="default">Workgroup Report by the Joint Task Force Involving American Academy of Allergy, Asthma &amp; Immunology (AAAAI); Food Allergy, Anaphylaxis, Dermatology and Drug Allergy (FADDA) (Adverse Reactions to Foods Committee and Adverse Reactions to Drugs, Biologicals, and Latex Committee); and the Centers for Disease Control and Prevention Botulism Clinical Treatment Guidelines Workgroup-Allergic Reactions to Botulinum Antitoxin: A Systematic Review</style></title><secondary-title><style face="normal" font="default">Clin Infect Dis</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Clin Infect Dis</style></abbr-1></periodical><pages end="S72" start="S65">S65-S72</pages><volume><style face="normal" font="default">66</style></volume><number><style face="normal" font="default">suppl_1</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Allergy</style></keyword><keyword><style face="normal" font="default"> Anaphylaxis</style></keyword><keyword><style face="normal" font="default"> Asthma</style></keyword><keyword><style face="normal" font="default"> Epinephrine</style></keyword><keyword><style face="normal" font="default"> Food allergy</style></keyword><keyword><style face="normal" font="default"> Guidelines</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword></keywords><dates><year Day="27" Month="12" Year="2017">2017/12/27</year></dates><abstract><style face="normal" font="default">Background: Naturally occurring botulism is rare, but a large number of cases could result from unintentional or intentional contamination of a commercial food. Despeciated, equine-derived, heptavalent botulinum antitoxin (HBAT) is licensed in the United States. Timely treatment reduces morbidity and mortality, but concerns that botulinum antitoxin can induce anaphylaxis exist. We sought to quantify the allergy risk of botulinum antitoxin treatment and the usefulness of skin testing to assess this risk. Methods: We conducted a systematic review of (1) allergic reactions to botulinum antitoxin and (2) the predictive value of skin testing (ST) before botulinum antitoxin administration. We searched 5 scientific literature databases, reviewed articles' references, and obtained data from the HBAT manufacturer and from the Centers for Disease Control and Prevention. Anaphylaxis incidence was determined for HBAT and previously employed botulinum antitoxins. We calculated the positive predictive value (PPV) and negative predictive value (NPV) of ST for anaphylaxis related to HBAT and other botulinum antitoxins. Results: Seven articles were included. Anaphylaxis incidence was 1.64% (5/305 patients) for HBAT and 1.16% (8/687 patients) for all other botulinum antitoxins (relative risk, 1.41 [95% confidence interval, .47-4.27]; P = .5). Observed values for both PPV and NPV for HBAT-ST (33 patients) were 100%. Observed PPVs and NPVs of ST for other botulinum antitoxins (302 patients) were 0-56% and 50%-100%, respectively. There were no reports of fatal anaphylaxis. Conclusions: Considering the &lt;2 % rate of anaphylaxis, fatal outcomes, modest predictive value of ST, resource requirements for ST, and the benefits of early treatment, data do not support delaying HBAT administration to perform ST in a mass botulinum toxin exposure. Anaphylactic reactions may occur among 1%-2% of botulinum antitoxin recipients and will require epinephrine and antihistamine treatment and, possibly, intensive care</style></abstract><notes><style face="normal" font="default">IS - 1537-6591 (Electronic)IS - 1058-4838 (Linking)LA - engPT - Journal ArticleCO - United States -</style></notes><work-type><style face="normal" font="default">10.1093/cid/cix827</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="29293931">PM:29293931</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Clin Infect Dis\2017-66S1-65-72.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Clin Infect Dis\2017-66S1-65-72.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171227, Schussler E</style></custom2><misc3><style face="normal" font="default">10.1093/cid/cix827</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86661</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Matricardi,P.M.</style></author><author><style face="normal" font="default"> Kleine-Tebbe,J.</style></author><author><style face="normal" font="default"> Hoffmann,H.J.</style></author><author><style face="normal" font="default"> Valenta,R.</style></author><author><style face="normal" font="default"> Hilger,C.</style></author><author><style face="normal" font="default"> Hofmaier,S.</style></author><author><style face="normal" font="default"> Aalberse,R.C.</style></author><author><style face="normal" font="default"> Agache,I.</style></author><author><style face="normal" font="default"> Asero,R.</style></author><author><style face="normal" font="default"> Ballmer-Weber,B.</style></author><author><style face="normal" font="default"> Barber,D.</style></author><author><style face="normal" font="default"> Beyer,K.</style></author><author><style face="normal" font="default"> Biedermann,T.</style></author><author><style face="normal" font="default"> Bilo,M.B.</style></author><author><style face="normal" font="default"> Blank,S.</style></author><author><style face="normal" font="default"> Bohle,B.</style></author><author><style face="normal" font="default"> Bosshard,P.P.</style></author><author><style face="normal" font="default"> Breiteneder,H.</style></author><author><style face="normal" font="default"> Brough,H.A.</style></author><author><style face="normal" font="default"> Caraballo,L.</style></author><author><style face="normal" font="default"> Caubet,J.C.</style></author><author><style face="normal" font="default"> Crameri,R.</style></author><author><style face="normal" font="default"> Davies,J.M.</style></author><author><style face="normal" font="default"> Douladiris,N.</style></author><author><style face="normal" font="default"> Ebisawa,M.</style></author><author><style face="normal" font="default"> EIgenmann,P.A.</style></author><author><style face="normal" font="default"> Fernandez-Rivas,M.</style></author><author><style face="normal" font="default"> Ferreira,F.</style></author><author><style face="normal" font="default"> Gadermaier,G.</style></author><author><style face="normal" font="default"> Glatz,M.</style></author><author><style face="normal" font="default"> Hamilton,R.G.</style></author><author><style face="normal" font="default"> Hawranek,T.</style></author><author><style face="normal" font="default"> Hellings,P.</style></author><author><style face="normal" font="default"> Hoffmann-Sommergruber,K.</style></author><author><style face="normal" font="default"> Jakob,T.</style></author><author><style face="normal" font="default"> Jappe,U.</style></author><author><style face="normal" font="default"> Jutel,M.</style></author><author><style face="normal" font="default"> Kamath,S.D.</style></author><author><style face="normal" font="default"> Knol,E.F.</style></author><author><style face="normal" font="default"> Korosec,P.</style></author><author><style face="normal" font="default"> Kuehn,A.</style></author><author><style face="normal" font="default"> Lack,G.</style></author><author><style face="normal" font="default"> Lopata,A.L.</style></author><author><style face="normal" font="default"> Makela,M.</style></author><author><style face="normal" font="default"> Morisset,M.</style></author><author><style face="normal" font="default"> Niederberger,V.</style></author><author><style face="normal" font="default"> Nowak-Wegrzyn,A.H.</style></author><author><style face="normal" font="default"> Papadopoulos,N.G.</style></author><author><style face="normal" font="default"> Pastorello,E.A.</style></author><author><style face="normal" font="default"> Pauli,G.</style></author><author><style face="normal" font="default"> Platts-Mills,T.</style></author><author><style face="normal" font="default"> Posa,D.</style></author><author><style face="normal" font="default"> Poulsen,L.K.</style></author><author><style face="normal" font="default"> Raulf,M.</style></author><author><style face="normal" font="default"> Sastre,J.</style></author><author><style face="normal" font="default"> Scala,E.</style></author><author><style face="normal" font="default"> Schmid,J.M.</style></author><author><style face="normal" font="default"> Schmid-Grendelmeier,P.</style></author><author><style face="normal" font="default"> van Hage,M.</style></author><author><style face="normal" font="default"> van Ree,R.</style></author><author><style face="normal" font="default"> Vieths,S.</style></author><author><style face="normal" font="default"> Weber,R.</style></author><author><style face="normal" font="default"> Wickman,M.</style></author><author><style face="normal" font="default"> Muraro,A.</style></author><author><style face="normal" font="default"> Ollert,M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Paediatric Pneumology and Immunology, Charite Medical University, Berlin, Germany</style></auth-address><titles><title><style face="normal" font="default">EAACI Molecular Allergology User's Guide</style></title><secondary-title><style face="normal" font="default">Pediatr Allergy Immunol</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Pediatr Allergy Immunol</style></abbr-1></periodical><pages end="250" start="1">1-250</pages><volume><style face="normal" font="default">27 Suppl 23</style></volume><reprint-status status="no-file"/><keywords/><dates><year Day="0" Month="5" Year="2016">2016/5</year></dates><abstract><style face="normal" font="default">The availability of allergen molecules ('components') from several protein families has advanced our understanding of immunoglobulin E (IgE)-mediated responses and enabled 'component-resolved diagnosis' (CRD). The European Academy of Allergy and Clinical Immunology (EAACI) Molecular Allergology User's Guide (MAUG) provides comprehensive information on important allergens and describes the diagnostic options using CRD. Part A of the EAACI MAUG introduces allergen molecules, families, composition of extracts, databases, and diagnostic IgE, skin, and basophil tests. Singleplex and multiplex IgE assays with components improve both sensitivity for low-abundance allergens and analytical specificity; IgE to individual allergens can yield information on clinical risks and distinguish cross-reactivity from true primary sensitization. Part B discusses the clinical and molecular aspects of IgE-mediated allergies to foods (including nuts, seeds, legumes, fruits, vegetables, cereal grains, milk, egg, meat, fish, and shellfish), inhalants (pollen, mold spores, mites, and animal dander), and Hymenoptera venom. Diagnostic algorithms and short case histories provide useful information for the clinical workup of allergic individuals targeted for CRD. Part C covers protein families containing ubiquitous, highly cross-reactive panallergens from plant (lipid transfer proteins, polcalcins, PR-10, profilins) and animal sources (lipocalins, parvalbumins, serum albumins, tropomyosins) and explains their diagnostic and clinical utility. Part D lists 100 important allergen molecules. In conclusion, IgE-mediated reactions and allergic diseases, including allergic rhinoconjunctivitis, asthma, food reactions, and insect sting reactions, are discussed from a novel molecular perspective. The EAACI MAUG documents the rapid progression of molecular allergology from basic research to its integration into clinical practice, a quantum leap in the management of allergic patients</style></abstract><notes><style face="normal" font="default">DA - 20160612IS - 1399-3038 (Electronic)IS - 0905-6157 (Linking)LA - engPT - Journal ArticleSB - IMLA - Germany -CO - Denmark -CO - Austria -CO - Luxembourg -CO - Romania -CO - Italy -CO - Switzerland -CO - Spain -CO - United Kingdom -CO - Colombia -CO - Australia -CO - Greece -CO - Japan -CO - United States -CO - Belgium -CO - Poland -CO - Slovenia -CO - Finland -CO - France -CO - Sweden -</style></notes><work-type><style face="normal" font="default">10.1111/pai.12563</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="27288833">PM:27288833</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Pediatr Allergy Immunol\2017-27S23-1-250.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Pediatr Allergy Immunol\2017-27S23-1-250.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20160612, Matricardi PM</style></custom2><misc3><style face="normal" font="default">10.1111/pai.12563</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86581</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Xu,F.</style></author><author><style face="normal" font="default"> Oruna-Concha,M.J.</style></author><author><style face="normal" font="default"> Elmore,J.S.</style></author></authors></contributors><titles><title><style face="normal" font="default">The use of asparaginase to reduce acrylamide levels in cooked food</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="171" start="163">163-171</pages><volume><style face="normal" font="default">210</style></volume><number><style face="normal" font="default">Supplement C</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Acrylamide</style></keyword><keyword><style face="normal" font="default"> Asparaginase</style></keyword><keyword><style face="normal" font="default"> Enzymes</style></keyword><keyword><style face="normal" font="default"> Asparagine</style></keyword><keyword><style face="normal" font="default"> Reducing sugars</style></keyword><keyword><style face="normal" font="default"> Maillard Reaction</style></keyword></keywords><dates><year Day="0" Month="0" Year="2016">2016</year></dates><isbn><style face="normal" font="default">0308-8146</style></isbn><abstract><style face="normal" font="default">Strategies proposed for reducing the formation of the suspected carcinogen acrylamide in cooked foods often rely on a reduction in the extent of the Maillard reaction, in which acrylamide is formed from the reaction between asparagine and reducing sugars. However, the Maillard reaction also provides desirable sensory attributes of cooked foods. Mitigation procedures that modify the Maillard reaction may negatively affect flavour and colour. The use of asparaginase to convert asparagine to aspartic acid may provide a means to reduce acrylamide formation, while maintaining sensory quality. This review collates research on the use of enzymes, asparaginase in particular, to mitigate acrylamide formation. Asparaginase is a powerful tool for the food industry and it is likely that its use will increase. However, the potential adverse effects of asparaginase treatment on sensory properties of cooked foods and the need to achieve sufficient enzyme</style><style face="normal" font="Symbol">G</style><style face="normal" font="default">Çôsubstrate contact remain areas for future research</style></abstract><notes><style face="normal" font="default">LA - ENGCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2016.04.105</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="27211635">PM:27211635</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\2016-210SC-163-71.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\2016-210SC-163-71.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Xu F</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2016.04.105</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87256</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Bonavita,A.</style></author><author><style face="normal" font="default"> Carratore,V.</style></author><author><style face="normal" font="default"> Ciardiello,M.A.</style></author><author><style face="normal" font="default"> Giovane,A.</style></author><author><style face="normal" font="default"> Servillo,L.</style></author><author><style face="normal" font="default"> D'Avino,R.</style></author></authors></contributors><auth-address><style face="normal" font="default">Institute of Biosciences and BioResources, C.N.R. , Napoli, Italy</style></auth-address><titles><title><style face="normal" font="default">Influence of pH on the Structure and Function of Kiwi Pectin Methylesterase Inhibitor</style></title><secondary-title><style face="normal" font="default">J Agric Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Agric Food Chem</style></abbr-1></periodical><pages end="5876" start="5866">5866-5876</pages><volume><style face="normal" font="default">64</style></volume><number><style face="normal" font="default">29</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Actinidia</style></keyword><keyword><style face="normal" font="default"> Amino Acid Sequence</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> antagonists &amp; inhibitors</style></keyword><keyword><style face="normal" font="default"> Carboxylic Ester Hydrolases</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> Circular Dichroism</style></keyword><keyword><style face="normal" font="default"> Enzyme Inhibitors</style></keyword><keyword><style face="normal" font="default"> enzymology</style></keyword><keyword><style face="normal" font="default"> genetics</style></keyword><keyword><style face="normal" font="default"> Hydrogen-Ion Concentration</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> Models,Molecular</style></keyword><keyword><style face="normal" font="default"> Molecular Sequence Data</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword><keyword><style face="normal" font="default"> Plant Proteins</style></keyword></keywords><dates><year Day="27" Month="7" Year="2016">2016/7/27</year></dates><abstract><style face="normal" font="default">Pectin methylesterase is a pectin modifying enzyme that plays a key role in plant physiology. It is also an important quality-related enzyme in plant-based food products. The pectin methylesterase inhibitor (PMEI) from kiwifruit inhibits this enzyme activity and is widely used as an efficient tool for research purposes and also recommended in the context of fruit and vegetable processing. Using several methodologies of protein biochemistry, including circular dichroism and fluorescence spectroscopy, chemical modifications, direct protein-sequencing, enzyme activity, and bioinformatics analysis of the crystal structure, this study demonstrates that conformational changes occur in kiwi PMEI by the pH rising over 6.0 bringing about structure loosening, exposure, and cleavage of a natively buried disulfide bond, unfolding and aggregation, ultimately determining the loss of ability of kiwi PMEI to bind and inhibit PME. pH-induced structural changes are prevented when PMEI is already engaged in complex or is in a solution of high ionic strength</style></abstract><notes><style face="normal" font="default">IS - 1520-5118 (Electronic)IS - 0021-8561 (Linking)LA - engPT - Journal ArticleRN - 0 (Enzyme Inhibitors)RN - 0 (Plant Proteins)RN - EC 3.1.1.- (Carboxylic Ester Hydrolases)RN - EC 3.1.1.11 (pectinesterase)SB - IMCO - Italy -</style></notes><work-type><style face="normal" font="default">10.1021/acs.jafc.6b01718</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="27335009">PM:27335009</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Agric Food Chem\2016-64-5866-76.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Agric Food Chem\2016-64-5866-76.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20160623, Bonavita A</style></custom2><misc3><style face="normal" font="default">10.1021/acs.jafc.6b01718</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86649</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Kukurova,K.</style></author><author><style face="normal" font="default"> Morales,F.J.</style></author><author><style face="normal" font="default"> Bednarikova,A.</style></author><author><style face="normal" font="default"> Ciesarova,Z.</style></author></authors></contributors><auth-address><style face="normal" font="default">VUP Food Research Institute, Bratislava, Slovak Republic</style></auth-address><titles><title><style face="normal" font="default">Effect of L-asparaginase on acrylamide mitigation in a fried-dough pastry model</style></title><secondary-title><style face="normal" font="default">Mol Nutr Food Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Mol Nutr Food Res</style></abbr-1></periodical><pages end="1539" start="1532">1532-1539</pages><volume><style face="normal" font="default">53</style></volume><number><style face="normal" font="default">12</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Acrylamide</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> Amino Acids</style></keyword><keyword><style face="normal" font="default"> Asparaginase</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> Color</style></keyword><keyword><style face="normal" font="default"> Cooking</style></keyword><keyword><style face="normal" font="default"> methods</style></keyword><keyword><style face="normal" font="default"> Dietary Proteins</style></keyword><keyword><style face="normal" font="default"> Dietary Sucrose</style></keyword><keyword><style face="normal" font="default"> Flour</style></keyword><keyword><style face="normal" font="default"> Food Analysis</style></keyword><keyword><style face="normal" font="default"> Food Contamination</style></keyword><keyword><style face="normal" font="default"> prevention &amp; control</style></keyword><keyword><style face="normal" font="default"> Food Technology</style></keyword><keyword><style face="normal" font="default"> Furaldehyde</style></keyword><keyword><style face="normal" font="default"> analogs &amp; derivatives</style></keyword><keyword><style face="normal" font="default"> Maillard Reaction</style></keyword><keyword><style face="normal" font="default"> Models,Chemical</style></keyword><keyword><style face="normal" font="default"> Spectrometry,Fluorescence</style></keyword><keyword><style face="normal" font="default"> Time Factors</style></keyword><keyword><style face="normal" font="default"> Water</style></keyword></keywords><dates><year Day="0" Month="12" Year="2009">2009/12</year></dates><abstract><style face="normal" font="default">A dough resembling traditional Spanish rosquillas was used as a model to represent classical fried-dough pastry to investigate the effects of asparaginase and heat treatment on amino acid levels and acrylamide mitigation. Wheat-based dough was deep fried at 180 and 200 degrees C for 4, 6, and 8 min. Two recipes were formulated by addition of different asparaginase levels (100 and 500 U/kg flour) to the dough. The temperature/time profile of the frying process, moisture, sugars, amino acids, acrylamide, and some indicators of the Maillard reaction (hydroxymethylfurfural, color, free fluorescence compounds, and browning) were determined to investigate the extent of the reaction and the effect on reactants. At the both levels of asparaginase used, 96-97% of the asparagine present was converted to aspartic acid, and consequently the acrylamide level was very efficiently reduced (up to 90%). The asparaginase also affected the content of glutamine and glutamic acid in dough, resulting in a 37% increase in glutamic acid compared with the untreated sample. Concerning color, browning and Maillard reaction parameters, no significant changes between untreated and enzymatically treated samples were observed, pointing out the potential industrial and domestic enzyme application</style></abstract><notes><style face="normal" font="default">DA - 20091209IS - 1613-4133 (Electronic)IS - 1613-4125 (Linking)LA - engPT - Journal ArticlePT - Research Support, Non-U.S. Gov'tRN - 0 (Amino Acids)RN - 0 (Dietary Proteins)RN - 0 (Dietary Sucrose)RN - 059QF0KO0R (Water)RN - 20R035KLCI (Acrylamide)RN - 70ETD81LF0 (5-hydroxymethylfurfural)RN - DJ1HGI319P (Furaldehyde)RN - EC 3.5.1.1 (Asparaginase)SB - IMCO - Slovakia -</style></notes><work-type><style face="normal" font="default">10.1002/mnfr.200800600</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="19824015">PM:19824015</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Mol Nutr Food Res\2009-53-1532-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Mol Nutr Food Res\2009-53-1532-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20091209, Kukurova K</style></custom2><misc3><style face="normal" font="default">10.1002/mnfr.200800600</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86580</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Pedreschi,F.</style></author><author><style face="normal" font="default"> Kaack,K.</style></author><author><style face="normal" font="default"> Granby,K.</style></author></authors></contributors><titles><title><style face="normal" font="default">The effect of asparaginase on acrylamide formation in French fries</style></title><secondary-title><style face="normal" font="default">Food Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Food Chem</style></abbr-1></periodical><pages end="392" start="386">386-392</pages><volume><style face="normal" font="default">109</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Par-fried potatoes</style></keyword><keyword><style face="normal" font="default"> Frying</style></keyword><keyword><style face="normal" font="default"> Acrylamide</style></keyword><keyword><style face="normal" font="default"> French fries</style></keyword><keyword><style face="normal" font="default"> Reducing sugar</style></keyword><keyword><style face="normal" font="default"> Glucose</style></keyword><keyword><style face="normal" font="default"> Asparagine</style></keyword><keyword><style face="normal" font="default"> Asparaginase</style></keyword></keywords><dates><year Day="0" Month="0" Year="2008">2008</year></dates><isbn><style face="normal" font="default">0308-8146</style></isbn><abstract><style face="normal" font="default">Acrylamide formation in French fries was investigated in relation to blanching and asparaginase soaking treatments before final frying. Par-fried potatoes of Bintje variety were prepared by cutting strips (0.8+ù0.8+ù5cm) which were blanched at 75-¦C for 10min. Unblanched strips were used as the control. Control or blanched strips were then dried at 85-¦C for 10min and immediately partially fried at 175-¦C for 1min. Finally, frozen par-fried potatoes were fried at 175-¦C for 3min to obtain French fries. Pre-drying of raw or blanched potato strips did not generate acrylamide formation as expected. Partial frying of pre-dried control potato strips generated 370++g/kg of acrylamide and the final frying determined French fries with 2075++g/kg of acrylamide. When control potato strips were treated with a 10000 ASNU/l asparaginase solution at 40-¦C for 20min, the acrylamide formation in French fries was reduced by 30%. When blanched potato strips were treated in the same way, the produced French fries have 60% less acrylamide content than blanched strips without the enzyme treatment. Soaking of blanched potato strips (75-¦C, 10min) in an 10000 ASNU/l asparaginase solution at 40-¦C for 20min is an effective way to reduce acrylamide formation after frying by reducing the amount of one of its important precursors such as asparagine</style></abstract><notes><style face="normal" font="default">LA - ENGCO - Chile -CO - Denmark -</style></notes><work-type><style face="normal" font="default">10.1016/j.foodchem.2007.12.057</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="26003362">PM:26003362</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Food Chem\2008-109-386-92.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Food Chem\2008-109-386-92.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20171114, Pedreschi F</style></custom2><misc3><style face="normal" font="default">10.1016/j.foodchem.2007.12.057</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86958</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Mizushima,Y.</style></author><author><style face="normal" font="default"> Amano,Y.</style></author><author><style face="normal" font="default"> Kitagawa,H.</style></author><author><style face="normal" font="default"> Ogata,K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Autoimmune Diseases Project, Discovery Research Laboratories, Hoechst Japan, Ltd., Saitama, Japan.</style></auth-address><titles><title><style face="normal" font="default">Oral administration of leflunomide (HWA486) results in prominent suppression of immunoglobulin E formation in a rat type 1 allergy model</style></title><secondary-title><style face="normal" font="default">J Pharmacol Exp Ther</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Pharmacol Exp Ther</style></abbr-1></periodical><pages end="857" start="849">849-857</pages><volume><style face="normal" font="default">288</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Administration,Oral</style></keyword><keyword><style face="normal" font="default"> allergic diseases</style></keyword><keyword><style face="normal" font="default"> Allergy</style></keyword><keyword><style face="normal" font="default"> Aniline Compounds</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> Antibody Specificity</style></keyword><keyword><style face="normal" font="default"> autoimmune diseases</style></keyword><keyword><style face="normal" font="default"> biosynthesis</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Disease Models,Animal</style></keyword><keyword><style face="normal" font="default"> Drug Administration Schedule</style></keyword><keyword><style face="normal" font="default"> drug effects</style></keyword><keyword><style face="normal" font="default"> drug therapy</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Hydroxybutyrates</style></keyword><keyword><style face="normal" font="default"> Hypersensitivity,Immediate</style></keyword><keyword><style face="normal" font="default"> IgE</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin E</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin G</style></keyword><keyword><style face="normal" font="default"> Immunoglobulin M</style></keyword><keyword><style face="normal" font="default"> immunology</style></keyword><keyword><style face="normal" font="default"> Immunosuppressive Agents</style></keyword><keyword><style face="normal" font="default"> Isoxazoles</style></keyword><keyword><style face="normal" font="default"> Lymphocyte Activation</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> Ovalbumin</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword><keyword><style face="normal" font="default"> Rats,Inbred BN</style></keyword><keyword><style face="normal" font="default"> Uridine</style></keyword></keywords><dates><year Day="0" Month="2" Year="1999">1999/2</year></dates><abstract><style face="normal" font="default">Leflunomide, a drug being developed for use in the treatment of rheumatoid arthritis, was evaluated in an ovalbumin (OVA)-induced rat type 1 allergy model. In a dose of 1 mg/kg/day, it strongly suppressed the formation of OVA-specific IgE, thus preventing the elevation of the plasma histamine level and induction of anaphylactic shock observed after i.v. challenge with OVA. Studies on leflunomide's effects on the secondary antibody response showed that administration during the primary immune response remarkably diminished the secondary antibody responses, except IgM, even without further drug administration. Furthermore, when administered during the secondary response after rechallenge, both the total IgE and OVA-specific IgE serum levels declined rapidly to nearly baseline levels. Although OVA-specific IgG1, IgG2a, and IgM did not decrease from their primary response levels, these classes' secondary responses were strongly suppressed. In an in vitro study, the proliferation and antibody production of OVA-stimulated spleen cells, derived from Brown Norway rats, were strongly inhibited by A77 1726, leflunomide's active metabolite. When uridine was added to the cell culture, this molecule's effect on cell proliferation was completely restored, whereas the antibody production was partially restored. These findings are consistent with data indicating that leflunomide is a dihydroorotate dehydrogenase inhibitor. Taken together, the above findings suggest the therapeutic potential of leflunomide against type 1 allergic diseases</style></abstract><notes><style face="normal" font="default">IS - 0022-3565 (Print)IS - 0022-3565 (Linking)LA - engPT - Journal ArticleRN - 0 (Aniline Compounds)RN - 0 (Hydroxybutyrates)RN - 0 (Immunoglobulin G)RN - 0 (Immunoglobulin M)RN - 0 (Immunosuppressive Agents)RN - 0 (Isoxazoles)RN - 108605-62-5 (A 771726)RN - 37341-29-0 (Immunoglobulin E)RN - 9006-59-1 (Ovalbumin)RN - G162GK9U4W (leflunomide)RN - WHI7HQ7H85 (Uridine)SB - IMCO - Japan -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9918599">PM:9918599</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Pharmacol Exp Ther\1999-288-849-57.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Pharmacol Exp Ther\1999-288-849-57.pdf</url></text-urls></urls><custom2><style face="normal" font="default">19990210, Mizushima Y</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86956</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Willumsen,J.F.</style></author><author><style face="normal" font="default"> Simmank,K.</style></author><author><style face="normal" font="default"> Filteau,S.M.</style></author><author><style face="normal" font="default"> Wagstaff,L.A.</style></author><author><style face="normal" font="default"> Tomkins,A.M.</style></author></authors></contributors><auth-address><style face="normal" font="default">Centre for International Child Health, Institute of Child Health, London, WC1N 1EH, United Kingdom</style></auth-address><titles><title><style face="normal" font="default">Toxic damage to the respiratory epithelium induces acute phase changes in vitamin A metabolism without depleting retinol stores of South African children</style></title><secondary-title><style face="normal" font="default">J Nutr</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Nutr</style></abbr-1></periodical><pages end="1343" start="1339">1339-1343</pages><volume><style face="normal" font="default">127</style></volume><number><style face="normal" font="default">7</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Acute-Phase Proteins</style></keyword><keyword><style face="normal" font="default"> Acute-Phase Reaction</style></keyword><keyword><style face="normal" font="default"> administration &amp; dosage</style></keyword><keyword><style face="normal" font="default"> adverse effects</style></keyword><keyword><style face="normal" font="default"> Aging</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> blood</style></keyword><keyword><style face="normal" font="default"> Case-Control Studies</style></keyword><keyword><style face="normal" font="default"> chemically induced</style></keyword><keyword><style face="normal" font="default"> Child,Preschool</style></keyword><keyword><style face="normal" font="default"> drug effects</style></keyword><keyword><style face="normal" font="default"> Epithelium</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Follow-Up Studies</style></keyword><keyword><style face="normal" font="default"> Food,Fortified</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Infant</style></keyword><keyword><style face="normal" font="default"> Kerosene</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> pathology</style></keyword><keyword><style face="normal" font="default"> physiopathology</style></keyword><keyword><style face="normal" font="default"> Respiratory System</style></keyword><keyword><style face="normal" font="default"> Retinol-Binding Proteins</style></keyword><keyword><style face="normal" font="default"> Retinol-Binding Proteins,Plasma</style></keyword><keyword><style face="normal" font="default"> South Africa</style></keyword><keyword><style face="normal" font="default"> Vitamin A</style></keyword></keywords><dates><year Day="0" Month="7" Year="1997">1997/7</year></dates><abstract><style face="normal" font="default">Whereas there is much information concerning the effects of vitamin A status on response to infectious challenge, the effects of infection or trauma on vitamin A metabolism and status are less well documented. These relationships need to be understood to optimize clinical and public health programs to improve vitamin A status and health of children in less-developed countries. We measured acute changes in retinol and retinol-binding protein in 57 young South African children hospitalized following respiratory epithelial damage resulting from accidental ingestion of kerosene. In addition, vitamin A status, as measured by the modified relative dose response test, of these children 3 mo later was compared with that of neighborhood control children to determine whether their illness had depleted retinol stores. Plasma retinol was already significantly below control levels when children were admitted [geometric mean (95% CI): 0.57 micromol/L (0.48-0.67) compared with 1.15 micromol/L (1.02-1.30) for controls] and decreased further the following morning [0.38 micromol/L (0.31-0.46)]. Significant differences in retinol-binding protein were not detected until the next morning [5.99 mg/L (4.70-7.63) compared with 14.0 mg/L (11.8-16.6) for controls] and were not as large as the relative differences in retinol. This dissociation between changes in retinol and its binding protein suggests that there may be increased retinol uptake by certain tissues during the acute phase response. The proportion of case children (37/46, 80%) with inadequate liver retinol stores 3 mo after the illness was slightly, but not significantly (chi2 = 2.16, P = 0.14), greater than the proportion of control children (28/42, 67%). Acute respiratory illness therefore did not further deplete retinol stores in this population in which stores were already frequently inadequate</style></abstract><notes><style face="normal" font="default">IS - 0022-3166 (Print)IS - 0022-3166 (Linking)LA - engPT - Journal ArticlePT - Research Support, Non-U.S. Gov'tRN - 0 (Acute-Phase Proteins)RN - 0 (Kerosene)RN - 0 (Retinol-Binding Proteins)RN - 0 (Retinol-Binding Proteins, Plasma)RN - 11103-57-4 (Vitamin A)SB - IMCO - United KIngdom -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9202088">PM:9202088</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Nutr\1997-127-1339-43.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Nutr\1997-127-1339-43.pdf</url></text-urls></urls><custom2><style face="normal" font="default">19979596, Willumsen JF</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86941</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Goyal,J.</style></author><author><style face="normal" font="default"> Wang,K.</style></author><author><style face="normal" font="default"> Liu,M.</style></author><author><style face="normal" font="default"> Subbaiah,P.V.</style></author></authors></contributors><auth-address><style face="normal" font="default">Departments of Medicine and Biochemistry, Rush Medical College, Chicago, Illinois 60612, USA</style></auth-address><titles><title><style face="normal" font="default">Novel function of lecithin-cholesterol acyltransferase. Hydrolysis of oxidized polar phospholipids generated during lipoprotein oxidation</style></title><secondary-title><style face="normal" font="default">J Biol Chem</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">J Biol Chem</style></abbr-1></periodical><pages end="16239" start="16231">16231-16239</pages><volume><style face="normal" font="default">272</style></volume><number><style face="normal" font="default">26</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">1-Alkyl-2-acetylglycerophosphocholine Esterase</style></keyword><keyword><style face="normal" font="default"> Adult</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> antagonists &amp; inhibitors</style></keyword><keyword><style face="normal" font="default"> Chickens</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Hydrolysis</style></keyword><keyword><style face="normal" font="default"> Isoflurophate</style></keyword><keyword><style face="normal" font="default"> Lipoproteins</style></keyword><keyword><style face="normal" font="default"> metabolism</style></keyword><keyword><style face="normal" font="default"> Middle Aged</style></keyword><keyword><style face="normal" font="default"> Oxidation-Reduction</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword><keyword><style face="normal" font="default"> Phosphatidylcholines</style></keyword><keyword><style face="normal" font="default"> Phospholipases A</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword><keyword><style face="normal" font="default"> Sterol O-Acyltransferase</style></keyword></keywords><dates><year Day="27" Month="6" Year="1997">1997/6/27</year></dates><abstract><style face="normal" font="default">Although the major function of lecithin-cholesterol acyltransferase (LCAT) is cholesterol esterification, our previous studies showed that it can also hydrolyze platelet-activating factor (PAF). Because of the structural similarities between PAF and the truncated phosphatidylcholines (polar PCs) generated during lipoprotein oxidation, we investigated the possibility that LCAT may also hydrolyze polar PCs to lyso-PC during the oxidation of plasma. PAF acetylhydrolase (PAF-AH), which is known to hydrolyze polar PCs in human plasma, was completely inhibited by 0.2 mM p-aminoethyl benzenesulfonyl fluoride (Pefabloc), a new serine esterase inhibitor, which had no effect on LCAT at this concentration. On the other hand, 1 mM diisopropylfluorophosphate (DFP) completely inhibited LCAT but had no effect on PAF-AH. Polar PC accumulation during the oxidation of plasma increased by 44% in the presence of 0.2 mM Pefabloc and by 30% in the presence of 1 mM DFP. The formation of lyso-PC was concomitantly inhibited by both of the inhibitors. The combination of the two inhibitors resulted in the maximum accumulation of polar PCs, suggesting that both PAF-AH and LCAT are involved in their breakdown. Oxidation of chicken plasma, which has no PAF-AH activity, also resulted in the formation of lyso-PC from the hydrolysis of polar PC, which was inhibited by DFP. Polar PCs, either isolated from oxidized plasma or by oxidation of labeled synthetic PCs, were hydrolyzed by purified LCAT, which had no detectable PAF-AH activity. These results demonstrate a novel function for LCAT in the detoxification of polar PCs generated during lipoprotein oxidation, especially when the PAF-AH is absent or inactivated</style></abstract><notes><style face="normal" font="default">IS - 0021-9258 (Print)IS - 0021-9258 (Linking)LA - engPT - Journal ArticlePT - Research Support, Non-U.S. Gov'tPT - Research Support, U.S. Gov't, P.H.SRN - 0 (Lipoproteins)RN - 0 (Phosphatidylcholines)RN - 12UHW9R67N (Isoflurophate)RN - EC 2.3.1.26 (Sterol O-Acyltransferase)RN - EC 3.1.1.32 (Phospholipases A)RN - EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase)SB - IMCO - United States -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9195924">PM:9195924</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\J Biol Chem\1997-272-16231-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\J Biol Chem\1997-272-16231-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">19970627, Goyal J</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86972</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Wells,J.E.</style></author></authors></contributors><titles><title><style face="normal" font="default">Cannabis uses in young New Zealanders</style></title><secondary-title><style face="normal" font="default">N Z Med J</style></secondary-title></titles><periodical><full-title><style face="normal" font="System">N Z Med J</style></full-title></periodical><pages end="175" start="174">174-175</pages><volume><style face="normal" font="default">110</style></volume><number><style face="normal" font="default">1043</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Adolescent</style></keyword><keyword><style face="normal" font="default"> Adult</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Marijuana Abuse</style></keyword><keyword><style face="normal" font="default"> New Zealand</style></keyword><keyword><style face="normal" font="default"> Unemployment</style></keyword><keyword><style face="normal" font="default"> Violence</style></keyword></keywords><dates><year Day="9" Month="5" Year="1997">1997/5/9</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 0028-8446 (Print)IS - 0028-8446 (Linking)LA - engPT - LetterSB - IMCO - New Zealand -</style></notes><work-type><style face="normal" font="default">NO-DOI</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9196507">PM:9196507</url></web-urls></urls><custom2><style face="normal" font="default">19971010, Wells JE</style></custom2><misc3><style face="normal" font="default">NO-DOI</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86971</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Williams,G.</style></author><author><style face="normal" font="default"> Gill,G.V.</style></author></authors></contributors><titles><title><style face="normal" font="default">Eating disorders and diabetic complications</style></title><secondary-title><style face="normal" font="default">N Engl J Med</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">N Engl J Med</style></abbr-1></periodical><pages end="1906" start="1905">1905-1906</pages><volume><style face="normal" font="default">336</style></volume><number><style face="normal" font="default">26</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">blood</style></keyword><keyword><style face="normal" font="default"> Blood Glucose</style></keyword><keyword><style face="normal" font="default"> complications</style></keyword><keyword><style face="normal" font="default"> Diabetes Mellitus,Type 1</style></keyword><keyword><style face="normal" font="default"> Diabetic Angiopathies</style></keyword><keyword><style face="normal" font="default"> epidemiology</style></keyword><keyword><style face="normal" font="default"> Feeding and Eating Disorders</style></keyword><keyword><style face="normal" font="default"> Female</style></keyword><keyword><style face="normal" font="default"> Glucose</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> Risk factors</style></keyword></keywords><dates><year Day="26" Month="6" Year="1997">1997/6/26</year></dates><abstract><style face="normal" font="default">No Abstract Available</style></abstract><notes><style face="normal" font="default">IS - 0028-4793 (Print)IS - 0028-4793 (Linking)LA - engPT - CommentPT - EditorialRN - 0 (Blood Glucose)SB - AIMSB - IMCO - United States -</style></notes><work-type><style face="normal" font="default">10.1056/NEJM199706263362609</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9197220">PM:9197220</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\N Engl J Med\1997-336-1905-6.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\N Engl J Med\1997-336-1905-6.pdf</url></text-urls></urls><custom2><style face="normal" font="default">19970612, Williams G</style></custom2><misc3><style face="normal" font="default">10.1056/NEJM199706263362609</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>86845</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Peoples,L.L.</style></author><author><style face="normal" font="default"> Uzwiak,A.J.</style></author><author><style face="normal" font="default"> Gee,F.</style></author><author><style face="normal" font="default"> West,M.O.</style></author></authors></contributors><auth-address><style face="normal" font="default">Department of Psychology, Rutgers, The State University of New Jersey, New Brunswick 08903, USA.</style></auth-address><titles><title><style face="normal" font="default">Operant behavior during sessions of intravenous cocaine infusion is necessary and sufficient for phasic firing of single nucleus accumbens neurons</style></title><secondary-title><style face="normal" font="default">Brain Res</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Brain Res</style></abbr-1></periodical><pages end="284" start="280">280-284</pages><volume><style face="normal" font="default">757</style></volume><number><style face="normal" font="default">2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Animals</style></keyword><keyword><style face="normal" font="default"> Behavior,Animal</style></keyword><keyword><style face="normal" font="default"> Cocaine</style></keyword><keyword><style face="normal" font="default"> Conditioning,Operant</style></keyword><keyword><style face="normal" font="default"> cytology</style></keyword><keyword><style face="normal" font="default"> Electrophysiology</style></keyword><keyword><style face="normal" font="default"> Infusions,Intravenous</style></keyword><keyword><style face="normal" font="default"> Male</style></keyword><keyword><style face="normal" font="default"> Narcotics</style></keyword><keyword><style face="normal" font="default"> Neurons</style></keyword><keyword><style face="normal" font="default"> Nucleus Accumbens</style></keyword><keyword><style face="normal" font="default"> pharmacology</style></keyword><keyword><style face="normal" font="default"> physiology</style></keyword><keyword><style face="normal" font="default"> Rats</style></keyword><keyword><style face="normal" font="default"> Rats,Inbred Strains</style></keyword><keyword><style face="normal" font="default"> Self Administration</style></keyword></keywords><dates><year Day="23" Month="5" Year="1997">1997/5/23</year></dates><abstract><style face="normal" font="default">The activity of individual accumbens neurons in rats was recorded in relation to intravenous cocaine infusions that were either response (i.e., lever press) contingent or response non-contingent. Neural firing was additionally recorded in relation to non-reinforced lever presses. Comparisons of firing under the three conditions showed that operant behavior was necessary and sufficient for preinfusion firing to occur. Surprisingly, the same was true, in many cases, for firing that occurred during the infusion. For other neurons, firing during the infusion was unrelated to operant behavior and possibly related to infusion stimuli. The relationship to operant behavior exhibited by the majority of NAcc neurons is consistent with previous studies that demonstrated a necessary relationship between NAcc neurons and cocaine reinforced operant behavior</style></abstract><notes><style face="normal" font="default">IS - 0006-8993 (Print)IS - 0006-8993 (Linking)LA - engPT - Journal ArticlePT - Research Support, U.S. Gov't, P.H.SRN - 0 (Narcotics)RN - I5Y540LHVR (Cocaine)SB - IMCO - United States -</style></notes><work-type><style face="normal" font="default">10.1016/S0006-8993(97)00299-0</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9200758">PM:9200758</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Brain Res\1997-757-280-84.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Brain Res\1997-757-280-84.pdf</url></text-urls></urls><custom2><style face="normal" font="default">20170523, Peoples LL</style></custom2><misc3><style face="normal" font="default">10.1016/S0006-8993(97)00299-0</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87015</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Urzhumtsev,A.</style></author><author><style face="normal" font="default"> Tete-Favier,F.</style></author><author><style face="normal" font="default"> Mitschler,A.</style></author><author><style face="normal" font="default"> Barbanton,J.</style></author><author><style face="normal" font="default"> Barth,P.</style></author><author><style face="normal" font="default"> Urzhumtseva,L.</style></author><author><style face="normal" font="default"> Biellmann,J.F.</style></author><author><style face="normal" font="default"> Podjarny,A.</style></author><author><style face="normal" font="default"> Moras,D.</style></author></authors></contributors><auth-address><style face="normal" font="default">UPR-de Biologie Structurale 9004 IGMBC CNRS/INSERM/ULP 1 rue Laurent Fries, B.P. 163, 67404, Illkirch, France</style></auth-address><titles><title><style face="normal" font="default">A 'specificity' pocket inferred from the crystal structures of the complexes of aldose reductase with the pharmaceutically important inhibitors tolrestat and sorbinil</style></title><secondary-title><style face="normal" font="default">Structure</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Structure</style></abbr-1></periodical><pages end="612" start="601">601-612</pages><volume><style face="normal" font="default">5</style></volume><number><style face="normal" font="default">5</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Aldehyde Reductase</style></keyword><keyword><style face="normal" font="default"> Animals</style></keyword><keyword><style face="normal" font="default"> antagonists &amp; inhibitors</style></keyword><keyword><style face="normal" font="default"> Binding Sites</style></keyword><keyword><style face="normal" font="default"> chemistry</style></keyword><keyword><style face="normal" font="default"> complications</style></keyword><keyword><style face="normal" font="default"> Computer Simulation</style></keyword><keyword><style face="normal" font="default"> Conformation</style></keyword><keyword><style face="normal" font="default"> Crystallography</style></keyword><keyword><style face="normal" font="default"> Enzyme Inhibitors</style></keyword><keyword><style face="normal" font="default"> enzymology</style></keyword><keyword><style face="normal" font="default"> Imidazoles</style></keyword><keyword><style face="normal" font="default"> Imidazolidines</style></keyword><keyword><style face="normal" font="default"> Lens,Crystalline</style></keyword><keyword><style face="normal" font="default"> Models,Molecular</style></keyword><keyword><style face="normal" font="default"> Molecular Conformation</style></keyword><keyword><style face="normal" font="default"> Molecular Sequence Data</style></keyword><keyword><style face="normal" font="default"> Nadp</style></keyword><keyword><style face="normal" font="default"> Naphthalenes</style></keyword><keyword><style face="normal" font="default"> Swine</style></keyword></keywords><dates><year Day="15" Month="5" Year="1997">1997/5/15</year></dates><abstract><style face="normal" font="default">BACKGROUND: Aldose reductase (AR) is an NADPH-dependent enzyme implicated in long-term diabetic complications. Buried at the bottom of a deep hydrophobic cleft, the NADPH coenzyme is surrounded by the conserved hydrophilic residues of the AR active site. The existence of an anionic binding site near the NADP+ has been determined from the structures of the complexes of AR with citrate, cacodylate and glucose-6-phosphate. The inhibitor zopolrestat binds to this anionic site, and in the hydrophobic cleft, after a change of conformation which opens a 'specificity' pocket. RESULTS: The crystal structures of the porcine AR holoenzyme and its complexes with the inhibitors tolrestat and sorbinil have been solved; these structures are important as tolrestat and sorbinil are, pharmaceutically, the most well-studied AR inhibitors. The active site of the holoenzyme was analyzed, and binding of the inhibitors was found to involve two contact zones in the active site: first, a recognition region for hydrogen-bond acceptors near the coenzyme, with three centers, including the anionic site; and second, a hydrophobic contact zone in the active-site cleft, which in the case of tolrestat includes the specificity pocket. The conformational change leading to the opening of the specificity pocket upon tolrestat binding is different to the one seen upon zopolrestat binding; this pocket binds inhibitors that are more effective against AR than against aldehyde reductase. CONCLUSIONS: The active site of AR adapts itself to bind tightly to different inhibitors; this happens both upon binding to the inhibitor's hydrophilic heads, and at the hydrophobic and specificity pockets of AR, which can change their shape through different conformational changes of the same residues. This flexibility could explain the large variety of possible substrates of AR</style></abstract><notes><style face="normal" font="default">IS - 0969-2126 (Print)IS - 0969-2126 (Linking)LA - engPT - Comparative StudyPT - Journal ArticlePT - Research Support, Non-U.S. Gov'tRN - 0 (Enzyme Inhibitors)RN - 0 (Imidazoles)RN - 0 (Imidazolidines)RN - 0 (Naphthalenes)RN - 0T93LG5NMK (tolrestat)RN - 53-59-8 (NADP)RN - EC 1.1.1.21 (Aldehyde Reductase)RN - G4186B906P (sorbinil)SB - IMCO - Russia -CO - France -</style></notes><work-type><style face="normal" font="default">10.1016/S0969-2126(97)00216-5</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9195881">PM:9195881</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Structure\1997-5-601-12.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Structure\1997-5-601-12.pdf</url></text-urls></urls><custom2><style face="normal" font="default">19970613, Urzhumtsev A</style></custom2><misc3><style face="normal" font="default">10.1016/S0969-2126(97)00216-5</style></misc3></record><record><database name="HMW 1 Allergens" path="D:\Bibliografia Generale\HMW 1 Allergens">HMW 1 Allergens</database><source-app name="Reference Manager 11.0" version="11.0.1.1709">Reference Manager 11.0</source-app><rec-number>87012</rec-number><ref-type name="Journal">17</ref-type><contributors><authors><author><style face="normal" font="default">Dyne,D.</style></author><author><style face="normal" font="default"> Cocker,J.</style></author><author><style face="normal" font="default"> Wilson,H.K.</style></author></authors></contributors><auth-address><style face="normal" font="default">Health and Safety Executive, London, England</style></auth-address><titles><title><style face="normal" font="default">A novel device for capturing breath samples for solvent analysis</style></title><secondary-title><style face="normal" font="default">Sci Total Environ</style></secondary-title></titles><periodical><abbr-1><style face="normal" font="System">Sci Total Environ</style></abbr-1></periodical><pages end="89" start="83">83-89</pages><volume><style face="normal" font="default">199</style></volume><number><style face="normal" font="default">1-2</style></number><reprint-status status="no-file"/><keywords><keyword><style face="normal" font="default">Absorption</style></keyword><keyword><style face="normal" font="default"> Air Pollutants,Occupational</style></keyword><keyword><style face="normal" font="default"> analysis</style></keyword><keyword><style face="normal" font="default"> Breath Tests</style></keyword><keyword><style face="normal" font="default"> Environmental Monitoring</style></keyword><keyword><style face="normal" font="default"> Gas Chromatography-Mass Spectrometry</style></keyword><keyword><style face="normal" font="default"> Humans</style></keyword><keyword><style face="normal" font="default"> instrumentation</style></keyword><keyword><style face="normal" font="default"> Occupational Exposure</style></keyword><keyword><style face="normal" font="default"> Reproducibility of Results</style></keyword><keyword><style face="normal" font="default"> Safety</style></keyword><keyword><style face="normal" font="default"> Solvents</style></keyword></keywords><dates><year Day="20" Month="6" Year="1997">1997/6/20</year></dates><abstract><style face="normal" font="default">We have developed a novel breath sampling device suitable for capturing a portion of end-tidal air. This breath sample is then transferred onto a Perkin Elmer automated thermal desorption (ATD) sampling tube which is subsequently analysed by ATD-gas chromatography-mass spectrometry (GCMS). The breath sampler has been evaluated in the laboratory, in brief field trials and in human volunteer studies. The method is sensitive with a typical detection limit of 1 nmol/l and reproducible with an overall coefficient of variation between 5% and 15% for collection and analysis of breath samples from volunteers. The field trials used the sampler to assess exposure to solvents in several industries including the shoe manufacturing industry, the inks and coatings industry and at dry cleaning establishments. The sampler was found easy to use and reliable. Solvents detected include ethyl acetate (6.4-25.5 nmol/l), propan-2-ol (3.4-39.3 nmol/l), 2-butanone (0-6.6 nmol/l) and tetrachloroethene (0-557 nmol/l). The breath sampler was also used to monitor the elimination of solvents in breath from human volunteers after exposure chamber studies. More than 500 breath samples have been analysed from 24 volunteers in exposures to 10 different solvents (toluene, trimethyl benzene, tetrachloroethene, tetrahydrofuran, acetone, propan-2-ol, xylene, 2-butanone, 1-methoxy-2-propanol and n-hexane). The breath sampler allowed the rapid and non-invasive collection of data on elimination of solvents</style></abstract><notes><style face="normal" font="default">IS - 0048-9697 (Print)IS - 0048-9697 (Linking)LA - engPT - Journal ArticleRN - 0 (Air Pollutants, Occupational)RN - 0 (Solvents)SB - IMCO - United Kingdom -</style></notes><work-type><style face="normal" font="default">10.1016/S0048-9697(97)05483-1</style></work-type><urls><web-urls><url has-ut="yes" ppv-app="PM" ppv-ref="yes" ppv-ut="9200850">PM:9200850</url></web-urls><pdf-urls><url ppv-ref="no">C:\A&amp;H HMW Papers\Sci Total Environ\1997-199-83-9.pdf</url></pdf-urls><text-urls><url ppv-ref="no">F:\A&amp;H HMW Papers\Sci Total Environ\1997-199-83-9.pdf</url></text-urls></urls><custom2><style face="normal" font="default">19979893, Dyne D</style></custom2><misc3><style face="normal" font="default">10.1016/S0048-9697(97)05483-1</style></misc3></record></records></xml>
