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  • 1
    Language: English
    In: The Journal of Allergy and Clinical Immunology, March 2017, Vol.139(3), pp.1052-1055
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jaci.2016.08.041 Byline: Rebecca Z. Krouse (a), Christine A. Sorkness (b), Jeremy J. Wildfire (a), Agustin Calatroni (a), Rebecca Gruchalla (c), Gurjit K. Khurana Hershey (d), Meyer Kattan (e), Andrew H. Liu (f)(g), Melanie Makhija (h), Stephen J. Teach (i), Joseph B. West (j), Robert A. Wood (k), Edward M. Zoratti (l), Peter J. Gergen (m) Author Affiliation: (a) Rho Federal Systems Division, Inc, Chapel Hill, NC (b) University of Wisconsin School of Medicine and Public Health, Madison, Wis (c) University of Texas Southwestern Medical Center, Dallas, Tex (d) Cincinnati Children's Hospital, Cincinnati, Ohio (e) College of Physicians and Surgeons, Columbia University, New York, NY (f) National Jewish Health, Denver, Colo (g) Children's Hospital Colorado and University of Colorado School of Medicine, Aurora, Colo (h) Ann and Robert H. Lurie Children's Hospital of Chicago, Chicago, Ill (i) Children's National Health System, Washington, DC (j) Boston University School of Medicine, Boston, Mass (k) Johns Hopkins University School of Medicine, Baltimore, Md (l) Henry Ford Health System, Detroit, Mich (m) National Institute of Allergy and Infectious Diseases, Bethesda, Md Article Note: (footnote) This project has been funded in whole or in part with federal funds from the National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Department of Health and Human Services (contract nos. HHSN272200900052C, HHSN272201000052I, and 1UM1AI114271-01). Additional support was provided by the National Center for Research Resources, and National Center for Advancing Translational Sciences, NIH (grant nos. NCRR/NIH UL1TR000451, UL1RR025780, UL1TR000075, UL1TR000154, UL1TR001082, UL1TR000077-04, UL1TR000040, UL1TR000150, and UL1TR001105). Glaxo SmithKline (GSK) provided Ventolin, Flovent, Advair, and Flonase under a clinical trial agreement with NIH-NIAID; GSK did not have a role in the development or approval of the protocol, conduct of the trial, data analysis, manuscript preparation, or the decision to submit the manuscript for publication., Disclosure of potential conflict of interest: R. Z. Krouse receives research support from the National Institutes of Health (NIH)-National Institute of Allergy and Infectious Diseases (NIAID). C. A. Sorkness receives research support from the NIH-NIAID and Novartis. J. J. Wildfire receives research support from the NIH-NIAID. A. Calatroni receives research support from the NIH-NIAID. R. Gruchalla serves as a consultant for Massachusetts Medical Society. G. K. K. Hershey receives grant support from the NIH. M. Kattan receives research support from the NIH-NIAID and serves on the board for Novartis Pharma. A. H. Liu receives research support from the NIH; has board membership for GlaxoSmithKine; and receives payments for lectures from Merck. M. Makhija receives research support from the NIH. S. J. Teach receives research support from the NIH-NIAID, PCORI, Fight for Children Foundation and EJF Philanthropies, and Novartis; serves as consultant for Novartis; and receives royalties from UpToDate. J. B. West receives research support from the NIH-NIAID. R. A. Wood receives research support from the NIH, DBV, and Aimmune; serves as a consultant for Sanofi and Stallergenes; and receives royalties from UpToDate. E. M. Zoratti receives research support from the NIH-NIAID. The rest of the authors declare that they have no relevant conflicts of interest.
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 2
    Language: English
    In: The Journal of Allergy and Clinical Immunology, February 2016, Vol.137(2), pp.AB177-AB177
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jaci.2015.12.714 Byline: Kari R. Brown, Rebecca A. Zabel, Agustin Calatroni, Cynthia Visness, Umasundari Sivaprasad, Elizabeth Matsui, Joseph B. West, Melanie M. Makhija, Michelle A. Gill, Haejin Kim, Meyer Kattan, Dinesh K. Pillai, James E. Gern, William W. Busse, Alkis Togias, Andrew H. Liu, Gurjit K. Khurana Hershey Author Affiliation: (1) Cincinnati Children's Hospital Medical Center, Cincinnati, OH (2) Rho Federal Systems Division Inc., Chapel Hill, NC (3) Cincinnati Children's Hospital Medical Center, Division of Asthma Research, Cincinnati, OH (4) Johns Hopkins University School of Medicine, Baltimore, MD (5) Boston University Medical Center, Boston, MA (6) Ann and Robert H. Lurie Children's Hospital of Chicago, Chicago, IL (7) UT Southwestern Medical Center, Dallas, TX (8) Henry Ford Health System, Division of Allergy and Clinical Immunology, Detroit, MI (9) College of Physicians and Surgeons, Columbia University, New York, NY (10) Children's National Health System, Washington, DC (11) University of Wisconsin-Madison, Madison, WI (12) University of Wisconsin School of Medicine and Public Health, Madison, WI (13) NIAID/NIH, Bethesda, MD (14) Children's Hospital Colorado, Aurora, CO (15) National Jewish Health, Denver, CO (16) Cincinnati Children's Hospital, Cincinnati, OH Article Note: (miscellaneous) 582
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 3
    Language: English
    In: The Journal of Allergy and Clinical Immunology, October 2016, Vol.138(4), pp.1042-1050
    Description: Pathway analyses can be used to determine how host and environmental factors contribute to asthma severity. To investigate pathways explaining asthma severity in inner-city children. On the basis of medical evidence in the published literature, we developed a conceptual model to describe how 8 risk-factor domains (allergen sensitization, allergic inflammation, pulmonary physiology, stress, obesity, vitamin D, environmental tobacco smoke [ETS] exposure, and rhinitis severity) are linked to asthma severity. To estimate the relative magnitude and significance of hypothesized relationships among these domains and asthma severity, we applied a causal network analysis to test our model in an Inner-City Asthma Consortium study. Participants comprised 6- to 17-year-old children (n = 561) with asthma and rhinitis from 9 US inner cities who were evaluated every 2 months for 1 year. Asthma severity was measured by a longitudinal composite assessment of day and night symptoms, exacerbations, and controller usage. Our conceptual model explained 53.4% of the variance in asthma severity. An allergy pathway (linking allergen sensitization, allergic inflammation, pulmonary physiology, and rhinitis severity domains to asthma severity) and the ETS exposure pathway (linking ETS exposure and pulmonary physiology domains to asthma severity) exerted significant effects on asthma severity. Among the domains, pulmonary physiology and rhinitis severity had the largest significant standardized total effects on asthma severity (−0.51 and 0.48, respectively), followed by ETS exposure (0.30) and allergic inflammation (0.22). Although vitamin D had modest but significant indirect effects on asthma severity, its total effect was insignificant (0.01). The standardized effect sizes generated by a causal network analysis quantify the relative contributions of different domains and can be used to prioritize interventions to address asthma severity.
    Keywords: Asthma ; Children ; Inner-City ; Allergy ; Sensitization ; Inflammation ; Lung Function ; Pulmonary Physiology ; Rhinitis ; Environmental Tobacco Smoke Exposure ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 4
    Language: English
    In: The Journal of Allergy and Clinical Immunology, May 2017, Vol.139(5), pp.1478-1488
    Description: Given the strong environmental influence on both epigenetic marks and allergic asthma in children, the epigenetic alterations in respiratory epithelia might provide insight into allergic asthma. We sought to identify DNA methylation and gene expression changes associated with childhood allergic persistent asthma. We compared genomic DNA methylation patterns and gene expression in African American children with persistent atopic asthma (n = 36) versus healthy control subjects (n = 36). Results were validated in an independent population of asthmatic children (n = 30) by using a shared healthy control population (n = 36) and in an independent population of white adult atopic asthmatic patients (n = 12) and control subjects (n = 12). We identified 186 genes with significant methylation changes, differentially methylated regions or differentially methylated probes, after adjustment for age, sex, race/ethnicity, batch effects, inflation, and multiple comparisons. Genes differentially methylated included those with established roles in asthma and atopy and genes related to extracellular matrix, immunity, cell adhesion, epigenetic regulation, and airflow obstruction. The methylation changes were substantial (median, 9.5%; range, 2.6% to 29.5%). Hypomethylated and hypermethylated genes were associated with increased and decreased gene expression, respectively (  〈 2.8 × 10 for differentially methylated regions and  〈 7.8 × 10 for differentially methylated probes). Quantitative analysis in 53 differentially expressed genes demonstrated that 32 (60%) have significant methylation-expression relationships within 5 kb of the gene. Ten loci selected based on the relevance to asthma, magnitude of methylation change, and methylation-expression relationships were validated in an independent cohort of children with atopic asthma. Sixty-seven of 186 genes also have significant asthma-associated methylation changes in nasal epithelia of adult white asthmatic patients. Epigenetic marks in respiratory epithelia are associated with allergic asthma and gene expression changes in inner-city children.
    Keywords: DNA Methylation ; Gene Expression ; Microarray ; Atopic Asthma ; Respiratory Epithelia ; Epigenetic Regulation ; Inner City ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 5
    Language: English
    In: The Journal of Allergy and Clinical Immunology, September 2015, Vol.136(3), pp.802-806
    Description: Regarding susceptibility loci reported exclusively in GWASs of Asian populations, 5 loci (GLB1, CCDC80, ZNF365, OR10A/3/NLRP10, and CYP24A1/PFDN4) showed evidence for association in Europeans for the first time. [...]21 of 23 reported AD risk loci could be confirmed.
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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