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Identifying pediatric lung disease: A comparison of forced oscillation technique outcomesThese findings suggest the utility of specific FOT outcomes is dependent on the respiratory disease being assessed
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Developmental regulation of type 1 and type 3 interferon production and risk for infant infections and asthma developmentType 1 and 3 interferon response capacity appears strongly developmentally constrained at birth
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Impaired airway epithelial cell responses from children with asthma to rhinoviral infectionHuman rhinovirus infection delays repair and inhibits apoptotic processes in epithelial cells from non-asthmatic and asthmatic children
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Basophil counts in PBMC populations during childhood acute wheeze/asthma are associated with future exacerbationsOur findings suggest that the proportion of degranulated basophils can also be associated with recurrent exacerbations
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Insights into respiratory disease through bioinformaticsHere, we review the basic concepts in bioinformatics and genomic data analysis and illustrate the application of these tools to further our understanding of lung diseases
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Prevention of Allergy/Asthma - New StrategiesThis review focuses on the scientific rationale for early intervention aimed at asthma prophylaxis and discusses therapeutic approaches
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Identification of epithelial phospholipase A2 receptor 1 as a potential target in asthmaPLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation
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Differential gene network analysis for the identification of asthma-associated therapeutic targets in allergen-specific T-helper memory responsesDifferential network analysis of allergen-induced CD4 T cell responses can unmask covert disease-associated genes and pin point novel therapeutic targets
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The genetic and epigenetic landscapes of the epithelium in asthmaGenetic factors in airway epithelial cells that are functionally associated with asthma pathogenesis
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Accumulation mode particles and LPS exposure induce TLR-4 dependent and independent inflammatory responses in the lungWe aimed to delineate the effects of LPS and AMP on airway inflammation, and potential contribution to airway disease by measuring airway inflammatory responses