Data Administration and Analysis (DAA) Core support will be provided in all projects of this grant. Core personnel have worked, and will continue to work, closely with project leaders for assuring that each project receives state-of-the-art statistical and data-management support.
The specific aims of the DAA Core are: 1.1. To provide study design and review all laboratory, animal and clinical studies, including feasibility assessment, power analysis and sample size estimation. To collaborate in project data analysis, interpretation of results, and the writing of final study reports and manuscripts. 1.2. To provide relational database design, data entry, data tracking, forms, queries, and reports, and to maintain computer databases for information storage and retrieval for all projects. 1.3. To apply methods of longitudinal, survival data and nested-case control design analysis to the cohort of children who will be studied in Project 1. 1.4. To develop dendograms of the genetic relationship among the respiratory syncytial virus (RSV) strains that affect our study subjects in Project 2, and to model and assess the association between RSV genotype and bronchiolitis severity. 1.5. To use repeated measures analysis of variance to assess the effects of interleukin (IL)-17A and other cytokines on airway responsiveness in the in vivo murine model described in Project 3. Similar methods will be used to analyze data from the other specific aims of this project. 1.6. To work with the Clinical and Biospecimen Core to ensure that this core has excellent data management support and to ensure that the needed specimens are collected from the correct patients at the right time. 1.7. To develop and evaluate statistical methods for experimental design and data analysis.
RSV is the leading cause of bronchiolitis and causes >100,000 infant hopsitalizations in the US each year. Studies have also revealed that severe RSV infection in infancy is associated with the later development of childhood asthma. This application will examine both host genetic and immune response determinants, as well as the influence of specific RSV strains, on severity of RSV bronchiolitis and childhood asthma. In addition, we will define the role of a novel therapeutic target, PGI2, in RSV pathogenesis.
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|Mathias, Rasika Ann; Taub, Margaret A; Gignoux, Christopher R et al. (2016) A continuum of admixture in the Western Hemisphere revealed by the African Diaspora genome. Nat Commun 7:12522|
|Rosas-Salazar, Christian; Shilts, Meghan H; Tovchigrechko, Andrey et al. (2016) Nasopharyngeal Microbiome in Respiratory Syncytial Virus Resembles Profile Associated with Increased Childhood Asthma Risk. Am J Respir Crit Care Med 193:1180-3|
|Rostad, Christina A; Stobart, Christopher C; Gilbert, Brian E et al. (2016) A Recombinant Respiratory Syncytial Virus Vaccine Candidate Attenuated by a Low-Fusion F Protein Is Immunogenic and Protective against Challenge in Cotton Rats. J Virol 90:7508-18|
|Lee, Sujin; Nguyen, Minh Trang; Currier, Michael G et al. (2016) A polyvalent inactivated rhinovirus vaccine is broadly immunogenic in rhesus macaques. Nat Commun 7:12838|
|Stobart, Christopher C; Rostad, Christina A; Ke, Zunlong et al. (2016) A live RSV vaccine with engineered thermostability is immunogenic in cotton rats despite high attenuation. Nat Commun 7:13916|
|Tan, Yi; Hassan, Ferdaus; Schuster, Jennifer E et al. (2016) Molecular Evolution and Intraclade Recombination of Enterovirus D68 during the 2014 Outbreak in the United States. J Virol 90:1997-2007|
|Banathy, Alex; Cheung-Flynn, Joyce; Goleniewska, Kasia et al. (2016) Heat Shock-Related Protein 20 Peptide Decreases Human Airway Constriction Downstream of Î²2-Adrenergic Receptor. Am J Respir Cell Mol Biol 55:225-33|
|Zhou, Weisong; Zhang, Jian; Goleniewska, Kasia et al. (2016) Prostaglandin I2 Suppresses Proinflammatory Chemokine Expression, CD4 T Cell Activation, and STAT6-Independent Allergic Lung Inflammation. J Immunol 197:1577-86|
|Stier, Matthew T; Bloodworth, Melissa H; Toki, Shinji et al. (2016) Respiratory syncytial virus infection activates IL-13-producing group 2 innate lymphoid cells through thymic stromal lymphopoietin. J Allergy Clin Immunol 138:814-824.e11|
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