Abstract

The main responsibility of the Human Subjects Core will be to recruit, categorize, and then test human research subjects that will participate in the SCOR program. In that context, this core will conduct all clinical research protocols required by SCOR investigators, including those for baseline assessments of research subjects, segmental allergen-challenge, and inhaled glucocorticoid-withdrawal. In these protocols, the core will perform all necessary procedures (e.g., blood drawing, endobronchial biopsy, bronchial brushing, and bronchoalveolar lavage) and will be responsible for maintaining records of research subjects. The core (in conjunction with computer support from Core A) will also provide for statistical analysis of clinical data from each of the component projects and assist each project in correlating their findings with clinical data. Some record keeping will require the core to also interface with the St. Louis Area Asthma Database. As an extension of its work on human subjects, the core will also be responsible for coordinating procurement of human tracheal and bronchial specimens from lung transplant donors and autopsies and generating epithelial cells for use in SCOR projects.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Specialized Center (P50)
Project #
5P50HL056419-03
Application #
6110724
Study Section
Project Start
1998-09-01
Project End
1999-08-31
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
3
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
Washington University
Department
Type
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130

  Publications

Liu, Michael; Subramanian, Vijay; Christie, Chandrika et al. (2012) Immune responses to self-antigens in asthma patients: clinical and immunopathological implications. Hum Immunol 73:511-6
Holtzman, Michael J; Patel, Dhara A; Zhang, Yong et al. (2011) Host epithelial-viral interactions as cause and cure for asthma. Curr Opin Immunol 23:487-94
Mikols, Cassandra L; Yan, Le; Norris, Jin Y et al. (2006) IL-12 p80 is an innate epithelial cell effector that mediates chronic allograft dysfunction. Am J Respir Crit Care Med 174:461-70
Jung, Yong Woo; Schoeb, Trenton R; Weaver, Casey T et al. (2006) Antigen and lipopolysaccharide play synergistic roles in the effector phase of airway inflammation in mice. Am J Pathol 168:1425-34
Atkinson, Jeffrey J; Holmbeck, Kenn; Yamada, Susan et al. (2005) Membrane-type 1 matrix metalloproteinase is required for normal alveolar development. Dev Dyn 232:1079-90
Nabe, Takeshi; Zindl, Carlene L; Jung, Yong Woo et al. (2005) Induction of a late asthmatic response associated with airway inflammation in mice. Eur J Pharmacol 521:144-55
Wikenheiser-Brokamp, Kathryn A (2004) Rb family proteins differentially regulate distinct cell lineages during epithelial development. Development 131:4299-310
Surendran, Kameswaran; Simon, Theodore C; Liapis, Helen et al. (2004) Matrilysin (MMP-7) expression in renal tubular damage: association with Wnt4. Kidney Int 65:2212-22
Lorenz, Robin G; Chaplin, David D; McDonald, Keely G et al. (2003) Isolated lymphoid follicle formation is inducible and dependent upon lymphotoxin-sufficient B lymphocytes, lymphotoxin beta receptor, and TNF receptor I function. J Immunol 170:5475-82
Fu, Xiaoyun; Kassim, Sean Y; Parks, William C et al. (2003) Hypochlorous acid generated by myeloperoxidase modifies adjacent tryptophan and glycine residues in the catalytic domain of matrix metalloproteinase-7 (matrilysin): an oxidative mechanism for restraining proteolytic activity during inflammation. J Biol Chem 278:28403-9

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