Abstract

The Genetic Epidemiology and Biostatistics Core combines the expertise in genetic analysis of the Bowman Gray School of Medicine with the experience in biostatistics in Bowman Gray and the University of Alabama, Birmingham, to facilitate collection of experimental data, data management, statistical and genetic data analysis. The goals of the Genetic Epidemiology and Biostatistics Core are to promote interdisciplinary research in the area of SLE, with a focus on measured environmental risk factors, genetic risk factors and their interaction by (1) addressing appropriate experimental designs tailored to address specific genetic hypotheses, (2) facilitating an efficient data collection procedure at each project site for data transfer, (3) developing standardized data transfer procedures to allow efficient and useful data extraction for analysis, and (4) providing state-of-the-art longitudinal statistical and genetic data analysis. The long-term goals of the Genetic Epidemiology and Biostatistics Core are to utilize genetic and epidemiologic data collect on SLE patients and their family members in order to identify genes and environmental risk factors that singly and jointly contribute to the susceptibility for SLE.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Specialized Center (P50)
Project #
5P50AR045231-02
Application #
6201556
Study Section
Project Start
1999-07-01
Project End
2000-06-30
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
2
Fiscal Year
1999
Total Cost
Indirect Cost

  Institution

Name
University of Alabama Birmingham
Department
Type
DUNS #
004514360
City
Birmingham
State
AL
Country
United States
Zip Code
35294

  Publications

Vaughn, Samuel E; Kottyan, Leah C; Munroe, Melissa E et al. (2012) Genetic susceptibility to lupus: the biological basis of genetic risk found in B cell signaling pathways. J Leukoc Biol 92:577-91
Heinlen, Latisha D; Ritterhouse, Lauren L; McClain, Micah T et al. (2010) Ribosomal P autoantibodies are present before SLE onset and are directed against non-C-terminal peptides. J Mol Med (Berl) 88:719-27
Burgos, Paula I; Perkins, Elizabeth L; Pons-Estel, Guillermo J et al. (2009) Risk factors and impact of recurrent lupus nephritis in patients with systemic lupus erythematosus undergoing renal transplantation: data from a single US institution. Arthritis Rheum 60:2757-66
McClain, Micah T; Heinlen, Latisha D; Dennis, Gregory J et al. (2005) Early events in lupus humoral autoimmunity suggest initiation through molecular mimicry. Nat Med 11:85-9
Bruner, Benjamin F; Wynn, Donny M; Reichlin, Morris et al. (2005) Humoral antigenic targets of the ribosomal P0 lupus autoantigen are not limited to the carboxyl region. Ann N Y Acad Sci 1051:390-403
Su, Kaihong; Li, Xiaoli; Edberg, Jeffrey C et al. (2004) A promoter haplotype of the immunoreceptor tyrosine-based inhibitory motif-bearing FcgammaRIIb alters receptor expression and associates with autoimmunity. II. Differential binding of GATA4 and Yin-Yang1 transcription factors and correlated receptor expre J Immunol 172:7192-9
McClain, Micah T; Arbuckle, Melissa R; Heinlen, Latisha D et al. (2004) The prevalence, onset, and clinical significance of antiphospholipid antibodies prior to diagnosis of systemic lupus erythematosus. Arthritis Rheum 50:1226-32
McClain, Micah T; Lutz, Carol S; Kaufman, Kenneth M et al. (2004) Structural availability influences the capacity of autoantigenic epitopes to induce a widespread lupus-like autoimmune response. Proc Natl Acad Sci U S A 101:3551-6
Su, Kaihong; Wu, Jianming; Edberg, Jeffrey C et al. (2004) A promoter haplotype of the immunoreceptor tyrosine-based inhibitory motif-bearing FcgammaRIIb alters receptor expression and associates with autoimmunity. I. Regulatory FCGR2B polymorphisms and their association with systemic lupus erythematosus. J Immunol 172:7186-91
Nath, Swapan K; Namjou, Bahram; Kilpatrick, Jeff et al. (2004) A candidate region on 11p13 for systemic lupus erythematosus: a linkage identified in African-American families. J Investig Dermatol Symp Proc 9:64-7

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