Abstract

The objective of the Biostatistics Core is to help make quantitative inferences based on research about the causes and control of diabetes and related endocrine and metabolic disorders by consulting and collaborating on relevant research. The Core provides experimental design, data management and data analysis in support of approved projects in the Center. Core personnel also develop novel biostatistical techniques, including models in statistical genetics, that are necessary to improve the analysis of such data. Examples of such biostatistical techniques include; improved estimation of hormone levels in sera from assays, including RIA's; development of a model to identify pulses in hormone secretion from a sequential series of assays; improved methods to include data from dropouts in 'intent to treat' analyses of controlled clinical trials; methods to combine information from multiple endpoints into a single overall test of efficacy; and analysis of pedigree data with emphasis on linkage analysis. Members of this Core will provide expertise in developing additional models in collaboration with investigators from the Michigan Diabetes Center.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Comprehensive Center (P60)
Project #
3P60DK020572-22S1
Application #
6105083
Study Section
Project Start
1999-05-03
Project End
1999-11-30
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
22
Fiscal Year
1999
Total Cost
Indirect Cost

  Institution

Name
University of Michigan Ann Arbor
Department
Type
DUNS #
791277940
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109

  Publications

Kumar, Navasuja; Pop-Busui, Rodica; Musch, David C et al. (2018) Central Corneal Thickness Increase Due to Stromal Thickening With Diabetic Peripheral Neuropathy Severity. Cornea 37:1138-1142
Wilson, Matthew J; Sen, Ananda; Bridges, Dave et al. (2018) Higher baseline expression of the PTGS2 gene and greater decreases in total colonic fatty acid content predict greater decreases in colonic prostaglandin-E2 concentrations after dietary supplementation with ?-3 fatty acids. Prostaglandins Leukot Essent Fatty Acids 139:14-19
Sucularli, Ceren; Thomas, Peedikayil; Kocak, Hande et al. (2018) High-throughput gene expression analysis identifies p53-dependent and -independent pathways contributing to the adrenocortical dysplasia (acd) phenotype. Gene 679:219-231
Kady, Nermin M; Liu, Xuwen; Lydic, Todd A et al. (2018) ELOVL4-Mediated Production of Very Long-Chain Ceramides Stabilizes Tight Junctions and Prevents Diabetes-Induced Retinal Vascular Permeability. Diabetes 67:769-781
Malik, Ahmed M; Miguez, Roberto A; Li, Xingli et al. (2018) Matrin 3-dependent neurotoxicity is modified by nucleic acid binding and nucleocytoplasmic localization. Elife 7:
Lee, Pearl G; Ha, Jinkyung; Blaum, Caroline S et al. (2018) Patterns of physical activity in sedentary older individuals with type 2 diabetes. Clin Diabetes Endocrinol 4:7
Ramos, Carla J; Lin, Chengmao; Liu, Xuwen et al. (2018) The EPAC-Rap1 pathway prevents and reverses cytokine-induced retinal vascular permeability. J Biol Chem 293:717-730
Djuric, Zora; Bassis, Christine M; Plegue, Melissa A et al. (2018) Colonic Mucosal Bacteria Are Associated with Inter-Individual Variability in Serum Carotenoid Concentrations. J Acad Nutr Diet 118:606-616.e3
Vollbrecht, Peter J; Nesbitt, Kathryn M; Mabrouk, Omar S et al. (2018) Cocaine and desipramine elicit distinct striatal noradrenergic and behavioral responses in selectively bred obesity-resistant and obesity-prone rats. Behav Brain Res 346:137-143
Jiang, Lin; Su, Haoran; Keogh, Julia M et al. (2018) Neural deletion of Sh2b1 results in brain growth retardation and reactive aggression. FASEB J 32:1830-1840

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