This is a proposal for continuation of a research training program for physicians and postdoctoral basic scientists in Nephrology. The overall goal of this Program continues to be the development of our trainees for careers in academic nephrology. Investigations will be performed using state-of-the-art tools aimed at defining the basic biology underlying normal kidney function, and mechanisms that mediate renal diseases. A key goal is to develop the independent research abilities of trainees which we will foster by our focus upon techniques of contemporary molecular biology, immunology and cell biology, as well as cultivation of intellectual skill in the critical reading of scientific papers, analysis and reporting of research data, as well as oral presentation at scientific meetings. Although we emphasize basic research techniques, we apply them to health-related problems. These include molecular immunopathology, the complement system in renal diseases, apoptosis and autoimmunity (especially in systemic lupus erythematosis), ischemic renal reperfusion injury, endotoxin-induced acute renal failure, mouse models of renal disease, transgenic and knockout mouse technologies, mouse renal transplantation, gene expression in experimental glomerular cell injury, function genomics, bioinformatics, epithelial cell growth factors, regulation of Na:K ATPase along the nephron, renal hemodynamics in acute renal failure using direct human clinical protocols, clinical studies of human nephrolithiasis, and renal transplantation. Applications will have an M.D., Ph.D. degree, or both, and physicians will have completed clinical training in Internal Medicine and one year in Nephrology. Selection of the applicants by the Nephrology Training Faculty is based upon interviews, letters of recommendation, and past research performance where applicable. Progress of the trainees is assessed by the Program Director, Co-Director, individual faculty sponsors, and yearly seminars given by the trainees. All training will be carried out in the Section of Nephrology of the Department of Medicine. Individual training can be arranged as needed in basic science departments at the University of Chicago.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Institutional National Research Service Award (T32)
Project #
3T32DK007510-25S1
Application #
8722679
Study Section
Special Emphasis Panel (ZDK1-GRB-S (J3))
Program Officer
Rys-Sikora, Krystyna E
Project Start
1986-09-29
Project End
2014-06-30
Budget Start
2012-07-01
Budget End
2014-06-30
Support Year
25
Fiscal Year
2013
Total Cost
$68,072
Indirect Cost
$5,042
Name
University of Chicago
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
005421136
City
Chicago
State
IL
Country
United States
Zip Code
60637
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Eadon, Michael T; Koyner, Jay L (2012) Autologous creatinine clearance in a case of necrotizing fasciitis and anuria. Am J Nephrol 35:225-9
Eadon, Michael T; Hack, Bradley K; Xu, Chang et al. (2012) Endotoxemia alters tight junction gene and protein expression in the kidney. Am J Physiol Renal Physiol 303:F821-30
Dhar, Promila; Eadon, Michael; Hallak, Patrick et al. (2012) Whole blood viscosity: Effect of hemodialysis treatment and implications for access patency and vascular disease. Clin Hemorheol Microcirc 51:265-75
Murray, Patrick; Udani, Suneel; Koyner, Jay L (2011) Does renal replacement therapy improve outcome? Controversies in acute kidney injury. Contrib Nephrol 174:212-21
Antoni, Angelika; Patel, Vimal A; Fan, Hanli et al. (2011) Macrophages from lupus-prone MRL mice have a conditional signaling abnormality that leads to dysregulated expression of numerous genes. Immunogenetics 63:291-308
Jacob, Alexander; Hack, Bradley; Bai, Tao et al. (2010) Inhibition of C5a receptor alleviates experimental CNS lupus. J Neuroimmunol 221:46-52
Puri, Tipu S; Shakaib, Mohammed I; Chang, Anthony et al. (2010) Chronic kidney disease induced in mice by reversible unilateral ureteral obstruction is dependent on genetic background. Am J Physiol Renal Physiol 298:F1024-32
Jacob, A; Bao, L; Brorson, J et al. (2010) C3aR inhibition reduces neurodegeneration in experimental lupus. Lupus 19:73-82

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