This proposal is for renewal of a research training program in academic nephrology, under the directorship of Dr. Vikas P. Sukhatme, Chief of Nephrology, Beth Israel Deaconess Medical Center (BIDMC), Harvard Medical School (HMS). Support is requested for six trainees (an increase from the current level of five) who will spend at least 2 years in the program. Most candidates will have received the MD degree or the MD-PhD degree but prospective trainees with a PhD background in either immunology, biochemistry, physiology, or cell and molecular biology are also considered. The major criterion for selection is evidence of an interest, ability and commitment to investigative nephrology. Following their training, trainees have generally begun independent research programs as faculty in academic medical schools. *** Research activities span studies in patients with renal disease, to animal models, to cultured cells, to molecular biological investigations and include programs in acute renal failure, the molecular basis for ion transport, cellular immunology, mammalian gene regulation, kidney development and cancer, gene therapy directed to the kidney, mechanisms of protein degradation, renal fibrosis, and podocyte injury. *** The chief method of instruction is intensive personal involvement in a program of basic research under the close supervision of a senior scientist. Moreover, a structured program of research seminars, journal club, and laboratory presentations is mandatory participation for all trainees. *** The primary facilities for training are in the Renal, Immunology, Rheumatology and Molecular Medicine Divisions at BIDMC, in the Department of Cell Biology (HMS) and at MIT. A clinical research center has capabilities for experimental studies in normal volunteers and patients. A transgenic core, located only two floors below the Renal Division, is also utilized by These sites are close to each other, thus facilitating trainees, as is a new NIDDK supported Genomics Core. These sites are close to each other, thus facilitating didactic and research interactions.

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 #
5T32DK007199-28
Application #
6800341
Study Section
Diabetes, Endocrinology and Metabolic Diseases B Subcommittee (DDK)
Program Officer
Rankin, Tracy L
Project Start
1977-07-01
Project End
2007-06-30
Budget Start
2004-07-01
Budget End
2005-06-30
Support Year
28
Fiscal Year
2004
Total Cost
$331,293
Indirect Cost
Name
Beth Israel Deaconess Medical Center
Department
Type
DUNS #
071723621
City
Boston
State
MA
Country
United States
Zip Code
02215
Lynch, Matthew R; Tran, Mei T; Parikh, Samir M (2018) PGC1? in the kidney. Am J Physiol Renal Physiol 314:F1-F8
Poyan Mehr, Ali; Tran, Mei T; Ralto, Kenneth M et al. (2018) De novo NAD+ biosynthetic impairment in acute kidney injury in humans. Nat Med 24:1351-1359
Feng, Di; Notbohm, Jacob; Benjamin, Ava et al. (2018) Disease-causing mutation in ?-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch. Proc Natl Acad Sci U S A 115:1517-1522
Musah, Samira; Mammoto, Akiko; Ferrante, Thomas C et al. (2017) Mature induced-pluripotent-stem-cell-derived human podocytes reconstitute kidney glomerular-capillary-wall function on a chip. Nat Biomed Eng 1:
Olabisi, Opeyemi A; Heneghan, John F (2017) APOL1 Nephrotoxicity: What Does Ion Transport Have to Do With It? Semin Nephrol 37:546-551
Chen, Christina W; Drechsler, Christiane; Suntharalingam, Pirianthini et al. (2017) High Glycated Albumin and Mortality in Persons with Diabetes Mellitus on Hemodialysis. Clin Chem 63:477-485
Olabisi, Opeyemi A; Zhang, Jia-Yue; VerPlank, Lynn et al. (2016) APOL1 kidney disease risk variants cause cytotoxicity by depleting cellular potassium and inducing stress-activated protein kinases. Proc Natl Acad Sci U S A 113:830-7
Feng, Di; Steinke, Julia M; Krishnan, Ramaswamy et al. (2016) Functional Validation of an Alpha-Actinin-4 Mutation as a Potential Cause of an Aggressive Presentation of Adolescent Focal Segmental Glomerulosclerosis: Implications for Genetic Testing. PLoS One 11:e0167467
Lynch, Katherine E; Ghassemi, Fatimah; Flythe, Jennifer E et al. (2016) Sodium modelling to reduce intradialytic hypotension during haemodialysis for acute kidney injury in the intensive care unit. Nephrology (Carlton) 21:870-7
Ralto, Kenneth M; Parikh, Samir M (2016) Mitochondria in Acute Kidney Injury. Semin Nephrol 36:8-16

Showing the most recent 10 out of 47 publications