Cardiovascular disease is a leading cause of mortality in the United States. Understanding the physiology and pathology of the heart and circulation is the foundation for improving the treatment and prevention of cardiovascular diseases. Wayne State University has an outstanding track record in providing extensive training in the cardiovascular sciences and an exceptional record in the training of minority students in the Detroit metropolitan area, contributing a major role in research education in the region. This new T32 proposal seeks financial support to strengthen our research training effort in the development of a new generation of scientists who will not only pursue cardiovascular research to improve health care, but also strengthen our economic base by innovations that will be translated to medical practice. This proposal encompasses a focused program of excellence in training predoctoral graduate students in cardiovascular research. Based on a selective team of 14 training faculty with complementary scientific expertise in cardiovascular physiology and diseases, the new Detroit Cardiovascular Training Program will emphasize preparing 21st century scientists with strong backgrounds in molecular mechanisms of cardiovascular health and diseases, who are equipped with integrative and translational approaches to scientific investigation. The goal of this new program is to support 4 predoctoral trainees per year. Trainees will be selected from an excellent pool of candidates, including under-represented minorities who may come from an NIH-supported Initiative for Maximizing Student Diversity (IMSD) program. In addition to externally funded active individual research programs with proven training productivity, our training faculty has a long-standing history of joint research an training collaborations. This strong research environment enables us to provide multidisciplinary training in cardiovascular science through a combination of didactic courses and mentored research in areas including hypertension, cardiac muscle contractility, heart failure, myocardial ischemia-reperfusion injury, and cardiovascular adaptation. The training program provides comprehensive didactic and practical instructions in the responsible conduct of research. Career development training will include research seminars and workshops focusing on writing and presentation skills and fellowship and research grant writing and evaluation. Exceptional institutional commitment is in place to support our Program. Operation of the Program will be monitored by a Steering Committee consisting of the Program Director, Program Coordinator, and three training faculty members. The Program will be reviewed regularly by an Internal Advisory Committee in consultation with external advisors. The Department of Physiology Office staff will provide administrative support to the personnel, accounting, and programmatic operations of the Program.

Public Health Relevance

Cardiovascular diseases are leading causes of deaths in the United States. The Detroit Cardiovascular Training Program will be the first NIH program in the region to provide research training for predoctoral graduate students in integrative and translational cardiovascular sciences. This training effort will contribute in a timely fashion to the education of a new generation of scientists who will pursue biomedical research to improve health care and medical innovations for the economic recovery in Detroit.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
5T32HL120822-03
Application #
8984910
Study Section
NHLBI Institutional Training Mechanism Review Committee (NITM)
Program Officer
Wang, Wayne C
Project Start
2014-01-01
Project End
2018-12-31
Budget Start
2016-01-01
Budget End
2016-12-31
Support Year
3
Fiscal Year
2016
Total Cost
$166,358
Indirect Cost
$9,126
Name
Wayne State University
Department
Physiology
Type
Schools of Medicine
DUNS #
001962224
City
Detroit
State
MI
Country
United States
Zip Code
48202
Wider, Joseph; Undyala, Vishnu V R; Whittaker, Peter et al. (2018) Remote ischemic preconditioning fails to reduce infarct size in the Zucker fatty rat model of type-2 diabetes: role of defective humoral communication. Basic Res Cardiol 113:16
Bryson, Timothy D; Gu, Xiaosong; Khalil, Remonda M et al. (2018) Overexpression of prostaglandin E2 EP4 receptor improves cardiac function after myocardial infarction. J Mol Cell Cardiol 118:1-12
Holcomb, Joshua; Doughan, Maysaa; Spellmon, Nicholas et al. (2018) SAXS analysis of a soluble cytosolic NgBR construct including extracellular and transmembrane domains. PLoS One 13:e0191371
Holcomb, Joshua; Spellmon, Nicholas; Zhang, Yingxue et al. (2017) Protein crystallization: Eluding the bottleneck of X-ray crystallography. AIMS Biophys 4:557-575
Mahapatra, Gargi; Varughese, Ashwathy; Ji, Qinqin et al. (2017) Phosphorylation of Cytochrome c Threonine 28 Regulates Electron Transport Chain Activity in Kidney: IMPLICATIONS FOR AMP KINASE. J Biol Chem 292:64-79
Barupala, Dulmini P; Dzul, Stephen P; Riggs-Gelasco, Pamela Jo et al. (2016) Synthesis, delivery and regulation of eukaryotic heme and Fe-S cluster cofactors. Arch Biochem Biophys 592:60-75
Gunther, Laura K; Feng, Han-Zhong; Wei, Hongguang et al. (2016) Effect of N-Terminal Extension of Cardiac Troponin I on the Ca(2+) Regulation of ATP Binding and ADP Dissociation of Myosin II in Native Cardiac Myofibrils. Biochemistry 55:1887-97
Smith, Aaron T; Barupala, Dulmini; Stemmler, Timothy L et al. (2015) A new metal binding domain involved in cadmium, cobalt and zinc transport. Nat Chem Biol 11:678-84
Marshall, John; Wong, Kwoon Y; Rupasinghe, Chamila N et al. (2015) Inhibition of N-Methyl-D-aspartate-induced Retinal Neuronal Death by Polyarginine Peptides Is Linked to the Attenuation of Stress-induced Hyperpolarization of the Inner Mitochondrial Membrane Potential. J Biol Chem 290:22030-48
Hong-Hermesdorf, Anne; Miethke, Marcus; Gallaher, Sean D et al. (2014) Subcellular metal imaging identifies dynamic sites of Cu accumulation in Chlamydomonas. Nat Chem Biol 10:1034-42