Our program is well suited to generate the needed investigators for multi-disciplinary training. We have specific training programs for clinically trained physician postdoctoral investigators and research trained PhD postdoctoral investigators. To facilitate the development of a cohesive training environment we integrate the three major cardiovascular research centers at the University of Utah School of Medicine: The University of Utah Molecular Medicine Program at the Eccles Institute of Human Genetics, Heart Failure and Regeneration Initiatives in the Divisions of Cardiology and Cardiothoracic Surgery at the School of Medicine, Nora Eccles Harrison Cardiovascular Research and Training Institute that specializes in cardiac electrophysiology and ion transport. These three centers of cardiovascular research are located near to one another on our campus and form the three legs of a tripod that support the T32 in Cardiovascular Research. Nineteen members of the faculty of the School of Medicine will form the 'core training faculty' for the program. All are experts in their fields and are successful in training post doctoral fellows. We wish to support eight post-doctoral MD and PhD scientist-trainees each year. We anticipate that each trainee will be supported for a minimum of two years by the T32.

Public Health Relevance

The basis for this program's existence and continuation is the need for well-trained investigators in cardiovascular medicine. There are too few well trained cardiovascular investigators to take advantage of today's enormous growth in genetics, imaging, and technological advances. The University of Utah has successfully trained cardiovascular investigators and is well-equipped to continue this success.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
3T32HL007576-30S1
Application #
9384838
Study Section
Program Officer
Wang, Wayne C
Project Start
1994-07-01
Project End
2017-01-31
Budget Start
2015-07-01
Budget End
2017-01-31
Support Year
30
Fiscal Year
2017
Total Cost
Indirect Cost
Name
University of Utah
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
009095365
City
Salt Lake City
State
UT
Country
United States
Zip Code
84112
Gibbons, Eric K; Hodgson, Kyler K; Chaudhari, Akshay S et al. (2018) Simultaneous NODDI and GFA parameter map generation from subsampled q-space imaging using deep learning. Magn Reson Med :
Wei, Peng; Dove, Katja K; Bensard, Claire et al. (2018) The Force Is Strong with This One: Metabolism (Over)powers Stem Cell Fate. Trends Cell Biol 28:551-559
Abdul-Wajid, Sarah; Demarest, Bradley L; Yost, H Joseph (2018) Loss of embryonic neural crest derived cardiomyocytes causes adult onset hypertrophic cardiomyopathy in zebrafish. Nat Commun 9:4603
Chaudhari, Akshay S; Fang, Zhongnan; Kogan, Feliks et al. (2018) Super-resolution musculoskeletal MRI using deep learning. Magn Reson Med 80:2139-2154
Warren, Mark; Sciuto, Katie J; Taylor, Tyson G et al. (2017) Blockade of CaMKII depresses conduction preferentially in the right ventricular outflow tract and promotes ischemic ventricular fibrillation in the rabbit heart. Am J Physiol Heart Circ Physiol 312:H752-H767
Nielson, Jason R; Fredrickson, Eric K; Waller, T Cameron et al. (2017) Sterol Oxidation Mediates Stress-Responsive Vms1 Translocation to Mitochondria. Mol Cell 68:673-685.e6
Schlaberg, Robert; Queen, Krista; Simmon, Keith et al. (2017) Viral Pathogen Detection by Metagenomics and Pan-Viral Group Polymerase Chain Reaction in Children With Pneumonia Lacking Identifiable Etiology. J Infect Dis 215:1407-1415
Schlaberg, Robert; Ampofo, Krow; Tardif, Keith D et al. (2017) Human Bocavirus Capsid Messenger RNA Detection in Children With Pneumonia. J Infect Dis 216:688-696
Gomez, Arnold D; Zou, Huashan; Bowen, Megan E et al. (2017) Right Ventricular Fiber Structure as a Compensatory Mechanism in Pressure Overload: A Computational Study. J Biomech Eng 139:
Sommakia, Salah; Houlihan, Patrick R; Deane, Sadiki S et al. (2017) Mitochondrial cardiomyopathies feature increased uptake and diminished efflux of mitochondrial calcium. J Mol Cell Cardiol 113:22-32

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