This is a competitive renewal of a multi-disciplinary, post-doctoral cardiovascular research program Sponsored by the Cardiology Unit of the Dept. of Medicine and the Depts. of Molecular Physiology and Biophysics and Pharmacology of the University of Vermont College of Medicine. This grant has been funded since 1988. The goal of the program is to provide rigorous training for both MDs and PhDs that will equip them for productive research careers in cardiovascular science. MD trainees are recruited primarily in conjunction with the clinical Cardiology Fellowship Program at the University of Vermont, while PhDs are mainly recruited through the two basic science departments. The 18 participating faculty are divided into four thematic groups: 1) Cardiac Muscle and Heart Failure, 2) Smooth Muscle, 3) Vascular Biology, and 4) Clinical Cardiology and Epidemiology. Training is centered around a focussed laboratory or clinical research experience under the supervision of a primary mentor and a secondary mentor. Interactions with participating faculty within each thematic group and across boundaries are encouraged and facilitated. Trainees in Clinical Cardiology and Epidemiology take required seminar courses in study design and biostatistics, which are open to other trainees if they are deemed useful or necessary. All trainees attend a seminar series on responsible conduct of research. Administrative and policy decisions and overall oversight of trainees'progress is accomplished by a Steering Committee composed of the Pland Drs. David Warshaw and Mark Nelson, Chairs of Molecular Physiology and Biophysics and Pharmacology, respectively. The philosophy of the training program is to provide both focus and flexibility, a collaborative environment, and carefully designed, supportive mentoring relationships.

Public Health Relevance

The ulitmate goal of this Training Program Is to train phyisicans and scientists who will make meaningful contributions to the understanding, diagnosis and treatment of human cardiovascular disease.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
5T32HL007647-25
Application #
8456080
Study Section
NHLBI Institutional Training Mechanism Review Committee (NITM)
Program Officer
Carlson, Drew E
Project Start
1994-07-01
Project End
2014-06-30
Budget Start
2013-07-01
Budget End
2014-06-30
Support Year
25
Fiscal Year
2013
Total Cost
$262,816
Indirect Cost
$21,136
Name
University of Vermont & St Agric College
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
066811191
City
Burlington
State
VT
Country
United States
Zip Code
05405
Moon, Thomas M; Sheehe, Jessica L; Nukareddy, Praveena et al. (2018) An N-terminally truncated form of cyclic GMP-dependent protein kinase I? (PKG I?) is monomeric and autoinhibited and provides a model for activation. J Biol Chem 293:7916-7929
Rengo, Jason L; Callahan, Damien M; Savage, Patrick D et al. (2016) Skeletal muscle ultrastructure and function in statin-tolerant individuals. Muscle Nerve 53:242-51
Heppner, Thomas J; Tykocki, Nathan R; Hill-Eubanks, David et al. (2016) Transient contractions of urinary bladder smooth muscle are drivers of afferent nerve activity during filling. J Gen Physiol 147:323-35
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Moon, Thomas M; Tykocki, Nathan R; Sheehe, Jessica L et al. (2015) Synthetic Peptides as cGMP-Independent Activators of cGMP-Dependent Protein Kinase I?. Chem Biol 22:1653-61
Callahan, Damien M; Tourville, Timothy W; Slauterbeck, James R et al. (2015) Reduced rate of knee extensor torque development in older adults with knee osteoarthritis is associated with intrinsic muscle contractile deficits. Exp Gerontol 72:16-21
Meyer, Markus; McEntee, Rachel K; Nyotowidjojo, Iwan et al. (2015) Relationship of exercise capacity and left ventricular dimensions in patients with a normal ejection fraction. An exploratory study. PLoS One 10:e0119432
Tykocki, Nathan R; Nelson, Mark T (2015) Location, Location, Location: Juxtaposed calcium-signaling microdomains as a novel model of the vascular smooth muscle myogenic response. J Gen Physiol 146:129-32
Tanner, Bertrand C W; McNabb, Mark; Palmer, Bradley M et al. (2014) Random myosin loss along thick-filaments increases myosin attachment time and the proportion of bound myosin heads to mitigate force decline in skeletal muscle. Arch Biochem Biophys 552-553:117-27

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