This is an amended application for a renewal of a long standing (31 year) pre- and postdoctoral training program, the theme of which is molecular and cellular mechanisms in cardiovascular disease. The environment is multi-disciplinary consisting of well-funded faculty (total of 21) established in research and training from basic and clinical departments in the College of Medicine (COM) and in several divisions in the Children's Hospital Medical Research Center & Foundation. The administrative structure of the amended grant has been revised. The Internal Advisory Committee (IAC) has been expanded to 5 with a specific rotation plan. Two Co- Pis now assist in the overall functioning of the Program. The External Advisory Committee (EAC) consists of 4 senior outside investigators and convenes semiannually. Collaboration amongst the faculty and trainees is outstanding, with over 187 multi-authored publications in the past 10 years. The faculty provides a vast repertoire of approaches and methods, ranging from the gene to the organism, and the human cardiovascular system, thus providing a wide educational experience for trainees. The transgenic approach is utilized by most faculty, and integrated translational biology is emphasized. The program has been highly successful in training and retention of the highest quality of predoctoral and postdoctoral candidates, and in emphasizing health professionals (Physician/Scientists). The current proposal requests funding for 5 pre- and 5 postdoctoral trainees. Predocs are selected by the IAC from a wide pool arising from departments, the successful """"""""Flex"""""""" program, a funded PSTP and a Short-Term Medical Student & ASPET -supported programs. Postdoctoral fellows, are nominated by faculty, and must be approved by the IAC. A specific plan and benchmarks for successful progress are in place. The mentoring is detailed, and includes mentoring of junior faculty. Evaluation (annually) of the mentoring of trainees utilizes the NHLBI Mentoring Evaluation Form sent to the IAC. Recruitment of minorities has been very successful. A new URL, http://heartrresearch.minority. opp., has been developed. In the post genomic era our challenge as cardiovascular biomedical scientists is to meaningfully characterize how genes function and underlie critical physiologic processes and disease. ? ? ? ?

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Institutional National Research Service Award (T32)
Project #
Application #
Study Section
NHLBI Institutional Training Mechanism Review Committee (NITM)
Program Officer
Carlson, Drew E
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of Cincinnati
Schools of Medicine
United States
Zip Code
Zhou, Long; Hinerman, Jennifer M; Blaszczyk, Michal et al. (2016) Structural basis for collagen recognition by the immune receptor OSCAR. Blood 127:529-37
Bodi, Ilona; Nakayama, Hiroyuki; Schwartz, Arnold (2016) Tetrodotoxin-sensitive Ca2+ Currents, but No T-type Currents in Normal, Hypertrophied, and Failing Mouse Cardiomyocytes. J Cardiovasc Pharmacol 68:452-464
Deng, Xiaodi; Walker, Ryan G; Morris, Jamie et al. (2015) Role of Conserved Proline Residues in Human Apolipoprotein A-IV Structure and Function. J Biol Chem 290:10689-702
Waltmann, Meaghan D; Basford, Joshua E; Konaniah, Eddy S et al. (2014) Apolipoprotein E receptor-2 deficiency enhances macrophage susceptibility to lipid accumulation and cell death to augment atherosclerotic plaque progression and necrosis. Biochim Biophys Acta 1842:1395-405
McLendon, Patrick M; Ferguson, Bradley S; Osinska, Hanna et al. (2014) Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy. Proc Natl Acad Sci U S A 111:E5178-86
Pritchard, Tracy J; Kawase, Yoshiaki; Haghighi, Kobra et al. (2013) Active inhibitor-1 maintains protein hyper-phosphorylation in aging hearts and halts remodeling in failing hearts. PLoS One 8:e80717
Schulz, Emily M; Wieczorek, David F (2013) Tropomyosin de-phosphorylation in the heart: what are the consequences? J Muscle Res Cell Motil 34:239-46
Schulz, Emily M; Wilder, Tanganyika; Chowdhury, Shamim A K et al. (2013) Decreasing tropomyosin phosphorylation rescues tropomyosin-induced familial hypertrophic cardiomyopathy. J Biol Chem 288:28925-35
Koch, Sheryl E; Tranter, Michael; Robbins, Nathan et al. (2013) Probenecid as a noninjurious positive inotrope in an ischemic heart disease murine model. J Cardiovasc Pharmacol Ther 18:280-9
Deng, Xiaodi; Morris, Jamie; Chaton, Catherine et al. (2013) Small-angle X-ray scattering of apolipoprotein A-IV reveals the importance of its termini for structural stability. J Biol Chem 288:4854-66

Showing the most recent 10 out of 154 publications