This application is for the revision of a competing renewal in the Cardiovascular Pathophysiology training program at UAB for 6 pre-doctoral students which is currently in its 14th year. Since the appointment of the first trainees in late 1999 36 students have entered the training program with 28 having completed their graduate studies and developed science related careers in respected national research centers and universities. Students over the last ten years have graduated within 5 years, have an average of 6 publications and the cumulative H factor for all trainee publications (120) is 41. The training will be undertaken by faculty from six separate departments at the institution (four basic science and two clinical) with a expertise in a broad range of research areas relevant to cardiovascular research. This training program recognizes the integrated and multi-disciplinary nature of modern cardiovascular research and includes faculty from six research centers at UAB encompassing institutional areas of strength in Free Radical Biology, Nephrology Research, Clinical Nutrition, Cardiovascular and Diabetes and Hypertension. The students will earn degrees in the graduate programs in pathology, physiology or cell biology. Students supported by the proposal will have completed the first year, selected a project and mentor with cardiovascular relevance and demonstrated excellence in their studies and research potential. The program plan consists of a didactic component that emphasizes cardiovascular disease in the context of other pathologies with a particular emphasis on molecular mechanisms of disease. Trainees will be able to observe key cardiovascular interventions including angioplasty and flow mediated dilatation. An area of increasing significance in cardiovascular research and a strength at UAB is the integration of bioinformatics into many aspects of research. We also include courses that encompass career enhancement components including preparation for research applications, public presentations, review of papers, and preparation of review articles. In addition we have included an emerging and important area in graduate education in the development of the management and personnel skills necessary to direct a research group. No overlap between this application with current training programs at this institution exist.
Cardiovascular disease is a major cause of morbidity and mortality in developed countries including the United States. This proposal is designed to provide the training for the next generation of cardiovascular researchers.
|Holdbrooks, Andrew T; Britain, Colleen M; Bellis, Susan L (2018) ST6Gal-I sialyltransferase promotes tumor necrosis factor (TNF)-mediated cancer cell survival via sialylation of the TNF receptor 1 (TNFR1) death receptor. J Biol Chem 293:1610-1622|
|Owusu, Benjamin Y; Zimmerman, Kurt A; Murphy-Ullrich, Joanne E (2018) The role of the endoplasmic reticulum protein calreticulin in mediating TGF-?-stimulated extracellular matrix production in fibrotic disease. J Cell Commun Signal 12:289-299|
|Lambert, James A; Carlisle, Matthew A; Lam, Adam et al. (2017) Mechanisms and Treatment of Halogen Inhalation-Induced Pulmonary and Systemic Injuries in Pregnant Mice. Hypertension 70:390-400|
|Willig, Amanda L; Kramer, Philip A; Chacko, Balu K et al. (2017) Monocyte bioenergetic function is associated with body composition in virologically suppressed HIV-infected women. Redox Biol 12:648-656|
|Kandasamy, Jegen; Olave, Nelida; Ballinger, Scott W et al. (2017) Vascular Endothelial Mitochondrial Function Predicts Death or Pulmonary Outcomes in Preterm Infants. Am J Respir Crit Care Med 196:1040-1049|
|Fetterman, Jessica L; Sammy, Melissa J; Ballinger, Scott W (2017) Mitochondrial toxicity of tobacco smoke and air pollution. Toxicology 391:18-33|
|Grabner, Alexander; Schramm, Karla; Silswal, Neerupma et al. (2017) FGF23/FGFR4-mediated left ventricular hypertrophy is reversible. Sci Rep 7:1993|
|Quiles, Justin M; Narasimhan, Madhusudhanan; Mosbruger, Timothy et al. (2017) Identification of transcriptome signature for myocardial reductive stress. Redox Biol 13:568-580|
|Kesterson, Robert A; Johnson, Larry W; Lambert, Laura J et al. (2016) Generation of Mitochondrial-nuclear eXchange Mice via Pronuclear Transfer. Bio Protoc 6:|
|Fetterman, Jessica L; Holbrook, Monica; Westbrook, David G et al. (2016) Mitochondrial DNA damage and vascular function in patients with diabetes mellitus and atherosclerotic cardiovascular disease. Cardiovasc Diabetol 15:53|
Showing the most recent 10 out of 89 publications