This pre- and post-doctoral training program, now in its 25th year, will provide the scientific background and methodologic experience that will enable successful trainees to pursue investigative careers in biochemistry, molecular genetics and other areas of experimental pathology. The emphasis of the program will be in the areas of atherosclerosis, angiogenesis, and thrombosis research. This program will provide intensive research opportunities employing basic techniques in molecular/structural biology, cell culture, protein and lipid biochemistry, enzymology and molecular pharmacology. Specific areas under active investigation by the 13 program faculty include the study of: macrophage function; angiogenesis; fibrinolysis; lipoprotein receptor structure and function; mechanisms of platelet adhesion; nitric oxide biology; cellular transformation by viruses; relationship of nerve growth factors and neurotrophins to vascular cell proliferation and differentiation; the role of smooth muscle proteins in developmental aspects of the vasculature and in hypertrophic cardiomyopathies. There is a close working relationship that exists between the 5 basic science departments and the Department of Medicine at Cornell with our 3 NIH Program Project Grants on Vascular Cell Signaling, Atherosclerosis, and Angiogenesis. The close proximity of the vascular biology program faculty to each other in the Center of Vascular Biology will indeed contribute to a fertile research environment which emphasizes the application of basic research to problems in human arterial disease. Five postdoctoral research trainees (M.D., M.D./Ph.D., or Ph.D.) will be expected to attend and participate in a series of didactic courses such as ethics, statistics, and scientific writing, weekly research seminars, journal clubs, and research-in-progress sessions. Three pre-doctoral fellows admitted to our Cornell University Graduate Program will take graduate courses according to program requirements, participate in seminars and journal clubs, undertake 3 laboratory rotations, and will train in laboratories which emphasize either a biochemical, cellular, molecular or structural biology approach to vascular diseases. They are also expected to take courses in ethics, scientific writing and statistics. Since the Weill Cornell Medical College is located on a large campus in Manhattan that includes the Graduate School of Medical Sciences of Cornell University, The New York Presbyterian Hospital, Rockefeller University and Memorial Sloan-Kettering Cancer Center, our pre-and post-doctoral trainees will be in an intellectually-rich environment to pursue rigorous graduate and post-graduate studies in cardiovascular biology.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
5T32HL007423-29
Application #
7460738
Study Section
Special Emphasis Panel (ZHL1-CSR-G (F1))
Program Officer
Commarato, Michael
Project Start
1979-07-01
Project End
2010-06-30
Budget Start
2008-07-01
Budget End
2009-06-30
Support Year
29
Fiscal Year
2008
Total Cost
$340,715
Indirect Cost
Name
Weill Medical College of Cornell University
Department
Pathology
Type
Schools of Medicine
DUNS #
060217502
City
New York
State
NY
Country
United States
Zip Code
10065
Israely, Edo; Ginsberg, Michael; Nolan, Daniel et al. (2014) Akt suppression of TGF? signaling contributes to the maintenance of vascular identity in embryonic stem cell-derived endothelial cells. Stem Cells 32:177-90
Dassah, Maryann; Almeida, Dena; Hahn, Rebecca et al. (2014) Annexin A2 mediates secretion of collagen VI, pulmonary elasticity and apoptosis of bronchial epithelial cells. J Cell Sci 127:828-44
Higgins, Christina E; Gross, Steven S (2011) The N-terminal peptide of mammalian GTP cyclohydrolase I is an autoinhibitory control element and contributes to binding the allosteric regulatory protein GFRP. J Biol Chem 286:11919-28
Moussai, Dariush; Mitsui, Hiroshi; Pettersen, Julia S et al. (2011) The human cutaneous squamous cell carcinoma microenvironment is characterized by increased lymphatic density and enhanced expression of macrophage-derived VEGF-C. J Invest Dermatol 131:229-36
Pettersen, Julia S; Fuentes-Duculan, Judilyn; Suarez-Farinas, Mayte et al. (2011) Tumor-associated macrophages in the cutaneous SCC microenvironment are heterogeneously activated. J Invest Dermatol 131:1322-30
Morrey, Christopher; Brazin, Jacqueline; Seyedi, Nahid et al. (2010) Interaction between sensory C-fibers and cardiac mast cells in ischemia/reperfusion: activation of a local renin-angiotensin system culminating in severe arrhythmic dysfunction. J Pharmacol Exp Ther 335:76-84
Lamon, Brian D; Upmacis, Rita K; Deeb, Ruba S et al. (2010) Inducible nitric oxide synthase gene deletion exaggerates MAPK-mediated cyclooxygenase-2 induction by inflammatory stimuli. Am J Physiol Heart Circ Physiol 299:H613-23
Deeb, Ruba S; Cheung, Cynthia; Nuriel, Tal et al. (2010) Physical evidence for substrate binding in preventing cyclooxygenase inactivation under nitrative stress. J Am Chem Soc 132:3914-22
Jacovina, Andrew T; Deora, Arunkumar B; Ling, Qi et al. (2009) Homocysteine inhibits neoangiogenesis in mice through blockade of annexin A2-dependent fibrinolysis. J Clin Invest 119:3384-94
Lamon, Brian D; Summers, Barbara D; Gotto Jr, Antonio M et al. (2009) Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells. Eur J Pharmacol 606:72-6

Showing the most recent 10 out of 39 publications