Project Description:
The principle objectives of our research are elucidation of biochemical mechanisms responsible for thrombosis in the coronary arterial tree, mechanisms underlying effective coronary thrombolysis and development of novel plasminogen activators to enhance clot dissolution and mechanisms responsible for accelerated coronary artery disease associated with diabetes. The ultimate objective in each area is to define cause/consequence connections that permit identification and development of promising pharmacologic targets and agents for reduction of the toll from coronary artery disease and its sequelae.

Nordt, T.K.; Sawa, H.; Fujii, S.; & Sobel, B.E. (1995) Induction of plasminogen activator inhibitor type-1 (PAI-1) by proinsulin and insulin in vivo. Circulation 91: 764-770.

Kruszynska, Y., Yu, J.G., Sobel, B.E. and Olefsky, J.M.: Effects of troglitazone on blood concentrations of plasminogen activator inhibitor 1 in patients with type 2 diabetes mellitus and in lean and obese normal subjects. Diabetes 49:633-639, 2000.

Taatjes, D.J., Wadsworth, M.P., Schneider, D.J. and Sobel, B.E.: Improved quantitative characterization of atherosclerotic plaque composition with immunohistochemistry, confocal fluorescence microscopy and computer-assisted image analysis. Histochem. Cell Biol. 113:161-173, 2000.

Schneider, D.J., Bauman, P.Q., Holmes, M.B., Taatjes, D.T. and Sobel, B.E.: Time and dose dependent augmentation of inhibitory effects of abciximab by aspirin. Thromb. Haemost. 85:309-313, 2001.

Challenges in Acute Coronary Syndromes. Edited by David de Bono and Burton E. Sobel, Blackwell Science, London, 2001.