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Bradford C. Berk, M.D., Ph.D.
Dr. Berk's laboratory is focused on defining the mechanisms by which cells in the vascular wall respond to hemodynamic and hormonal stimuli. |
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Mark B. Taubman, M.D.
Dr. Taubman's laboratory is focused on the role of vascular smooth muscle cells (SMC) in regulating inflammation and thrombosis in the arterial wall. There are three major areas of investigation: |
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Jun-ichi Abe, M.D., Ph.D.
In the last four years, I have been interested in the mechanism of atherosclerosis and myocardial infarction, especially in the role of oxidative stress, hypoxia, and hyperglycemia. |
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Jeffrey Alexis, M.D.
The research in my lab focuses on key signaling pathways involved in the development of transplant arteriopathy. Transplant arteriopathy is the leading cause of long term morbidity and mortality following heart transplantation. |
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Burns Blaxall , Ph.D.
Our laboratory has a long-standing interest in the development, progression and regression (treatment) of heart failure, particularly as it relates to b(beta)-adrenergic receptor (b-AR) signaling. |
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Keigi Fujiwara, Ph.D.
Dr. Fujiwara's major research is on mechanosignaling by vascular endotehlial cells. Mechanical forces such as fluid flow and stretch trigger unique responses in endothelial cells, indicating that they are capable of sensing mechanical forces. |
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Zheng-Gen Jin , Ph.D.
Dr. Jin’s research has been focused on molecular regulation of vascular endothelial function. Vascular endothelial cells in blood vessels produce a number of vasodilator and vasoconstrictor substances that not only physiologically regulate vasomotor tone and vascular homeostasis, but also mediate the recruitment and activity of inflammatory cells and the propensity towards atherosclerotic lesion formation and thrombosis in the pathological condition. |
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Coeli Lopes , Ph.D.
The major focus of Dr. Lopes current work involves the regulation of the slow delayed rectifier-like current (IKs) in the heart and the pathogenesis of the Long QT (LQT1) syndrome. |
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Joseph Miano, Ph.D.
Perturbations in programs of cellular differentiation underlie numerous human ailments. Within the vasculature, for example, smooth muscle cells (SMC) exhibit phenotypic plasticity in which their normal differentiated program is subverted to one of growth, migration, and matrix secretion. |
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Jane Sottile , Ph.D.
Remodelling of extracellular matrices occurs during development, wound healing, and in a variety of pathological processes including atherosclerosis, ischemic injury, and angiogenesis. Perturbing matrix remodelling events by preventing the turnover of extracellular matrix molecules, or by increasing the levels of matrix degrading proteases or inhibitors has been shown to result in fibrosis, arthritis, reduced angiogenesis, and developmental abnormalities. |
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R. James White, M.D., Ph.D.
The overall goal of my laboratory is to understand the pathobiology which causes vascular remodeling in severe human pulmonary hypertension. Severe pulmonary hypertension (PH) occurs in idiopathic form and is also observed in diseases as diverse as chronic venous thromboembolism, scleroderma, HIV infection, and cirrhosis. |
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Chen Yan , Ph.D.
Regulation and function of cyclic nucleotide phosphodiesterases in the cardiovascular system. Second messenger cyclic nucleotides (cAMP and cGMP) regulate many signaling pathways in the cardiovascular system. |
