David J. Schneider, MD, FACC, FAHA

Education:

Training:

Residency

Fellowship

Specialty:

Certifications:

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Biography:

Dr. Schneider is the Director of the Cardiology and the Vascular Biology Units in the Department of Medicine at the University of Vermont. He has won awards as both a student and a physician/scientist and has been named teacher of the year three times. He is very active in national and international professional societies and is a member of the editorial boards of Coronary Artery Disease and the American Journal of Cardiology.  Dr. Schneider is an active researcher and holds a patent for determining platelet reactivity in a whole blood sample. His research is focused on causal connections between diabetes and heart disease, and the role of platelets in the development and progression of atherosclerosis. Dr. Schneider has published more than 100 manuscripts, authored numerous chapters and edited a book entitled Diabetes and Heart Disease.

Major Research Interests:

Delineated mechanisms responsible for altered fibrinolysis in the blood of patients with diabetes.  Demonstrated that the combination of hyperinsulinemia, hyperglycemia and increased concentrations of free fatty acids in blood of healthy subjects increases the concentration and activity of the primary inhibitor of fibrinolysis, plasminogen activator inhibitor type 1 (PAI-1).  With studies in vitro that demonstrated increased concentrations in blood of insulin increase expression of PAI-1 through stabilization of mRNA.  In addition demonstrated that free fatty acids increase expression of PAI-1 by increasing transcription of PAI-1 through a fatty acid response region in the 5’ untranslated region of the PAI-1 gene.

Participated in the development of a semi-quantitative method to assess plaque morphology in mice.  This model has been implemented to determine the role of genetic modifications such as increased vascular smooth muscle expression of PAI-1 in the genesis of atherosclerotic lesions.  Demonstrated that increased vascular smooth muscle cell (VSMC) expression of PAI-1 limits VSMC migration and promotes formation of vulnerable atherosclerotic plaques thus decreasing neointimal VSMC content.

Developed and implemented a sensitive and specific assessment of platelet function that utilizes flow cytometry to characterize specific components of platelet reactivity.  Utilized this method to demonstrate the prognostic implications of platelet reactivity and to characterize the effects of selected condition, and treatments on platelet function.

Major Recent Grant Support

NIH: (U01 HL61744) “BARI 2D” - 1/01-12/07 Kathryn Detre, Principal Investigator, Schneider, Co-Investigator

NIH: (R01 HL69146) "Mechanisms of Pro-Thrombosis in Diabetes Mellitus" - 7/01/01-12/31/05

Centocor: "Platelet Function, GP IIIa Polymorphism, and PCI in BARI 2D An Ancillary Study to BARI 2D" - 1/02 - 12/07 Schneider, Principal Investigator

Publications:

Representative Publications from a total of 108

Schneider DJ, Sobel BE:  Augmentation of synthesis of plasminogen activator inhibitor type-1 by insulin and insulin-like growth factor type-I:  Implications for vascular disease in hyperinsulinemic states.  Proc. Natl. Acad. Sci. USA 88:9959-9963, 1991.

McGill JB, Schneider DJ, Arfken CL, Lucore CL, Sobel BE:  Factors responsible for impaired fibrinolysis in obese subjects and NIDDM patients.  Diabetes 43:104-109, 1994.

Calles-Escandon J, Mirza S, Sobel BE, Schneider DJ:  Induction of hyperinsulinemia combined with hyperglycemia and hypertriglyceridemia increases plasminogen activator inhibitor type-1 (PAI-1) in blood in normal human subjects.  Diabetes 47:290-293, 1998.

Holmes MB, Schneider DJ, Hayes M,  Sobel BE, Mann KG: A novel bedside, tissue factor-dependent clotting assay permitting improved assessment of both antithrombotic and antiplatelet therapy.  Circulation 102:2051-2057, 2000.

Chen Y, Billadello JJ, Schneider DJ:  Identification and localization of a fatty acid response region in human plasminogen activator inhibitor-1 gene.  Arterioscler. Thromb. Vasc. Biol. 20:2696-2701, 2000.

Schneider DJ, Baumann PQ, Holmes MB, Taatjes DJ, Sobel BE: Time and dose dependent augmentation of inhibitory effects of abciximab by aspirin.  Thromb. Haemost. 85:309-313, 2001.

Chen Y, Kelm RJ, Budd RC, Sobel BE, Schneider DJ: Inhibition of apoptosis and caspase-3 in vascular smooth muscle cells by plasminogen activator inhibitor type-1. J. Cell Biochem.  92:178-188, 2004.

Schneider DJ, Hayes M, Taatjes H, Wadsworth M, Rincon M, Taatjes DJ, Sobel BE: Attenuation of neointimal vascular smooth muscle cellularity in atheroma by plasminogen activator inhibitor type-1 (PAI-1). J. Histochem. Cytochem. 52:1091-1099, 2004.

Keating FK, Dauerman HL, Whitaker DA, Sobel BE, Schneider DJ: Increased expression of platelet P-selectin and formation of platelet-leukocyte aggregates in blood from patients treated with unfractionated heparin plus eptifibatide compared with bivalirudin. Thromb. Res. 118:361-369, 2006.

Schneider DJ, Keating F, Sobel BE:  Greater inhibitory effects of bivalirudin compared with unfractionated heparin plus eptifibitide on thrombin-induced platelet activation.  Coron. Artery Dis. 17:471-476, 2006.