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.
Developed assays for assessing platelet function that utilize flow cytometry to characterize specific components of platelet reactivity. Demonstrated the prognostic implications of platelet reactivity to characterize the effects of selected condition, and treatments on platelet function. Assessing new methods to identify patients likely to exhibit consistently increased platelet reactivity.
Identified factors that influence platelet function by increasing platelet reactivity.
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. 1991;88:9959-63.
McGill JB, Schneider DJ, Arfken CL, Lucore CL, Sobel BE. Factors responsible for impaired fibrinolysis in obese subjects and NIDDM patients. Diabetes. 1994;43:104-109.
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. 2004;52:1091-9.
Schneider DJ, Hardison RM, Lopes N, Sobel BE, Brooks MM. Association between increased platelet P-selectin expression and obesity in patients with type 2 diabetes: A BARI 2D sub-study. Diabetes Care. 2009;32:944-9.
Ades PA, Savage PD, Lischke S, Toth MJ, Harvey-Berino J, Bunn JY, Ludlow M, Schneider DJ. The effect of weight loss and exercise training on flow-mediated dilatation in coronary heart disease: A randomized trial. Chest. 2011;140:1420-7.
Keating FK, Butenas S, Fung MK, Schneider DJ. Platelet-leukocyte interaction, leukocyte apoptosis and procoagulant activity in stored red blood cells. Transfusion. 2011;51:1086-95.
Ringwala SM, Dibattiste PM, Schneider DJ. Effects on platelet function of a direct acting antagonist of coagulation factor Xa. J Thromb Thrombolysis. 2012;34:291-6.
Schneider DJ, Sobel BE. PAI-1 and diabetes: A journey from the bench to the bedside. Diabetes Care. 2012;35:1961-7.
Keating FK, Schneider DJ, Savage PD, Bunn JY, Harvey-Berino J, Ludlow M, Toth MJ, Ades PA. Effect of exercise training and weight loss on platelet reactivity in overweight patients with coronary artery disease. J Cardiopulm Rehabil Prev. 2013;33:371-7.
Brummel-Ziedins KE, Lam PH, Gissel M, Gauthier E, Schneider DJ. Depletion of systemic concentrations of coagulation factors in blood from patients with atherosclerotic vascular disease. Coron Artery Dis. 2013;24:468-74.
Donaldson CW, Schneider DJ, Bertges DJ, Adams JE, Elgharib NZ, Mueller EL, Prabhu W, Ashikaga T, Dauerman HL. Increased local cytokine production at culprit superficial femoral artery plaques. J Thromb Thrombolysis. 2013;36:293-9.
Schneider DJ, Agarwal Z, Seecheran N, Keating FK, Gogo P. Pharmacodynamic effects during the transition between cangrelor and ticagrelor. JACC Cardiovasc Interv. 2014;7:435-42.
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