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Kevin Baker

Kevin BakerCooperating Doctoral Program: Pharmacology and Toxicology

EITS Track: Biomedical Toxicology

Education: B.S. Microbiology, B.S. Genomics and Molecular Genetics, Japanese, Michigan State University

Research Interests:
The liver is an extraordinary organ in that it is capable several feats such as regeneration and detoxification. Yet, the liver also synthesizes several components of the coagulation cascade, which ultimately forms blood clots. This implies that small changes in the liver can have tremendous consequences on one’s ability to clot blood. I am interested in this intersection of liver disease and blood coagulation; how do changes in the liver during a diseased state influence our ability to form clots? One disease of interest is cholestatic liver disease (cholestasis), which is a blockage of the bile duct. In normal physiology, the bile duct passes bile from the liver to the intestines to aid in digestion. During cholestasis, this flow is blocked, which causes the buildup of bile in the liver. In the liver, a component of the coagulation cascade called tissue factor (TF) can exist in an inactive state that lacks the ability to form clots. TF is the primary activator for coagulation; if TF is activated, a blood clot will form. Interestingly, inactive TF is present on liver parenchymal cells (i.e. hepatocytes), and this TF is activated during cholestasis. However, the mechanisms whereby which tissue factor becomes activated during cholestasis remains poorly understood.  My tentative dissertation is to determine the mechanisms whereby the coagulation cascade is activated and the functional consequence of intrahepatic coagulation in acute obstructive cholestasis.

Major Professor: James Luyendyk, Pathobiology and Diagnostic Investigation