Ph.D. in Toxicology, Uniersity of Kansas Medical Center
B.S. in Biochemistry, University of Kansas
Clarence David Williams was born in Davenport, Iowa but grew up in Overland Park, Kansas. He received a B.S. degree in Biochemistry from the University of Kansas in 2002. After graduation, Dave worked at IBT Laboratories in Lenexa, KS primarily in the development of assays to determine the immunogenicity of new biological therapeutics. Dave entered the Ph.D. program in the Department of Pharmacology, Toxicology, and Therapeutics in 2007 and joined Hartmut Jaeschke’s laboratory. After graduating with a Ph.D. in toxicology in 2012 Dave has stayed in the Jaeschke lab and currently works on the mechanisms of acetaminophen induced liver injury and tissue repair.
Jaeschke, H., Williams C.D., McGill, M., Farhood, A. Herbal Extracts as hepatoprotecticants against acetaminophen hepatotoxicity (letter). World Journal of Gastroenterology. 16(19): 2448-50, 2010.
Williams, C.D., Farhood, A. Jaeschke H. Role of caspase-1 and interleukin-1beta in acetaminophen-induced hepatic inflammation and liver injury. Toxicology and Applied Pharmacology, 247: 169-178, 2010.
Williams, C.D., Bajt, M.L., Farhood, A. Jaeschke, H. Acetaminophen-induced hepatic neutrophil accumulation and inflammatory liver injury in CD18-deficient mice. Liver International. 30(9): 1280-1292, 2010.
Luyendyk, J.P., Flanagan, K.C., Williams, C.D., Jaeschke, H., Slusser, J.G., Mackman, N., Cantor, G.H. Tissue factor contributes to neutrophil CD11b expression in alpha-naphthylisothiocyanate-treated mice. Toxicology and Applied Pharmacology, 250(3): 256-262, 2011.
Williams, C.D., Jaeschke, H.: Liver toxicology. In: Nriagu JO (ed.) Encyclopedia of Environmental Health, volume 3, pp. 509-514, Burlington: Elsevier, 2011.
Jaeschke, H., Williams, C.D., Farhood, A. No evidence for caspase-dependent apoptosis in acetaminophen hepatotoxicity (letter). Hepatology, 52(2): 718-719, 2011.
Jaeschke, H., McGill, M.R., Williams, C.D., Ramachandran, A. Acetaminophen Hepatotoxicity- A clinically relevant model to test the efficacy of natural products. Life Sciences, 88(17-18): 737-745, 2011.
Williams, C.D., Antoine, D.J., Shaw, P.J., Benson, C., Farhood, A., Williams, D.P., Kanneganti, T.D., Park, B.K., Jaeschke, H. Role of the Nalp3 inflammasome in acetaminophen-induced sterile inflammation and liver injury. Toxicology and Applied Pharmacology, 252: 289-297, 2011.
Williams, C.D., Koerner, M.R., Lampe, J.N., Farhood, A., Jaeschke, H.: Mouse strain-dependent caspase activation during acetaminophen hepatotoxicity does not result in apoptosis or modulation of inflammation. Toxicology and Applied Pharmacology, 257: 449-458, 2011.
Jaeschke, H., Williams, C.D.: Cyclophilin A Is a Damage-Associated Molecular Pattern Molecule That Mediates Acetaminophen-Induced Liver Injury (Letter). Journal of Immunology, 187: 6168, 2011.
Jaeschke, H., Williams, C.D., Ramachandran, A., Bajt, M.L.: Acetaminophen hepatotoxicity and repair- role of sterile inflammation and innate immunity. Liver International, 32(1): 8-20, 2012.
McGill, M.R., Sharpe, M.R., Williams, C.D., Taha, M., Curry, S.C., and Jaeschke, H.: Mechanisms of acetaminophen hepatotoxicity in humans and mice involve mitochondrial damage and nuclear DNA fragmentation. Journal of Clinical Investigation, 122(4): 1574-1583, 2012.
Jaeschke, H., McGill, M.R., Williams, C.D.: The pathophysiological relevance of neutrophils in acetaminophen hepatotoxicity (Letter). Hepatology, doi:10.1002/hep.25877.
Williams, C.D., Jaeschke H.: Role of innate and adaptive immunity during drug-induced liver injury. Toxicology Research, doi:10.1039/c2tx20032e.
*McGill, M.R., *Williams, C.D., Xie, Y., Ramachandran, A., Jaeschke, H.: Comparison of rats and mice for the study of acetaminophen-induced liver injury: protein binding, mitochondrial dysfunction, and oxidative stress in the mechanisms of toxicity. Toxicology and Applied Pharmacology, doi:10.1016/j.taap.2012.08.015. (*co-first author)
*Xie, Y., *Williams, C.D., McGill, M.R., Lebofsky, M., Ramachandran, A., Jaeschke, H.: Purinergic receptor antagonist A438079 protects against acetaminophen-induced liver injury by inhibiting mitochondrial protein adduct formation not inflammasome activation. Toxicological Sciences, doi:10.1093/toxsci/kfs283. (*co-first author)
Jaeschke, H., Williams, C.D., McGill, M.R.: Caveats of using acetaminophen hepatotoxicity models for natural product testing. Toxicology Letters. doi:10.1016/j.toxlet.2012.09.023.
Dave Williams, PhD
4018 HLSIC; MS-1018
3901 Rainbow Blvd.
Kansas City, Kansas 66160
F: (913) 588-7501