The toxicology training program emphasizes two facets of environmental toxicology. One is to impart to students the status to toxicologic problems that are caused by chemicals in our environment, and the methods that are used to evaluate these problems. This aspect of training involves didactic material and contact with toxicologists who are engaged in this type of evaluation. Such general problems as evaluation of risk for chemicals in food and water, and development of tests for setting standards, will be covered throughout the training In depth training will be achieved through the advanced toxicology course and in the industrial technology techniques course taught in conjunction with the toxicologists at Bayer Chemical Company. The second aspect of environmental toxicology emphasized in the training program is to learn the general research approaches that are used to answer environmental questions that require the application of scientific research. The focus in toxicology by the faculty is on the biological and molecular mechanisms involved in the response of the organism to environmental chemicals (ie., heavy metals, pesticides, dioxin, and carcinogens) as well as the effect of the organism on the chemical (absorption, distribution, biotransformation and excretion). This training program is primarily targeted at the predoctoral and postdoctoral level, but a short-term training for students in health professions (medical students) is also included.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Institutional National Research Service Award (T32)
Project #
5T32ES007079-24
Application #
6498238
Study Section
Environmental Health Sciences Review Committee (EHS)
Program Officer
Shreffler, Carol K
Project Start
1979-07-01
Project End
2004-06-30
Budget Start
2002-07-01
Budget End
2003-06-30
Support Year
24
Fiscal Year
2002
Total Cost
$246,728
Indirect Cost
Name
University of Kansas
Department
Pharmacology
Type
Schools of Medicine
DUNS #
016060860
City
Kansas City
State
KS
Country
United States
Zip Code
66160
Woolbright, Benjamin L; Jaeschke, Hartmut (2018) Alcoholic Hepatitis: Lost in Translation. J Clin Transl Hepatol 6:89-96
Boxberger, Kelli H; Hagenbuch, Bruno; Lampe, Jed N (2018) Ligand-dependent modulation of hOCT1 transport reveals discrete ligand binding sites within the substrate translocation channel. Biochem Pharmacol 156:371-384
Borude, Prachi; Bhushan, Bharat; Apte, Udayan (2018) DNA Damage Response Regulates Initiation of Liver Regeneration Following Acetaminophen Overdose. Gene Expr 18:115-123
Li, Jibiao; Woolbright, Benjamin L; Zhao, Wen et al. (2018) Sortilin 1 Loss-of-Function Protects Against Cholestatic Liver Injury by Attenuating Hepatic Bile Acid Accumulation in Bile Duct Ligated Mice. Toxicol Sci 161:34-47
Zou, An; Magee, Nancy; Deng, Fengyan et al. (2018) Hepatocyte nuclear receptor SHP suppresses inflammation and fibrosis in a mouse model of nonalcoholic steatohepatitis. J Biol Chem 293:8656-8671
Huck, Ian; Beggs, Kevin; Apte, Udayan (2018) Paradoxical Protective Effect of Perfluorooctanesulfonic Acid Against High-Fat Diet-Induced Hepatic Steatosis in Mice. Int J Toxicol 37:383-392
McCracken, Jennifer M; Chalise, Prabhakar; Briley, Shawn M et al. (2017) C57BL/6 Substrains Exhibit Different Responses to Acute Carbon Tetrachloride Exposure: Implications for Work Involving Transgenic Mice. Gene Expr 17:187-205
McGreal, Steven R; Rumi, Karim; Soares, Michael J et al. (2017) Disruption of Estrogen Receptor Alpha in Rats Results in Faster Initiation of Compensatory Regeneration Despite Higher Liver Injury After Carbon Tetrachloride Treatment. Int J Toxicol 36:199-206
Bhushan, Bharat; Poudel, Samikshya; Manley Jr, Michael W et al. (2017) Inhibition of Glycogen Synthase Kinase 3 Accelerated Liver Regeneration after Acetaminophen-Induced Hepatotoxicity in Mice. Am J Pathol 187:543-552
Woolbright, Benjamin L; Williams, C David; Ni, Hongmin et al. (2017) Microcystin-LR induced liver injury in mice and in primary human hepatocytes is caused by oncotic necrosis. Toxicon 125:99-109

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