Understanding the cellular and molecular mechanisms of hazardous chemicals in our environment is a critical national objective. Comprehensive Environmental Response, Compensation and Liability Act of 1980 (CERCLA) was established to gain knowledge on the public health risks associated with exposure to Superfund site hazardous waste. Thus, a greater understanding of the exposure pathways and the health consequences resulting from human exposure to uncontrolled hazardous waste from Superfund and other hazardous waste sites are high priorities. The University of Californian at San Diego (UCSD) Superfund Research Program (SRP) Center's objective is to generate new perspectives on the molecular and genetic basis of the biological effects of toxicant exposure, leading to new methodologies for gauging health risks and assessing health effects;innovative detection and monitoring systems for toxicity;and novel models for bioremediation. Our findings have shown that chemical exposure leads to alterations in patterns of gene expression which are controlled and regulated by underlying signal transduction pathways. The investigators will test the hypothesis that "Alterations in biological response by Superfund site chemicals can be exploited to develop models for the detection and bioremediation of chemical toxicants". The UCSD SRP Center has developed a multidisciplinary effort consisting of six biomedical research projects, two non-biomedical research projects, two research support cores and Research Translation and Community Engagement cores. The research will be supported in part by a Ph.D. training program. The environmental problems unique to our coastal environment proximate to the populous U.S.-Mexico border create issues involving water born pollutants that are of special relevance. Through our Research Translation and Community Engagement cores, partnerships have been formed with local industry and community groups to utilize our developing technologies as applied biological tools for assessment of exposure levels and to predict health risk. Investigators with complimentary expertise from ten UCSD Departments, Organized Research Units and Centers are participating in this project, as well as two outside organizations. Our combined efforts are anticipated to provide new insights into the molecular mechanisms that lead to environmental illness, and improve our understanding of the consequences of exposure to Superfund site contaminants.
The UCSD SRP addresses each of the 4 mandates outlined in the Superfund Amendment Act. With the support of our cores, the biomedical programs are working to meet mandates 1 and 2 by developing a better understanding of the impact of toxicants on human health through the creation of models of exposure Mandates 3 and 4 are attained through the work of our non-biomedical projects, which focus on detecting the toxicity of environmental hazards and how to reduce their impact on the environment and human health.
|Wall, Christopher E; Yu, Ruth T; Atkins, Anne R et al. (2016) Nuclear receptors and AMPK: can exercise mimetics cure diabetes? J Mol Endocrinol 57:R49-58|
|Liu, Weilin; Struik, Dicky; Nies, Vera J M et al. (2016) Effective treatment of steatosis and steatohepatitis by fibroblast growth factor 1 in mouse models of nonalcoholic fatty liver disease. Proc Natl Acad Sci U S A 113:2288-93|
|Hirashima, Rika; Michimae, Hirofumi; Takemoto, Hiroaki et al. (2016) Induction of the UDP-Glucuronosyltransferase 1A1 during the Perinatal Period Can Cause Neurodevelopmental Toxicity. Mol Pharmacol 90:265-74|
|Park, Charlie C; Nguyen, Phirum; Hernandez, Carolyn et al. (2016) Magnetic Resonance Elastography vs Transient Elastography in Detection of Fibrosis and Noninvasive Measurement of Steatosis in Patients with Biopsy-proven Nonalcoholic Fatty Liver Disease. Gastroenterology :|
|Guo, Lan; Ganguly, Abantika; Sun, Lingling et al. (2016) Global Fitness Profiling Identifies Arsenic and Cadmium Tolerance Mechanisms in Fission Yeast. G3 (Bethesda) 6:3317-3333|
|Karin, Michael; Dhar, Debanjan (2016) Liver carcinogenesis: from naughty chemicals to soothing fat and the surprising role of NRF2. Carcinogenesis 37:541-6|
|Booth, D R; Ding, N; Parnell, G P et al. (2016) Cistromic and genetic evidence that the vitamin D receptor mediates susceptibility to latitude-dependent autoimmune diseases. Genes Immun 17:213-9|
|Umemura, Atsushi; He, Feng; Taniguchi, Koji et al. (2016) p62, Upregulated during Preneoplasia, Induces Hepatocellular Carcinogenesis by Maintaining Survival of Stressed HCC-Initiating Cells. Cancer Cell 29:935-48|
|Liu, Miao; Chen, Shujuan; Yueh, Mei-Fei et al. (2016) Cadmium and arsenic override NF-ÎºB developmental regulation of the intestinal UGT1A1 gene and control of hyperbilirubinemia. Biochem Pharmacol 110-111:37-46|
|Hsin, I-Fang; Montano, Erica; Seki, Ekihiro (2016) Finding a new role for NEMO: A key player in preventing hepatocyte apoptosis and liver tumorigenesis by inhibiting RIPK1. Hepatology 64:295-7|
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