The Center for Alcohol Studies (CAS) training program at the University of North Carolina at Chapel Hill is designed to promote the development of promising pre- and post-doctoral research fellows as independent investigators and future University faculty members who will investigate the pathogenesis of alcoholism and alcohol abuse using modern molecular medicine techniques. Training of the postdoctoral fellows will be individualized with the most important component being the research conducted by the trainee in the faculty mentor's laboratory. Particular emphasis will be on modern molecular biological and biochemical techniques. Additional training will include didactic courses, seminars and conferences, and activities on responsible conduct of research. The training faculty will consist of 13 funded investigators from 10 basic science and clinical departments and centers at the University of North Carolina at Chapel Hill. The faculty has a documented history of close interactions. The trainees will benefit from the unique strengths of alcohol research at the University of North Carolina, which include the CAS, center for Gastrointestinal Biology and Diseases (CGIBD), with its research cores, UNC-Neuroscience Center, a research-oriented Mental Health Research Center with its research cores in Psychiatry, a Gene Therapy Center and the Program in Molecular Biology and Biotechnology. The training program will be directed by Dr. Fulton T. Crews with the assistance of three senior alcohol researchers, Drs. David Brenner, George Breese and Leslie Morrow, who will constitute the Training Program Advisory Committee. The program proposes to recruit three post-doctoral fellows and one pre-doctoral fellow. The trainees will receive two and usually more years of research training with external support sought for later years. This institutional training grant will promote intensive training in molecular techniques and basic pathophysiology in a stimulating environment leading to broadly trained independent investigators capable of adapting to the rapid advances in research in the 21st century.

National Institute of Health (NIH)
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Institutional National Research Service Award (T32)
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Special Emphasis Panel (ZAA1-HH (10))
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Grandison, Lindsey
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University of North Carolina Chapel Hill
Schools of Medicine
Chapel Hill
United States
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Cook, Jason B; Dumitru, Ana Maria G; O'Buckley, Todd K et al. (2014) Ethanol administration produces divergent changes in GABAergic neuroactive steroid immunohistochemistry in the rat brain. Alcohol Clin Exp Res 38:90-9
Cook, Jason B; Werner, David F; Maldonado-Devincci, Antoniette M et al. (2014) Overexpression of the steroidogenic enzyme cytochrome P450 side chain cleavage in the ventral tegmental area increases 3?,5?-THP and reduces long-term operant ethanol self-administration. J Neurosci 34:5824-34
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Broadwater, Margaret A; Liu, Wen; Crews, Fulton T et al. (2014) Persistent loss of hippocampal neurogenesis and increased cell death following adolescent, but not adult, chronic ethanol exposure. Dev Neurosci 36:297-305
Qin, Liya; Crews, Fulton T (2014) Focal thalamic degeneration from ethanol and thiamine deficiency is associated with neuroimmune gene induction, microglial activation, and lack of monocarboxylic acid transporters. Alcohol Clin Exp Res 38:657-71
Fish, Eric W; Agoglia, Abigail E; Krouse, Michael C et al. (2014) Levetiracetam results in increased and decreased alcohol drinking with different access procedures in C57BL/6J mice. Behav Pharmacol 25:61-70
Fanelli, Rebecca R; Klein, Jeffrey T; Reese, Rebecca M et al. (2013) Dorsomedial and dorsolateral striatum exhibit distinct phasic neuronal activity during alcohol self-administration in rats. Eur J Neurosci 38:2637-48
Gizer, Ian R; Gilder, David A; Lau, Philip et al. (2013) Contributions of ethnicity to differential item functioning of cannabis abuse and dependence symptoms. J Stud Alcohol Drugs 74:320-8
Vetreno, Ryan P; Qin, Liya; Crews, Fulton T (2013) Increased receptor for advanced glycation end product expression in the human alcoholic prefrontal cortex is linked to adolescent drinking. Neurobiol Dis 59:52-62

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