The research training objective is to provide a proper environment for the development of independent investigators in the field of alcoholism as it relates to molecular and cellular pathology. Post-doctoral fellows will work closely with a preceptor on a project related to the research of the preceptor. The trainees will interact among themselves, with other preceptors in the program, and with the research community as a whole of the Institution. Also, they can obtain formal instruction in biochemistry, biostatistics, and research methodology, and will be exposed to lectures and interaction with established investigators in the field of alcoholism. The principal areas and significance of the research training offered are: 1. Hormonal regulation of the rat class I alcohol dehydrogenase (ADH). This study identifies the cis- and trans- acting elements that mediate the effect of hormones on the ADH gene. 2. Mechanisms of liver fibrogenesis. Investigation of factors that activate stellate cells to collagen producing myofibroblast-like cell and mechanisms whereby acetaldehyde stimulates fibrogenesis. 3. Alterations in water transport across membranes. Study of effects of ethanol on aquaporin water transport proteins and water permeability across cells. 4. Effects of ethanol on hepatic regenerative growth. Studies of possible factors that may accelerate recovery from ethanol-induced liver injury. 5. Differences in dynamics of the hypothalamic-pituitary-adrenal axis as a risk factor for alcoholism. 6. Molecular and biological analysis of adenyl cyclase in alcoholism. These studies include a search for markers of predisposition towards alcoholism. 7. Regulation of growth and differentiation of intestinal epithelial cells. Study of effects of ethanol in intestinal cell differentiation and function. These areas of research will provide extensive training in different methods of biochemistry, molecular biology and cell culture. Trainees will be exposed to the application of basic research to studies of patients with alcoholism. The final objective is to instill in the trainee the ability to approach original questions of research relating to the pathogenesis of damaging effects of alcoholism on the body.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Institutional National Research Service Award (T32)
Project #
5T32AA007467-12
Application #
6298805
Study Section
Health Services Research Review Subcommittee (AA)
Program Officer
Vanderveen, Ernestine
Project Start
1987-09-30
Project End
2004-05-31
Budget Start
2000-06-01
Budget End
2001-05-31
Support Year
12
Fiscal Year
2000
Total Cost
$96,380
Indirect Cost
Name
Johns Hopkins University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
045911138
City
Baltimore
State
MD
Country
United States
Zip Code
21218
Sanchez-Alvarez, Rosa; Martinez-Outschoorn, Ubaldo E; Lin, Zhao et al. (2013) Ethanol exposure induces the cancer-associated fibroblast phenotype and lethal tumor metabolism: implications for breast cancer prevention. Cell Cycle 12:289-301
Dippold, Rachael P; Vadigepalli, Rajanikanth; Gonye, Gregory E et al. (2013) Chronic ethanol feeding alters miRNA expression dynamics during liver regeneration. Alcohol Clin Exp Res 37 Suppl 1:E59-69
Sanchez-Alvarez, Rosa; Martinez-Outschoorn, Ubaldo E; Lamb, Rebecca et al. (2013) Mitochondrial dysfunction in breast cancer cells prevents tumor growth: understanding chemoprevention with metformin. Cell Cycle 12:172-82
Dippold, Rachael P; Vadigepalli, Rajanikanth; Gonye, Gregory E et al. (2012) Chronic ethanol feeding enhances miR-21 induction during liver regeneration while inhibiting proliferation in rats. Am J Physiol Gastrointest Liver Physiol 303:G733-43
Ding, Ming; Potter, James J; Liu, Xiaopu et al. (2010) Selenium supplementation decreases hepatic fibrosis in mice after chronic carbon tetrachloride administration. Biol Trace Elem Res 133:83-97
Aram, Ghazaleh; Potter, James J; Liu, Xiaopu et al. (2009) Deficiency of nicotinamide adenine dinucleotide phosphate, reduced form oxidase enhances hepatocellular injury but attenuates fibrosis after chronic carbon tetrachloride administration. Hepatology 49:911-9
Sysa, Polina; Potter, James J; Liu, Xiaopu et al. (2009) Transforming growth factor-beta1 up-regulation of human alpha(1)(I) collagen is mediated by Sp1 and Smad2 transacting factors. DNA Cell Biol 28:425-34
Aram, Ghazaleh; Potter, James J; Liu, Xiaopu et al. (2008) Lack of inducible nitric oxide synthase leads to increased hepatic apoptosis and decreased fibrosis in mice after chronic carbon tetrachloride administration. Hepatology 47:2051-8
Wang, Lan; Tankersley, Lynda Rennie; Tang, Mei et al. (2004) Regulation of alpha 2(I) collagen expression in stellate cells by retinoic acid and retinoid X receptors through interactions with their cofactors. Arch Biochem Biophys 428:92-8
Tang, Mei; Potter, James J; Mezey, Esteban (2003) Activation of the human alpha1(I) collagen promoter by leptin is not mediated by transforming growth factor beta responsive elements. Biochem Biophys Res Commun 312:629-33

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