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Evaluation of cell proliferation, apoptosis, and dna-repair genes as potential biomarkers for ethanol-induced cns alterations

Steven D Hicks13, Lambert Lewis1, Julie Ritchie1, Patrick Burke1, Ynesse Abdul-Malak2, Nyssa Adackapara1, Kelly Canfield2, Erik Shwarts1, Karen Gentile1, Zsuzsa Szombathyne Meszaros2 and Frank A Middleton123*

Author Affiliations

1 Departments of Neuroscience & Physiology, Upstate Medical University, 750 East Adams Street, Syracuse, NY, 13210, USA

2 Department of Psychiatry, Upstate Medical University, Syracuse, NY, USA

3 Developmental Exposure Alcohol Research Center, Binghamton University, Binghamton, NY, USA

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BMC Neuroscience 2012, 13:128  doi:10.1186/1471-2202-13-128

Published: 25 October 2012

Additional files

Additional file 1:

Figure S1. Experimental overview. The rationale for the present study was based on our recently published findings [15,16] regarding the in vitro effects of ethanol on mRNA expression in mouse neural stem cells (NSCs), where changes in a considerable portion of genes involved in p53 signaling, cell cycle regulation, apoptosis and DNA damage and repair were observed and independently confirmed using real-time quantitative RT-PCR (qRT-PCR). In the present study, we first examined whether there were similar changes in peripheral blood leukocytes (PBLs) in an in vivo rat binge drinking model using microarray data. Then, based on the considerable overlap and correlated changes, we confirmed several of the rat findings and tested their validity in two sets of human samples: PBLs from subjects with alcohol use disorders, and lymphoblasts (LBs) from a normal human subject. We noted that all four of these data sources showed evidence of dysregulation of the genes of interest, although the specific genes most affected could vary across models. In addition, several of the genes showed highly significant correlations with medical, neuropsychological, neuroimaging, and demographic traits in our human subjects.

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