Alcohol RSS feed: Articles in Press. Alcohol is an international, peer-reviewed journal that is devoted to publishing multi-disciplinary biomedical research on all aspects of the actions or effects of alcohol on the nervous system or on other organ systems. Emphasis is given to studies into the causes and consequences of alcohol abuse and alcoholism, and biomedical aspects of diagnosis, etiology, treatment or prevention of alcohol-related health effects. Intended for both research scientists and practicing clinicians, the journal publishes original research on the neurobiological, neurobehavioral, and pathophysiological processes associated with alcohol drinking, alcohol abuse, alcohol-seeking behavior, tolerance, dependence, withdrawal, protracted abstinence, and relapse. In addition, the journal reports studies on the effects alcohol on brain mechanisms of neuroplasticity over the life span, biological factors associated with adolescent alcohol abuse, pharmacotherapeutic strategies in the treatment of alcoholism, biological and biochemical markers of alcohol abuse and alcoholism, pathological effects of uncontrolled drinking, biomedical and molecular factors in the effects on liver, immune system, and other organ systems, and biomedical aspects of fetal alcohol spectrum disorder including mechanisms of damage, diagnosis and early detection, treatment, and prevention. Articles are published from all levels of biomedical inquiry, including the following: molecular and cellular studies of alcohol's actions in vitro and in vivo ; animal model studies of genetic, pharmacological, behavioral, developmental or pathophysiological aspects of alcohol; human studies of genetic, behavioral, cognitive, neuroimaging, or pathological aspects of alcohol drinking; clinical studies of diagnosis (including dual diagnosis), treatment, prevention, and epidemiology. The journal will publish 9 issues per year; the accepted abbreviation for Alcohol for bibliographic citation is Alcohol . Alcohol subscribes to the tenets of The Farmington Consensus (see http://www.elsevier.com/framework_products/promis_misc/525453fc.pdf or http://www1.elsevier.com/homepage/sab/alcohol/fconsensus.htm ). Submission of a paper to the journal will be taken as evidence that the authors have complied with the tenets set forth in the Consensus. All submitted material will be subject to peer review. Alcohol considers three types of manuscripts for publication: - Original research articles are full-length reports of the authors' original research addressing topics consistent with the Aims and Scope of the journal. Submissions outside the scope of the journal, or incomplete or fragmentary submissions, will not be considered. - Rapid communications are original, high-quality manuscripts that describe new data of high impact and major importance to the field. These contributions are typically short (e.g., 4 journal pages), and will be peer-reviewed by at least one expert in the field of the research and an Editor, and will be either accepted with minimal or no revisions or rejected. Publication of accepted rapid communications will be expedited. - Invited review articles will be considered for publication, upon invitation from the Editor-in-Chief, as full-length papers or mini-reviews. These contributions will be peer-reviewed. Contact the Editor-in-Chief concerning the suitability of a topic for an invited review. There are no page charges for articles published in Alcohol , and the current practice is to provide the corresponding author with 50 free reprints of his/her article. Effective May 2006, authors from all countries are invited to submit manuscripts, complete in all respects and following the Instructions to Authors (revised May 2006), to Charles R. Goodlett, Editor-in-Chief, via Elsevier electronic submission at http://ees.elsevier.com/alcohol Contact for questions: Charles R. Goodlett Editor-in-Chief, Alcohol Department of Psychology IUPUI 402 North Blackford Street Indianapolis, IN 46202-3275 Tel: +1-317 274-6772 Fax: +1-317 278-7181 E-mail: alcojrnl@iupui.edu http://www.alcoholjournal.org//inpress?rss=yesElsevier Inc.en © 2011 Elsevier Inc. All rights reserved. Alcohol0741-83292011-10-24 © 2011 Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.alcoholjournal.org/article/PIIS0741832911004356/abstract?rss=yesAbstract: Ethyl glucuronide (EtG) is a minor ethanol metabolite that confirms the absorption and metabolism of ethanol after oral or dermal exposure. Human data suggest that maximum blood EtG (BEtG) concentrations are reached between 3.5 and 5.5h after ethanol administration. This study was undertaken to determine if the Sprague–Dawley (SD) rat biotransforms ethanol to EtG after a single high oral dose of ethanol. SD rats (male, n=6) were gavaged with a single ethanol dose (4g/kg), and urine was collected for 3h in metabolic cages, followed by euthanization and collection of heart blood. Blood and urine were analyzed for ethanol and EtG by gas chromatography and enzyme immunoassay. Blood and urine ethanol concentrations were 195±23 and 218±19mg/dL, whereas BEtG and urine EtG (UEtG) concentrations were 1,363±98ng equivalents/mL and 210±0.29mg equivalents/dL .Sixty-six male SD rats were gavaged ethanol (4g/kg) and placed in metabolic cages to determine the extent and duration of ethanol to EtG biotransformation and urinary excretion. Blood and urine were collected up to 24h after administration for ethanol and EtG analysis. Maximum blood ethanol, urine ethanol, and UEtG were reached within 4h, whereas maximum BEtG was reached 6h after administration. Maximum concentrations were blood ethanol, 213±20mg/dL; urine ethanol, 308±34mg/dL; BEtG, 2,683±145ng equivalents/mL; UEtG, 1.2±0.06mg equivalents/mL . Areas under the concentration–time curve were blood ethanol, 1,578h∗mg/dL; urine ethanol, 3,096h∗mg/dL; BEtG, 18,284h∗ng equivalents/mL; and UEtG, 850h∗mg equivalents/dL. Blood ethanol and BEtG levels were reduced to below limits of detection (LODs) within 12 and 18h after ethanol administration. Urine ethanols were below LOD at 18h, but UEtG was still detectable at 24h after administration. Our data prove that the SD rat biotransforms ethanol to EtG and excretes both in the urine and suggest that it is similar to that of the human.Biotransformation of ethanol to ethyl glucuronide in a rat model after a single high oral dosage - Corrected ProofTrista H. Wright, Kenneth E. Ferslew10.1016/j.alcohol.2011.07.006Alcohol (2011)2011-10-24Alcohol2011-10-24http://www.alcoholjournal.org/article/PIIS0741832911004459/abstract?rss=yesAbstract: The Combined Pharmacotherapies and Behavioral Interventions (COMBINE) Study sought to answer questions about the benefits of combining behavioral and pharmacological interventions (naltrexone and acamprosate) in alcohol-dependent patients. Our goals were to identify trajectories of heavy drinking before randomization in COMBINE, to characterize patients in these trajectories, and to assess whether prerandomization trajectories predict drinking outcomes. We analyzed daily indicators of heavy drinking 90 days before randomization using a trajectory-based approach. Each patient was assigned to the most likely prerandomization heavy-drinking trajectory, and the baseline characteristics of participants in the baseline trajectories were compared. The main and interactive effects of these trajectories and treatment factors (acamprosate, naltrexone, or combined behavioral intervention) on summary drinking measures during active treatment (16 weeks) were assessed. We identified five trajectories of heavy drinking prerandomization: “T1: frequent heavy drinkers”; “T2: very frequent heavy drinkers”; “T3: nearly daily heavy drinkers”; “T4: daily heavy drinkers”; and “T5: daily heavy drinkers stopping early” before randomization. Trajectory membership was significantly associated with all drinking outcomes. Patients in “T5: daily heavy drinkers stopping early” had comparable drinking outcomes to those in “T1: frequent heavy drinkers,” whereas the remaining trajectories were associated with significantly worse outcomes. The baseline trajectory did not interact significantly with the treatment condition. These exploratory analyses confirmed the hypothesis that baseline trajectories predict postrandomization drinking outcomes. Interestingly, “T5: daily heavy drinkers stopping early” had outcomes that were comparable to the least severe baseline trajectory “T1: frequent heavy drinkers,” and baseline trajectories of heavy drinking did not moderate the treatment effects.Baseline trajectories of heavy drinking and their effects on postrandomization drinking in the COMBINE Study: empirically derived predictors of drinking outcomes during treatment - Corrected ProofRalitza Gueorguieva, Ran Wu, Dennis Donovan, Bruce James Rounsaville, David Couper, John Harrison Krystal, Stephanie Samples O’Malley10.1016/j.alcohol.2011.08.008Alcohol (2011)2011-09-19Alcohol2011-09-19http://www.alcoholjournal.org/article/PIIS0741832911004423/abstract?rss=yesAbstract: The 15th annual meeting of the Alcohol and Immunology Research Interest Group was held on November 19, 2010, at Loyola University Medical Center in Maywood, IL. This year, the focus of the meeting was on alcohol’s effect on the immune system in both clinical and experimental systems. The event consisted of three sessions, which featured plenary talks from invited speakers along with oral presentations from selected abstracts, in addition to a poster session. Participants presented a variety of information on ethanol-induced effects on infection susceptibility and resolution, oxidative stress, and organ inflammation. Specifically, speakers presented new insights on the mechanism of alcohol-mediated deleterious effects in the lung, liver, skin, and neuroendocrine system, as well as on immune cells in both in vivo and in vitro systems. Additional oral presentations suggested possible mechanisms of how alcohol-induced reactive oxygen species promote immune dysregulation both locally and systemically.Alcohol and inflammation and infection: clinical and experimental systems—summary of the 2010 Alcohol and Immunology Research Interest Group Meeting - Corrected ProofAnita Zahs, Robert T. Cook, Thomas J. Waldschimdt, Mashkoor A. Choudhry, Elizabeth J. Kovacs, Melanie D. Bird10.1016/j.alcohol.2011.07.009Alcohol (2011)2011-09-15Alcohol2011-09-15http://www.alcoholjournal.org/article/PIIS0741832911004381/abstract?rss=yesAbstract: Because of numerous limitations for liver biopsy, a noninvasive marker of liver cirrhosis is sought. Promising indicators seem to be matrix metalloproteinases (MMPs) that are responsible for degradation of extracellular matrix. The aim of the study was to evaluate the gelatinase activities (MMP-2 and MMP-9) in patients with different stages of alcoholic cirrhosis. Sixty-seven outpatients who presented various stages of alcoholic cirrhosis according to Child–Turcotte–Pugh criteria and 26 healthy control subjects were enrolled. Blood samples were collected for MMP-2 and MMP-9 activities. A significant decrease of serum MMP-2 activity was noted in stages B and C of cirrhosis in comparison with control. Serum MMP-9 activity did not depend on the stage of cirrhosis. The MMP-2 levels, but not those of MMP-9, may be of value in understanding the pathogenesis and progression of alcoholic cirrhosis.The decrease of serum MMP-2 activity corresponds to alcoholic cirrhosis stage - Corrected ProofAgnieszka Madro, Grazyna Czechowska, Maria Slomka, Krzysztof Celinski, Stanislawa Szymonik-Lesiuk, Jacek Kurzepa10.1016/j.alcohol.2011.07.008Alcohol (2011)2011-09-12Alcohol2011-09-12http://www.alcoholjournal.org/article/PIIS0741832911004435/abstract?rss=yesAbstract: The aim of the present study was to examine the association between alcohol, alcohol and tobacco, and mortality in a large adult population in the city of Mumbai. A total of 35,102 men aged 45 years and older were surveyed about their alcohol drinking as part of a cohort study. These respondents were followed up over time, and all deaths were recorded. Compared with those who never drank alcohol, alcohol drinkers had 1.22 times higher risk of mortality, with the highest risk observed for liver disease (hazard ratio [HR]=3.19). Among ever drinkers, risk of mortality varied according to types (country/desi), frequency (four or less times a week, HR=1.39), and quantity of alcohol consumed (>100mL) per day. In addition, country/desi drinkers (HR=1.34) had the highest mortality risk compared with all other types of alcohol (HR=0.97). Alcohol drinkers had increased risk of mortality for tuberculosis (HR=2.53), cerebrovascular disease (HR=1.83), and liver disease (HR=3.19). Synergistic joint effect of tobacco and alcohol on mortality was also observed, with lowest risk in never tobacco user drinkers (HR=1.02) and highest in mixed tobacco user drinkers (HR=1.79). The results of this study show a direct association between greater consumption of alcohol and increased risk of mortality from alcohol-specific causes. In addition to individual effect, this study demonstrates the synergistic interaction between alcohol and tobacco use in various forms on mortality.Association of alcohol, alcohol and tobacco with mortality: findings from a prospective cohort study in Mumbai (Bombay), India - Corrected ProofMangesh S. Pednekar, Genevieve Sansone, Prakash C. Gupta10.1016/j.alcohol.2011.08.006Alcohol (2011)2011-09-12Alcohol2011-09-12http://www.alcoholjournal.org/article/PIIS0741832911004447/abstract?rss=yesAbstract: Distraction osteogenesis (DO) is an orthopedic protocol, which induces direct new bone formation as a result of the stimulating effects of mechanical distraction. Chronic ethanol exposure has been demonstrated to inhibit bone formation in rodent models of DO. Further, it has been demonstrated that (1) tumor necrosis factor-α (TNF) blockers are protective against ethanol exposure and (2) recombinant mouse TNF (rmTNF) inhibits direct bone formation in ethanol naïve mice through TNF receptor 1 (TNFR1). These results suggest that the inhibitory effects are significantly mediated by TNF signaling. Therefore, we hypothesized that direct new bone formation in TNFR1 knockout (KO) mice would be protected from ethanol exposure. We used a unique model of mouse DO combined with liquid/chow diets to compare the effects of ethanol on both a strain of TNFR1 knockout (TNFR1 KO) mice and on mice of their C57BL/6 (B6) control strain. In the B6 study, and in concordance with previous work, both radiological and histological analyses of direct bone formation in the distraction gaps demonstrated significant osteoinhibition due to ethanol compared with chow- or pair-fed mice. In the TNFR1 KO study and in support of the hypothesis, both radiological and histological analyses of distraction gap bone formation demonstrated no significant differences between the ethanol, chow fed, or pair fed. We conclude that exogenous rmTNF and ethanol-induced endogenous TNF act to inhibit new bone formation during DO by signaling primarily through TNFR1.Distraction osteogenesis in TNF receptor 1 deficient mice is protected from chronic ethanol exposure - Corrected ProofElizabeth C. Wahl, James Aronson, Lichu Liu, Robert A. Skinner, Martin J.J. Ronis, Charles K. Lumpkin10.1016/j.alcohol.2011.08.007Alcohol (2011)2011-09-12Alcohol2011-09-12http://www.alcoholjournal.org/article/PIIS0741832911004137/abstract?rss=yesAbstract: This study compared differences in risk for suicidality among youth living in the community who met criteria for comorbid depression and binge drinking, depression without binge drinking, and binge drinking without depression relative to a reference group with neither condition. Logistic regression analysis was used to analyze data from the Canadian Community Health Survey, Cycle 3.1 (CCHS 3.1, 2005): a cross-sectional survey of respondents from the Canadian population. To restrict the sample to youth, respondents were excluded who were younger than 15 or older than 24 years. Over 17,000 respondents were assessed to determine whether they met criteria for depression, binge drinking, the comorbid condition, or neither condition (reference group). Binge drinking was defined as five drinks or more on an occasion. The 12-month prevalence rates for comorbid binge drinking and depression were 2.7% for male respondents and 2.1% for female respondents. When adjusted for demographic factors and when compared with the reference group, the risk of suicidality was increased for the depressed group (odds ratio [OR] 5.23, 95% confidence interval [CI]: 3.34–8.2) and the comorbid group (OR 6.28, 95% CI: 3.68–10.70), but not for the binge-drinking group. With the exception of increasing age, sociodemographic factors were not correlates of comorbidity. In conclusion, binge drinking was not associated with an increased risk of suicidality among Canadian youth living in the community, although depression and comorbidity were associated with suicidality.Concurrent binge drinking and depression among Canadian youth: prevalence, patterns, and suicidality - Corrected ProofSuzanne Archie, Azadeh Zangeneh Kazemi, Noori Akhtar-Danesh10.1016/j.alcohol.2011.07.001Alcohol (2011)2011-08-08Alcohol2011-08-08