Alcohol (Fayetteville, N.Y.)
Current impact factor: 2.01
Impact Factor Rankings
|2016 Impact Factor ||Available summer 2017 |
|2014 / 2015 Impact Factor ||2.006 |
|2013 Impact Factor ||2.038 |
|2012 Impact Factor ||2.255 |
|2011 Impact Factor ||2.468 |
|2010 Impact Factor ||2.423 |
|2009 Impact Factor ||2.407 |
|2008 Impact Factor ||2.363 |
|2007 Impact Factor ||2.14 |
|2006 Impact Factor ||2.02 |
|2005 Impact Factor ||1.743 |
|2004 Impact Factor ||1.874 |
|2003 Impact Factor ||1.585 |
|2002 Impact Factor ||1.693 |
|2001 Impact Factor ||1.31 |
|2000 Impact Factor ||1.495 |
|1999 Impact Factor ||1.433 |
|1998 Impact Factor ||1.32 |
|1997 Impact Factor ||1.264 |
|1996 Impact Factor ||1.324 |
|1995 Impact Factor ||1.753 |
|1994 Impact Factor ||1.373 |
|1993 Impact Factor ||1.523 |
|1992 Impact Factor ||1.5 |
Impact factor over time
|5-year impact ||2.32 |
|Cited half-life ||9.40 |
|Immediacy index ||0.29 |
|Eigenfactor ||0.00 |
|Article influence ||0.59 |
|ISSN ||1873-6823 |
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- Publisher last reviewed on 01/05/2015
- 'Elsevier Masson' is an imprint of 'Elsevier'
Publications in this journal
[Show abstract] [Hide abstract] ABSTRACT: The present study examined the effects of drinking intentions (DI) on alcohol expectancies (AE) and drink refusal self-efficacy (DRSE) in regard to alcohol consumption among heavy drinking undergraduates. Research shows that DRSE buffers against drinking (Young, Hasking, Oei, & Loveday, 2007) and interacts with AE to predict alcohol consumption (Oei & Burrow, 2000). Studies further show that DI is predicted by DRSE (Norman, 2011) and AE (Fleming, Thorson, & Atkin, 2004). However, additional research is needed to understand DI's influence on both DRSE and AE among heavy college drinkers. This research included 344 heavy drinking college students (mean age = 23.06 years, SD = 5.61, 74.71% female) from a large southern university who completed study material as part of a larger intervention. Findings showed that DI, DRSE, and AE interacted with respect to heavy drinking such that DRSE was negatively associated with alcohol consumption, particularly among those low in positive AE and high in negative AE. This relationship was stronger among individuals low in DI relative to those high in DI. DI seems to be an important factor influencing heavy drinking among undergraduate students. Present findings further support DI's associations with heavy drinking, regardless of an individual's DRSE or AE. Implications of this research suggest that it may be beneficial for interventions to target specific aspects of AE, including anxious drinking.
[Show abstract] [Hide abstract] ABSTRACT: Alcoholism is one of the most prevalent diseases in society and causes significant health and social problems. Alcohol consumption by pregnant women is reported to cause adverse effects on the physical and psychological growth of the fetus. However, the direct effect of chronic alcohol consumption on reproductive fitness has not been tested. In recent years, the zebrafish (Danio rerio) has emerged as a versatile model system to study the effects of alcohol on behavior and embryonic development. We utilized the zebrafish model system to address the effect of chronic alcohol exposure (0.5% alcohol in the holding tank for 9 weeks) on reproductive capacity. We found a dramatic decrease in fecundity, measured by counting the number of eggs laid, when at least one of the parents is subject to chronic alcohol exposure. Interestingly, a 9-week alcohol withdrawal program completely restored the reproductive capacity of the treated subjects. In agreement with observations on fecundity, the chronic alcohol exposure leads to increased anxiety, as measured by the novel-tank diving assay. Conversely, the withdrawal program diminished heightened anxiety in alcohol-exposed subjects. Our results highlight the adverse effects of chronic alcohol exposure on the reproductive capacity of both males and females, and underscore the utility of the zebrafish model system to understand the biology of chronic alcoholism.
[Show abstract] [Hide abstract] ABSTRACT: Drug addiction is a chronically relapsing disorder characterized by compulsion to seek and take the drug, loss of control in limiting intake and, eventually, the emergence of a negative emotional state when access to the drug is prevented. Both dopamine and corticotropin-releasing factor (CRF)-mediated systems seem to play important roles in the modulation of alcohol abuse and dependence. The present study investigated the effects of alcohol consumption on anxiety and locomotor parameters and on the activation of dopamine and CRF-innervated brain regions. Male Wistar rats were given a choice of two bottles for 31 days, one containing water and the other a solution of saccharin + alcohol. Control animals only received water and a solution of 0.2% saccharin. On the 31st day, animals were tested in the elevated plus-maze and open field, and euthanized immediately after the behavioral tests. An independent group of animals was treated with ethanol and used to measure blood ethanol concentration. Results showed that alcohol intake did not alter behavioral measurements in the plus-maze, but increased the number of crossings in the open field, an index of locomotor activity. Additionally, alcohol intake increased Fos-immunoreactivity (Fos-ir) in the prefrontal cortex, in the shell region of the nucleus accumbens, in the medial and central amygdala, in the bed nucleus of the stria terminalis, in the septal region, and in the paraventricular and dorsomedial hypothalamus, structures that have been linked to reward and to approach/withdrawal behavior. These observations might be relevant to a better understanding of the behavioral and physiological alterations that follow alcohol consumption.
[Show abstract] [Hide abstract] ABSTRACT: High rates of comorbidity for anxiety and alcohol-use disorders suggest a causal relationship between these conditions. Previous work demonstrates basal anxiety levels in outbred Long-Evans rats correlate with differences in voluntary ethanol consumption and that amygdalar Neuropeptide Y (NPY) systems may play a role in this relationship. The present work explores the possibility that differences in sensitivity to ethanol’s anxiolytic effects contribute to differential ethanol self-administration in these animals and examines the potential role of central and peripheral NPY in mediating this relationship. Animals were first exposed to the elevated plus maze (EPM) to assess individual differences in anxiety-like behaviors and levels of circulating NPY and corticosterone (CORT). Rats were then tested for anxiety-like behavior in the light-dark box (LD box) following acute ethanol treatment (1 g/kg; intraperitoneally [i.p.]), and neuronal activation in the amygdala and bed nucleus of the stria terminalis (BNST) was assessed using Fos immunohistochemistry. EPM exposure increased plasma CORT levels without altering plasma NPY levels. Acute ethanol treatment significantly increased light-dark transitions and latency to re-enter the light arena, but no differences were seen between high- and low-anxiety groups and no correlations were found between anxiety-like behaviors in the EPM and LD box. Acute ethanol treatment significantly increased Fos immunoreactivity in the BNST and the central amygdala. Although NPY neurons were not significantly activated following ethanol exposure, in saline-treated animals lower levels of anxiety-like behavior in the LD box (more time in the light arena and more transitions) were correlated with higher NPY-positive cell density in the central amygdala. Our results suggest that activation of the CeA and BNST are involved in the behavioral expression of ethanol-induced anxiolysis, and that differences in basal anxiety state may be correlated with NPY systems in the extended amygdala.
[Show abstract] [Hide abstract] ABSTRACT: To estimate the prevalence of any alcohol use and heavy alcohol drinking using the Alcohol Use Disorders Identification Test (AUDIT) and its correlates among men who have sex with men (MSM), a cross-sectional study was conducted among 391 MSM in Chongqing, China to collect data about sociodemographic characteristics, alcohol use, sexual behaviors, and other related factors through a computer-assisted self-administered questionnaire. Heavy alcohol drinking in the past 12 months was defined as an AUDIT-C score ≥4. Blood was collected from each potential participant to test for HIV and syphilis status. Twenty three percent of MSM had consumed a drink containing alcohol in the previous year. 7.2% had an AUDIT-C score ≥4, defined as heavy alcohol drinkers. 23.5% were unmarried, but planning to marry, who were more likely to report any alcohol drinking (adjusted odds ratio [AOR], 2.38; 95% confidence interval [CI], 1.40-4.06) and to have AUDIT-C scores ≥4 (AOR, 3.58; 95% CI, 1.60-8.00). MSM who had used any alcohol in the previous year, and MSM who were heavy alcohol drinkers, were more likely to have had anal sex with male casual partners in the previous 6 months, to have been tested for HIV, and to have decreased scores on the scales of general self-efficacy, increased scores on the scales of stigma and discrimination. Our findings provided further evidence of the associations of any alcohol use and heavy alcohol consumption with HIV-risky behaviors, lowered sense of general self-efficacy, and higher sense of HIV/AIDS-related stigma and discrimination among MSM in the city with the highest HIV epidemic among MSM in China.
[Show abstract] [Hide abstract] ABSTRACT: Our previous studies showed that ethanol elicited estrogen (E2)-dependent myocardial oxidative stress and dysfunction. In the present study we tested the hypothesis that E2 signaling via the estrogen receptor (ER), ERα, mediates this myocardial detrimental effect of alcohol. To achieve this goal, conscious female rats in proestrus phase (highest endogenous E2 level) received a selective ER antagonist (200 μg/kg; intra-venous [i.v.]) for ERα (MPP), ERβ (PHTPP) or GPER (G15) or saline 30 min before ethanol (1 g/kg; i.v.) or saline infusion. ERα blockade virtually abrogated ethanol-evoked myocardial dysfunction and hypotension, while ERβ blockade had little effect on the hypotensive response, but caused delayed attenuation of the ethanol-evoked reductions in left ventricular developed pressure and the rate of left ventricle pressure rise. GPER blockade caused delayed attenuation of all cardiovascular effects of ethanol. All three antagonists attenuated the ethanol-evoked increases in myocardial catalase and ALDH2 activities, Akt, ERK1/2, p38, eNOS, and nNOS phosphorylation, except for a lack of effect of PHTPP on p38. Finally, all three ER antagonists attenuated ethanol-evoked elevation in myocardial ROS, but this effect was most notable with ERα blockade. In conclusion, ERα plays a greater role in, and might serve as a molecular target for ameliorating, the E2-dependent myocardial oxidative stress and dysfunction caused by ethanol.
[Show abstract] [Hide abstract] ABSTRACT: Disturbances in the central signaling of reactive oxygen species (ROS) in response to energy intake are recognized as taking part in appetitive and consummative phases of eating disorders. This study aimed to verify the hypothesis that blood oxidoreductive balance can also affect demand for energy substances, such as alcoholic beverages in alcohol-dependent individuals, as well as the severity of their alcohol dependence and risk of drinking relapse. The following values were determined in the blood of 54 alcohol-dependent male patients after alcohol withdrawal, again after 4 weeks and after 6 months: the aldehyde products of lipid peroxidation (malonyl dialdehyde [MDA] and 4-hydroxynonenal [4-HNE]), nitric oxide (NO) metabolites, total antioxidant status (TAS), the blood activities of glutathione peroxidase (GSHpx), superoxide dismutase (SOD), glutathione reductase (GSHred), blood glucose, and lipids. Alcoholics who relapsed during 6 months of observation (n = 31, 57%) compared with patients who maintained alcohol abstinence for 6 months (n = 23, 43%) differed only in relation to initial and final NO metabolite serum concentrations. The risk of alcohol drinking relapse was lower in patients with an above-median initial blood concentration of NO metabolites and TAS. The oxidative stress parameters correlated with alcohol-dependence severity markers. No significant correlations between the studied antioxidant balance parameters and markers of nutritional status, including blood glucose and lipids, were found. Although the results of our study have some limitations and require further investigation, they suggest the role of oxidoreductive balance in the pathomechanisms of alcohol dependence and drinking relapse. In addition, due to a lack of association found between blood oxidative stress parameters and BMI, blood glucose, and lipid concentrations, they show the presence of disturbances in systemic ROS signaling in response to energy availability in alcoholics after alcohol withdrawal.
[Show abstract] [Hide abstract] ABSTRACT: Long-term alcohol use leads to persistent cognitive deficits that may be associated with maladaptive changes in the neurocircuitry that mediates executive functions. Impairments caused by these changes can persist well into abstinence and have a negative impact on quality of life and job performance, and can increase the probability of relapse. Many of the changes that affect cognitive function appear to involve dysregulation of the mesocortical dopamine system. This includes changes in dopamine release and alterations in dopamine receptor expression and function in the medial prefrontal cortex (PFC). This review summarizes the cellular effects of acute and chronic ethanol exposure on dopamine release and dopamine receptor function in the PFC with the goal of providing greater understanding of the effects of alcohol-use disorders on the dopamine system and how this relates to deficits in the executive function of the PFC.
[Show abstract] [Hide abstract] ABSTRACT: Larval zebrafish present unique opportunities to study the behavioral responses of a model organism to environmental challenges during early developmental stages. The purpose of the current study was to investigate the locomotor activities of AB strain zebrafish larvae at 5 and 7 days post-fertilization (dpf) in response to light changes under the influence of ethanol, and to explore potential neurological mechanisms that are involved in ethanol intoxication. AB strain zebrafish larvae at both 5 and 7 dpf were treated with ethanol at 0% (control), 0.1%, 0.25%, 0.5%, 1%, and 2% (v/v%). The locomotor activities of the larvae during alternating light-dark challenges, as well as the locomotor responses immediately following the light transitions, were investigated. The levels of various neurotransmitters were also measured in selected ethanol-treated groups. The larvae at 5 and 7 dpf demonstrated similar patterns of locomotor responses to ethanol treatment. Ethanol treatment at 1% increased the swimming distances of the zebrafish larvae in the dark periods, but had no effect on the swimming distances in the light periods. In contrast, ethanol treatment at 2% increased the swimming distances in the light periods, but did not potentiate the swimming activity in the dark periods, compared to controls. Differences in the levels of neurotransmitters that are involved in norepinephrine, dopamine, and serotonin pathways were also observed in groups with different ethanol treatments. These results indicated the behavioral studies concerning the ethanol effects on locomotor activities of zebrafish larvae could be carried out as early as 5 dpf. The 1% and 2% ethanol-treated zebrafish larvae modeled ethanol effects at different intoxication states, and the differences in neurotransmitter levels suggested the involvement of various neurotransmitter pathways in different ethanol intoxication states.
[Show abstract] [Hide abstract] ABSTRACT: Clinical data indicate that cutaneous burn injuries covering greater than 10% of the total body surface area are associated with significant morbidity and mortality, in which pulmonary complications, including acute respiratory distress syndrome (ARDS), contribute to nearly half of all patient deaths. Approximately 50% of burn patients are intoxicated at the time of hospital admission, which increases days on ventilators by 3-fold, and doubles the length of hospitalization, compared to non-intoxicated burn patients. The most common drinking pattern in the United States is binge drinking, where an individual rapidly consumes alcoholic beverages (4 for women, 5 for men) in 2 h. An estimated 38 million Americans binge drink, often several times per month. Experimental data demonstrate that a single binge-ethanol exposure, prior to scald injury, impairs innate and adaptive immune responses, thereby enhancing infection susceptibility and amplifying pulmonary inflammation, neutrophil infiltration, and edema, and is associated with increased mortality. Since these characteristics are similar to those observed in ARDS burn patients, our study objective was to determine whether ethanol intoxication and burn injury and the subsequent pulmonary congestion affect physiological parameters of lung function, using non-invasive and unrestrained plethysmography in a murine model system. Furthermore, to mirror young adult binge-drinking patterns, and to determine the effect of multiple ethanol exposures on pulmonary inflammation, we utilized an episodic binge-ethanol exposure regimen, where mice were exposed to ethanol for a total of 6 days (3 days ethanol, 4 days rest, 3 days ethanol) prior to burn injury. Our analyses demonstrate mice exposed to episodic binge ethanol and burn injury have higher mortality, increased pulmonary congestion and neutrophil infiltration, elevated neutrophil chemoattractants, and respiratory dysfunction, compared to burn or ethanol intoxication alone. Overall, our study identifies plethysmography as a useful tool for characterizing respiratory function in a murine burn model and for future identification of therapeutic compounds capable of restoring pulmonary functionality.
[Show abstract] [Hide abstract] ABSTRACT: The onset of puberty is the result of the increased secretion of hypothalamic luteinizing hormone-releasing hormone (LHRH). The pubertal process can be altered by substances that can affect the prepubertal secretion of this peptide. Alcohol is one such substance known to diminish LHRH secretion and delay the initiation of puberty. The increased secretion of LHRH that normally occurs at the time of puberty is due to a decrease of inhibitory tone that prevails prior to the onset of puberty, as well as an enhanced development of excitatory inputs to the LHRH secretory system. Additionally, it has become increasingly clear that glial-neuronal communications are important for pubertal development because they play an integral role in facilitating the pubertal rise in LHRH secretion. Thus, in recent years attempts have been made to identify specific glial-derived components that contribute to the development of coordinated communication networks between glia and LHRH cell bodies, as well as their nerve terminals. Transforming growth factor-α and transforming growth factor-β1 are two such glial substances that have received attention in this regard. This review summarizes the use of multiple neuroendocrine research techniques employed to assess these glial-neuronal communication pathways involved in regulating prepubertal LHRH secretion and the effects that alcohol can have on their respective functions.
[Show abstract] [Hide abstract] ABSTRACT: Identification of facial dysmorphology is essential for the diagnosis of fetal alcohol syndrome (FAS); however, most children with fetal alcohol spectrum disorders (FASD) do not meet the dysmorphology criterion. Additional objective indicators are needed to help identify the broader spectrum of children affected by prenatal alcohol exposure. Computed tomography (CT) was used in a sheep model of prenatal binge alcohol exposure to test the hypothesis that quantitative measures of craniofacial bone volumes and linear distances could identify alcohol-exposed lambs. Pregnant sheep were randomly assigned to four groups: heavy binge alcohol, 2.5 g/kg/day (HBA); binge alcohol, 1.75 g/kg/day (BA); saline control (SC); and normal control (NC). Intravenous alcohol (BA; HBA) or saline (SC) infusions were given three consecutive days per week from gestation day 4-41, and a CT scan was performed on postnatal day 182. The volumes of eight skull bones, cranial circumference, and 19 linear measures of the face and skull were compared among treatment groups. Lambs from both alcohol groups showed significant reduction in seven of the eight skull bones and total skull bone volume, as well as cranial circumference. Alcohol exposure also decreased four of the 19 craniofacial measures. Discriminant analysis showed that alcohol-exposed and control lambs could be classified with high accuracy based on total skull bone volume, frontal, parietal, or mandibular bone volumes, cranial circumference, or interorbital distance. Total skull volume was significantly more sensitive than cranial circumference in identifying the alcohol-exposed lambs when alcohol-exposed lambs were classified using the typical FAS diagnostic cutoff of ≤10th percentile. This first demonstration of the usefulness of CT-derived craniofacial measures in a sheep model of FASD following binge-like alcohol exposure during the first trimester suggests that volumetric measurement of cranial bones may be a novel biomarker for binge alcohol exposure during the first trimester to help identify non-dysmorphic children with FASD.
[Show abstract] [Hide abstract] ABSTRACT: The purpose of the study is to clarify the effect of 7 days of ethanol administration upon brain histaminergic neurons in rats. Male Wistar rats were injected intraperitoneally (i.p.) with 20% ethanol/saline (0.85% NaCl) daily, over 7 days, whereas control rats were given saline. The animals were decapitated 24 h after the 7th injection and samples of hypothalamus were prepared for light and electron microscopy, accompanied by morphometry to examine the histaminergic neurons. It was found that ethanol administration gradually decreased the duration of alcohol-induced sleep and decreased the total amount of histaminergic neurons and the amount of histologically normal neurons, but increased the amount of hypochromic neurons and shadow cells. The histaminergic neuron bodies and nuclei decreased in size. The ultrastructural changes in histaminergic neurons demonstrated activation of their nuclear apparatus, both destruction or hypertrophy and hyperplasia of organelles, especially lysosomes. The histochemical examination revealed the activation of lactate dehydrogenase and acid phosphatase, and inhibition of NADH-, NADPhH, and succinate dehydrogenases. Following 7 days of ethanol administration, histaminergic neurons exhibit the structural signs of hyperactivity, which can be related to neuronal adaptation to the actions of ethanol, and increased behavioral tolerance to ethanol.
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