bluuebunny/crossref_metadata_2025_split huggingface dataset:
Validity of Self‐Reported Alcohol Consumption in Nondependent Drinkers With Unintentional Injuries
Authors: Sommers Marilyn Sawyer , Dyehouse Janice M. , Howe Steven R. , Lemmink Jennifer , Volz Tina , Manharth Marjorie 
Published: April 2006

Background: Self‐report has become an anchor for alcohol assessment in the acute and primary care populations. The purpose of the study was to determine the validity of self‐reported alcohol consumption after unintentional injuries in hospitalized, nondependent drinkers.Methods: Non‐alcohol‐dependent subjects 18 years of age and older with unintentional injuries (n= 209) were enrolled in the study and were interviewed if they had either an admitting blood alcohol concentration (BAC) ≥ 10 mg/dl (0.01 g/dl) or a positive screen for a history of problem drinking. The self‐reported number of standard drinks, time that drinking commenced, sex, and weight were used to calculate estimated blood alcohol concentration (EBAC), which was then compared to the admission BAC.Results: We had data to calculate the EBAC on 141 of the 209 subjects. Seven men and no women with positive (≥10 mg/dl) BAC denied drinking. Of the 134 subjects for whom we had data to calculate EBAC and who acknowledged drinking, mean BAC was 147.06 mg/dl and mean EBAC was 68.66 mg/dl. For women (n= 30), mean BAC was 149.53 mg/dl and mean EBAC was 114.67 mg/dl; for men (n= 104), mean BAC was 146.35 mg/dl and mean EBAC was 55.38 mg/dl. The Spearman's ρ between laboratory BAC and EBAC was 0.461 (p < 0.001) for all subjects (n= 134), 0.275 (NS) for women (n= 30), and 0.532 (p < 0.001) for men (n= 104). For women and men separately, multiple regression analyses were performed to predict BAC by using weight and reported number of drinks. For women, weight and number of drinks accounted for 3% of the variance in laboratory BAC [r= 0.181, F (2,47) = 0.797, p= NS]. In contrast, for men these same predictors accounted for 34% of the variance [r= 0.585, F (2,135) = 35.203, p < 0.001).Conclusions: Most nondependent patients with unintentional injury acknowledged drinking before injury. After injury, women and men have different patterns of reporting their drinking, with men more frequently underreporting but reporting more accurately and women more random in their self‐reports.
Dose‐Dependent Effect of Ethanol on Hepatic Oxidative Stress and Interleukin‐6 Production After Burn Injury in the Mouse
Authors: Colantoni Alessandra , Duffner Lisa A. , de Maria Nicola , Fontanilla Christine V. , Messingham Kelly A. N. , Van Thiel David H. , Kovacs Elizabeth J. 
Published: April 2006

Background: Burned patients with detectable blood alcohol levels (BAL) show an elevated mortality rate. Interleukin (IL)‐6 and reactive oxygen species (ROS) production is stimulated independently by alcohol and burn injury. The aim of the study was to determine whether increasing levels of alcohol differentially enhance the hepatic production of IL‐6 and ROS after burn in a murine model of dorsal scald injury. Groups of mice received either saline or alcohol intraperitoneally to reach a BAL of 100 mg/dl or 300 mg/dl at the time of burn (15% total body surface scald) or sham injury.Results: Burn injury alone resulted in a low mortality rate at 24 hr after injury as did the burn group with a BAL of 100 mg/dl (15%), whereas 57% of the mice burned with a BAL of 300 mg/dl did not survive (p= 0.02). Twenty‐four hours after burn or sham injury, IL‐6 levels were measured by enzyme‐linked immunosorbent assay in serum and liver. In the saline‐treated group, IL‐6 circulating and hepatic levels rose after burn injury (p < 0.03). Circulating IL‐6 levels in sham mice increased 1.5‐fold in the group with a BAL of 100 mg/dl and 3‐fold in those with a BAL of 300 mg/ml (p= 0.005 versus burn‐injured, saline‐treated). IL‐6 hepatic production after burn injury was higher in the mice with a BAL of 300 mg/dl than in those with a BAL of 100 mg/dl and the saline‐treated group (p= 0.001). Among the burned mice, alcohol exposure increased hepatic ROS production, measured by lipid peroxidation and protein oxidation, in a dose‐dependent manner.Conclusions: Alcohol enhances in a dose‐dependent manner the hepatic production of IL‐6 induced by burn injury through the modulation of oxidative stress. The increased mortality rate of mice exposed to alcohol and burn injury may be due to the adverse effect on immune function induced by IL‐6 elevation.
Influence of Sex Hormonal Status on Alcohol‐Induced Oxidative Injury in Male and Female Rat Liver
Authors: Colantoni Alessandra , La Paglia Nancy , de Maria Nicola , Emanuele Mary Ann , Emanuele Nicholas V. , Idilman Ramazan , Harig James , Van Thiel David H. 
Published: April 2006

Background: Oxidative stress contributes to the development of liver injury after chronic alcohol intake. Women exhibit greater sensitivity to alcohol‐induced liver disease than do men. The aim of the study was to determine the relationship between the sex hormone status of male and female rats and the degree of alcohol‐induced oxidative stress in the liver.Methods: Male and female rats were pair‐fed a liquid diet that contained 36% of their total daily calories as ethanol (EtOH group) or maltose (control group). Blood and liver samples were collected at the end of 8 weeks of diet.Results: Male EtOH rats experienced a reduction in plasma testosterone (T) and an increase in estradiol (E2) levels, with an increase in their calculated E2/T ratio with respect to their controls. Malonaldehyde (MDA) levels, an index of lipid peroxidation, and protein carbonyl content, an index of protein oxidation, in the liver were greater among the EtOH groups in females than in males. In males, an inverse correlation was found between hepatic MDA and circulating T levels, and a direct correlation was disclosed between MDA and estradiol levels. In addition, the hepatic histopathological score correlated inversely with the plasma T levels and directly with the calculated E2/T ratio, an index of feminization.Conclusions: Alcohol‐induced oxidative injury, which contributes to hepatic injury in both male and female rats, is enhanced in females compared with males. A role for plasma T levels in protecting male rat liver from ethanol‐induced oxidative injury can be hypothesized.
A Comparison of Correlates of DSM‐IV Alcohol Abuse or Dependence Among More Than 400 Sons of Alcoholics and Controls
Authors: Schuckit M. A. , Smith Tom L. 
Published: April 2006

Background: Alcohol dependence and abuse are defined as separate disorders. However, relatively few data are available about whether the same characteristics predict both syndromes.Methods: Complete data were available from the 15 year follow‐up of 411 men who originally had been evaluated from a university population at about age 20. Both baseline data gathered prospectively and the retrospective ratings in six domains of life functioning were analyzed for their relationship to the development of alcohol abuse or dependence during the follow‐up.Results: Baseline characteristics of a family history of substance use disorders, the quantity and frequency of drinking, the history of alcohol‐related problems, and the level of response to alcohol all predicted future alcohol abuse or dependence, but only an alcoholic second‐degree relative or a first‐degree drug‐dependent family member differentially predicted dependence. Logistic regression analyses revealed that similar baseline characteristics combined to predict dependence and, separately, abuse. When the domains of functioning during the 15 years were included, positive alcohol expectancies, poor coping mechanisms, low level of social support, and drinking in the environment contributed to both dependence and abuse, although the relationship was stronger for dependence.Conclusions: The predictors and correlates of alcohol abuse and dependence in this group of men were similar. Further research in additional populations and on other drugs is needed to determine if the two syndromes overlap sufficiently to be combined.
Pretreatment With Hydromorphone, a μ‐Opioid Agonist, Does Not Alter the Acute Behavioral and Physiological Effects of Ethanol in Humans
Authors: Rush Craig R. 
Published: April 2006

Background: Endogenous opioid systems are thought to mediate at least some of the behavioral effects of ethanol. Opioid antagonists, like naloxone and naltrexone, decrease ethanol self‐administration under a variety of conditions in different species of laboratory animals (e.g., rodents and nonhuman primates). Opioid agonists, like morphine, also alter ethanol consumption. However, the dose‐response functions for opioid agonists are complex in that low doses increase ethanol self‐administration, whereas moderate to high doses decrease ethanol self‐administration. The results of prospective human laboratory studies that assessed the behavioral effects of ethanol after pretreatment with an opioid antagonist are mixed. The aim of the present study was to assess the acute subject‐rated effects of ethanol (0, 0.5, and 1 g/kg) after pretreatment with hydromorphone, a μ‐opioid agonist.Methods: In the present experiment, the acute subject‐rated, performance‐impairing, and physiological effects of ethanol (0, 0.5, and 1 g/kg) were examined after pretreatment with hydromorphone (0, 1, and 2 mg), a μ‐opioid agonist, in nine healthy volunteers. Volunteers received one of the nine possible ethanol‐hydromorphone combinations during each of nine experimental sessions.Results: Ethanol produced prototypical subject‐rated drug effects (e.g., dose dependently increased ratings of “high”), impaired performance, and increased heart rate. Hydromorphone pretreatment generally did not significantly alter the subject‐rated, performance‐impairing, or physiological effects of ethanol.Conclusions: The results of the present experiment suggest that hydromorphone pretreatment does not significantly affect the subject‐rated effects of ethanol. Future human laboratory studies should test higher doses of hydromorphone. Future studies also might use more sophisticated behavioral procedures like self‐administration, or perhaps drug discrimination, to determine if opioid agonists can modulate the behavioral effects of ethanol in humans.
Adverse Drinking Consequences Among Alcohol Abusing Intravenous Drug Users
Authors: Anderson Bradley J. , Gogineni Aruna , Charuvastra Anthony , Longabaugh Richard , Stein Michael D. 
Published: April 2006

Background: Heavy alcohol use is common among out‐of‐treatment injection drug users (IDUs); however, the relationship between alcohol and drug use behaviors in codependent populations is not well understood. Our specific objectives were (1) to describe the psychometric properties of the Drinker Inventory of Consequences (DrInC) in a sample of active IDUs, and (2) to compare DrInC scores of active IDUs with those reported for the alcohol treatment seeking sample on which the instrument was developed.Methods: Interview data were collected from 187 active IDUs who scored positively (≥ 8) on the Alcohol Use Disorders Identification Test, who were recruited from a Providence, RI, needle exchange program (1998–1999). DrInC total and subscale scores for the 159 (85%) participants who met DSM‐IV criteria for alcohol abuse/dependence were analyzed. Six‐month follow‐up data were used to estimate test‐retest reliability.Results: The DrInC total scale exhibited high internal consistency and test‐retest reliability. With the exception of adverse physical consequences, reliability estimates for DrInC subscales were good to very good. These data indicate higher subscale redundancy than reported for the development sample. Active IDUs had significantly higher adverse impulse control consequences than the alcohol treatment seeking population on which the instrument was developed.Conclusions: The DrInC exhibits desirable psychometric properties for assessing adverse drinking consequences in active IDU populations. IDUs who met DSM‐IV criteria for alcohol abuse/dependence reported overall levels of adverse drinking consequences comparable with non‐IDU alcohol treatment populations but were more likely to exhibit adverse impulse control consequences.
Effects of Chronic Alcohol Consumption on the Broad Phospholipid Signal in Human Brain: An In Vivo 31P MRS Study
Authors: Estilaei M. R. , Matson G. B. , Payne G. S. , Leach M. O. , Fein G. , Meyerhoff D. J. 
Published: April 2006

Background: Phosphorus magnetic resonance spectroscopy (31P MRS) allows for the measurement of phospholipids and their breakdown products in the human brain. Fairly mobile membrane phospholipids give rise to a broad signal that co‐resonates with metabolic phosphodiesters. Chronic alcohol exposure increases the rigidity of isolated brain membranes and, thus, may affect the amount and transverse relaxation times (T2) of MRS‐detectable phospholipids. We tested the hypothesis that subjects who were heavy drinkers have stiffer membranes than controls who were light drinkers, as reflected in a smaller broad signal component and a shorter T2 of the broad signal in 31P MR spectra of the brain.Methods: Thirteen alcohol‐dependent heavy drinkers (mean age 44 years) were studied by localized 31P MRS in the centrum semiovale and compared with 17 nondependent light drinkers of similar age. The broad component signal was separated from the metabolite signal by convolution difference, which is based on the large difference in line widths of these two signals. Longitudinal and T2 relaxation times were measured using standard methods.Results: The broad component integral was 13% lower in the brain of heavy drinkers compared with light drinkers (p < 0.001) and remained significantly smaller after corrections for both longitudinal and transverse relaxations (p < 0.01). The T2 distribution of the broad component consistently showed two resolvable components in both groups. The fast relaxing component had the same T2 in both groups (T2= 1.9 msec). The slower relaxing component T2 was 0.6 msec shorter in heavy drinkers compared with light drinkers (p= 0.08).Conclusions: These results, observed in the absence of white matter volume loss, are consistent with biochemical alterations and higher rigidity of white matter phospholipids associated with long‐term chronic alcohol abuse. The observed smaller broad signal component in these relatively young heavy drinkers is a sensitive measure of white matter phospholipid damage.
Thiamin Treatment and Working Memory Function of Alcohol‐Dependent People: Preliminary Findings
Authors: Ambrose Margaret L. , Bowden Stephen C. , Whelan Greg 
Published: April 2006

Background: Wernicke‐Korsakoff syndrome (WKS) is most often seen in people who are alcohol dependent. Treatment with thiamin may rapidly resolve acute symptoms. However, much evidence suggests that identification of WKS on clinical examination is relatively insensitive when compared with diagnosis at postmortem. No study has investigated the therapeutic effect of thiamin in a sample of alcohol‐dependent people without the clinical triad of acute WKS.Methods: We conducted a randomized, double‐blind, multidose study of thiamin treatment in 107 subjects who were detoxifying from alcohol. Five groups of subjects were assessed with the Mini‐Mental State Examination and were examined for the presence of neurological signs. Subjects were given different doses of intramuscular thiamin for two consecutive days. The posttreatment performance of these groups then was examined on a test of working memory derived from comparative neuropsychology, namely, the delayed alternation task. This test has been established as sensitive to the neuropathology of WKS.Results: Pretreatment measures of mental status and neurological signs were equivalent across groups. Groups were equated with respect to the background variables of age, education, typical daily alcohol consumption, and years of drinking. On the posttreatment measure, a superior performance was found in the group that received the highest dose of thiamin, compared with the other four treatment groups.Conclusions: A therapeutic relationship between dose and working memory performance was indicated. These results have important implications for the management and prevention of WKS, but further investigations are needed to substantiate the nature of the therapeutic relationship.
Association of Neuropeptide Y Polymorphism With the Occurrence of Type 1 and Type 2 Alcoholism
Authors: Ilveskoski Erkki , Kajander Olli A. , Lehtimäki Terho , Kunnas Tarja , Karhunen Pekka J. , Heinälä Pekka , Virkkunen Matti , Alho Hannu 
Published: April 2006

Background: The susceptibility to alcoholism can be explained partially by genetic factors. Neuropeptide Y (NPY) has emerged as one potential factor contributing the development of alcoholism. A recent study indicated that the NPY gene variant producing a leucine‐to‐proline substitution (T to C at position 1128) was associated with 34% higher average alcohol consumption.Methods: The subjects consisted of 122 alcoholics classified as type 1 and type 2 subtypes by psychiatric evaluation. A random sample of 59 social drinkers was used as a control group to compare the distribution of NPY genotypes with those of alcoholics.Results: In a logistical regression model, there was a significantly lower frequency of the leucine(7)/proline(7) heterozygotes among well characterized type 2 alcoholics, compared with the controls (10.8 vs. 24.1%, p= 0.028).Conclusions: We speculate that the genetic polymorphism producing the proline(7) substitution of NPY might not predispose to alcoholism, but indeed retard the transition to alcoholism.
Effects of Raclopride in the Nucleus Accumbens on Ethanol Seeking and Consumption
Authors: Czachowski Cristine L. , Chappell Ann M. , Samson Herman H. 
Published: April 2006

Background: Nucleus accumbens dopamine has been shown to play a role in the processing of behaviorally relevant stimuli and to mediate ethanol‐reinforced responding. Previous research that used a fixed‐ratio schedule of responding maintained by the presentation of small dippers (0.1 ml) of ethanol demonstrated that the dopamine D2 antagonist, raclopride, decreased total responding for ethanol by both delaying the onset of responding and causing the early termination of lever‐press behavior. Because these studies required animals to continuously respond to obtain access to small amounts of ethanol over a period of self‐administration, this procedure assessed a combination of appetitive (seeking) and consummatory (drinking) behavior. The paradigm used in the present study separated the appetitive or seeking response from the consummatory response to assess the effects of raclopride on both types of ethanol‐related behaviors.Methods: Male Long‐Evans rats were trained to emit a fixed number of lever‐press responses that resulted in access to a drinking tube that contained 10% ethanol for 20 min, once each day. We measured the effects of microinjections of raclopride (1.0, 3.0, and 10.0 μg/subject) into the nucleus accumbens, before the sessions, on appetitive and consummatory responding.Results: Raclopride delayed the onset of ethanol‐seeking (appetitive responding) at all doses and decreased the number of responses made at the low and high doses. The rate of responding, however, was unaffected. Raclopride had no effect on the latency to begin consuming ethanol or on any of the characteristics of the initial bout of ethanol intake at all doses tested. Total ethanol intake was decreased, after an initially “normal” pattern of self‐administration, following only the highest dose of raclopride. Mean ethanol intake (g/kg) was 0.54 (±0.03) after no injection, 0.51 (±0.04) after sham treatment, and 0.38 (±0.05) after 10 μg of raclopride.Conclusions: The procedural separation of the seeking and intake responses used in this experiment allowed us to assess the effects of dopamine receptor antagonism in the nucleus accumbens on these two different behaviors. Overall, appetitive responding that preceded the delivery of an ethanol solution was more sensitive to raclopride treatment than was consummatory responding. These findings are consistent with a stimulus‐processing function of the mesolimbic dopamine system.
Allopregnanolone and Pentobarbital Infused Into the Nucleus Accumbens Substitute for the Discriminative Stimulus Effects of Ethanol
Authors: Hodge Clyde W. , Nannini Michelle A. , Olive M. Foster , Kelley Stephen P. , Mehmert Kristin K. 
Published: April 2006

Background: The discriminative stimulus effects of ethanol are mediated in part by the γ‐aminobutyric acid type A (GABAA) receptor system. We have previously shown that microinjections of the competitive GABAA agonist muscimol in the nucleus accumbens and amygdala fully substitute for the discriminative stimulus effects of systemic ethanol. However, it is not known whether allosteric binding sites on GABAA receptors located within specific limbic brain regions contribute to the discriminative stimulus effects of ethanol.Methods: Male Long‐Evans rats were trained to discriminate between intraperitoneal injections of ethanol (1 g/kg) and saline under a fixed‐ratio 10 schedule of sucrose (10% w/v) reinforcement. Injector guide cannulae, aimed at both the nucleus accumbens core and the hippocampus area CA1, were then implanted to allow site‐specific infusion of GABAA‐positive modulators.Results: Infusion of the neurosteroid 3α‐hydroxy‐5α‐pregnan‐20‐one (allopregnanolone, or 3α‐5α‐P) in the nucleus accumbens resulted in dose‐dependent full substitution for intraperitoneal ethanol (50% effective dose = 0.38 ng/μl per side). Likewise, injection of the barbiturate pentobarbital into the nucleus accumbens also substituted dose‐dependently for ethanol (50% effective dose = 1.55 μg/μl per side). However, infusions of either 3α‐5α‐P or pentobarbital in the hippocampus failed to substitute for ethanol and produced inverted U‐shaped dose‐response curves.Conclusions: These results demonstrate that allosteric positive modulation of GABAA receptors in the nucleus accumbens produces full substitution for the stimulus effects of ethanol. This suggests that GABAA receptors in the nucleus accumbens may play a more influential role in the discriminative stimulus effects of ethanol than those in the hippocampus.