bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ethanol‐induced Hydrolysis of Brain Sialoglycoconjugates in the Rat: Effect pf Sialic Acid in Antagonizing Ethanol Intoxication
Authors: Cherian L. , Mathew J. , Klemm W.R. 
Published: April 2006

Several reports indicate that acute ethanol promotes the cleavage of brain sialoglycoconjugates (SGC). We attempted to confirm this effect by monitoring cleavage of sialic acid (SA) that had been radiolabeled by pretreatment with the specific precursor of SA, N‐[3H]acetyl‐d‐mannosamine, injected intracerebroventricuhrly into rats 20 h prior to ethanol injection (2 or 3 g/kg, given four times in a simulated “binge drinking” protocol).Analysis of the residual labeled material revealed a significant reduction of radiolabel (p < 0.01), as compared to saline controls. A dose of 3 g/kg diminished the total labeled SGC by half. Brain sialidase activity was not affected by the ethanol treatment.Since ethanol intoxication is associated with enhanced SA cleavage, one hypothesis needing testing is that loss of SA might help to cause intoxication. If so, pretreatment with SA might antagonize intoxication, presumably by offsetting loss due to cleavage of SA. Consistent with our earlier results, we found that when sialic acid was given i.p. (25 mg/kg), 1, 6, or 24 h prior to ethanol injection (4 g/kg, i.p.), the sleep time was reduced by 35‐40% and the performance on rotorod was significantly enhanced (p < 0.01). When ethanol was replaced by pentobarbital (40 mg/kg), the sleep time was increased (∼30%) at 6 h after injection with either 25 or 100 mg/kg sialic acid, whereas at the 24 h postinjection it was decreased (∼20%) at both doses. The results suggest that sialic acid is a key component in mediating ethanol effects and perhaps also, in a different way, anesthetic effects.
Paternal and Maternal Alcohol Consumption: Effects on Offspring in Two Strains of Rats
Authors: Abel Ernest L. 
Published: April 2006

Long‐Evans and Sprague‐Dawley male rats were given liquid alcohol diets containing 35%, 17.5%, or 0% ethanol‐derived calories (EDC). The latter two groups were pair fed to the higher alcohol diet group. A fourth group received lab chow and water ad libitum to assess the role of paternal undernutrition associated with alcohol consumption. After three or four weeks of diet Consumption, these males were bred to females of the same strain. Pregnant females were divided into similarly treated alcohol groups and were fed these diets beginning on gestation Day 8, thus creating a factorial study with strain, paternal, and maternal alcohol consumption as main factors.Paternal alcohol consumption was associated with decreased litter size, decreased testosterone levels, and a strain‐related effect on offspring activity. Offspring activity decreased for those sired by 35% and 17.5% EDC Long‐Evans fathers. Activity also decreased for offspring sired by 17.5% EDC Sprague‐Dawley fathers but increased for those sired by 35% EDC fathers. Paternal alcohol consumption did not affect postnatal mortality or passive avoidance learning of offspring.Maternal alcohol consumption was associated with lower birth weights, lower offspring weights at weaning, increased postnatal mortality, and poorer passive avoidance learning. However, offspring activity was not affected.In a separate study, levels of alcohol in the testes were found to be somewhat, but not significantly, lower than blood alcohol levels. DNA taken from sperm of Long‐Evans males consuming alcohol, migrated farther under pulsed field electrophoresis than DNA from control fathers, suggestive of an alcohol‐related effect on sperm DNA.
Comparative Study on Ethanol Elimination and Blood Acetaldehyde between Alcoholics and Control Subjects
Authors: Adachi Junko , Mizoi Yasuhiko , Fukunaga Tatsushige , Ogawa Yumi , Imamichi Hiroyuki 
Published: April 2006

Factors influencing ethanol elimination rate and Mood acetaldehyde concentration with regard to age, blood ethanol concentration, and degrees of alcoholic liver disorder were studied in alcoholic patients vis‐à‐vis healthy subjects.Ninety‐four male alcoholic patients were divided into five groups according to age and into three groups according to blood ethanol concentration which ranged between 4.21 and 0.29 mg/ml. It was noted that as age increased, Mood ethanol concentration decreased. Groups A, B, and C consisted of subjects whose ethanol levels were more than 2.5, between 1.0 and 2.5, and less than 1.0 mg/ml, respectively. Average values of ethanol elimination rate in Groups A, B, and C were 0.26, 0.23, and 0.18 mg/ml/hr, respectively. The rate Increased as blood ethanol concentration elevated. The rate In group B was significantly higher than that in the healthy control subjects who had blood ethanol levels between 1.0 and 2.5 mg/ml. The rate of ethanol elimination was independent of liver disorder judged by liver function test values.Blood acetaldehyde concentrations in the patients were less than 1.48 μg/ml, with an average value of 0.58 μg/ml, and were significantly correlated with blood ethanol levels in both alcoholics and healthy subjects.
Derivation and Validation of a Prediction Rule for Identifying Heavy Consumers of Alcohol
Authors: Lichtenstein Michael J. , Burger M. Candice , Yarned John W. G. , Elwood Peter C. , Sweetnam Peter M. 
Published: April 2006

Using two population‐based cohorts of men aged 45‐59, we sought to derive and validate a prediction rule for identifying heavy consumers of alcohol. Eighty‐five percent of eligible men on electoral rolls in Caerphilly, Wales (derivation set, N = 2512) and 90% of eligible men on the practice lists of 16 Speedwell, England, general practitioners participated (validation set, N = 2348).Alcohol consumption was assessed by questionnaire with heavy alcohol consumption defined as the top 10% of the Caerphilly population's alcohol usage (>525 cc ethanol per week).The prediction rule, Score = (mean corpuscular volume × 1.00) + (body mass index × 0.31) + (systolic blood pressure × 0.08) + HDL‐cholesterol × 9.24) + (fasting triglyceride × 2.20) was derived by multiple linear regression in the Caerphilly cohort and validated in the Speedwell cohort. Comparing the lower 20% of the Score distribution with the upper 5%, likelihood ratios increased from 0.15 to 5.29 and 0.06 to 7.42 in the Caerphilly and Speedwell cohorts, respectively. Having a score of 136.30 or greater yielded a relative risk of being a heavy drinker of 23.1 (95% CI = 10.1‐53.0) in Caerphilly and 99.3 (95% CI = 12.8‐769.5) in Speedwell. The derived prediction rule is a valid diagnostic aid to help clinicians identify heavy alcohol consumers.
Exposure of Rats to Ethanol from Postnatal Days 4 to 8: Alterations of Cholinergic Neurochemistry in the Hippocampus and Cerebellum at Day 20
Authors: Light Kim E. , Serbus Dellan C. , Santiago Melissa 
Published: April 2006

Brief neonatal ethanol exposure (3.0 g/kg/dose, twice daily; postnatal day (PN) 4 to PN8) resulted in cholinergic neurochemical alterations in the cerebellum, but not the hippocampus of rats assayed on PN20. Analysis revealed that the binding affinity of cerebellar muscarinic receptors for [3H]quinuclidinyl benzilate was decreased by ethanol, but only in female pups. Other gender‐specific but treatment‐independent cerebellar differences were identified as well, including lower levels of choline acetyltransferase activity and St‐level (1,000 × g) crude protein in males and females, respectively.No evidence of ethanol‐induced cholinergic change was noted in the hippocampus of the same pups on PN20. However, collapsed across treatment, male hippocampi were found to contain less S1‐level protein than their female counterparts.Neither muscarinic receptor density nor acetyl cholinesterase activity were found to differ between treatments or genders, in either brain region. Consistent with the developmental timetables for regional cholinergic synaptogenesis in the rat, observations on PN20 confirm a hypothesis of cerebellar cholinergic vulnerability and hippocampal cholinergic resilience to neonatal ethanol insult.
Human Leukocyte β‐Adrenergic Stimulated Cyclic AMP in Ethanol Intoxication and Withdrawal
Authors: Swift R. M. , DePetrillo P. 
Published: April 2006

The effects of ethanol were examined on cyclic AMP production in intact human leukocytes in vitro. In leukocytes isolated from alcohol abstinent subjects, ethanol enhances isoproterenol‐stimulated and prostaglandin E1‐stimulated cyclic AMP formation. Without agonist, ethanol is able to stimulate cyclic AMP production at concentrations of 160 mM and above.Leukocytes isolated from subjects undergoing alcohol detoxification showed increases in basal levels of leukocyte cyclic AMP, in isoproterenol‐stimulated cyclic AMP, and in ethanol‐stimulated cyclic AMP on the 2nd or 3rd day of withdrawal in comparison to the first day of withdrawal and in comparison to abstinent subjects. The data suggest that increased β‐adrenergic activity seen in alcohol withdrawal may be in part due to an increased responsiveness of β‐adrenergic stimulated cyclic AMP in tissues.
Clinical Characteristics of Female Alcoholics with Low Platelet Monoamine Oxidase Activity
Authors: Hallman Jarmila , von Knorring Anne‐Liis , von Knorring Lars , Oreland Lars 
Published: April 2006

The aim of the present study was to see if female alcoholics had low platelet MAO activity and whether there was a correlation between low MAO activity in female alcoholics and specific clinical characteristics often observed in type II male alcoholics. In earlier studies, male alcoholics have been subdivided into type I and type II alcoholics. Type II alcoholics were characterized by early onset, a high frequency of depression and alcoholism in first degree relatives, a high frequency of drug abuse and social complications, sensation seeking behavior, extraversion, impulsive sensation seeking psychopathy, and low platelet MAO activity.In the present series it was demonstrated that the female alcoholics had significantly lower platelet MAO activities than the female healthy volunteers. The subgroup of female alcoholics with low platelet MAO activity, however, did not differ from female alcoholics with normal platelet MAO activity in the same way as male alcoholics with low platelet MAO activity have been shown to differ from male alcoholics with normal platelet activity. They did not have early onset, higher frequency of depression or alcoholism in their first degree relatives, nor more social complications than the female alcoholics with normal platelet MAO activity. Furthermore, they did not differ from the female alcoholics with normal platelet MAO activity in any personality trait covered by the Karolinska Scales of Personality (KSP).
Hypothalamic‐Pituitary and Thyroid Function in Chronic Alcoholics with Neurological Complications
Authors: Knudsen G. Moos , Christensen H. , Berild D. , Melgaard B. , Kirkegaard C. , Hasselbalch H. 
Published: April 2006

Endocrinological tests were performed in 14 chronic alcoholic men with signs of intellectual impairment and/or peripheral neuropathy. All had been abstinent from alcohol for at least 1 month.Basal serum growth hormone (GH) was consistently increased in only one patient whereas the GH responses to insulin hypoglycemia stimulation was normal in all patients. Thyroid function values (T4, T3, rT3, TSH) were normal in all patients whereas baseline serum prolactin values were significantly increased in alcoholics as compared with a control group. In a combined TRH‐ and GnRH‐stimulation tests, GH‐responses were also normal whereas TSH and prolactin responses were blunted or absent in about half of the patients, the responses correlating significantly (p < 0.01). It is concluded that disturbances in the hypothalamic‐pituitary axis may occur in chronic alcoholics with nervous impairment independently of the physical deterioration, which often is associated with chronic alcoholism.
Initiating Ethanol Drinking in a Simian Social Group in a Naturalistic Setting
Authors: Crowley Thomas J. , Williams Elizabeth A. , Jones Richard H. 
Published: April 2006

We examined in nine group‐living, male Japanese Snow monkeys the initiation of alcohol‐drinking behavior in an enriched environment where both social and nonsocial stimuli could influence drinking. The monkeys usually could move freely between an indoor shelter and a large outdoor corral, which contained three drinkometers. During daily 2‐hr sessions in pre‐ and post‐training periods (with food and water available ad libitum), the drinkometers held (on different days) Koolaid‐saccharin, water, water with 5% ethanol, Koolaid‐saccharin with 5% ethanol, or Koolaid‐sucrose with acetic acid (matched in calories and palatability to Koolaid‐saccharin with 5% ethanol). Between pre‐and post‐training periods was a long training period, in which Koolaid‐saccharin with various ethanol concentrations was presented with the daily food ration in 2‐hr drinking sessions. On other selected training days, water with 5% ethanol was presented.During training sessions some monkeys drank high doses; others did not. During the period of peak drinking, the daily mean ethanol consumption ranged among animals from 0.54‐1.99 ml/kg. Blood ethanol concentrations then sometimes exceeded 100 mg/dl. During the post‐training period, with return to ad libitum food and water, consumption declined from these peaks, but remained significantly higher than pretraining consumption; the ethanol solution was established as a reinforcer. Monkeys differed significantly in the extent of this pre/post increase. In both pre‐ and post‐training periods, consumption was significantly greater when all three drinkometers operated, compared with only one. On pretraining days when only one drinkometer operated, more dominant animals drank significantly more than less dominant animals; this difference disappeared by the post‐training period, as less dominant animals learned to use the drinkometers at times when the dominant animals eschewed the machines. Pretraining consumption did not predict (among animals) post‐training consumption. Before, during, and after training, these animals drank less of both alcohol and control solutions than did members of another species, which we had studied in smaller indoor pens. We discuss possible explanations and implications.
Maternal Genetic Effects on Ethanol Teratogenesis and Dominance of Relative Embryonic Resistance to Malformations
Authors: Gilliam David M. , Irtenkauf Keith T. 
Published: April 2006

Maternal genetic factors and/or fetal genetic factors contribute to variations in response to prenatal alcohol exposure. To assess the contribution of maternal genotype to ethanol teratogenesis, a reciprocal cross study was conducted in an animal model using C57BL/6J (B6) and long‐sleep (LS) mice. B6 mice are more susceptible than LS mice to prenatal ethanol‐induced malformations but both mouse stocks are susceptible to fetal weight deficits following in utero alcohol exposure. B6 and LS dams were reciprocally mated to B6 or LS males producing four embryonic genotype groups: the true‐bred B6B6 and LSLS genotypes, and the genetically similar B6LS and LSB6 genotypes (the F1 genotype). Dams were intubated with either 5.8 g/kg ethanol (E) or an isocaloric amount of sucrose (S) on day 9 of pregnancy. Fetuses were removed on gestation day 18, weighed, and assessed for soft tissue or skeletal malformations. Results showed a greater litter weight deficit and increased total malformation rate in ethanol‐exposed F1 litters carried by B6 mothers compared to ethanol‐exposed F1 litters carried by LS mothers. This result would be expected only if maternal genetic factors contribute significantly towards susceptibility to ethanol teratogenesis. The influence of the LS mother was to decrease susceptibility to ethanol teratogenesis compared to the B6 mother while the influence of the B6 mother was to increase susceptibility to ethanol teratogenesis compared to the LS mother.The average malformation rate for F1 litters was significantly less than the predicted midparental value. This shows that the F1 genotype exhibited dominance towards resistance to prenatal alcohol effects. There was no differential effect of prenatal treatment on male and female fetuses for any embryonic genotype, indicating that the differential teratogenic response between F1 litters was not due to sex‐linked traits. Likewise, weight gain due to pregnancy and maternal blood ethanol levels did not differ among genotypes.It was concluded that genetic factors differentially influence maternal physiological response to ethanol, which in turn affects teratogenic responses in F1 litters. Separation of maternal physiological mechanisms from fetal mechanisms responsible for ethanol teratogenic susceptibility is needed for targeting women and infants at risk. Such knowledge will help in formulating effective therapeutic intervention strategies.
Detection of a New Acetaldehyde‐Induced Hemoglobin Fraction HbA1ach by Cation Exchange Liquid Chromatography
Authors: Sillanaukee Pekka , Koivula Timo 
Published: April 2006

We developed a sensitive cation exchange liquid chromatographic method for analysis of acetaldehyde binding with hemoglobin. When human hemolysates were incubated in vitro with micromolar concentrations of acetaldehyde without reducing agents, HbAo was found to form two new fractions. One of them was eluated with HbA1c, whereas a novel, previously undescribed fraction was detected between HbF and HbA1c. This new fraction was termed HbA1sch. The mean within‐assay variation for the different hemoglobin fractions varied from 0.45 (HbA0) to 8.2% (HbA1ach) and the between‐assay variation from 0.6 to 19.3%, respectively. After incubation with [1,214C]acetaldehyde the specific radioactivity of HbA1ach was about 10 times higher than that of HbA0 and twice as high as the activity of the HbA1c fraction.The reaction kinetics of the formation of hemoglobin adducts were studied in vitro by incubation of hemolysates with various acetaldehyde concentrations. Acetaldehyde caused both short‐term and permanent changes in hemoglobin. Even low acetaldehyde concentrations from 10 to 100 μmol/liter caused detectable changes in hemoglobin. During incubation the amount of HbA1ach and HbA1c fractions increased rapidly within the first 10 min and decreased slowly during the next hr but did not return to the initial levels. This suggests that only the part of binding of acetaldehyde with hemoglobin is irreversible and the changes can be already detected after incubation with physiological acetaldehyde concentrations.
Videotape versus Computer Interactive Education in Alcoholic and Nonalcoholic Controls
Authors: Alterman Arthur I. , Baughman Timothy G. 
Published: April 2006

Few studies have evaluated the ability of the alcoholic patient to learn treatment‐related information and all have involved conventional educational modalities such as videotape or lecture. Since computer interactive (Cl) programs allow for individualization, feedback, and active learning, we were interested in determining whether Cl would prove to be a more effective educational/treatment modality for male alcoholic patients than the conventional videotape (V) modality. The current study compared the relative effectiveness of the CI and V educational interventions for VA alcoholic patients and a cognitively and sociodemographically matched sample of nonalcoholic VA patients.The 91 male alcoholic subjects (46 V, 45 Cl) were lower socioeconomic outpatients in a VA Alcoholism Treatment program. Control subjects were 35 nonalcoholic men (18 V, 17 Cl) attending an outpatient medical clinic at the same facility. All subjects were individually exposed in a single session to a 1 hr intervention on the Medical Effects of Alcohol. Baseline knowledge was measured prior to the intervention using a 21‐item multiple choice test, while learning and retention were assessed with the same instrument 24 hr after the intervention. All four subgroups (two types of subjects x two types of intervention) identified approximately three more items correctly at the post‐test than at baseline. Thus, neither alcoholics for nonalcoholics acquired more information when exposed to the CI intervention. Further, no differences were found overall in the learning of the alcoholic and nonalcoholic subjects. The implications of these findings and their limitations are discussed.
Suppression of Immune Responsiveness: Sex Differences in Prenatal Ethanol Effects
Authors: Weinberg Joanne , Jerrells Thomas R. 
Published: April 2006

Exposure to ethanol in utero results in changes in the offspring's developing immune system, including thymus lymphocyte subpopulation shifts and functional lymphocyte changes that persist in adult animals. The present study was designed to define further the extent of changes in the immune system that result from fetal ethanol exposure and to compare effects in male and female offspring. In adulthood, male and female offspring from Sprague‐Dawley dams fed an ethanol‐containing liquid diet (alcohol, A), an isocaloric liquid control diet (pair‐fed, PF), or laboratory chow and water (control, C) during pregnancy were tested for several measures of immune competency. Prenatal ethanol exposure differentially affected male and female offspring. Fetal ethanol‐exposed males exhibited a decrease in thymocyte number as well as a decreased splenic lyrnphocyte proliferative response to the T‐cell mitogen, concanavalin A (Con A), with a concomitant decrease in recoverable blast cells, when compared with PF and C males. Further, the defect in T‐cell proliferation of A males was not due to an inability to produce the critical growth factor, interleukin‐2 (IL‐2), but to an inability of lymphoblasts to utilize exogenous IL‐2. Fetal ethanol‐exposed females showed some suggestion of lower thymocyte counts and decreased splenic T‐cell proliferative responses to Con A compared to PF and C females. For most of the immune measures, however, no significant differences occurred among A, PF, and C females. In utero ethanol exposure did not significantly alter spleen cell counts or IL‐2 production, splenic B‐cell proliferation to bacterial lipopolysaccharide (LPS), or thymocyte response to IL‐2 in animals of either sex. As expected, however, all females had lower lymphoid organ cell counts and generally better lymphocyte responses than males from the corresponding groups.These data demonstrate that exposure to ethanol during fetal development results in a number of deficits in immune competency that persist in the adult animal. Of particular importance are the observations that these deficits were observed in T‐cell‐dependent aspects of immunity and were found primarily in male offspring.