bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of Acute in Vivo Ethanol Exposure on Follicle Stimulating Hormone Transcription and Translation
Authors: Emanuele M. A. , Tentler J. J. , Halloran M. M. , Emanuele N. V. , Wallock L. , Kelley M. R. 
Published: April 2006

The impact of ethanol (EtOH) on male rodent reproduction has been well characterized for luteinizing hormone (LH) with suppression of LH release from the pituitary being reported. We have previously reported that acute ethanol (EtOH) exposure in vivo results in rapid and marked suppression of β‐LH gene expression and protein release from the pituitary. This suppression of β‐LH gene expression was unaccompanied by a change in the common α‐subunit mRNA. To further explore the impact of ethanol on male rodent reproduction, we have expanded our studies to follicle stimulating hormone (FSH) and hypothalamic luteinizing hormone releasing hormone (LHRH) as well as of pituitary protein kinase C (PKC).Previously castrated male rats were acutely exposed to EtOH and a dramatic reduction in both serum FSH and LH levels was noted at 1.5 and 3 hr after treatment. These levels returned to saline injected control values at 6 and 24 hr. Despite the fall in serum FSH, there was no change in intrapituitary FSH content at any time point; this lack of pituitary FSH depletion in the face of a fall in serum levels is suggestive of impaired FSH release. In contrast to the fall in β‐LH steady‐state mRNA levels seen previously and confirmed in the present studies, there was no change in β‐FSH steady‐state mRNA at any time point suggesting that EtOH has dichotomous effects on the expression of these two gonadotropins.Pituitary PKC levels were also assessed and found to be unaffected by EtOH at any time point. This enzyme is important in transmembrane signaling for the gonadotropins, and while ETOH is known to affect PKC in other cells, it appears that the effect of EtOH on the gonadotrops is not mediated at this level. Finally, hypothalamic luteinizing hormone releasing hormone (LHRH) content was assessed by radioimmunoassay, and no change was found at any time point in this hypothalamic peptide.We conclude that the effect of EtOH on pituitary gonadotropin gene expression is not uniform, with β‐LH suppression occurring selectively while β‐FSH is unaltered. The release of both gonadotropins appears to be impaired by EtOH, while pituitary PKC and hypothalamic LHRH content are unchanged.
Membrane Biogenesis in the Presence of Ethanol
Authors: Slomiany Amalia , Grabska Maria , Grzelinska Ewa , Yamaki Ken‐ichiro , Kasinathan Chinnaswamy , Slomiany Beatrix A. , Slomiany Bronislaw L. 
Published: April 2006

To investigate the effect of ethanol on the intracellular transport in gastric epithelial cells, the in vitro system, generating transport vesicles which transfer mucus glycoprotein apopeptide (apomucin) from rough endoplasmic reticulum (RER) to Golgi, was assembled. The vesicles, generated from gastric mucous cell RER microsomes and labeled with [3H]palmitic acid, were isolated from the maternal RER and characterized. The electron microscopy revealed that these RER products consisted of 80 to 100 nm smooth membrane vesicles, while the immunochemical analyses showed that they contain apomucin but were devoid of the characteristic integral proteins of the RER membrane. Incubation of apomucin transporting vesicles with Golgi in the presence of UDP‐[3H]galactose resulted in the formation of glycosylated mucin and fusion of the vesicles with Golgi.Formation of ER transport vesicles was dependent on the supply of lipid precursors, and the activity of phosphoglyceride and sphingolipid synthesizing enzymes. In the presence of 60 and 120 MM ethanol, the vesicles were formed, but their lipid composition was modified. The results suggest that ethanol‐induced membrane alterations are initiated at the early stages of the membrane biogenesis and are first reflected in the lipid composition of the intracellular transport vesicles.
Characteristics of a New Urine, Serum, and Saliva Alcohol Reagent Strip
Authors: Tu Guang‐chou , Kapur Bhushan , Israel Yedy 
Published: April 2006

We have tested an ethanol reagent strip developed at the Addiction Research Foundation of Ontario. Alcohol dehydrogenase and nicotinamide adenine dinucleotide, in the presence of pyrazole, react with ethanol to yield acetaldehyde plus reduced nicotinamide adenine dinucleotide. The latter reduces iodonitrotetrazolium chloride in the presence of diaphorase, generating an intense red color. The rate of color development is proportional to the concentration of ethanol. Color is compared at a specific time against a calibrated color scale ranging from green (negative) to red, representing alcohol concentrations of 0, 25,50, 100, 200, and 400 mg/dI(0‐0.4%; 0–87 mmol/liter).We were able to interpolate the color observed between the calibrated blocks. When tested on urine, serum/plasma, and saliva, ethanol concentration determined by the reagent strip correlates well with ethanol concentration as determined by gas chromatography or by automated enzymatic analysis (r= 0.92–0.98, p < 0.001; slope 0.83–1.16). The reagent strip was shown to be used appropriately by nonexperienced individuals following a 1‐min explanation (reagent strip values, r= 0.92; p < 0.001, slope = 0.97, versus gas chromatography). The reagent strip does not react with methanol (wood alcohol), isopropanol (rubbing alcohol), and ethylene glycol (antifreeze) often found in accidental poisonings. In 379 clinical samples obtained without exclusion criteria from 12 hospital emergency rooms and a liver clinic, the sensitivity of the reagent strip in detecting ethanol was 98%. Specificity was 99%. The reagent strip was found to have virtually unlimited stability under refrigeration (4°C) and to be stable for 3 to 4 months at room temperature (22‐23°C). The reagent strip should be valuable in a number of clinical settings in which rapid assessment of alcohol intoxication or of alcohol consumption, using either of the biological fluids (urine/serum/saliva), is wanted and in which a specific and sensitive method to determine alcohol requiring no instrumentation is needed.
Obsessive and Compulsive Characteristics of Craving for Alcohol in Alcohol Abuse and Dependence
Authors: Modell Jack G. , Glaser Frederick B. , Cyr Louis , Mountz James M. 
Published: April 2006

The purpose of this study was to quantify the extent to which subjective ratings of craving for alcohol in the alcohol‐abusing or dependent person (herein, alcoholic) correlate with measurable and specific characteristics of obsessions and compulsions. The Yale‐Brown Obsessive Compulsive Scale modified to reflect obsessionality and compulsivity specifically related to heavy drinking (Y‐BOCS‐hd) was used for this purpose.Highly significant correlations were found in the alcoholic population (n= 62) between subjectively rated craving for alcoholic beverages and several of the Y‐BOCS‐hd questions regarding alcohol‐related thoughts and drinking behavior. Additionally, mean craving scores were considerably greater in the alcoholic population than the matched control population (n= 62). The data suggest that craving shares specific features in common with the obsessions of obsessive‐compulsive disorder and that the existence of craving is dependent on the presence of obsessive thoughts about drinking. Positive correlations between craving and measures of compulsive drinking behavior also were found; compulsive drinking behavior, however, may reflect the consequences of craving rather than a fundamental characteristic of craving itself. The data show that despite difficulties in defining the term craving, it is clearly a phenomenon that is experienced or endorsed by most alcoholic subjects and is not by most persons who do not abuse alcohol.
Alterations in Brain Polyribosomal RNA Translation and Lymphocyte Proliferation in Prenatal Ethanol‐Exposed Rats
Authors: Tewari Sujata , Diano Marcel , Bera Rimal , Nguyen Quoc , Parekh Hemalatha 
Published: April 2006

The long‐term effects of prenatal ethanol exposure on the properties of brain polysomes and the proliferative responses of lymphocytes to mitogenic stimulation in adult offspring were assessed. Female Sprague‐Dawley rats either ingested the control or 6.6% ethanol‐containing Lieber‐DeCarli liquid diet during the 3rd trimester of pregnancy. Controls were age‐matched and pair‐fed. At 42 to 72 days of age, ethanol effects were evaluated on the (1) polysomal properties in the cerebral hemispheres, cerebellum, and hippocampal regions of the brain after translation in a messenger RNA (mRNA)‐dependent rabbit reticulocyte lysate system and (2) immunologic functions of lymphocytes cultured from spleen cells by measuring their responses to mitogenic stimulation.Results showed long‐term adverse effects of in utero ethanol exposure on the polysomal RNA translation in each of the three brain regions tested with free polysomal mRNAs affected more than the bound polysomal mRNAs. Of these, the hippocampal region appeared to sustain the most injurious effects. In addition, a suppression of the mitogen‐induced lymphocyte proliferative responses were present under these conditions. The degree of suppression varied with the specific mitogen used. Data suggest that the ethanol effects on the CNS and lymphocyte proliferation are most possibly irreversible, and in the case of the CNS, a post‐translational modification by ethanol is indicated. The reduced lymphocyte responses are suggestive of a possible interference by ethanol of the synthesis of interleukin‐2 (IL‐2) and/or a reduced binding of IL‐2 with its receptor (IL‐2 receptors).
Isradipine and Other Calcium Channel Antagonists Attenuate Ethanol Consumption in Ethanol‐Preferring Rats
Authors: Fadda F. , Garau B. , Colombo G. , Gessa G. L. 
Published: April 2006

The present work is concerned with studying of the ability of different calcium channel antagonists to modify voluntary ethanol ingestion by rats selectively bred for high ethanol preference. The compounds were given S.C. thrice daily for 5 days at doses that did not produce locomotor impairment. While nifedipine, darodipine, and verapamil (each at the dose of 20 mg/kg thrice daily) produced a modest reduction in ethanol intake, isradipine (at the dose of 1 mg/kg three times a day) reduced ethanol intake by over 70%.For all compounds, the reduction in ethanol intake was compensated by a proportional increase in water consumption and the inhibitory effect persisted throughout the 5 days of treatment. The data indicate that calcium channel antagonists exhibit quite different potency in reducing ethanol preference, however this action is a general property of this class of compounds.
Alcohol Availability and the Formal Power and Resources of State Alcohol Beverage Control Agencies
Authors: Gruenewald Paul J. , Madden Pat , Janes Kathy 
Published: April 2006

The formal powers and resources of state alcohol beverage control agencies place them in a position to regulate access to alcoholic beverages through restrictions on retail distribution and sales. For example, monopoly states restrict access to spirits, and sometimes wine, by allowing retail sales only through state stores. On the other hand, license and monopoly states share in restricting sales through the use of price posting and fixing provisions. The degree to which these powers are realized in restrictions on alcohol outlets (e.g., licenses) and subsequent alcohol consumption (e.g., sales) was investigated in the current study.In a cross‐sectional analysis of data available from 44 alcohol beverage control (ABC) jurisdictions in the United States, it was shown that states with greater restrictions on retail sales had greater resources for the conduct of ABC activities and lower densities of spirit outlets. These states, however, had greater densities of wine and beer outlets. States with greater marketplace restrictions had more resources for ABC enforcement activities and lower outlet densities across all beverage types. Further, supporting the suggestion that availability and demand may be simultaneously related, greater outlet densities were related to greater alcohol consumption (for beer) and greater levels of consumption were related to greater outlet densities (for wine).
Enzymatic Production of Acetaldehyde from Ethanol in Rat Brain Tissue
Authors: Gill K. , Menez J. F. , Lucas D. , Deitrich R. A. 
Published: April 2006

The capacity for the brain to produce acetaldehyde (AcHO) from ethanol was determined in rat brain homogenates. Rat brains were perfused with saline‐heparin solution and homogenized in a phosphate buffer. Varying amounts of tissue were incubated with ethanol (0–100 mM) for periods of up to 60 min. The reaction was stopped by the addition of desferrioxamine and ice‐cold perchloric acid. Supernatants were treated with dinitrophenylhydrazine reagent, extracted with isooctane in the presence of an internal standard, and the derivatives were separated by HPLC.The addition of 4‐methyl pyrazole (an alcohol dehydrogenase inhibitor) or metyrapone (a cytochrome P450 inhibitor) had no effect on the amount of recovered AcHO. On the other hand, treatment with the catalase inhibitors sodium azide, cyanamide, or 3‐amino‐1,2,4‐triazole blocked the production of AcHO while the addition of exogenous peroxide or a peroxide‐generating system enhanced the production of AcHO. Overall, these results suggest that AcHO may be produced in the brain during alcohol intoxication, through the action of the enzyme catalase.
The Relationship of Outlet Densities to Alcohol Consumption: A Time Series Cross‐Sectional Analysis
Authors: Gruenewald Paul J. , Ponicki William R. , Holder Harold D. 
Published: April 2006

The implementation of regulations on access to alcoholic beverages, whether through beverage taxes or restrictions on the availability of this commodity through alcohol outlets, has often been proposed as a legitimate and politically feasible approach to the prevention of alcohol‐related problems. Empirical studies of the effects of these approaches to regulation on alcohol consumption and problems, however, have not been unanimous in their support of these preventive measures. While support exists for the suggestion that increases in alcohol beverage prices reduce consumption and have preventive effects upon the occurrence of problems, relatively little evidence exists for the supposition that the regulation of alcohol availability will have similar preventive effects. The lack of evidence in support of the latter thesis rests primarily upon the difficulty of obtaining sufficient data to examine comprehensive models of access to alcohol.The current paper analyzes aggregate time series cross‐sectional data from states of the U.S. to evaluate the relationships between alcohol beverage prices, availability, and alcohol sales within one analytic model. The model relates beverage prices and alcohol availability directly to alcohol sales in the context of an assumed simultaneous relationship between sales and availability. The results show that, independent of the effects of beverage prices, and controlling for the endogeneity of sales and availability, physical availability of alcohol was directly related to sales of spirits and wine.
Effects of Ethanol Concentration and Fixed‐Ratio Requirement on Ethanol Self‐Administration by P Rats in a Continuous Access Situation
Authors: Files Forrest J. , Andrews Christine M. , Lewis Roderic S. , Samson Herman H. 
Published: April 2006

Rats, from the alcohol preferring (P) line, were placed in operant chambers in which food pellets, water, and 10% ethanol (v/v) were available continuously for 23 hr/day. During Experiment 1, the effects of changing ethanol concentration and response requirement for ethanol were examined. Ten percent and 20% ethanol (v/v) were available on two fixed ratio (FR) schedules, FR 1 and FR 4, for 2 weeks each. During Experiment 2, the effects of increasing the response requirement for ethanol were investigated. Starting with FR 4, the FR requirement for ethanol doubled during 2‐week intervals until FR 32 was in effect. For the final phase of these studies, water was placed in the dipper for 1 week followed by a return to 10% ethanol in the dipper.The results from Experiment 1 indicated that when the FR requirement was decreased from FR 4 to FR 1, ethanol‐reinforced responding decreased but total daily intake increased. Lowering the FR requirement did not affect the number of ethanol bouts per day but bout size increased. Ethanol concentration had no effect on bout size but the number of bouts per day decreased when the concentration was increased to 20%. Since bout size was unchanged by increasing the ethanol concentration, intake per bout increased at 20% ethanol. The results from Experiment 2 indicated that increasing the response requirement for ethanol decreases ethanol intake. When water was placed in the dipper, responding decreased to the lowest levels observed in the experiment. When ethanol was returned to the dipper, responding returned to baseline levels. Overall, the results indicate that while P rats may consume more ethanol than other lines of rats, their behavior can be modified by environmental variables in a manner somewhat similar to heterogeneous nonselected Long‐Evans rats.
Effects of Ethanol on Cultured Fetal Serotonergic Neurons
Authors: Lokhorst Denise K. , Druse Mary J. 
Published: April 2006

In utero ethanol exposure impairs the development of several neurotransmitter systems, including the serotonergic system. However, at present the mechanism by which in utero ethanol exposure damages the developing brain is unknown. This research examined the possibility that ethanol directly impairs the development of serotonergic neurons. This hypothesis was assessed by examining the content of serotonin (5‐HT), 5‐HT uptake, and 5‐HT immunopositive neurons in cultures of fetal rhombencephalic neurons that were exposed to ethanol for 4 days in vitro. In addition, the effects of in vitro ethanol exposure on protein and DNA content of cultured rhombencephalic neurons were determined.These studies demonstrated that a 4‐day exposure of cultured rhombencephatic neurons to 50 to 300 mg ethanol/dl did not affect 5‐HT content, 5‐HT uptake, or the proportion of 5‐HT immunopositive neurons. In addition, this ethanol exposure had no significant effect on protein or DNA content. Additional studies, using a 4‐day exposure to 450 mg ethanol/dl also did not detect significant differences in 5‐HT uptake or in protein or DNA content.The marked differences in the findings of the present in vitro and previous in vivo studies may be due to the fact that the ethanol exposure in vivo was longer than that in vitro, and included the period of early development of serotonergic neurons and their progenitors. Alternatively, the differences may be due to ethanol‐associated alterations in maternal or fetal factors (e.g., hormones, amino acids, and growth factors) that are necessary for the normal development of the serotonergic system in vivo. Normal concentrations of such factors in the serum‐containing media may have protected the cultured neurons from the damaging effects of ethanol.
Personality Characteristics of Sisters and Spouses of Male Alcoholics
Authors: Hill Shirley Y. 
Published: April 2006

Sisters of alcoholics from high‐density multigenerational families were assessed to determine personality characteristics. Spousal similarity was evaluated in proband/spouse pairs and in spouse pairs from the parental generation, allowing for comparisons of selection versus contagion as explanations for this similarity.Sisters were found to differ from control women with respect to Alienation and Social Closeness from the Multidimensional Personality Questionnaire, and Scale 6 (Paranoia) from the Minnesota Multiphasic Personality Inventory. Only spouses from the parental generation were similar on Alienation, suggesting that exposure over time (contagion) leads to greater similarity in parents from High‐Risk families. Modest correlations in spouse pairs from both generations suggest that assortative mating for Social Closeness occurs among the parents of these individuals from High‐Risk families, and further suggest that a diminished level of Social Closeness for sisters of alcoholics may be mediated in part by additive genetic variance. It is concluded that assortative mating for particular traits may contribute to increased risk for alcoholism. Also, failure to mate assortatively for other traits (e.g., Traditionalism, Harm Avoidance) may also contribute to increased rates in High‐Risk families.
Atypical Liver Alcohol Dehydrogenase in the Spanish Population: Its Relation with the Development of Alcoholic Liver Disease
Authors: Vidal Francesc , Perez Jaume , Panisello Joima , Toda Roca , Gutierrez Cristina , Richart Cristobal 
Published: April 2006

The presence of atypical liver alcohol dehydrogenase (ADH) was determined in samples of liver tissue from 222 alcoholic and nonalcoholic subjects to determine its prevalence in the Spanish population, and to evaluate the possible relationship between the presence of this isoenzyme and the development of alcoholism and alcoholic liver disease. Alcoholic patients were classified into the following groups: control subjects, with normal liver pathology (group 1), patients with noncirrhotic liver disease (group 2), and patients with cirrhosis of the liver (group 3). Nonalcoholic subjects were also divided, following the same criteria, into groups 4, 5, and 6, respectively.The prevalence of atypical ADH in the population analyzed was 16.2%. Atypical ADH was present in 14.9% of alcoholics and in 17.4% of nonalcoholics (P=ns). There were no significant differences when the prevalence of atypical ADH of alcoholic and nonalcoholic patients with similar degrees of liver pathology was compared (group 1 vs. 4, group 2 vs. 5, and group 3 vs. 6). The prevalence of atypical ADH was also similar in cirrhotic patients with respect to those of noncirrhotic liver disease and control patients, either in alcoholic or nonalcoholic groups.Our findings indicate that the prevalence of atypical ADH in the Spanish population is similar to that reported for other Caucasian groups. Moreover, the presence of atypical ADH does not play a role in the development of alcoholism nor in the development of alcoholic liver disease in the population analyzed.
Effects of Ethanol on Cultured Fetal Astroglia
Authors: Lokhorst Denise K. , Druse Mary J. 
Published: April 2006

This study investigated the effects of a 4‐day ethanol exposure on cultured rhombencephalic astroglia. The contents of astroglial protein and DNA, and astroglial uptake of serotonin (5‐HT) were determined. Fetal rhombencephalic astroglia were examined because of this laboratory's evidence that in utero ethanol exposure markedly impairs the development of serotonergic neurons, which are located in this fetal brain area, and because of the recently demonstrated importance of local support glia in neuronal development.The results of these experiments demonstrated that protein was significantly reduced in astroglia cultured in ethanol at either 150 or 300 mg/dl. In addition, these astroglia exhibited decreased [3H]5‐HT uptake per well. However, no significant ethanol‐associated differences were detected when [3H]5‐HT uptake was expressed per mg protein rather than per well. In contrast to the effects of a 4‐day ethanol exposure, the acute ethanol exposure did not significantly alter astroglial uptake of [3H]5‐HT/well. In addition, the 4‐day exposure to 50 to 300 mg/dl of ethanol did not significantly alter astroglial DNA content.In summary, it appears that a 4‐day exposure of cultured fetal rhombencephalic astroglia to 150 to 300 mg/dl of ethanol reduces astroglial protein content and astroglial 5‐HT uptake. A reduction in total astroglial proteins, potentially including those that act as essential growth factors, could contribute to some of the ethanolassociated alterations in central nervous system development.