bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Stress on Alcohol Consumption in Rats Selectively Bred for High or Low Alcohol Drinking
Authors: Chester Julia A. , Blose Annette M. , Zweifel Mark , Froehlich Janice C. 
Published: March 2004

Abstract: Background: Stress has long been thought to influence the initiation and maintenance of alcohol drinking in humans. However, results of studies in animals suggest that the relationship between stress and alcohol drinking is not well understood. The purpose of this study was to examine the effect of unpredictable and uncontrollable restraint stress on alcohol consumption in two sets of rat lines selectively bred for alcohol preference (P) and high alcohol drinking (HAD1) and for alcohol nonpreference (NP) and low alcohol drinking (LAD1).Methods: Male P (n= 26) and NP (n= 26) and HAD1 (n= 17) and LAD1 (n= 20) rats were counterbalanced on the basis of alcohol intake and assigned, in matched pairs, to either a stress (Stress) or a no‐stress (Control) group. All rats were given a free choice between a 10% v/v alcohol solution and water, with food freely available. Unpredictable, uncontrollable stress, which consisted of immobilization in a nylon restraint sleeve for 30 to 120 min/day, was applied for 10 consecutive days.Results: Stress moderately reduced alcohol intake in both P and HAD1 rats versus controls and had no effect on alcohol intake in either the NP or the LAD1 rats during the 10 days of stress application. Alcohol intake was increased for the first 5 days after stress termination in P rats but not in HAD1 rats. Alcohol intake remained stable for several weeks in both the NP and LAD1 lines after stress termination and then increased during the last 15 days of the 35‐day poststress period in NP rats, but not in LAD1 rats.Conclusions: A reduction in alcohol intake during stress in rats with a genetic predisposition toward high alcohol intake seems to be a moderate but consistent finding, whereas an increase in alcohol intake after stress termination is less consistent and may be influenced by genetic background.
Possible Interaction of Alcohol Dehydrogenase and Aldehyde Dehydrogenase Genes With the Dopamine D2 Receptor Gene in Anxiety‐Depressive Alcohol Dependence
Authors: Huang San‐Yuan , Lin Wei‐Wen , Ko Huei‐Chen , Lee Jia‐Fu , Wang Tso‐Jen , Chou Yuan‐Hwa , Yin Shih‐Jiun , Lu Ru‐Band 
Published: March 2004

Abstract:Background:The role of the dopamine D2 receptor (DRD2) gene in the development of alcohol abuse or dependence is controversial. The controversy is due in part to the disparate definitions pertaining to the control groups used and to the definitions of subtypes in alcohol dependence. In the Han Chinese population, the alcohol dehydrogenase 1B*2/*2 (ADH1B*2/*2) genotype and the aldehyde dehydrogenase 2*2 (ALDH2*2) allele have been considered as protective factors against alcohol abuse or dependence. Moreover, theADH1BandALDH2genes might be involved in dopamine metabolism. We hypothesized that theADH1BandALDH2genes might interact with theDRD2gene and that the association between theDRD2gene and alcohol dependence might be affected by differentADH1BandALDH2genotypes. This study examined whether theDRD2gene is associated with specific subtypes of alcohol dependence and evaluated the relationship between theDRD2gene and alcohol‐metabolizing genes in a specific subtype of alcohol dependence.Methods:Of the 465 Han Chinese subjects who were recruited for the study, 71 were classified with pure alcohol dependence, 113 with both alcohol dependence and anxiety‐depression (ANX/DEP ALC), and 129 with anxiety‐depression but without alcohol dependence (ANX/DEP). The remaining 152 subjects were supernormal controls. All subjects were interviewed with the Chinese version of the modified Schedule of Affective Disorders and Schizophrenia‐Lifetime; all alcohol dependence, anxiety, and major depressive diagnoses were made according to DSM‐IV criteria.Results:TheDRD2gene was not found to be associated with pure alcohol dependence or ANX/DEP, but was found to be associated with ANX/DEP ALC. Furthermore, the association between theDRD2gene and ANX/DEP ALC was shown to be under the control of theALDH2*1/*1andADH1B*1/*2genotypes.Conclusions:ANX/DEP ALC is a specific subtype of alcohol dependence. Because ANX/DEP ALC was associated with theDRD2gene only under the stratification ofADH1B*1/*2orALDH2*1/*1, theDRD2gene might interact with theADH1Bgene and theALDH2gene, respectively, in the development of ANX/DEP ALC in the Taiwan Han Chinese population.
Alcohol Affects Eye Movements Essential for Visually Guided Stepping
Authors: Crowdy K. A. , Marple‐Horvat D. E. 
Published: March 2004

Abstract: Background: To understand how and why alcohol intoxication affects visually guided stepping, the eye movements and performance of 6 subjects (aged 22–35 years) were monitored as they progressed along a pathway of 18 irregularly placed stepping stones before and after consumption of an acute oral dose of alcohol.Methods: Horizontal eye movements were measured with infrared reflectometry; footfall on or off target was monitored via copper fabric soles stuck to subjects’ footwear. Breath alcohol concentration was monitored with an Alco‐Sensor III breathalyzer.Results: After alcohol loading, both locomotor and oculomotor deficits were evident. All subjects increased their step cycle duration—with prolonged stance, swing, and double support phases—and occasionally missed footfall targets. A large proportion of saccades made to fixate successive stepping stones were inaccurate and were accompanied by one or more corrective saccades. These problems with looking and stepping to footfall targets tended to occur together and were comparable to those seen previously in cerebellar patients undertaking the same task.Conclusions: The fact that healthy subjects acutely intoxicated by alcohol show symptoms of cerebellar dysfunction suggests that alcohol acutely and adversely affects the cerebellar contribution to performance of visually guided movements.
Using Alcohol Screening Results and Treatment History to Assess the Severity of At‐Risk Drinking in Veterans Affairs Primary Care Patients
Authors: Bradley Katharine A. , Kivlahan Daniel R. , Zhou Xiao‐Hua , Sporleder Jennifer L. , Epler Amee J. , McCormick Kinsey A. , Merrill Joseph O. , McDonell Mary B. , Fihn Stephan D. 
Published: March 2004

Abstract: Background: Primary care providers need practical methods for managing patients who screen positive for at‐risk drinking. We evaluated whether scores on brief alcohol screening questionnaires and patient reports of prior alcohol treatment reflect the severity of recent problems due to drinking.Methods: Veterans Affairs general medicine outpatients who screened positive for at‐risk drinking were mailed questionnaires that included the Alcohol Use Disorders Identification Test (AUDIT) and a question about prior alcohol treatment or participation in Alcoholics Anonymous (“previously treated”). AUDIT questions 4 through 10 were used to measure past‐year problems due to drinking (PYPD). Cross‐sectional analyses compared the prevalence of PYPD and mean Past‐Year AUDIT Symptom Scores (0–28 points) among at‐risk drinkers with varying scores on the CAGE (0–4) and AUDIT‐C (0–12) and varying treatment histories.Results: Of 7861 male at‐risk drinkers who completed questionnaires, 33.9% reported PYPD. AUDIT‐C scores were more strongly associated with Past‐Year AUDIT Symptom Scores than the CAGE (p < 0.0005). The prevalence of PYPD increased from 33% to 46% over the range of positive CAGE scores but from 29% to 77% over the range of positive AUDIT‐C scores. Among subgroups of at‐risk drinkers with the same screening scores, patients who reported prior treatment were more likely than never‐treated at‐risk drinkers to report PYPD and had higher mean Past‐Year AUDIT Symptom Scores (p < 0.0005). We propose a simple method of risk‐stratifying patients using AUDIT‐C scores and alcohol treatment histories.Conclusions: AUDIT‐C scores combined with one question about prior alcohol treatment can help estimate the severity of PYPD among male Veterans Affairs outpatients.
Verbal and Visuospatial Learning and Memory Function in Children With Moderate Prenatal Alcohol Exposure
Authors: Willford Jennifer A. , Richardson Gale A. , Leech Sharon L. , Day Nancy L. 
Published: March 2004

Abstract: Background: This study investigated the effects of moderate prenatal alcohol exposure on learning and memory in 14‐year‐old adolescents. The Children's Memory Scale was used to assess learning and memory function in the verbal/auditory and visual/spatial domains. In addition, both short‐ and long‐term memory function were assessed.Methods: Data were collected as part of the Maternal Health Practices and Child Development Project, a longitudinal study including 580 children and their mothers. Women were assessed during each trimester of pregnancy and with their children from birth to 16 years of age. At age 14, memory function was evaluated using the Children's Memory Scale, an assessment tool that measures learning and immediate and delayed memory function in the verbal and visual‐spatial domains.Results: Prenatal alcohol exposure during the first trimester predicted deficits in learning, short‐term memory, and long‐term memory, specifically in the verbal domain. Deficits in performance were specific to learning and memory of word‐pairs. In addition, deficits in memory were mediated by learning performance.Conclusions: Results demonstrated that prenatal alcohol exposure lead to deficits in encoding processes as indicated by deficits in verbal learning. Initial deficits in acquisition were responsible for deficits in immediate and delayed recall of verbal information in children who were exposed to alcohol during pregnancy but did not have fetal alcohol syndrome.
Cumulative Lifelong Alcohol Consumption Alters Auditory Brainstem Potentials
Authors: Smith Elisabeth Stephanie , Riechelmann Herbert 
Published: March 2004

Abstract: Background: Alcohol is one of the most widely abused substances in the United States and Europe. It is believed that alcohol causes brain damage that may influence the central auditory tracts. Brainstem auditory evoked potentials (BAEPs) are a common method for measuring central auditory pathways. Therefore, the influence of cumulative lifelong alcohol consumption on BAEPs in subjects with normal hearing was investigated both qualitatively and quantitatively.Methods: BAEPs were measured in 38 male subjects, 19 of whom were head and neck tumor patients with an ECOG (Eastern Cooperative Oncology Group) scale of zero and 19 plastic surgery patients. A self‐report questionnaire on alcohol and nicotine consumption together with blood tests and pure tone audiometry were obtained for all subjects before the BAEP measurement.Results: The alcohol consumption of the head and neck tumor patients corresponded to high‐risk, dangerous, and risky alcohol consumption behavior, whereas that of the plastic surgery patients corresponded to risky and low‐risk consumption behavior. In this way, a wide spectrum of alcohol consumption was covered. The latency I–V of the high‐risk, dangerous, and risky drinkers was found to be significantly delayed compared with low‐risk drinkers. A logarithmic relationship between BAEP latencies and cumulative lifelong alcohol consumption was obtained.Conclusion: Alcohol consumption leads to damage in the brainstem. The logarithmic behavior between BAEP latencies and cumulative lifelong alcohol consumption reveals that even alcohol consumption within the range of low‐risk drinkers may alter auditory evoked brainstem potentials significantly.
Effect of Duration of Maternal Alcohol Consumption on Calcium Metabolism and Bone in the Fetal Rat
Authors: Keiver Kathy , Weinberg Joanne 
Published: March 2004

Abstract: Background: Prenatal ethanol exposure can retard fetal growth and delay skeletal development. Ethanol also impairs maternal calcium (Ca) homeostasis and this impairment could mediate some of ethanol's effects on the fetal skeleton. Our previous studies suggest that the duration of maternal ethanol consumption may be an important factor for determining the severity of ethanol's effects on Ca homeostasis and fetal skeletal development. The purpose of this study was, therefore, to determine the effect of the duration of maternal ethanol consumption on fetal growth and skeletal development and to investigate the possibility that ethanol's effects may be related to perturbations in fetal/maternal Ca homeostasis.Methods: Rats were fed ethanol (36% ethanol‐derived calories) in liquid diets for 3 weeks (days 1–21 of gestation) or 6 weeks (for 3 weeks before and throughout gestation). Fetuses were collected on day 21 of gestation, and body weight and length were measured. Fetuses were stained to determine the degree of skeletal ossification, and fetal blood was analyzed for ethanol, Ca (total and ionic Ca), albumin, parathyroid hormone (PTH), and osteocalcin.Results: Maternal ethanol consumption decreased fetal growth and delayed fetal skeletal development. Although there was a trend for fetal body length and serum osteocalcin levels to be more severely affected with an increased duration of maternal ethanol consumption, duration had no effect on fetal body weight or skeletal ossification. Fetal Ca homeostasis was also affected by ethanol exposure, with fetal hypocalcemia apparent after 6 weeks of maternal ethanol intake. A significant inverse relationship was found between fetal blood Ca levels and blood alcohol concentration (BAC), suggesting that the severity of the fetal hypocalcemia may have been related to differences in fetal BAC, rather than duration of maternal ethanol intake. Fetal serum PTH levels did not differ significantly among treatment groups indicating that the fetal hypocalcemia was not caused by a decrease in PTH levels.Conclusions: Prenatal ethanol exposure impaired Ca homeostasis and skeletal development in the fetal rat. The severity of ethanol's effects was only marginally dependent on the duration of maternal ethanol consumption per se and seemed to be more related to the relative exposure of the fetus to ethanol (fetal BAC). The relationship between the ethanol‐induced fetal hypocalcemia and skeletal effects remains to be determined.
Inhibitory Effect of Alcohol on Osteogenic Differentiation in Human Bone Marrow–Derived Mesenchymal Stem Cells
Authors: Gong Zhaodi , Wezeman Frederick H. 
Published: March 2004

Abstract: Background: Alcohol‐induced osteoporosis is characterized by a considerable suppression of osteogenesis. The objective of this investigation was to determine the effect of alcohol on gene expression, protein synthesis, and mineralization in human bone marrow–derived mesenchymal stem cells induced toward osteogenic differentiation in vitro.Methods: Human bone marrow–derived mesenchymal stem cells induced toward osteogenesis were cultured in the presence or absence of 50 mM alcohol. Stem cells were characterized by using SH2 antibody to the cell‐surface antigen CD105/endoglin, and their proliferation in the presence of alcohol was quantified. The expression of genes for early, middle, and late markers of the osteogenic lineage was quantified by Northern analysis, and bone matrix protein synthesis was assayed. The effect of alcohol on cell‐mediated matrix mineralization in terminally differentiated cultures was determined by von Kossa staining.Results: Fluorescence‐activated cell sorting analysis of human mesenchymal stem cells separated with a Percoll gradient proved 99% homogeneity by using SH2 antibody to the surface antigen CD105. Dose‐dependent inhibition of proliferation of these stem cells occurred at concentrations greater than 50 mM alcohol. Gene expression of osteoblast‐specific factor 2/core binding factor a1 (Osf2/Cbfa1), type I collagen, alkaline phosphatase, and osteocalcin (early, middle, and late markers for osteogenesis, respectively) was analyzed with and without osteogenic induction and treatment with 50 mM alcohol. After induction, Osf2/Cbfa1 levels were unresponsive to alcohol. To determine the effect of alcohol on human mesenchymal stem cell progression along the osteogenic pathway, messenger RNA (mRNA) levels for type I collagen, alkaline phosphatase, and osteocalcin were examined after osteogenic induction. After osteogenic induction, alcohol down‐regulated the gene expression of type I collagen and significantly reduced its synthesis. Alcohol did not alter mRNA expression of alkaline phosphatase, a midstage marker for osteogenesis, but significantly decreased its activity compared with osteogenic induction alone. After induction, osteocalcin remained unchanged by alcohol at both the mRNA and protein levels. Histochemistry revealed decreased alkaline phosphatase staining and fewer alkaline phosphatase–positive cells in alcohol‐treated human mesenchymal stem cell cultures. von Kossa staining revealed a reduction in the number of mineralizing nodules in stem cell cultures after alcohol treatment.Conclusions: Collectively, the data suggest that alcohol alters osteogenic differentiation in human bone marrow–derived mesenchymal stem cell cultures during lineage progression and provide further insight into alcohol‐induced reduced bone formation.
A Follow‐up Survey on Seizures Induced by Animated Cartoon TV Program “Pocket Monster”
Authors: Ishiguro Yoshiko , Takada Hiroyuki , Watanabe Kazuyoshi , Okumura Akihisa , Aso Kosaburo , Ishikawa Tatsuya 
Published: March 2004

Summary:  Purpose
: To identify the short‐term outcome of patients who had seizures while watching an animated cartoon TV program, “Pocket Monster,” on December 16, 1997. Methods: One and three years after the incident, questionnaires were sent to physicians of each patient about seizure recurrence, EEGs, and medication. Results: Among 103 patients in whom epileptic seizures occurred during the TV program and information on the outcomes was available, 25 (24%) patients had a history of unprovoked seizures before the incident (Epilepsy Group), and 78 (76%) did not (Non‐Epilepsy Group). Twenty‐three (22%) patients were reported to have seizures after the incident, and 15 of them had visually induced seizures. Patients of the Epilepsy Group had more seizure recurrence than did those of the Non‐Epilepsy Group (56% vs. 9%; p < 0.0001), either for unprovoked (44% vs. 4%; p < 0.0001) or visually induced seizures (28% vs. 9%; p < 0.05). Of nine patients of the Non‐Epilepsy Group who had seizures after the incident, only three developed recurrent unprovoked seizures. In the Non‐Epilepsy Group, no difference was found in seizure recurrence between patients in whom valproate (VPA) was prescribed immediately after the incident and in those without medication (one of five (20%) vs. seven of 73 (10%); p > 0.05). EEG was performed at least once in 98 patients after the incident. Photoparoxysmal response (PPR) was present in 45 (46%) patients, and spontaneous epileptiform discharges, in 49 (50%). PPR did not have any correlation with recurrence of seizures, neither spontaneous nor visually induced seizures, whereas spontaneous epileptiform discharges showed a good correlation with seizure recurrence (34% vs. 8%; p < 0.01), including visually induced seizures (24% vs. 2%; p < 0.01). Conclusions: Short‐term outcomes showed that 70 (68%) of 103 patients who had a seizure during the incident had no seizures before and during ≤3 years of follow‐up.
Development of Amygdaloid Kindling in Histidine Decarboxylase–deficient and Histamine H1 Receptor–deficient Mice
Authors: Hirai Tadashi , Okuma Chihiro , Harada Chie , Mio Mitsunobu , Ohtsu Hiroshi , Watanabe Takeshi , Kamei Chiaki 
Published: March 2004

Summary:  Purpose: This study attempted to clarify the role of histamine or histamine H1 receptors in the development of amygdaloid kindling by using histidine decarboxylase (HDC)‐deficient and histamine H1 receptor (H1R)‐deficient mice. Methods: Under pentobarbital anesthesia, mice were fixed to a stereotaxic apparatus, and bipolar electrodes were implanted into the right amygdala. Electrodes were connected to a miniature receptacle, which was embedded in the skull with dental cement. A bipolar electroencephalogram was recorded; bipolar stimulation of the amygdala was applied every day with a constant‐current stimulator and continued until a generalized convulsion was obtained. Results: The development of amygdaloid kindling in HDC‐deficient and H1R‐deficient mice was significantly accelerated compared with that in their respective wild‐type mice. In addition, the afterdischarge (AD) duration and generalized seizure duration in HDC‐deficient and H1R‐deficient mice were prolonged. Intraperitoneal injection of histidine resulted in an inhibition of amygdaloid kindled seizures in wild‐type mice at doses that caused an increase in the histamine contents of the brain. However, no significant effect was observed with histidine in H1R‐deficient mice at the same dose. Conclusions: These findings suggest that histaminergic mechanisms through H1 receptors play a crucial role not only in amygdaloid kindled seizures but also in the development of amygdaloid kindling.
Identification of Abnormal Neuronal Metabolism Outside the Seizure Focus in Temporal Lobe Epilepsy
Authors: Mueller Suzanne G. , Laxer Kenneth D. , Cashdollar Nathan , Flenniken Derek L. , Matson Gerald B. , Weiner Michael W. 
Published: March 2004

Summary:  Purpose: The aim of this study was to identify metabolically abnormal extrahippocampal brain regions in patients with temporal lobe epilepsy with (TLE‐MTS) and without (TLE‐no) magnetic resonance imaging (MRI) evidence for mesial‐temporal sclerosis (MTS) and to assess their value for focus lateralization by using multislice 1H magnetic resonance spectroscopic imaging (MRSI). Methods: MRSI in combination with tissue segmentation was performed on 14 TLE‐MTS and seven TLE‐no and 12 age‐matched controls. In controls, N‐acetylaspartate/(creatine + choline) [NAA/(Cr+Cho)] of all voxels of a given lobe was expressed as a function of white matter content to determine the 95% prediction interval for any additional voxel of a given tissue composition. Voxels with NAA/(Cr+Cho) below the lower limit of the 95% prediction interval were defined as “pathological” in patients and controls. Z‐scores were used to identify regions with a higher percentage of pathological voxels than those in controls. Results: Reduced NAA/(Cr+Cho) was found in ipsilateral temporal and parietal lobes and bilaterally in insula and frontal lobes. Temporal abnormalities identified the epileptogenic focus in 70% in TLE‐MTS and 83% of TLE‐no. Extratemporal abnormalities identified the epileptogenic focus in 78% of TLE‐MTS but in only 17% of TLE‐no. Conclusions: TLE is associated with extrahippocampal reductions of NAA/(Cr+Cho) in several lobes consistent with those brain areas involved in seizure spread. Temporal and extratemporal NAA/(Cr+Cho) reductions might be helpful for focus lateralization.