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G Ethanol (g + ethanol)
Selected AbstractsA computerized harm minimization prevention program for alcohol misuse and related harms: randomized controlled trialADDICTION, Issue 4 2009Laura Vogl ABSTRACT Aims Hazardous alcohol use is a leading cause of death among adolescents and young adults world-wide, yet few effective prevention interventions exist. This study was the first to examine a computerized harm minimization intervention to reduce alcohol misuse and related harms in adolescents. Design Cluster randomized controlled trial of a six-session curriculum-integrated harm minimization prevention program. The intervention was delivered by computer in the form of a teenage drama, which provided education through alcohol-related scenarios to which young people could relate. Setting Schools in Australia. Participants A total of 1466 year 8 students (13 years) from 16 high schools in Australia were allocated randomly to a computerized prevention program (n = 611, eight schools) or usual classes (n = 855, eight schools). Measurements Change in knowledge, alcohol use, alcohol-related harms and alcohol expectancies. Findings A computerized prevention program was more effective than usual classes in increasing alcohol-related knowledge of facts that would inform safer drinking choices and decreasing the positive social expectations which students believed alcohol may afford. For females it was effective in decreasing average alcohol consumption, alcohol-related harms and the frequency of drinking to excess (more than four standard drinks; 10 g ethanol). For males the behavioural effects were not significant. Conclusions A harm minimization approach is effective in educating young people about alcohol-related risks and is effective in reducing risky drinking and harms among girls. Reduction of problems among boys remains a challenge. [source] Bioethanol production from bio- organosolv pulps of Pinus radiata and Acacia dealbataJOURNAL OF CHEMICAL TECHNOLOGY & BIOTECHNOLOGY, Issue 8 2007Claudio Muñoz Abstract Wood chips from Pinus radiata and Acacia dealbata were pretreated with the white-rot fungi Ceriporiopsis subvermispora and Ganoderma australe, respectively, for 30 days at 27 °C and 55% relative humidity, followed by an organosolv delignification with 60% ethanol solution at 200 °C for 1 h to produce pulps with high cellulose and low lignin content. Biotreatment for 30 days was chosen based on low weight and cellulose losses (lower than 4%) and lignin degradation higher than 9%. After organosolv delignification, pulp yield for P. radiata and A. dealbata pulps was 45,49% and 31,51%, respectively. P. radiata bio-pulps showed higher glucan (93%) and lower lignin content (6%) than control pulps (82% glucan and 13% lignin). A. dealbata bio-pulps also showed higher glucan (95%) and lower lignin content (2%) than control pulps (92% glucan and 4% lignin). Pulp suspensions at 2% consistency were submitted either to separate enzymatic hydrolysis and fermentation (SHF) or simultaneous enzymatic saccharification and fermentation (SSF) for bioethanol production. The yeast Saccharomyces cerevisiae was used for fermentation. Glucan-to-glucose conversion in the enzymatic hydrolysis of control and bio-pulps of P. radiata was 55% and 100%, respectively, and it was 100% for all pulp samples case of A. dealbata. The highest ethanol yield (calculated as percentage of theoretical yield) during SHF of P. radiata control and bio-pulps was 38% and 55%, respectively, and for A. dealbata control and bio-pulps 62% and 69%, respectively. The SSF of P. radiata control and bio-pulps yielded 10% and 65% of ethanol, respectively, and 77% and 82% for A. dealbata control and bio-pulps, respectively. In wood basis, the maximum conversion obtained (g ethanol per kg wood) in SHF was 37% and 51% (for P. radiata and A. dealbata pulps, respectively) and 44% and 65% in SSF (for P. radiata and A. dealbata pulps, respectively) regarding the theoretical yield. The low wood-to-ethanol conversion was associated with low pulp yield (A. dealbata pulps), high residual lignin amount (P. radiata pulps) and the low pulp consistency (2%) used for SHF and SSF. Copyright © 2007 Society of Chemical Industry [source] Alcohol and Colorectal Cancer: The Role of Alcohol Dehydrogenase 1C PolymorphismALCOHOLISM, Issue 3 2009Nils Homann Background:, Chronic alcohol consumption is a risk factor for colorectal cancer. Animal experiments as well as genetic linkage studies in Japanese individuals with inactive acetaldehyde dehydrogenase leading to elevated acetaldehyde concentrations following ethanol ingestion support the hypothesis that acetaldehyde may be responsible for this carcinogenic effect of alcohol. In Caucasians, a polymorphism of alcohol dehydrogenase 1C (ADH1C) exists resulting in different acetaldehyde concentrations following ethanol oxidation. Methods:, To evaluate whether the association between alcohol consumption and colorectal tumor development is modified by ADH1C polymorphism, we recruited 173 individuals with colorectal tumors diagnosed by colonoscopy and 788 control individuals without colorectal tumors. Genotyping was performed using genomic DNA extracted from whole blood followed by polymerase chain reaction. Results:, Genotype ADH1C*1/1 was more frequent in patients with alcohol-associated colorectal neoplasia compared to patients without cancers in the multivariate model controlling for age, gender, and alcohol intake (odds ratio = 1.674, 95% confidence interval = 1.110,2.524, 2-sided p from Wald test = 0.0139). In addition, the joint test of the genetic effect and interaction between ADH1C genotype and alcohol intake (2-sided p = 0.0007) indicated that the difference in ADH1C*1 polymorphisms between controls and colorectal neoplasia is strongly influenced by the alcohol consumption and that only individuals drinking more than 30 g ethanol per day with the genotype ADH1C*1/1 had an increased risk for colorectal tumors. Conclusions:, These data identify ADH1C homozygosity as a genetic risk marker for colorectal tumors in individuals consuming more than 30 g alcohol per day and emphasize the role of acetaldehyde as a carcinogenic agent in alcohol-related colorectal carcinogenesis. [source] Increased Interleukin-10 and Cortisol in Long-term Alcoholics after Cardiopulmonary Bypass: A Hint to the Increased Postoperative Infection Rate?ALCOHOLISM, Issue 9 2005Michael Sander Background: Previous studies have shown that 20% of all patients admitted to the hospital abuse alcohol and have increased morbidity after surgery. Long-term alcoholic patients are shown to suffer from immune alterations, which might be critical for adequate postoperative performance. Cardiac surgery with cardiopulmonary bypass (CPB) also leads to pronounced immune alteration, which might be linked with patients' ability to combat infections. Therefore, the aim of our study was to investigate the perioperative levels of TNF-alpha, interleukin-6, interleukin-10, and cortisol in long-term alcoholic and nonalcoholic patients undergoing cardiac surgery to elucidate a possible association with postoperative infections. Methods: Forty-four patients undergoing elective cardiac surgery were included in this prospective study. Long-term alcoholic patients (n= 10) were defined as having a daily ethanol consumption of at least 60 g and fulfilling the Diagnostic and Statistical Manual of Mental Disorders for alcohol abuse. The nonalcoholic patients (n= 34) were defined as drinking less than 20 g ethanol per day. Blood samples were obtained to analyze the immune status upon admission to hospital, the morning before surgery and on admission to the ICU, the morning of days one and three after surgery. Results: Basic characteristics of patients did not differ between groups. Long-term alcoholics had a fourfold increase in postsurgery infection rate and prolonged need for ICU treatment and mechanical ventilation. Postoperative levels of interleukin-10 and cortisol were significantly increased in long-term alcoholic patients compared with nonalcoholic patients. These observations were in line with postoperative interleukin-10 being predictive for postoperative infectious complications. Conclusions: The increased infection rate in long-term alcoholics strengthens the urgent need for interventional approaches providing modulation of the perioperative immune and HPA response in these high-risk patients to counteract their postoperative immune suppression. [source] Development of Industrial-Medium-Required Elimination of the 2,3-Butanediol Fermentation Pathway To Maintain Ethanol Yield in an Ethanologenic Strain of Klebsiellaoxytoca,BIOTECHNOLOGY PROGRESS, Issue 5 2005Brent E. Wood Fermentation efficiency and nutrient costs are both significant factors in process economics for the microbial conversion of cellulosic biomass to commodity chemicals such as ethanol. In this study, we have developed a more industrial medium (OUM1) composed of 0.5% corn steep liquor (dry weight basis) supplemented with mineral salts (0.2%), urea (0.06%), and glucose (9%). Although the growth of strain P2 was vigorous in this medium, approximately 14% of substrate carbon was diverted into 2,3-butanediol and acetoin under the low pH conditions needed for optimal cellulase activity during simultaneous saccharification. Deleting the central region of the budAB genes encoding ,-acetolactate synthase and ,-acetolactate decarboxylase eliminated the butanediol and acetoin coproducts and increased ethanol yields by 12%. In OUM1 medium at pH 5.2, strain BW21 produced over 4% ethanol in 48 h (0.47 g ethanol per g glucose). Average productivity (48 h), ethanol titer, and ethanol yield for BW21 in OUM1 medium (pH 5.2) exceeded that of the parent (strain P2) in rich laboratory medium (Luria broth). [source] Alcohol Consumption, Social Support, and Risk of Stroke and Coronary Heart Disease Among Japanese Men: The JPHC StudyALCOHOLISM, Issue 6 2009Satoyo Ikehara Background:, It is unclear whether the association between alcohol consumption and risk of cardiovascular disease is affected by social support. Methods:, The prospective data for 19,356 men aged 40 to 69 years who participated in the Japan Public Health Center-Based Prospective Study. Alcohol consumption was classified into 7 categories: never, past, occasional, 1 to 149, 150 to 299, 300 to 449, or ,450 g ethanol/wk. Associations between alcohol consumption and risk of cardiovascular disease were stratified by the median level of social support score, which was measured in emotional support score of this cohort study. Results:, During an average follow-up of 9.9 years, 629 total strokes and 207 coronary heart diseases were documented. Light-to-moderate alcohol consumption was associated with reduced risks of coronary heart disease and total cardiovascular disease, while heavy alcohol consumption was associated with increased risk of total stroke, in particular hemorrhagic stroke. When stratified by social support score, the multivariable hazard ratios of total cardiovascular disease associated with light-to-moderate alcohol consumption (1 to 299 g/wk) were 0.99 (0.72 to 1.37) in the low social support group and 0.56 (0.44 to 0.70) in the high social support group (p for interaction = 0.002), while the multivariable hazard ratios of hemorrhagic stroke associated with heavy alcohol consumption (,300 g/wk) were 2.09 (1.03 to 4.27) in the low social support group and 1.25 (0.72 to 2.15) in the high social support group (p for interaction = 0.44). There was no interaction between alcohol consumption and social support in relation to risk of coronary heart disease. Conclusions:, Social support may enhance the beneficial effect of light-to-moderate alcohol consumption on risk of cardiovascular disease. [source] Effect of Chronic Ethanol on Enkephalin in the Hypothalamus and Extra-Hypothalamic AreasALCOHOLISM, Issue 5 2010Guo-Qing Chang Background:, Ethanol may be consumed for reasons such as reward, anxiety reduction, or caloric content, and the opioid enkephalin (ENK) appears to be involved in many of these functions. Previous studies in Sprague,Dawley rats have demonstrated that ENK in the hypothalamic paraventricular nucleus (PVN) is stimulated by voluntary consumption of ethanol. This suggests that this opioid peptide may be involved in promoting the drinking of ethanol, consistent with our recent findings that PVN injections of ENK analogs stimulate ethanol intake. To broaden our understanding of how this peptide functions throughout the brain to promote ethanol intake, we measured, in rats trained to drink 9% ethanol, the expression of the ENK gene in additional brain areas outside the hypothalamus, namely, the ventral tegmental area (VTA), nucleus accumbens shell (NAcSh) and core (NAcC), medial prefrontal cortex (mPFC), and central nucleus of the amygdala (CeA). Methods:, In the first experiment, the brains of rats chronically drinking 1 g/kg/d ethanol, 3 g/kg/d ethanol, or water were examined using real-time quantitative polymerase chain reaction (qRT-PCR). In the second experiment, a more detailed, anatomic analysis of changes in gene expression, in rats chronically drinking 3 g/kg/d ethanol compared to water, was performed using radiolabeled in situ hybridization (ISH). The third experiment employed digoxigenin-labeled ISH (DIG) to examine changes in the density of cells expressing ENK and, for comparison, dynorphin (DYN) in rats chronically drinking 3 g/kg/d ethanol versus water. Results:, With qRT-PCR, the rats chronically drinking ethanol plus water compared to water alone showed significantly higher levels of ENK mRNA, not only in the PVN but also in the VTA, NAcSh, NAcC, and mPFC, although not in the CeA. Using radiolabeled ISH, levels of ENK mRNA in rats drinking ethanol were found to be elevated in all areas examined, including the CeA. The experiment using DIG confirmed this effect of ethanol, showing an increase in density of ENK-expressing cells in all areas studied. It additionally revealed a similar change in DYN mRNA in the PVN, mPFC, and CeA, although not in the NAcSh or NAcC. Conclusions:, While distinguishing the NAc as a site where ENK and DYN respond differentially, these findings lead us to propose that these opioids, in response to voluntary ethanol consumption, are generally elevated in extra-hypothalamic as well as hypothalamic areas, possibly to carry out specific area-related functions that, in turn, drive animals to further consume ethanol. These functions include calorie ingestion in the PVN, reward and motivation in the VTA and NAcSh, response-reinforcement learning in the NAcC, stress reduction in the CeA, and behavioral control in the mPFC. [source] Alterations in Circadian Rhythm Phase Shifting Ability in Rats Following Ethanol Exposure During the Third Trimester Brain Growth SpurtALCOHOLISM, Issue 5 2006Hiromi Sakata-Haga Background: Disruptions in sleep and feeding rhythms are among the consequences of prenatal alcohol exposure. Previously, we reported that ethanol exposure during the second trimester equivalent in rats produces long-lasting impairments in circadian system functioning. In the present study, we examined the effects of ethanol exposure during the third trimester equivalent brain growth spurt on the development of the circadian clock system. Methods: Sprague,Dawley male rat pups were exposed to 6.0 g/kg/d ethanol via an artificial rearing procedure on postnatal days (PD) 4 through 9 (EtOH). An artificially reared gastrostomized control group and a normally reared suckle control group were also included. At 10 to 12 weeks of age, wheel-running behavior was measured continuously under a 12-hour/12-hour light/dark (LD) cycle. Thereafter, subjects were exposed to a 6-hour phase delay of the LD cycle, and the ability to adjust to the new LD cycle was evaluated. Results: Before the phase delay, onset time of activity and acrophases of activity in all 3 groups were not significantly different from one another. After the 6-hour LD cycle delay, EtOH subjects were slower to adapt to the new cycle compared with both control groups, as measured by both activity onset and acrophase. Throughout the experiment, activity levels of EtOH subjects tended to be higher compared to both controls. Conclusions: These data demonstrate that ethanol exposure during the third trimester disrupts the ability to synchronize circadian rhythm to light cues. Disruptions in circadian regulation may cause abnormal behavioral rhythmicity, such as disrupted sleep and feeding patterns, as seen in individuals prenatally exposed to ethanol. [source] Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol ConsumptionALCOHOLISM, Issue 1 2009Garth A. Hargreaves Background:, Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood. Methods:, Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g/kg/day ethanol). The 4 weeks of alcohol access were followed by a 2-week alcohol-free washout period after which the hippocampus was analyzed using 2-DE proteomics. Results:, Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naïve adult controls. The only changes observed were an up-regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1) and a decrease in the expression of 10 other proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha-enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate-semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl-terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release). Conclusions:, These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure. [source] | ||||||||||