bluuebunny/crossref_metadata_2025_split huggingface dataset:
Polyenylphosphatidylcholine Protects Against Alcohol but Not Iron‐Induced Oxidative Stress in the Liver
Authors: Aleynik Semyon I. , Leo Maria Anna , Aleynik Maria K. , Lieber Charles S. 
Published: May 2006

Background:We reported before that, in baboons, the alcohol‐induced oxidative stress in the liver is associated with depletion of dilinoleoylphosphatidylcholine [the major component of polyenylphosphati‐dylcholine (PPC)] and that both can be corrected by the administration of PPC, but we did not determine whether this protection extended to iron‐induced oxidative stress.Methods:To compare the effects of PPC on alcohol‐ and iron‐induced hepatic oxidative stress, 56 Sprague Dawley® male rats were pair‐fed nutritionally adequate liquid diets containing ethanol (36% of energy) or isocaloric carbohydrate and PPC (3 mg/ml) or safflower oil (2.73 mg/ml), with or without 5 mg/ml carbonyl iron for 2 months. Markers of oxidative stress (4‐hydroxynonenal and reduced glutathione), antioxidants (vitamin E, ubiquinol‐9, and ubiquinol‐10), and phosphatidylcholine (PC) species were assessed by HPLC and/or gas chromatography/mass spectrometry.Results:Alcohol feeding increased hepatic 4‐hydroxynonenal 3‐fold and decreased glutathione by 19%, ubiquinol‐10 by 53%, and PC species containing arachidonate (palmitoyl‐ and stearoylarachidonoylphosphatifidylcholines by 24% and 21%, respectively) and total phospholipids by 14%. PPC feeding prevented the rise of 4‐hydroxynonenal, restored glutathione, and increased the hepatic content of dilinolcoylphosphatidylcholine and of some other PC carrying polyunsaturated fatty acids. Administration of iron alone increased hepatic iron, doubled 4‐hydroxynonenal and glutathione, whereas it decreased vitamin E, ubiquinol‐9, total phospholipids, and several polyunsaturated PC. Alcohol given with iron further exacerbated the hepatic oxidative stress, as documented by the increase of 4‐hydroxynonenal and the decrease in glutathione and ubiquinols‐10. PPC did not prevent this oxidative stress, although it increased hepatic glutathione. Hepatic dilinoleoylphosphatidylcholine content was comparable with and without dietary iron.Conclusions:PPC prevents the alcohol‐induced oxidative stress but only in the absence of iron overload.
Analysis of Heritability of Hormonal Responses to Alcohol in Twins: Beta‐Endorphin as a Potential Biomarker of Genetic Risk for Alcoholism
Authors: Froehlich J. C. , Zink R. W. , Li T.‐K. , Christian J. C. 
Published: May 2006

Background:Hormonal responses to alcohol have been reported to differ in subjects with and without a family history of alcoholism which suggests that alcohol‐induced hormonal changes might be used to identify individuals who are at elevated genetic risk for developing alcoholism. However, before a biological response can be used as a marker of genetic risk for disease, it must first be demonstrated that the response is, in fact, heritable. The present study was designed to determine whether hormonal responses to alcohol are heritable.Methods:The adrenocorticotropic hormone (ACTH), beta‐endorphin (β‐E), cortisol (CORT), and prolactin (PRL) responses to alcohol were examined in male and female identical (monozygotic or MZ) and fraternal (dizygotic or DZ) twin pairs. Male subjects consumed 0.35g ethanol/kg body weight (BW) and female consumed 0.325 g ethanol/kg BW in each of two alcohol drinking sessions administered 1 hr apar (total dose of 0.7 g/kg BW in males and 0.65 g/kg BW in females). Plasma hormone content was analyzed in samples collected before (resting conditions) and at 15, 60, 75, 120, 180, and 240 min after onset of drinking. Hormonal responses to alcohol were examined with twin analyses using the TWINAN90 program. A separate analysis was performed for each of the four hormones. A subset of subjects from each zygosity was seen on two separate occasions to establish retest reliability. Heritability of hormonal responses to alcohol was estimated using the intraclass correlation approach before and after removing the contribution of covariates that have the potential of influencing the plasma levels of these hormones.Results:Resting plasma levels of all four hormones were within the expected range, and the β‐E, ACTH, and PRL responses to the alcohol challenge evidenced good test‐retest reliability. Of the four hormones examined, the only one that showed significant heritability after alcohol drinking was β‐E. Heritability estimates were not altered for any of the four hormones after removal of the variance contributed by covariates, such as gender and age.Conclusions:Taken together with other recent findings, the results suggest that the β‐E response to alcohol may represent a new biomarker that can be used to identify individuals who are at elevated genetic risk for developing alcoholism.
Ethanol Suppresses NK Cell Activation by Polyinosinic‐Polycytidylic Acid (Poly I:C) in Female B6C3F1 Mice: Role of Endogenous Corticosterone
Authors: Collier Stephanie D. , Wu Wen‐Jun , Pruett Stephen B. 
Published: May 2006

Background: Acute administration of EtOH suppresses basal NK cell lytic function in mice, and this suppression is caused, in part, by neuroendocrine mediators induced by EtOH. There is also evidence that a smaller part of the suppression is caused by direct action of EtOH. However, activation of NK cells to higher levels of lytic activity may be more important than basal NK cell lytic function in resistance to cancer or infectious agents. Therefore, the study described here examined the effects of acute EtOH exposure on activation of NK cells by polyinosinic‐polycytidilic acid (poly I:C).Methods: Ethanol was administered by gavage as a 32% solution in water, and poly I:C was administered to activate NK cells. NK cell activity was measured using a standard 4 hr 51Cr release assay with YAC‐1 tumor cells. The effects of corticosterone were evaluated by administration of a glucocorticoid antagonist (RU 486) or a dosage of corticosterone previously shown to induce similar blood levels as treatment with EtOH.Results: EtOH at 5–7 g/kg suppressed poly I:C‐induced increases in NK cell lytic activity, and at least the lower end of this dosage range yields bloud EtOH levels that are relevant for humans (0.25–0.3%). This suppression was partially blocked in mice that were pretreated with a glucocorticoid antagonist, and administration of exogenous corticosterone also suppressed NK cell activation.Conclusions: EtOH‐induced increases in corticosterone are apparently involved in the suppression of NK cell activation. This conclusion was supported by the lack of a direct effect of EtOH or its major metabolites (acetaldehyde and acetate) on NK cell activation by poly I:n vitro.
Japanese National Survey of Adolescent Drinking Behavior in 1996
Authors: Suzuki Kenji , Minowa Masumi , Osaki Yoneatsu 
Published: May 2006

Background: Despite legal prohibition of drinking by minors, there has been no systematic attempt to monitor drinking by young Japanese. This research, the first Japanese national survey of Japanese adolescent drinking behaviors, was conducted in 1996.Methods: In this survey, information on drinking frequency was obtained from questionnaires completed by 42,183 junior high school and 72,396 senior high school students in randomly selected schools representing all areas of Japan.Results: Sixty percent of junior high school students and 70% of senior high school students reported having drinking experiences; 5% of junior high school students and 10% of senior high school students drank one or more times per week. Many of the junior high school students usually drank with their families and consumed small amounts, but many of senior high school students drank on various occasions and consumed larger amounts. These Japanese high school students reported being offered alcohol frequently by their parents, found it easy to buy alcoholic beverages, and believed that they had the right to determine whether to drink. Japanese adolescents' drinking has increased over the past 20 years, whereas drinking by U.S. adolescents has decreased.Conclusions: Japanese policies aimed at decreasing adolescent drinking are inadequate. A system for monitoring and potentially modifying adolescent drinking behavior is needed.
Acute Effects of Ethanol and the First Suckling Episode in the Newborn Rat
Authors: Cheslock Sarah J. , Varlinskaya Elena I. , Silveri Marisa M. , Petrov Evgeniy S. , Spear Linda P. , Spear Norman E. 
Published: May 2006

Background: In humans, early postnatal experience with alcohol is far from rare and includes exposure to alcohol through breast milk or through the bottle to attain sedative effects (Croce, 1987). Exposure to alcohol though mother's milk alters the infant's suckling behavior. However, acute effects of alcohol on suckling behavior using animal models remain to be investigated.Methods: The present study was designed to examine the effects of neonatal alcohol exposure on attachment to a surrogate nipple and ingestion of milk in rat pups, nafve both to suckling and to maternal care. Cesarean‐delivered rat pups were pre‐exposed to four dosages of ethanol (0, 1, 2, and 3 g/kg intragastrically) and tested 30 min after ethanol administration.Results: Suckling behavior was impaired only in pups exposed to a dosage of 3 g/kg of ethanol. Pups in this group demonstrated longer latency to attach followed by less efficient suckling–the pups maintained contact with the nipple but showed decreased ingestion of milk from it. Pups treated with 1 g/kg of ethanol showed the greatest suckling efficiency, ingesting far more milk per minute attached to the surrogate nipple than pups in all other groups. At the same time, nonevoked motor activity was significantly suppressed by all three dosages of ethanol. Blood alcohol levels showed a linear relationship with dose at 30 min postintubation.Conclusions: These findings suggest a dissociation between acute ethanol effects on suckling and overall motor activity, with suckling apparently less sensitive to suppressive and more sensitive to activating effects of ethanol.
Occupational Stress Factors and Alcohol‐Related Behavior in Urban Transit Operators
Authors: Ragland David R. , Greiner Birgit A. , Yen Irene H. , Fisher June M. 
Published: May 2006

Background: If alcohol consumption mitigates psychological and physiological aspects of the response to stressors, then alcohol consumption might be elevated for individuals exposed to high occupational stressors. Frequency of work stressors and reaction to those stressors were studied in relation to several alcohol‐related outcomes.Methods: During the period 1993–1995, 1979 transit operators underwent medical examinations for commercial driver's license renewal. Questionnaire and interview data concerning occupational stress factors and alcohol‐related outcomes were available for 1386 (70.2%) of the operators.Results: A positive association was found between the two job stressor‐related measures and each of six alcohol‐related outcomes. Of these 12 associations, ten were statistically significant. Individuals experiencing high self‐reported frequency of job stressors and a higher perceived severity of those job stressors were more likely to drink and more likely to be heavy drinkers. They reported more consequences of alcohol consumption, reported increased consumption since beginning work as transit drivers, and were more likely to report drinking to deal with work stress. They also drank more, but this effect was not significant for either job stress measure. There was virtually no association between either stressor‐related measure and alcohol dependency (CAGE).Conclusions: Together with other published findings, these results suggest increased alcohol‐related outcomes in the presence of work stressors. This conclusion has potential implications for worksite health promotion and job design. Because our findings are cross‐sectional, further research is needed to clarify the causal nature of the work stressor‐alcohol association. Further research also is needed to clarify the role of individual differences and context.
A Mutation in Mitochondrial Complex I Increases Ethanol Sensitivity inCaenorhabditis elegans
Authors: Kayser Ernst‐Bernhard , Hoppel Charles L. , Morgan Phil G. , Sedensky Margaret M. 
Published: May 2006

Background:The genegas‐1encodes the 49‐kDa subunit of complex I of the mitochondrial electron transport chain inCaenorhabditis elegans. A mutation ingas‐1profoundly increases sensitivity to ethanol and decreases complex I‐dependent metabolism in mitochondria.Methods:Mitochondria were isolated from wild‐type andgas‐1strains ofC. elegans. The effects of ethanol on complex I‐, II‐, and III‐dependent oxidative phosphorylation were measured for mitochondria from each strain. Reversibility of the effects of ethanol was determined by measuring oxidative phosphorylation after removal of mitochondria from 1.5 M ethanol. The effects of ethanol on mitochondrial structure were visualized with electron microscopy.Results:We found that ethanol inhibited complex I–, II–, and III–dependent oxidative phosphorylation in isolated wild‐type mitochondria at concentrations that immobilize intact worms. It is important to note that the inhibitory effects of ethanol on mitochondria from eitherC. elegansor rat skeletal muscle were reversible even at molar concentrations. Complex I activity was lower in mitochondria fromgas‐1animals than in mitochondria from wild‐type animals at equal ethanol concentrations. Complex II activity was higher ingas‐1than in wild‐type mitochondria at all concentrations of ethanol. No difference was seen between the strains in the sensitivity of complex III to ethanol.Conclusions:The difference in ethanol sensitivities betweengas‐1and wild‐type nematodes results solely from altered complex I function. At the respective concentrations of ethanol that immobilize whole animals, mitochondria from each strain of worms displayed identical rates of complex I‐dependent state 3 respiration. We conclude that a threshold value of complex I activity controls the transition from mobility to immobility ofC. elegans.
Alcohol Effects on Motor Vehicle Crash Injury
Authors: Waller Patricia F. , Hill Elizabeth M. , Maio Ronald F. , Blow Frederic C. 
Published: May 2006

Context: Although alcohol is frequently present in injured patients, whether it exacerbates injury and whether tolerance to alcohol changes such a relationship is less clear. Most clinical studies do not consider other important predictors of injury, making interpretation of their findings problematic.Objective: To examine alcohol's role in injuries, taking into account other important factors, and to examine the effect of tolerance, if any.Design: Prospective cohort study.Setting: University hospital and community hospital emergency departments and morgue.Patients: 1362 Motor Vehicle Crash patients age ≥18, treated and released, admitted, and deceased.Main Outcome Measures: Excess injury measured by Injury Severity Scale (ISS) 90, Weighted Revised Trauma Score (WRTS), and G‐Score.Results: Using regression analysis, the best predictors of injury severity were vehicle crush (TAD), safety belt use, and their interaction, and age. Alcohol use further predicted injury. Using the final regression model, the effect of alcohol was to increase ISS90, on average, by about 30% (from a predicted ISS90 of 5.1 to 6.8, all else being equal). The adjusted odds ratio for serious injury (ISS90>15), was 1.59 for a patient with a positive blood alcohol concentration (alc+) compared to a alc− patient. This potentiating effect is seen even for patients with low levels of alcohol (<22mmol/liter; <0.100 BAC) but is not linear with increasing alcohol level. Tolerance to alcohol did not affect the potentiation of injury by alcohol.Conclusion: When other relevant variables are considered, alcohol increases injury, but the effects of alcohol level and alcohol tolerance are less clear. These findings have important implications for injury prevention, treatment, and research.
The Management of Risk: Application to the Welding Industry
Authors: Stern Richard M. 
Published: May 2006

The management of health risk in the welding industry is considered based on a discussion of the major sources of harm to welders arising from their employment (e.g., accidents and inhalation of fumes and gases). It is shown that present methods neither enable the assessment of the societal and human costs involved, nor permit the specific association of delayed health effects to occupational fume exposures. Reported accidents usually occur early in the working experience and contribute to a large number of working days lost, while fume exposures may contribute to a reduction in life quality which is poorly defined. It is concluded that risk management can only be attempted after much more information is made available concerning the origin, nature, and duration of health effects, especially as related to individual welding technologies and applications.SUMMARY AND CONCLUSIONSThe reduction of risk in the welding industry requires the development of an approach to risk management. Although it is difficult to demonstrate that welders on the average suffer excess risk when compared to similar skilled manual occupations, there is some evidence of possible high risk associated with certain welding operations: currently available information is extremely limited.It is extremely difficult to rank various types of potential risk. On the other hand it is possible to try to identify certain situations, individuals, combinations of circumstances which lead to excess occupational health risk.A complete picture of the risk infrastructure can be obtained by a proper survey of each enterprise. Steps can immediately be taken for the elimination of unnecessary risk, especially from accidents. The problems with respect to delayed health effects, especially cancer, are less tractable. In particular much effort must be placed in the strategies for the management of small excess risks of delayed health effects and large variations in inter‐individual risk susceptibilities.
Environmental Tobacco Smoke: Exposure‐Response Relationships in Epidemiologic Studies
Authors: Wu‐Williams Anna H. , Samet Jonathan M. 
Published: May 2006

Demonstration of a dose‐response relationship for environmental tobacco smoke (ETS) is an important indication of causality. Central to the analysis and interpretation of dose‐response relations as described in epidemiological studies is the relationship between dose and exposure. It must be recognized that in studies of ETS we have only surrogate measures of dose, and these surrogate measures (based on exposure) are imperfect. The question‐based measures of ETS exposure generally have not been standardized, may have limited validity and reliability, and cannot comprehensively describe total ETS exposure, exposure to individual ETS components, nor doses of biologically relevant agents at target sites. Nevertheless, useful data have been yielded in epidemiologic studies linking ETS exposure to increased respiratory infection and symptoms, reduced lung growth in children, and increased lung cancer in nonsmoking adults. The more consistent exposure‐response data for studies on acute health in children may reflect the greater difficulty in measuring exposure in studies of chronic health in adults.SUMMARYFor children, adverse effects have been causally associated with exposure to ETS. The epidemiological evidence and the supporting toxicological data link ETS to increased lower respiratory illness, increased respiratory symptoms, and reduced lung growth. Exposure‐response relationships have been described for these effect; errors in exposure estimates would tend to lessen rather than to exaggerate these relationships. By contrast, in adults, the evidence for adverse cardiopulmonary effects of ETS exposures, other than lung cancer, it's presently less conclusive. Misclassification of exposure may be more severe for adults than for children, and the resulting bias toward the null may obscure effects of respiratory symptoms and lung function. Research on adults is hindered by the difficulty of estimating exposures received in diverse environments over a lengthy period. Continued controversy related to the effects of ETS exposure in the workplace and in public locations provides a rationale for further research. However, more valid methods for assessing the exposures of adults to ETS are needed for such research.
Chinese and Americans Agree on What Is Fair, but Disagree on What Is Best in Societal Decisions Affecting Health and Safety Risks
Authors: Bian Wen‐Qiang , Keller L. Robin 
Published: May 2006

Through surveys of students and junior professionals and interviews with business and government executives, we studied Chinese choices and fairness perceptions in risky health and safety decisions. The survey responses were compared with American responses from an earlier study by Keller and Sarin.The survey results show that the American and Chinese respondents had similar fairness perceptions, but the Chinese did not make decisions that were consistent with their fairness perceptions, whereas the Americans did. We found that the middle‐age Chinese professionals tended to make choices that were more different from the Americans than were the choices of the young Chinese management students. It is likely that these discrepancies were caused by cultural differences, with the younger Chinese tending to face a stronger Western influence.The insights from the survey results were enriched by interviews that revealed fairness perceptions of Chinese business and government executives.A framework to interpret cultural influences on decision making was also proposed.
Stock Options and the Corporate Demand for Insurance
Authors: Han Li‐Ming , MacMinn Richard 
Published: May 2006

AbstractThis article shows that a corporate manager compensated in stock options makes corporate decisions to maximize stock option value. Overinvestment is a consequence if risk increases with investment. Facing the choice of hedging corporate risk with forward contracts on a stock market index fund and insuring pure risks the manager will choose the latter. Hedging with forwards reduces weight in both tails of corporate payoff distribution and thus reduces option value. Insuring pure risks reduces the weight in the left tail where the options are out‐of‐the‐money and increases the weight in the right tail where the options are in‐the‐money; the effect is an increase in the option value. Insurance reduces the overinvestment problem but no level of insurance coverage can reduce investment to that which maximizes the shareholder value.
Ocular complications in a child with acute graft‐versus‐host disease following cord blood stem cell transplantation: therapeutic challenges
Authors: Uchino Miki , Ogawa Yoko , Kawai Masataka , Shimada Hiroyuki , Kameyama Kaori , Okamoto Shinichiro , Dogru Murat , Tsubota Kazuo 
Published: May 2006

AbstractWe present the first child case of pseudomembranous conjunctivitis accompanied by an extensive corneal ulcer with acute graft‐versus‐host disease (GVHD) after cord blood stem cell transplantation (CBSCT). The histopathology of the pseudomembrane and the ocular changes following its excision were investigated specifically. One week after the excision of pseudomembrane, the extensive corneal epithelial defects had totally disappeared. Pseudomembrane excision may be an effective method of treatment in corneal epithelial defects observed after GVHD.