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ANTIBODIES FROM ALCOHOLICS, ETHANOL-FED RATS AND A RABBIT IMMUNISED WITH PROTEINS MODIFIED BY ACETALDEHYDE IN VITRO REACT WITH LIVER CYTOSOLIC PROTEINS FROM ETHANOL-FED RATS
WORRALL, SIMON
JERSEY, JOHN DE
WILCE, PETER A.
Articles
In previous studies we have shown that ethanol-fed rats generate antibodies reactive with proteins modified by acetaldehyde <it>in</it> <it>vitro</it> and that their livers contain proteins modified by acetaldehyde. In this study we demonstrate that the antibodies from these animals react with the modified proteins found in their livers. Furthermore, when the antibodies reactive with specific proteins were isolated, they were found to react with all of the modified proteins detected by the whole serum. This suggests that all of the proteins modified by acetaldehyde in vivo carry the same or similar epitope(s). In addition, antibodies from alcoholics and a rabbit immunised with proteins modified by acetaldehyde in vitro also reacted with the liver cytosolic proteins from ethanol-fed rats. Therefore it appears that similar epitopes are generated in alcoholics as a result of ethanol misuse, in rat liver due to prolonged ethanol feeding and by the <it>in</it> <it>vitro</it> modification procedure used to produce the immunogen for the rabbit.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/513
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Copyright (C) 1993, Medical Council on Alcohol
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EFFECT OF ACUTE ETHANOL DOSAGE ON NUCLEOTIDE LEVELS IN THE RAT JEJUNUM: RELATIONSHIP TO PROTEIN SYNTHESIS
MARWAY, JASPAUL S.
RODRIGUES, LORETA M.
GRIFFITHS, JOHN R.
PREEDY, VICTOR R.
Articles
In previous studies we have shown that ethanol-fed rats generate antibodies reactive with proteins modified by acetaldehyde <it>in</it> <it>vitro</it> and that their livers contain proteins modified by acetaldehyde. In this study we demonstrate that the antibodies from these animals react with the modified proteins found in their livers. Furthermore, when the antibodies reactive with specific proteins were isolated, they were found to react with all of the modified proteins detected by the whole serum. This suggests that all of the proteins modified by acetaldehyde in vivo carry the same or similar epitope(s). In addition, antibodies from alcoholics and a rabbit immunised with proteins modified by acetaldehyde in vitro also reacted with the liver cytosolic proteins from ethanol-fed rats. Therefore it appears that similar epitopes are generated in alcoholics as a result of ethanol misuse, in rat liver due to prolonged ethanol feeding and by the <it>in</it> <it>vitro</it> modification procedure used to produce the immunogen for the rabbit.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/521
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5292015-05-19HighWireOUPalcalc:28:5
LACK OF EFFECT OF ACETALDEHYDE ON THE CARDIOVASCULAR SYSTEM IN RATS
PAWLAK, DARIUSZ
MORELOWSKA-SPIERZAK, DOROTA
AZZADIN, ARSALAN
WRÓBEL, KAZIMIERZ
BUCZKO, WLODZIMIERZ
Articles
The present study was destgned to evaluate the kinetics of acetaldehyde (ACT) and its action on the cardiovascular system in rats. ACT (3, 6, 12 mg/kg i.p.) causes accumulation of this metabolite in the blood, at a concentration corresponding to that obtained from ethanol metabolism after its administration in doses of 1, 2, 4 g/kg p.o., respectively. After intraperitoneal injection of ACT there were no significant changes in blood pressure and heart rate in comparison to the control group. It appears that, in rats, ACT has no influence on the function of the cardiovascular system after the ingestion of ethanol.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/529
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5352015-05-19HighWireOUPalcalc:28:5
PROBLEMS INVOLVED IN THE DETERMINATION OF ENDOGENOUS ACETALDEHYDE IN HUMAN BLOOD
FUKUNAGA, TATSUSHIGE
SILLANAUKEE, PEKKA
ERIKSSON, C. J. PETER
Articles
Little is known about the possible existence of endogenous acetaldehyde in human blood. This has partly been due to analytical difficulties preventing accurate determination of blood acetaldehyde levels with and without the presence of ethanol. In the present study the possible existence of endogenous acetaldehyde in human blood was investigated with headspace gas chromatography using three different procedures for the treatment of samples: (1) no treatment of whole blood, cells, or plasma (direct headspace method), (2) hemolysation, and (3) perchloric acid (PCA) precipitation, prior to the headspace determinations. In <it>in</it> <it>vilro</it> experiments, with the direct headspace and the hemolysation methods, higher acetaldehyde peaks were obtained depending on the headspace incubation time, temperature and ethanol concentration. Both methods displayed about the same values of acetaldehyde in blood cells, ranging between 0 and 40 μM, at incubation times between 15 and 180 min, an incubation temperature of 65°C, and ethanol concentrations less than 5 μM. Less acetaldehyde formation (0–15 μM) was obtained with PCA precipitates of whole blood and cell components. Very low acetaldehyde levels (0–1 μM) were obtained in the supernatants without precipitates from either whole blood or cells after headspace equilibration. Substantially less acetaldehyde was formed in plasma preparations than with whole blood and cell fractions. In human experiments, the disturbance of endogenous or exogenous ethanol was minimized by separating and washing the blood cells followed by PCA treatment. No differences in acetaldehyde concentrations were observed in blood samples taken before, during, or after ethanol intoxication (1.5 g/kg dose) of four healthy non-alcoholic volunteers. The present results demonstrated substantial artefactual acetaldehyde formation during the analytical procedures, with the PCA method being least problematic. No evidence was obtained for the release of acetaldehyde possibly bound during ethanol intoxication. Whether real endogenous acetaldehyde, especially in a bound form, was present initially and then released during the present conditions, remains also to be proven.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/535
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5432015-05-19HighWireOUPalcalc:28:5
RELATIONSHIP BETWEEN ETHANOL-RELATED DISEASES AND NUTRITIONAL STATUS IN CHRONICALLY ALCOHOLIC MEN
ESTRUCH, RAMÓN
NICOLÁS, JOSE M.
VILLEGAS, EULALIA
JUNQUÉ, ANTONIO
URBANO-MÁRQUEZ, ALVARO
Articles
Two-hundred and fifty chronically alcoholic men (mean age, 41 ± 11 years) entering an alcoholism treatment program were studied. Detailed clinical history, nutritional assessment and measurement of muscle strength by electronic myometer were performed in each case. In addition, hepatic ultrasonography and liver biopsy, echocardiography and radionuclide cardiac scanning, and electrophysiological testing of peripheral nerves were performed when there was clinical evidence of liver disease, cardiomyopathy or neuropathy, respectively. Alcoholic cirrhosis was diagnosed in 20 cases, skeletal myopathy in 117, dilated cardiomyopathy in 20 and peripheral neuropathy in 41 cases. No patients with chronic myopathy or cardiomyopathy showed either clinical or laboratory evidence of malnutrition. Patients with cirrhosis showed a significantly lower lean body mass than controls (P = 0.03) and significantly lower nutritional protein levels than those alcoholics without cirrhosis. Alcoholics with peripheral neuropathy had significantly lower anthropometric parameters and nutrition protein levels than their counter parts (P < 0.001). However, in the multivariate analysis, the only independent factor for developing these complications of alcoholism was the total lifetime dose of ethanol (P < 0.001). We conclude that alcohol-related diseases are common in asymptomatic alcoholic men and these diseases appear to be due to an accumulative toxic effect of ethanol. Age and nutritional status do not seem to play a part in the development of such diseases.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/543
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5512015-05-19HighWireOUPalcalc:28:5
NUTRITIONAL STATUS IN CHRONICALLY ALCOHOLIC MEN FROM THE MIDDLE SOCIOECONOMIC CLASS AND ITS RELATION TO ETHANOL INTAKE
NICOLÁS, JOSE M.
ESTRUCH, RAMÓN
ANTUNEZ, EMILIA
SACANELLA, EMILIO
URBANO-MÁRQUEZ, ALVARO
Articles
Two-hundred and fifty chronically alcoholic men (mean age, 41 ± 11 years) entering an alcoholism treatment program were studied. Detailed clinical history, nutritional assessment and measurement of muscle strength by electronic myometer were performed in each case. In addition, hepatic ultrasonography and liver biopsy, echocardiography and radionuclide cardiac scanning, and electrophysiological testing of peripheral nerves were performed when there was clinical evidence of liver disease, cardiomyopathy or neuropathy, respectively. Alcoholic cirrhosis was diagnosed in 20 cases, skeletal myopathy in 117, dilated cardiomyopathy in 20 and peripheral neuropathy in 41 cases. No patients with chronic myopathy or cardiomyopathy showed either clinical or laboratory evidence of malnutrition. Patients with cirrhosis showed a significantly lower lean body mass than controls (<it>P</it> = 0.03) and significantly lower nutritional protein levels than those alcoholics without cirrhosis. Alcoholics with peripheral neuropathy had significantly lower anthropometric parameters and nutrition protein levels than their counter parts (<it>P</it> < 0.001). However, in the multivariate analysis, the only independent factor for developing these complications of alcoholism was the total lifetime dose of ethanol (<it>P</it> < 0.001). We conclude that alcohol-related diseases are common in asymptomatic alcoholic men and these diseases appear to be due to an accumulative toxic effect of ethanol. Age and nutritional status do not seem to play a part in the development of such diseases
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/551
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Copyright (C) 1993, Medical Council on Alcohol
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CHRONIC ETHANOL EXPOSURE INCREASES LIPOPIGMENT ACCUMULATION IN HUMAN HEART
JAATINEN, P.
SAUKKO, P.
HERVONEN, A.
Articles
The amount and distribution of myocardial lipoptgments ( ‘age pigments’) were studied in alcoholic and control human hearts, to test the hypothesis of ethanol-induced long- term oxidative damage in myocardium. The amount of myocardial lipopigments was measured by image analysis in six men (age 34–60 years) who had a history of chronic alcohol misuse and who died of acute ethanol intoxication, and in their age-matched, non-alcoholic controls. Lipopigmentation in the intoxication cases was 33.5 ± 2.8% (mean ± SEM) higher compared to the controls in the eight myocardial areas studied (<it>P</it> < 0.001). A linear correlation of myocardial lipopigmentation with age was noticed in both the intoxication group (<it>R</it> = 0.894) and the controls (<it>R</it> = 0.927). The amount of lipopigments varied largely from one myocardial area to another, being highest in the most strained areas (left ventricle, interventricular septum). The accumulation of lipopigments is considered a marker of oxidative stress and ageing in the myocardium. The results support the role of free radical-induced oxidative stress in the pathogenesis of ethanol-induced cardiac abnormalities.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/559
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5712015-05-19HighWireOUPalcalc:28:5
MINERAL METABOLISM, OSTEOBLASTIC FUNCTION AND BONE MASS IN CHRONIC ALCOHOLISM
GONZALEZ-CALVIN, JORGE L.
GARCIA-SANCHEZ, ANTONIO
BELLOT, VICENTE
MUNOZ-TORRES, MANUEL
RAYA-ALVAREZ, ENRIQUE
SALVATIERRA-RIOS, DOMINGO
Articles
The role of ethanol as a risk factor for osteopenia was studied in alcoholic subjects without liver cirrhosis. The study was carried out in 58 male subjects classified into three groups: (1) 26 heavy drinkers, alcohol intake more than 100 g ethanol/day for more than 10 years; (2) 13 moderate drinkers, 60–100 g ethanol/day; (3) 19 healthy non-drinkers who served as control subjects. None of the drinkers had liver cirrhosis (normal clinical and biochemical data and/or liver biopsy). Mineral metabolism and serum bone Gla-protein (BGP) were studied while they were active drinkers and after they had abstained from ethanol for 7 days. Bone mineral density (BMD) was determined at the beginning of the study. Osteopenia was observed in 23% of the heavy drinkers. We found a significant inverse correlation between BMD and an index of cumulative alcohol intake. Heavy and moderate drinkers had significantly lower mean BGP values (1.6 ± 0.4 and 1.9 ± 0.3 ng/ml) (<it>P</it> <0.01 for both) than controls (3.5 ± 0.4 ng/ml); these values increased significantly (2.9 ± 0.4 ng/ml; <it>P</it> < 0.01) after 7 days of abstinence. The data show that chronic ethanol ingestion can induce osteopenia regardless of the absence of liver cirrhosis, and that some relationship can be expected between the amount and duration of ethanol consumption and the degree of bone loss. The low serum BGP levels in drinkers are reversible upon withdrawal of ethanol, suggesting that reduction of osteoblastic activity is probably the main factor responsible for alcohol-associated bone disease.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/571
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5812015-05-19HighWireOUPalcalc:28:5
PREVALENCE OF CHOLELITHIASIS IN ALCOHOLIC AND GENETIC HAEMOCHROMATOTIC CIRRHOSIS
CONTE, D.
BARISANI, D.
MANDELLI, C.
FARGION, S.
FRACANZANI, A. L.
CESARINI, L.
BODINI, P.
PISTOSO, S.
BIANCHI, P. A.
Articles
The prevalence of cholelithiasis and possible related factors was evaluated in 350 consecutive patients with alcoholic cirrhosis (218 cases, 174 male and 44 female, mean age 58 ± 9 years) or genetic haemochromatotic cirrhosis (132 cases, 115 male and 17 female, mean age 53 ± 10 years). At enrolment patients with alcoholic cirrhosis were significantly older than those with genetic haemochromatottc cirrhosis (<it>P</it> < 0.01), and their clinical status was more severe (Child's class B/C in 99 alcoholic cirrhosis cases versus 27 genetic haemochromatotic cirrhosis cases, <it>P</it> < 0.01). The overall frequency of cholelithiasis was 31% (67 cases) in the alcoholic cirrhosis group and 30% (40 cases) in the genetic haemochromatotic cirrhosis group, without differences according to gender, classes of age ( ≤49, 50–59, ≥60 years), or HBsAg positivity in either group. In addition, in the genetic haemochromatotic cirrhosis group the presence of diabetes (45 cases), alcohol misuse (38 cases) and β-thalassemia trait (13 cases) did not influence the prevalence of cholelithiasis. Body mass index, serum cholesterol and triglycerides, and the severity of the underlying liver disease (Child's class) did not distinguish patients with or without cholelithiasis. In conclusion, the frequency of cholelithiasis was high in both alcoholic cirrhosis and genetic haemochromatotic cirrhosis, and was three times higher than that reported in controls from the general population of the same area.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/581
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5852015-05-19HighWireOUPalcalc:28:5
QUESTION-ASKING STRATEGIES IN ABSTINENT ALCOHOLICS: A STUDY OF LEARNING POTENTIAL
SAARNIO, PEKKA
Articles
The question-asking strategies of 90 Finnish alcoholics were measured on a Vygotskian version of the Twenty Questions procedure. There were two questions to analyse: (1) can the performance of alcoholics be improved by means of instruction in question-asking; and (2) how does the duration of abstinence affect test performance? The results indicated that instruction had a positive effect on the performance of alcoholics. The duration of abstinence had no general effect; its effect was evident only in one type of question, i.e. pseudoconstraint questions. There were marked interindividual differences in both the pre-test and the post-test. About 15% of the subjects showed no noticeable improvement in their post-test performance in spite of the instruction they received.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/585
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Copyright (C) 1993, Medical Council on Alcohol
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THE KINDLING HYPOTHESIS: FURTHER EVIDENCE FROM A U.S. NATIONAL STUDY OF ALCOHOLIC MEN
BOOTH, BRENDA M.
BLOW, FREDERIC C.
Articles
A sample of 6818 alcoholic men participating in a short in-patient detoxification episode was studied to examine the kindling effect of repeated prior alcohol withdrawals on occurrence of seizures or severe withdrawal problems observed during the hospitalization. Subjects studied were hospitalized in one of 172 U.S. Department of Veterans Affairs medical centers. Patients with seizures and withdrawal problems had more prior detoxifications and other alcohol-specific hospitalizations. They were also more likely to be later readmitted for an alcoholism diagnosis. Patients with withdrawal problems during the detoxification episode studied were more likely to have such problems again as well as seizures during the readmission; those with seizures during the index detoxification were more likely to have repeated seizures during the readmission. These results confirm the kindling effect in a large, multi-site patient sample and suggest that alcohol detoxification programs may need to consider anticonvulsant therapy in patients with many prior detoxifications or withdrawals.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/593
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/5992015-05-19HighWireOUPalcalc:28:5
AN INVENTORY OF THE ALCOHOL RESEARCH LITERATURE
RUYVEN, MONIQIJE VAN
VEENSTRA, JAN
Articles
This paper provides an inventory of the literature on alcohol research. The aim is to provide the readers of this literature with data on the quantity and types of papers published. For this purpose, over 4000 scientific papers on biomedical and social aspects of alcohol consumption, which had been collected in our Alcohol Documentation Centre over the past 2 years, were surveyed. They were classified according to three criteria: (I) the subject under investigation, (2) the type of study, and (3) whether the study concerned normal consumption, alcohol misuse or both. Furthermore, information is given on sources of alcohol research literature, authorship, and countries of origin.
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/599
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/6072015-05-19HighWireOUPalcalc:28:5
LETTER TO THE EDITOR
WAINWRIGHT, PATRICIA E.
Letter to the Editor
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/607
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/6082015-05-19HighWireOUPalcalc:28:5
RESPONSE
REITZ, RONALD C.
Response
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/608
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/609-a2015-05-19HighWireOUPalcalc:28:5
BOOK REVIEWS
PEARSON, GEOFFREY
Book Reviews
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/609-a
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
COOK, C. C. H.
Book Reviews
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/609-b
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/6092015-05-19HighWireOUPalcalc:28:5
BOOK REVIEWS
LYDON, STEVIE
Book Reviews
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/609
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/6102015-05-19HighWireOUPalcalc:28:5
BOOK REVIEWS
BUXTON-THOMAS, M.
Book Reviews
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/610
en
Copyright (C) 1993, Medical Council on Alcohol
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CALENDAR
Calendar
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/611
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/5/6122015-05-19HighWireOUPalcalc:28:5
MEDICAL COUNCIL ON ALCOHOLISM SUBSCRIPTION RATES
Notices
Oxford University Press
1993-09-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/5/612
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Copyright (C) 1993, Medical Council on Alcohol