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oai:open-archive.highwire.org:alcalc:27/2/1012015-05-19HighWireOUPalcalc:27:2
OBITUARIES: Dr Oliver Pratt and Professor Trevor Slater
Obituaries
Oxford University Press
1992-03-01 00:00:00.0
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/101
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Copyright (C) 1992, Medical Council on Alcohol
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INVITED REVIEW: ALCOHOLIC LIVER DISEASE: TO TRANSPLANT OR NOT TO TRANSPLANT?
LUCEY, MICHAEL R.
BERESFORD, THOMAS P.
Articles
Liver transplantation for patients with alcoholic liver disease remains very controversial. We review recent data which suggest that, contrary to earlier reports, many alcoholic patients with end-stage liver disease are able to meet stringent selection criteria and that these selected alcoholics achieve a good result from a liver transplant. Conversely, non-selected alcoholics have a significantly poorer survival. This raises the question as to what is the most appropriate method to select alcoholic patients for liver transplantation. We advocate a selection process which considers the potential recipients' medical, surgical and psychiatric suitability rather than their diagnosis. We outline how we have arrived at this approach in part because of the heterogeneity of patients who carry the diagnosis ‘alcoholic liver disease’. We describe how we try to estimate prognosis for future abstinence, which is based on a profile of historical features rather than a fixed period of sobriety. Using this approach, the incidence of recidivism in the first 2 years after transplantation has been low. Prospective longitudinal studies are needed to improve methods of selection for the management of alcoholic patients undergoing liver transplantation.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/103
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/1092015-05-19HighWireOUPalcalc:27:2
INVITED REVIEW: A BURNING ISSUE? ADOLESCENT ALCOHOL USE IN BRITAIN 1970-1991
MAY, CARL
Articles
A review is presented of British research related to alcohol use and misuse by adolescents in the period 1970 to 1991. The stability of alcohol use among this age group is emphasised by a succession of studies which indicate the <it>normality</it> of alcohol consumption among its members, most of whom drink in moderation. It is noted that a succession of ‘moral panics’ amplified in the popular media have led to public concern about an ‘epidemic’ of alcohol misuse by young people, but that research evidence does not sustain this popular supposition. Nevertheless, the available evidence does support the conclusion that alcohol misuse is a major problem for a small proportion of young people.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/109
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/1172015-05-19HighWireOUPalcalc:27:2
INVITED REVIEW: DRINKING AND THE BRAIN: CURRENT EVIDENCE
DELIN, CATHERINE R.
LEE, TERRY H.
Articles
There is no question, as accumulating evidence reveals, that alcohol in excess negatively affects the brain and neuropsychological functioning, both immediately and in the long-term. The important question for social drinkers, however, is whether moderate amounts of alcohol can have deleterious effects on the brain or performance in either the medium- or longterm. It has been proposed that there is a continuum of negative consequences with light drinkers at one end and chronic alcoholics at the other end. Three levels of study of this hypothesis are distinguished; behavioural, structural, and cellular. Research into effects at these three levels is reviewed both for alcoholics and for social drinkers. A further hypothesis relates to the possibility that cognitive functioning is impaired even after blood alcohol concentration has returned to zero. It is concluded that while neither the continuity hypothesis nor a ‘hangover’ hypothesis is supported by current evidence, considerably more research is needed.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/117
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/1272015-05-19HighWireOUPalcalc:27:2
RAPID COMMUNICATION: ALCOHOL-PREFERRING RATS HAVE FEWER DOPAMINE D2 RECEPTORS IN THE LIMBIC SYSTEM
STEFANINI, ENNIO
FRAU, MICHELA
GARAU, MARIA GIULIA
GARAU, BRUNO
FADDA, FABIO
GESSA, GIAN LUIGI
Articles
Dopamine D<inf>2</inf> receptors in nucleus accumbens, olfactory tubercle and caudate nucleus of Sardinian ethanol-preferring (SP), and non-preferring (SNP) rats were compared by using [3H]YM-09151-2 binding. SP rats exhibited, in each area, lower density of D<inf>2</inf> receptors than SNP and unselected Wistar (UW) rats. The results suggest that reduction in D<inf>2</inf> receptors in SP rats may be relevant to their innate preference for alcohol.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/127
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Copyright (C) 1992, Medical Council on Alcohol
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OCCURRENCE IN VIVO OF 5-HYDROXYTRYPTOPHOL IN THE BRAIN OF RATS TREATED WITH ETHANOL
YOSHIMOTO, KANJI
KOMURA, SETSUO
KAWAMURA, KEIJI
Articles
The effect of ethanol (EtOH) on the release of dopamine (DA) and 5-hydroxytryptamine (5-HT) and the efflux of their metabolites, 3, 4-dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindol-3-ylacetic acid (5-HIAA) and 5-hydroxytryptophol (5-HTOL) from the striatum of the freely moving rat were studied <it>in vivo</it> using brain microdialysis. Striatal DA and 5-HT release was maximally enhanced at first fraction after the administration of EtOH (2 g/ kg, i.p.). The level of the DA-oxidized metabolite, DOPAC, decreased significantly. In the 5-HT metabolic pathway, the oxidized metabolite, 5-HIAA, did not show significant changes, whereas levels of the biogenic alcohol 5-HTOL were increased to 180% at 90 min following EtOH administration. It is suggested that EtOH, most probably via acetaldehyde, could shift 5-HT metabolism from the oxidative to the reductive pathway in the rat brain.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/131
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/1372015-05-19HighWireOUPalcalc:27:2
MODIFICATION OF THE BEHAVIOURAL EFFECTS OF ETHANOL BY NIFEDIPINE
WHITE, JASON M.
SMITH, ANGELA M.
Articles
Nifedipine (10.0 mg/kg) was administered to mice together with graded doses of ethanol (0, 2.5, 3.0, 3.5, 4.0 and 4.5 g/kg), and activity measured over a 2-hr period following administration. Low ethanol doses increased activity, whereas the highest dose decreased it. By itself, nifedipine had no effect on activity, but when combined with ethanol it produced a consistent decrease in comparison with ethanol alone. This occurred irrespective of whether the ethanol dose alone increased or decreased activity. These results demonstrate a clear interaction between nifedipine and ethanol which cannot be characterized as simple potentiation or antagonism. Time-course data showed that the effects of nifedipine were apparent within 10–20 min of drug administration, but, in the case of the highest ethanol dose, increased toward the end of the 2-hr period. Retardation of the development of acute tolerance may contribute to the interaction between ethanol and nifedipine.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/137
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Copyright (C) 1992, Medical Council on Alcohol
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BENZODIAZEPINE METABOLISM IN ETHANOL-TREATED MALE RATS: USE OF PAIR-FED AND AGE-MATCHED CONTROLS
MASON, STEVEN R.
REILLY, PAUL E. B.
WARD, LEIGH C.
Articles
The effects of chronic moderate (15%) ethanol consumption and ageing on rat hepatic cytochrome P450 monooxygenase activities were examined using diazepam, nordazepam, <it>d</it>-benzphetamine, erythromycin, ethylmorphine and nitrosodimethylamine (NDMA) as substrates. In addition, the effects of moderate ethanol alone on the oxidation of metoprolol, morphine and temazepam were examined. Cytochrome P450 specific content increased significantly only in the 6-week ethanol-treated rats, and no changes in percentage liver to body weights were apparent in any of the ethanol-treated animals compared with pair-fed controls. Only cytochrome P450IIIA enzyme activities displayed age-related decreases, these being identified in the pair-fed animals. <it>C</it><inf>3</inf>-hydroxylation of diazepam and nordazepam (36% of controls) and N-demethylation of erythromycin and ethylmorphine (58% and 64% of controls) were decreased in 6-week ethanol-treated animals, these effects being less pronounced in the 12, 24 and 48-week ethanol-treated groups. The decrease seen for diazepam and <it>d</it>-benzphetamine <it>N</it>-demethylation caused by ethanol consumption was approximately 80% of control groups for the duration of the treatment. NDMA and morphine <it>N</it>-demethylations were increased to 120% of control activities and metoprolol α-hydroxylase was increased to 140% of control activities at 6 weeks, whilst metoprolol <it>O</it>-demethylase activity remained unaltered. NDMA <it>N</it>-demethylase activity showed a two-fold induction at 24 and 48 weeks of ethanol treatment, compared with corresponding pair-fed control groups. These results support previous findings from this laboratory showing that the same or similar P450IIIA family isozymes are involved in the <it>C</it><inf>3</inf>-hydroxylation of diazepam and nordazepam. In addition, this study indicates that moderate ethanol consumption causes decreased activities of cytochrome P450IIIA family enzymes as evidenced by decreased <it>C</it><inf>3</inf>-hydroxylation of benzodiazepines and decreased <it>N</it>-demethylation of erythromycin and ethylmorphine.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/143
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CARBAMAZEPINE VERSUS OXAZEPAM IN THE TREATMENT OF ALCOHOL WITHDRAWAL: A DOUBLE-BLIND STUDY
STUPPAECK, C. H.
PYCHA, R.
MILLER, C.
WHITWORTH, A. B.
OBERBAUER, H.
FLEISCHHACKER, W. W.
Articles
The use of more than 130 drugs and drug combinations against the alcohol withdrawal syndrome reflects the fact that views on its treatment are far from being unequivocal. Benzodiazepines are the first choice treatment but it should not be disregarded that they have side effects and, above all, a varying risk of dependency themselves. In recent years many trials have focused on carbamazepine in this respect. Its efficacy was proven in various open and double-blind studies, most of them using concomitant sedative drugs, thereby diminishing the reliability of the results. In a double-blind study we compared the efficacy of carbamazepine with that of oxazepam, in 60 in-patients suffering from alcohol withdrawal syndrome. The main rating instrument was the Clinical Institute Withdrawal Scale —Alcohol (CIWA-A). The 7-day trial showed equal efficacy of carbamazepine and oxazepam during the first 5 days and a statistically significant superiority of carbamazepine on days 6 and 7. Four patients in each group had to be dropped from the study due to side effects or after having withdrawn informed consent. There was no decrease in white blood counts under carbamazepine. The experiences with carbamazepine up to now suggest a more widespread use, especially in non-delirious withdrawal states.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/153
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Copyright (C) 1992, Medical Council on Alcohol
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RELATIVE AND COMBINED ROLES OF ETHANOL AND PROTEIN MALNUTRITION ON SKELETAL MUSCLE
CONDE, A.
GONZALEZ-REIMERS, E.
GONZÁLEZ-HERNÁNDEZ, T.
SANTOLARIA, F.
MARTINEZ-RIERA, A.
ROMERO-PEREZ, J. C.
RODRIGUEZ-MORENO, F.
Articles
The aim of the present study is to analyse the relative and combined effect of ethanol and protein malnutrition on muscle changes in ethanol-fed rats. The study was performed in 32 animals divided into four groups, fed with the Lieber-DeCarli control, 36% ethanol, 2% protein, and 36% ethanol/2% protein-containing diets, respectively. Right gastrocnemius muscle was removed two months later, and histochemical-morphometrically studied. Type IIb fibre atrophy was observed both in the alcoholic and protein-deficient animals. The combination of these factors led to a slightly more marked atrophy. Malnutrition led to a decrease in type I fibre diameter; ethanol caused an increase in their size; whereas concurrent administration of ethanol and a protein deficient diet led to type I fibre atrophy. The proportion of type IIb fibre decreased in the three experimental groups with respect to the control group, especially in the alcoholic, protein-deficient animals. Thus, malnutrition potentiates the effect of ethanol except for changes in type I fibre diameter, in which the effects are opposite.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/159
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/1652015-05-19HighWireOUPalcalc:27:2
NON-INVASIVE LASER-DOPPLER ASSESSMENT OF CUTANEOUS BLOOD-FLOW IN ALCOHOL STUDIES: EFFECTS OF CHRONIC ETHANOL CONSUMPTION ON PERIPHERAL BLOOD-FLOW IN UNANAESTHETISED RATS
PREEDY, VICTOR R.
COOK, ELISABETH B.
SIDDIQ, TAHIR
Articles
We investigated the use of a microprocessor-controlled laser-Doppler monitor to measure blood-flow in unanaesthetised animals. The apparatus permitted real-time assessment of cutaneous blood-flow, identified artifactual changes due to limb and body movements and was able to calculate rapidly the average value for blood-flux between two selected time points. The practical applicability of the apparatus was appraised by determining the effects of chronic ethanol toxicity. Male Wistar rats were fed nutritionally adequate liquid diets containing 35% of dietary calories as ethanol, or pair-fed identical amounts of the same diet in which ethanol was replaced isocalorically by glucose. After 2 weeks of treatment, peripheral cutaneous flux was reduced in all ethanol-fed rats by 25%, from a mean of 322 arbitrary units (control rats) to 243 arbitrary units (ethanol-fed rats; <it>P</it><0.05); the laser-Doppler studies also indicated that there was no alteration in blood cellular contents.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/165
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/1712015-05-19HighWireOUPalcalc:27:2
EFFECTS OF CHRONIC ETHANOL INTOXICATION ON ALDEHYDE DEHYDROGENASE IN MOUSE LIVER
TOMITA, YUKARI
HASEBA, TAKESHI
KUROSU, MITSUYASU
WATANABE, TOKINORI
Articles
Effects of chronic ethanol treatment with liquid diet (ethanol constituted 28% of the calories) on hepatic aldehyde dehydrogenase (ALDH) isozymes were studied in mice. One week of ethanol feeding caused 66% loss of mitochondrial low Km ALDH activity and 80% loss of mitochondrial high Km ALDH activity, compared with the control-fed group. However, these decreases recovered after 4 weeks of ethanol feeding. The cytosolic ALDH activity increased up to 140% after 10 weeks of ethanol feeding, compared with the control-fed group. Effects of acute ethanol injection on ALDH activity after prolonged ethanol feeding were studied. The severe acute ethanol injection (4.5 g/kg body wt) after 4 weeks of ethanol feeding caused a drastic decrease of the mitochondrial low Km ALDH activity; however, that did not affect the ethanolfed group. After 10 weeks of ethanol feeding, acute ethanol injection (4.5 g/kg body wt) caused about twofold increase in mitochondrial low Km ALDH activity. From the agarose IEF study, it was found that ethanol intoxication does not affect the number and pI value of ALDH isozymes.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/171
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Copyright (C) 1992, Medical Council on Alcohol
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RELATIONSHIP BETWEEN BLOOD CATALASE ACTIVITY AND DRINKING HISTORY IN A HUMAN POPULATION, A POSSIBLE BIOLOGICAL MARKER OF THE AFFINITY TO CONSUME ALCOHOL
KOECHLING, ULRIKE M.
AMIT, ZALMAN
Articles
The relationship between blood catalase activity and alcohol consumption was investigated in a group of Caucasian volunteers (<it>N</it> = 191). Subjects individually attended a 1-hr session, during which they were asked to complete the Michigan Alcoholism Screening Test (MAST) and MacAndrew Scale (MAC), supply information on alcohol consumption (averaged over the most recent and typical 30-day periods: Recent and Typical Q-Values) and other drug use by answering the Concordia Alcohol Screening Questionnaire (CASQ), and provide a 100-μl blood sample from the fingertip. Results showed a significant positive relationship between typical Q-Value and catalase activity (<it>r</it> = 0.43, <it>P</it> < 0.001), which improved after eliminating multiple drug users from the analysis (<it>r</it> = 0.65, <it>P</it> < 0.001). Multiple regression analyses showed that catalase activity combined with being male, using cocaine or crack, scoring highly on the MAC scale and having alcohol-related problems (MAST), explained a significant portion of the variance in Typical Q-Value. These results support the notion that catalase activity is a strong positive determinant of alcohol intake and support the hypothesis that the enzyme catalase plays a role in regulating voluntary ethanol consumption.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/181
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Copyright (C) 1992, Medical Council on Alcohol
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FREQUENCY OF ALCOHOL-ASSOCIATED MANDIBULAR FRACTURES IN NORTHERN FINLAND IN THE 1980s
OIKARINEN, KYÖSTI
SILVENNOINEN, URPO
IGNATIUS, EINO
Articles
In order to evaluate the frequency of alcohol-associated mandibular fractures, information on patients treated and diagnosed at a University Hospital and Dental Institute in northern Finland between 1981 and 1990 was analysed. Altogether, 117 male patients (out of 239) and 23 female patients (out of 78) were under the influence of alcohol at the time of accident. The annual risk for men receiving a mandibular fracture under the influence of alcohol (odds ratio) varied between 0.6 and 6.6, compared with female patients. More alcohol-associated mandibular fractures occurred in late summer and autumn and fewer in spring. Patients suffering mandibular fractures at weekends were more often under the influence of alcohol than those injured on weekdays. There seemed to be a tendency for the proportion of alcohol-associated mandibular fractures to decrease towards the end of the decade.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/189
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/1952015-05-19HighWireOUPalcalc:27:2
ALCOHOL CONSUMPTION IN TELEVISION PROGRAMMING IN THREE ENGLISH-SPEAKING CULTURES
WAXER, P. H.
Articles
Previous research relating television advertising and alcohol consumption indicates no meaningful relationships. This study focused on observed drinking behaviour in comedy, soap opera, drama, and police/detective programmes produced for British, American and Canadian television. Results indicated British television fiction had three times the amount of alcohol consumption seen in either American or Canadian programming. In spite of this more frequent portrayal of alcohol consumption, examination of World Drinking Trends and other alcohol-related statistics (i.e. cirrhosis and alcohol-related auto accidents) indicated no greater level of alcohol misuse in the U.K. than in Canada or the United States. In fact, available statistics indicate significantly lower rates of liver cirrhosis in Britain as opposed to Canada and the United States. Hypotheses regarding the absence of relation between fictional and actual alcohol consumption were discussed.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/195
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Copyright (C) 1992, Medical Council on Alcohol
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BOOK REVIEWS
RUSSELL, M. A. H.
Book Reviews
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/201-a
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Copyright (C) 1992, Medical Council on Alcohol
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BOOK REVIEWS
ÖJESJÖ, L.
Book Reviews
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/201
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Copyright (C) 1992, Medical Council on Alcohol
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BOOK REVIEWS
HOWELLS, LIZ
Book Reviews
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/202-a
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Copyright (C) 1992, Medical Council on Alcohol
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BOOK REVIEWS
HILL, FAITH
Book Reviews
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/202
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Copyright (C) 1992, Medical Council on Alcohol
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BOOK REVIEWS
GLUCKSMAN, E.
Book Reviews
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/203-a
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Copyright (C) 1992, Medical Council on Alcohol
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BOOK REVIEWS
DAVIES, GAIUS
Book Reviews
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/203
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Copyright (C) 1992, Medical Council on Alcohol
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CALENDAR
Calendar
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/205
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/2062015-05-19HighWireOUPalcalc:27:2
MEDICAL COUNCIL ON ALCOHOLISM SUBSCRIPTION RATES 1992
NOTICES
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/206
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CORRIGENDUM
Cook, C. C. H.
Walden, R. J.
Graham, B. R.
Gillham, C.
Davies, S.
Prichard, B. N. C.
Corrigendum
Trace element and vitamin deficiency in alcoholic and control subjects. In Table 3 of the above article, the mean level of plasma magnesium should read 0.85, not 0.03 as shown.
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/207
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Copyright (C) 1992, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:27/2/992015-05-19HighWireOUPalcalc:27:2
ESBRA AWARD 1992
Announcement
Oxford University Press
1992-03-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/27/2/99
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Copyright (C) 1992, Medical Council on Alcohol