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MEETING REPORT
MEAD, ANNETTE
ESBRA News
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/613
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Copyright (C) 1993, Medical Council on Alcohol
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THE DEFINITION OF ALCOHOLISM
MADDEN, J. S.
INVITED REVIEW
Formulations of alcohol dependence are continuously refreshed, in line with changing concepts and altered needs. Two new descriptions have been prepared: the revised WHO criteria for substance use disorders and an educative definition of alcoholism. The major Sets of diagnostic criteria provided by WHO and by the American Psychiatric Association are moving closer together but have not solved all the semantic problems. More refined assessments are also available to quicken fulfilment of the long-awaited hope that treatments can be matched to patients.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/617
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Copyright (C) 1993, Medical Council on Alcohol
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ALCOHOL-ASSOCIATED GENERATION OF OXYGEN FREE RADICALS AND TUMOR PROMOTION
MUFTI, SIRAJ I.
ESKELSON, CLEAMOND D.
ODELEYE, OLALEKAN E.
NACHIAPPAN, VASANTHI
INVITED REVIEW
We discuss evidence indicating how ethanol could generate oxygen free radicals. Recent use of techniques such as spin trapping and EPR spectroscopy have demonstrably confirmed that both acute and chronic alcohol use by laboratory animals would generate free radical intermediates. These radicals are of biological origin and presumably involve lipids. However, an exact identification of the intermediates produced has not been worked out with the currently available methodologies. Also not known is the mechanism whereby ethanol could initiate free radicals. The relationship between generation of free radicals and cell toxicity or carcinogenesis is also not understood. Using a variety of systems that included different species, strains and gender (male Sprague-Dawley and Fisher-344 rats, female C57BL/6 mice, male Syrian golden hamsters) and carcinogens (NMB<inf>x</inf>A, NNN, NNK, DMBA and LP-BM5 retrovirus) we have shown an association of lipid peroxidation with ethanol tumor promotionability. However, the process of tumor promotion in general is not very clear and the role played by ethanol in this process is still more unclear. Here we are reviewing evidence that could possibly be involved in such promotion processes.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/621
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Copyright (C) 1993, Medical Council on Alcohol
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MODULATION OF ALCOHOL PREFERENCE BY NMDA ANTAGONISTS IN MALE RATS
LAMBLIN, FABIENNE
DEUCEUNINCK, DAVID
DE WITTE, PHILIPPE
Articles
Chronic alcoholization by alcohol inhalation was used to study the properties of magnesium, a non-competitive NMDA receptor antagonist, and CGP 39551, a competitive NMDA receptor antagonist, on behavioural dependence as estimated by the free-choice paradigm [alcohol 10% (v/v) vs. water], on the hypermotility after alcohol withdrawal, and finally on the cortical vascularization. The first experimental group received the drugs per os during the whole alcoholization period. Magnesium (20 mg/kg/day) decreased the alcohol dependence while CGP 39551 (5 and 10 mg/kg/day) increased, in a dose-dependent manner, the dependence to alcohol. A second group of animals received the same drugs at the same dosages, not simultaneously during chronic alcoholization, but immediately after alcoholization in one shot i.p. injection. In this case, rats receiving 5 mg/kg CGP 39551 never showed any dependence towards alcohol, while 10 mg/kg CGP 39551 or 20 mg/kg magnesium prolonged the number of days of alcohol dependence. These results thus indicate the close interaction between NMDA receptor function and dependence for alcohol. Magnesium had no effects on hypermotility, while CGP 39551-treated animals presented a decrease in the hypermotility observed after alcohol withdrawal. Neither drug affected the hypervasculanzation accompanying the chronic alcoholization.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/639
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/6/6492015-05-19HighWireOUPalcalc:28:6
EFFECTS OF CALCIUM ANTAGONISTS ON CENTRAL ACTIONS OF ETHANOL: COMPARATIVE STUDIES WITH NIFEDIPINE, VERAPAMIL AND CINNARIZINE
CZARNECKA, ELZBIETA
KUBIK-BOGUCKA, ELZBIETA
Articles
The effects of nifedipine (17.5 and 50 mg/kg), verapamil (5 and 15 mg/kg) and cinnarizine (75 and 200 mg/kg) on acute toxicity and central actions of ethanol (i.e. ethanol-induced sleep and hypothermia, disturbances of rota-rod performance and spontaneous activity) were investigated in mice. Additionally, effects of these drugs on the development of tolerance to hypothermic and sleep-inducing action of ethanol were studied in rats. Calcium antagonists were given acutely 30 min before ethanol administration, or chronically once daily (lower dose) for 10 days, and on the 11th day the animals received an ethanol injection. Single doses of nifedipine increased the acute toxicity of ethanol and potentiated its central effects. After long-term administration of nifedipine no significant alterations in the central actions of ethanol were observed. Verapamil and cinnarizine antagonized the ethanolinduced sleep and impairment of locomotor activity. Nifedipine did not affect the development of tolerance to hypnotic and hypothermic action of ethanol. Verapamil prevents the development of tolerance to hypnotic action of ethanol, whereas cinnarizine prevents the development of tolerance to the hypnotic and hypothermic action of ethanol.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/649
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Copyright (C) 1993, Medical Council on Alcohol
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MATERNAL ETHANOL CONSUMPTION INDUCES TRANSIENT COMPENSATORY HYPERPLASIA OF DEVELOPING CARDIAC TISSUE IN THE NEONATAL RAT
FUSELER, JOHN W.
Articles
The effect of continuous exposure to ethanol <it>in utero</it> and postpartum on growth and cell division in developing cardiac tissue was studied in neonatal Fischer rats. Pregnant and lactating females were maintained on three dietary regimens; a control group fed rat chow <it>ad libirum</it>, an experimental group receiving an ethanol-containing (6% by volume) liquid diet, and a pair-fed control group, which received an isocaloric amount of control liquid diet. At days 1, 5, and 10 postpartum, five litters of pups from each control and experimental group were sacrificed and the body weights, heart weights, heart-to-body weight ratios, and mitotic frequency of the ventricular myocardium were measured. When compared to either group of controls, pups continuously exposed to dietary ethanol expressed significantly (<it>P</it> < 0.01) lower body weights. Pups maintained by the pair-fed females had significantly (<it>P</it> < 0.01) lower body weights at days 5 and 10 than pups maintained by the chow-fed females, indicating a pair-fed effect of suboptimal nutrition of the model. As the pups developed, the heart weights of pups maintained by the chow-fed females became progressively greater (<it>P</it> < 0.01) than the heart weights of pups maintained by the pair-fed and ethanol-fed females, which expressed no weight difference. The reduction of heart weight present in the ethanol-fed and pair-fed pups represents a pair-fed effect of suboptimal nutrition and not an obvious effect of exposure to dietary ethanol. The ratio of heart weight to body weight and mitotic frequency were significantly greater (<it>P</it> < 0.01) in 1- to 5-day-old pups exposed to ethanol. Following day 5, these parameters decreased and approached the control values. This indicates that growth of cardiac tissue is not suppressed in the 1- to 5-day-old rat pups exposed continuously to dietary ethanol. These observations further suggest the presence of a mechanism intrinsic to the heart which can provide stage-dependent protection from the adverse effects of ethanol during early development. The decline in heart weight to body weight ratios and mitotic frequency in pups of ethanol-fed females also suggests that ethanol may initiate suppression of the growth of cardiac tissue or may incur stage-dependent injury during the later stages of development. The possible mechanism of this stage-dependent protection during early neonatal development is an increased mitotic activity of the cardiac myocytes.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/657
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Copyright (C) 1993, Medical Council on Alcohol
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ETHANOL-INDUCED ALTERATIONS IN GONADOTROPHINS SECRETION DURING THE ESTROUS CYCLE OF RATS
ALFONSO, M.
DURÁN, R.
MARCÓ, J.
Articles
The effects of ethanol administration during a preovulatory period on both serum and pituitary gonadotrophin concentrations were studied in female rats. The animals were injected with 2 g/kg of ethanol (30% v/v, in saline solution) at 18:00 hr of diestrous 2. Hormonal levels were measured by RIA at different times during the estrous cycle, especially during the proestrus day. The preovulatory LH surge was inhibited using ethanol. Serum LH levels decreased between 16.00 and 20.00 hr of proestrus (<it>P</it> < 0.01). The levels of FSH in serum were slightly depressed by ethanol between 12.00 and 17.00 hr of proestrus (P < 0.05 with respect to the control set), but the values during the proestrus surge (18.00–20.00 hr) were unaffected. Ethanol augmented pituitary hormonal content during the periods in which serum hormonal levels decreased (<it>P</it> < 0.05 with respect to the control set) but it did not affect gonadotrophins synthesis. The increase in pituitary gonadotrophin concentrations induced by ethanol during the proestrus day is due to the accumulation of the hormone which was not released before. The preovulatory LH surge was re-established in the next cycle (5th day after treatment). These effects of ethanol on gonadotrophin levels could explain the previously observed anovulatory effects induced by ethanol administration in diestrous.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/667
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Copyright (C) 1993, Medical Council on Alcohol
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THE IMPACT OF AGE ON ALCOHOL TOXICITY IN THE RAT
MENDENHALL, C. L.
ROUSTER, S. D.
GROSSMAN, C. J.
ROSELLE, G. A.
GHOSN, S.
GARTSIDE, P.
Articles
This study was performed to determine whether the severity of chronic alcohol toxicity is altered by age and duration of drinking. Alcohol as 35% of calorie intake (ED treatment) was administered to Sprague-Dawley rats at predetermined ages beginning at 1, 6, 12, 18, 24 and 27 months for a duration of treatment varying from 1 to 3 months. The degree of injury was compared to controls (CD treatment) of comparable age and duration of treatment. ED was associated with significantly higher serum levels of AST, total bilirubin and alkaline phosphatase (<it>P</it> < 0.0001 for each test) without detectable differences due to age and duration of treatment. Liver triglycerides (as a measure of alcoholic fatty steatosis) were significantly increased by ED (<it>P</it> < 0.0001) and influenced by both age and duration of treatment The greatest toxicity was observed in young animals. ED treatment beginning at 1 month of age was associated with an AST level 69% above CD and liver triglycerides 463% above CD; beginning at 18 months of age, ED produced an increase of 24% in AST and 175% in liver triglycerides. The heparic regenerative capacity, as measured by 3H uptake into nuclear DNA, was similarly affected by both ED and age. Regeneration was significantly higher in youth. ED produced a 62% increase above CD at 1 month compared to an 11% increase beginning at 18 months of age. These observations suggest that juveniles develop more severe injury from alcohol but that a greater regenerative capacity exists in youth. This may explain the observed clinical relationship between age and prognosis seen in patients with severe alcoholic liver injury.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/675
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Copyright (C) 1993, Medical Council on Alcohol
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EFFECTS OF SEED SAPONINS OF THEA SINENSIS L. (RYOKUCHA SAPONIN) ON ALCOHOL ABSORPTION AND METABOLISM
TSUKAMOTO, SHOJIRO
KANEGAE, TAKASHI
NAGOYA, TADAKI
SHIMAMURA, MASAO
KATO, TAMAKO
WATANABE, SHINICHIRO
KAWAGUCHI, MAKOTO
Articles
We evaluated the effects of the seed saponins of <it>Thea sinensis</it> L. on alcohol absorption and metabolism in rats and mice. An ethanolic extract from the seeds of <it>T. sinensis</it> was orally administered to the rats 1 hr before or 0.5 hr after administration of ethanol (2 g/kg), and the blood ethanol assayed 0.5, 1, 2, 3, and 4 hr after ethanol administration. The ethanol level decreased after both pie- and post- administration of the extract. The extract was further purified to obtain a saponin fraction which was orally administered to mice 1 hr before ethanol administration. Blood, liver, and stomach were obtained 0, 1, 3, and 6 hr after ethanol administration, and the ethanol, acetaldehyde, acetate, and acetone concentrations in each specimen were measured by head space gas chromatography. The saponin fraction decreased the ethanol levels in the blood and liver but increased that in the stomach five-fold over the control level, suggesting inhibition of alcohol absorption. The ethanol disappearance time from the blood was shortened, suggesting the promotion of alcohol disappearance. The acetate and acetone levels were unaffected. However, the acetaldehyde level decreased in the blood, liver, and stomach. The decreases in the ethanol and acetaldhyde levels in the liver suggested the protective effects of the seed saponins on the liver. The saponins did not directly inhibit hepalic alcohol dehydrogenase activity. The seed saponins of <it>T. sinensis</it> seem to suppress alcohol absorption by slowing gastric emptying and by inhibiting absorption across the cell membranes of the digestive tract.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/687
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/6/6932015-05-19HighWireOUPalcalc:28:6
PLASMA XANTHTNE OXIDASE LEVEL AND ALCOHOL ADMINISTRATION
ZIMA, T.
NOVÁK, L.
STÍPEK, S.
Articles
The acute administration of ethanol by gastric cathether significantly increases the plasma xanthine oxidase activity in both rats and hamsters without changing other enzyme activities — alanine aminotransferase and aspartate aminotransferase. The plasma xanthine oxidase level seems to be a sensitive marker of liver damage. Its higher activity due to the acute ethanol intoxication may have an impact on ethanol organ damage.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/693
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Copyright (C) 1993, Medical Council on Alcohol
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FAMILIAL ALCOHOLISM AND ERPs: DIFFERENCES IN PROBABILITY SENSITIVITY?
BERMAN, S. M.
MARTINEZ, R. A.
NOBLE, E. P.
Articles
Event-related potentials (ERPs) were recorded from sons (age 11–14) of families that were positive (FH+) and negative (FH−) for alcoholism in response to circles, triangles and squares presented in four colors with a single central digit A button was pressed for successive presentations of identical stimuli (target probability = 0.2). Reduced late positivity in FH+ boys has been previously reported. This positivity was shown to increase with the number of features that match target requirements. FH− boys responded more quickiy, but no less accurately, than FH− boys, and were characterized by reduced ERP stimulas selectivity. That is, FH+ boys not only produced less P3 than FH− boys in response to targets, but generally produced more late positivity than FH− boys in response to nontargets. The pattern of group differences was most consistent with FH+ boys exhibiting both reduced ERP effects of target features in general, and a specific insensitivity to matching digits. It is hypothesized that these effects result from reduced sensitivity to information about the frequency with which categories of events occur, and that this may be characteristic of those at high risk for alcoholism.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/695
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/6/7092015-05-19HighWireOUPalcalc:28:6
HIP FRACTURES IN MIDDLE-AGED MEN: A CONSEQUENCE OF EARLY RETIREMENT AND ALCOHOL MISUSE?
JÓNSSON, B.
SERNBO, I.
KRISTENSSON, H.
JOHNELL, O.
Articles
From the 1950s to the 1980s the incidence of hip fractures in women aged 50–64 and cervical fractures in men of the same age In Malmö did not increase, whereas the incidence of trochanteric fracture in men aged 50–64 increased significantly. Significant background factors in men were alcohol misuse, living alone, early retirement, previous fractures, low weight/height ratio and less severe trauma — more in men with trochanteric than in men with cervical fracture. The deviant lifestyle and suspected physical inertia in this group of middle-aged men probably predisposes to osteoporosis and increased fracture risk.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/709
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Copyright (C) 1993, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:28/6/7152015-05-19HighWireOUPalcalc:28:6
CONSUMPTION AND HARM: DRINKING PATTERNS OF THE IRISH, THE ENGLISH AND THE IRISH IN ENGLAND
HARRISON, LARRY
CARR-HILL, ROY
SUTTON, MATT
Articles
These has been controversy over the relationship between alcohol consumption and related problems amongst the Irish in England. Irish migrants have high Standardised Mortality Ratios for chronic liver disease and cirrhosis and high hospital admission rates for alcohol-related diagnoses in England. Yet it has been considered that people from the Republic of Ireland, whether living in Ireland (Conniffe <it>et al</it>., 1990) or in England (Pearson <it>et al</it>., 1991), actually drink less than the English. This paper reviews the evidence. In recent years Irish <it>per capita</it> volume alcohol consumption has been comparable to that of the U.K., although the distribution of consumption differs. Women in Ireland are less likely to drink than women in England and Wales, while men in Ireland are more likely to drink at high-risk levels than men in England and Wales: their average weekly consumption levels are closer to those of high-consuming men in Yorkshire and Humberside, who also drink more than the U.K. national average. Men in Ireland also appear to be more likely to experience drinking problems than their counterparts in England and Wales, although this may be related to factors other than the total amount of alcohol consumed. Although a previous study of General Household Survey data indicated low-risk alcohol consumption levels for people from the Irish Republic living in Britain, a reanalysis of these data adjusting for age and gender shows drinking rates that are very high. While it is important to avoid unhelpful stereotypes about Irish drunkenness, attempts to minimise or deny the scale of problems faced by a disadvantaged migrant group will result in the Irish community not receiving the resources and help that it needs.
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/715
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
CLEARE, A.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/725-a
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
RAISTRICK, D.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/725-b
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
DORÉ, C. J.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/725
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
HORE, B. D.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/726-a
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
WORLD, M. J.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/726
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
FORSYTHE, M.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/727-a
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
GORMAN, D. M.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/727
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Copyright (C) 1993, Medical Council on Alcohol
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BOOK REVIEWS
SHAW, G. K.
Book Reviews
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/728
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Copyright (C) 1993, Medical Council on Alcohol
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CALENDAR
Calendar
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/729
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Copyright (C) 1993, Medical Council on Alcohol
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NOTICES
Notices
Oxford University Press
1993-11-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/28/6/730
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Copyright (C) 1993, Medical Council on Alcohol