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ALCOHOL AND THIAMINE OF THE BRAIN
RINDI, GIANGUIDO
Editorial
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/493
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Copyright (C) 1989, Medical Council on Alcohol
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SEARCH FOR ASSOCIATION BETWEEN MCV AND MISCARRIAGE, REFLECTING ETHANOL CONSUMPTION OR OTHERWISE
FERNANDEZ-FONTECHA, MARIA L.
RENWICK, J. H.
Rapid Communication
In 38 miscarrying women and 38 pair-matched controls, all studied retrospectively, the mean pair-difference in MCV is +1.2 fl, <it>P</it>÷0.05 (one-tailed). As ethanol elevates MCV, this might weakly support the suggested role of ethanol in some miscarriages, although folate/B12 deficiencies cannot be excluded. The paper demonstrates only the feasibility of a first step in defining the possible role of ethanol in some miscarriages. It identifies a difficulty encountered from earlier attendance in the miscarrying group so that a later study could circumvent it and perhaps lead to a case for funding of a prospective enquiry into the dose-response relations of any association that might exist.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/497
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Copyright (C) 1989, Medical Council on Alcohol
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SUPEROXIDE DISMUTASE IN THE ERYTHROCYTES OF ACUTE ALCOHOLICS DURING DETOXIFICATION
ROOPRAI, H. K.
PRATT, O. E.
SHAW, G. K.
THOMASON, A. D.
Rapid Communication
The activity of erythrocyte superoxide dismutase in acute alcoholic patients on admission does not form a single population but clusters in two groups either above or below the normal range. The values in both groups revert towards the normal after a week of treatment. The divergent activities of this free radical scavenging enzyme between the two groups could not be explained by differences in age, haematology or liver function tests but are likely to be acute responses, possibly to diverse drinking pattern in the period immediately preceeding admission.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/503
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5092015-05-19HighWireOUPalcalc:24:6
IS 'DISEASE MODEL' AN APPROPRIATE TERM TO DESCRIBE THE ALCOHOL DEPENDENCE SYNDROME?
GORMAN, D. M.
Articles
Caetano (Concepts of alcohol dependence: the two worlds of research and treatment. <it>Alcohol and Alcoholism</it> <b>23</b>, 225–227, 1988) has suggested that in the U.S.A. opposition from the disease model has been the main reason for the limited application of the alcohol dependence syndrome. In Britain, the charge that the syndrome is a poorly disguised version of the disease model has had a similar effect. This paper describes the main features of the crude biomedical disease model, which critics equate with the alcohol dependence syndrome. It is concluded that the alcohol dependence syndrome does not conform to this, in that it is not presented by its proponents as a discrete entity identified by a core psycho-biological pathology and carries no built-in assumptions about causal processes. It is argued that instead of setting-up and championing competing all-embracing conceptual models, both clinicians and researchers should be flexible and imaginative in their use of concepts.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/509
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5132015-05-19HighWireOUPalcalc:24:6
SUBSTANCE P AGAINST ETHANOL-INDUCED ALTERATIONS IN CENTRAL MECHANISMS OF FEEDING AND ESCAPE IN RABBITS
ZILOV, VADIM G.
ROGACHEVA, SVETLANA K.
IVANOVA, LYUDMILA I.
Articles
Rabbits were treated with 0.5 g/kg ethanol intravenously and alterations of limbicmidbrain interactions in both feeding and escape elicited by threshold electrical stimulation of the lateral (LH) and ventromedial hypothalamus (VMH) were observed. Decrease of the VMH excitability and abolishing of inhibitory effects of the dorsal hippocampus (HPC) and facilitatory influences of the midbrain reticular formation (MRF) on both motivational hypothalamic centres were found in animals after ethanol administration. Subsequent single injection of substance P (SP) (30 μg-kg i.v.) just at the height of alcohol manifestations in central mechanisms of feeding and escape led to restoration of the VMH excitability and facilitatory MRF influences on this motivational centre. SP administration was also found to restore the inhibitory hippocampal and facilitatory MRF effects on the excitability of the LH feeding centre. Partial and selective SP restoration of ethanol-induced alterations in feeding and escape which are observed in the present study, as well as the data of some other researchers, led to the suggestion that peptides could be used as factors of enhancing tolerance to ethanol or curing deleterious acute alcohol-induced effects in motivated behaviour in animals.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/513
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5192015-05-19HighWireOUPalcalc:24:6
BUTHIONINE SULFOXIMINE INHIBITION OF GLUTATHIONE BIOSYNTHESIS ENHANCES HEPATIC LIPID PEROXIDATION IN RATS DURING ACUTE ETHANOL INTOXICATION
KERA, YOSHIO
OHBORA, YUMIKO
KOMURA, SETSUO
Articles
A single intraperitoneal injection of DL-buthionine-<it>S,R</it>-sulfoximine (BSO) (4 mmol/ kg) to overnight-starved rats caused a 70% inhibition of hepatic γ-glutamylcysteine synthetase and induced a decrease in liver-reduced glutathione (GSH) for several hours. There was, however, no difference in hepatic lipid peroxidation, assessed by malondialdehyde accumulation, between the control and BSO groups. During acute ethanol intoxication (5 g/kg), hepatic lipid peroxidation was increased by approx. 40% within 6 hr. Hepatic [GSH] was also signifiicantly decreased by ethanol. The effect of ethanol on GSH level was not observed in rats pretreated with BSO, though the ethanol-induced enhancement of hepatic lipid peroxidation was potentiated by the BSO pretreatment. Under these conditions there were no apparent effects on blood concentrations of ethnol and acetaldehyde nor on activities of hepatic alcohol dehydrogenase, aldehyde dehydrogenase, glutathione-dependent detoxifymg enzymes, superoxide dismutase or catalase. These results suggest that, although a decrease (by BSO) in GSH by itself does not alter the degree of endogenous lipid peroxidation, it is associated with a potentiation of the enhancement of hepatic lipid peroxidation caused by acute ethanol intoxication.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/519
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5252015-05-19HighWireOUPalcalc:24:6
THE EFFECT OF CHRONIC ETHANOL INTAKE ON LEUCINE ABSORPTION FROM THE RAT SMALL INTESTINE
MARTINES, D.
MORRIS, A. I.
BILLINGTON, D.
Articles
Total (active + diffusion) absorption of leucine from the entire small intestine of rats or from segments of upper jejunum and lower ileum was unaffected by chronic ethanol feeding for 4 weeks. However, because of ethanol-induced mucosal atrophy, specific absorption (expressed per g dry weight of mucosa) was almost doubled in ethanol-fed rats. In the upper jejunum, the active component of leucine uptake was significantly greater in ethanol-fed rats 72% vs. 52%), whereas in the lower ileum the relative contributions of active uptake and diffusion were unaltered. We propose that the increase in active uptake in the upper jejunum is the result of a higher concentration of aged enterocytes having a greater transport capacity at the villus surface.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/525
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5332015-05-19HighWireOUPalcalc:24:6
ETHANOL-INDUCED SKELETAL MUSCLE MYOPATHY: BIOCHEMICAL AND HISTOCHEMICAL MEASUREMENTS ON TYPE I AND TYPE II FIBRE-RICH MUSCLES IN THE YOUNG RAT
PREEDY, VICTOR R.
BATEMAN, CHRISTINE J.
SALISBRY, JONATHAN R.
PRICE, ASHLEY B.
PETERS, TIMOTHY J.
Articles
Rats were pair-fed either a nutritionally complete liquid diet containing 36% of total calories as ethanol or isovolumetric amounts of the same diet in which ethanol was substituted by isocaloric glucose. Chronic ethanol feeding caused a preferential decline in the wet weight of the plantaris (predominantly Type II muscle fibre) which was accompanied by a reduction in the total DNA content. The soleus (a predominantly Type I fibre muscle) was relatively unaffected. Chronic ethanol exposure had no effect on the biochemical index of cell size protein/DNA ratio) in either the plantaris or soleus. Quantitative histochemistry of Type II fibres in the plantaris demonstrated that ethanol caused an increase in the proportion of fibres with smaller diameters. Similar effects were observed for Type II fibres in the soleus. In contrast, ethanol exposure was associated with an increase in the relative proportion of Type I fibres with higher diameters, in both plantaris and soleus. Light microscopic examination of myopathic muscle sections demonstrated that lesions occurred without evidence of inflammation, fibrosis or other infiltration by non-muscle cells. It is concluded that chronic exposure of rats to ethanol is associated with skeletal muscle atrophy. The lesion appears to be specific for Type II fibres, irrespective of the predominant fibre type in the particular muscle.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/533
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5412015-05-19HighWireOUPalcalc:24:6
CONTRASTS IN INTERLEUKIN-1 AND INTERLEUKIN-2 ACTIVITY IN ALCOHOLIC HEPATITIS AND CIRRHOSIS
BIRD, G. L. A.
ARIA, KAYHAN NOURI
DANIELS, HELENA
ALEXANDER, G.J. M.
WILLIAMS, ROGER
Articles
To investigate whether disordered immune function, as shown by abnormalities in lymphokine production, is present in alcoholic liver disease, interleukin-1 and interleukin-2 activity were assayed in a group of patients with acute alcoholic hepatitis in the absence of underlying cirrhosis, and a group of patients with inactive alcoholic cirrhosis. Activitia of both IL-1 and IL-2 in alcoholic hepatitis were similar to those of normal individuals, although in abstinent patients with alcoholic cirrhosis, IL-1 activity was increased and IL-2 activity decreased. Lymphocyte transformation in response to PHA in patients with alcoholic hepatitis was significantly impaired when compared with normal controls, and addition of exogenous IL-2 did not correct this impaired response over a wide range of concentrations of both PHA and IL-2. These observations suggest the underlying defects in cell mediated immunity in acute alcoholic hepatitis, assessed by blast transformation, could be fundamentally different from those of alcoholic cirrhosis and could be secondary to the metabolic effects of acetaldehyde or altered redox potentials on the behaviour of proliferating cells.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/541
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5472015-05-19HighWireOUPalcalc:24:6
STUDIES ON ALDEHYDE DEHYDROGENASE TYPE V-A ISOZYMES IN LIVER DISEASE
TAKASE, SHUJIRO
URASHIMA, SACHIO
YASUHARA, MINORU
TAKADA, AKIRA
Articles
Aldehyde dehydrogenase (ALDH) V-A isozymes in saliva were detected in 96 patients with or without liver disease in order to clarify the relationships of the presence or absence of ALDH V-A isozymes to the metabolism of acetaldehyde (Ac-CHO) and alcoholic liver disease. The incidence of ALDH V-A deficiency was not different between the patients with alcoholic liver disease and those with non-alcoholic liver disease, nor between the patients with liver disease and without liver disease in no relation to alcohol misuse. Ac-CHO metabolism was not different between ALDH V-A deficient and non-deficient patients even in the ALDH I- deficient patients. These results indicated that ALDH V-A isozymes play virtually no role in the metabolism of Ac-CHO and its deficiency is not related to the development of alcoholic liver disease.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/547
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5552015-05-19HighWireOUPalcalc:24:6
PARAMETERS Vm'. AND Km FOR ELIMINATION OF ALCOHOL IN YOUNG MALE SUBJECTS FOLLOWING LOW DOSES OF ALCOHOL
WAGNER, JOHN G.
WILKINSON, PAUL K.
GANES, DEREK A.
Articles
Seventy-four (44 under fasting conditions and 30 following oral liquid meals) sets of post-absorptive human capillary blood alcohol concentration-time data were computer-fitted to the integrated form of the Michaelis-Menten equation by numerical integration by nonlinear least squares to provide 74 pairs of the kinetic <it>V<inf>m'</inf></it> and <it>K<inf>m</inf></it>, parameter values. The parameters were highly correlated (<it>r</it> = 0.915) by orthogonal least squares. Eight of the fasting subjects received four different oral doses of alcohol and fourteen subjects each received three different alcohol treatments. Intra-subject variances of <it>V<inf>m'</inf></it>, <it>K<inf>m</inf></it>, and the ratio <it>V<inf>m'</inf></it>, <it>K<inf>m</inf></it> were calculated from the multiple treatments. Inter-subjed variances were calculated from the 22 mean values of each parameter. Each parameter and the intra-subject variances of the parameters were found to be log normally distributed. The Liquid meals (carbohydrate, fat and protein separately) appeared not to affect the parameter values. The computer fittings were all excellent as evidenced by the relatively small standard deviations of the estimated parameters and other statistical measures of fit.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/555
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5652015-05-19HighWireOUPalcalc:24:6
THE ROLE OF ALCOHOL IN MORTALITY AND MORBIDITY FROM INTERPERSONAL VIOLENCE
NORTON, ROBYN N.
MORGAN, MARSHA Y.
Articles
Alcohol is regarded widely as a causal factor in interpersonal violence in Great Britain. However, much of the evidence used to support this association is anecdotal, or at best, based on descriptive studies. Data calculated from cross-sectional, case-control and cohort studies, undertaken in Great Britain, show that individuals who consume alcohol are several times more likely to perpetrate violence, or to be the victims of violence, than individuals who do not consume alcohol. If criteria for causality are used to assess these findings, then it would appear that alcohol is likely to be a causal factor in both violence perpetration and violence victimization. However, the proportion of interpersonal violence caused by alcohol and the levels of alcohol consumption associated with significantly increased risks of involvement in interpersonal violence cannot be identified from the data available to date.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/565
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5772015-05-19HighWireOUPalcalc:24:6
IMPROVING INFORMATION ON THE ROLE OF ALCOHOL IN INTERPERSONAL VIOLENCE IN GREAT BRITAIN
NORTON, ROBYN N.
MORGAN, MARSHA Y.
Articles
In Great Britain, at present, no valid or reliable estimate can be made of the proportion of interpersonal violence caused by alcohol, nor can an assessment be made of the levels of alcohol consumption associated with an increased risk of involvement in interpersonal violence. A critical review of existing British studies and surveillance systems has been undertaken, which indicates that the role of alcohol in interpersonal violence could be defined more precisely, if new and better analytical studies were conducted, if ongoing longitudinal studies and existing surveillance systems were improved or better exploited, and if new surveillance systems were implemented.
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/577
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Copyright (C) 1989, Medical Council on Alcohol
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BOOK REVIEWS
HORE, B. D.
Book Reviews
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/591-a
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Copyright (C) 1989, Medical Council on Alcohol
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BOOK REVIEWS
COOK, C. C. H.
Book Reviews
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/591
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/5922015-05-19HighWireOUPalcalc:24:6
BOOK REVIEWS
THOMSON, ALLAN D.
Book Reviews
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/592
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Copyright (C) 1989, Medical Council on Alcohol
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CALENDAR
Calendar
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/593
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Copyright (C) 1989, Medical Council on Alcohol
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INSTRUCTIONS TO AUTHORS
Instructions to Authors
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/594-a
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Copyright (C) 1989, Medical Council on Alcohol
oai:open-archive.highwire.org:alcalc:24/6/594-b2015-05-19HighWireOUPalcalc:24:6
MEDICAL COUNCIL ON ALCOHOLISM SUBSCRIPTION RATES
Notice
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/594-b
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Copyright (C) 1989, Medical Council on Alcohol
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AUTHOR INDEX
Author index
Oxford University Press
1989-01-01 00:00:00.0
TEXT
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http://alcalc.oxfordjournals.org/cgi/content/short/24/6/594
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Copyright (C) 1989, Medical Council on Alcohol