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1. |
Ethanol‐Induced Inhibition of Chick Brain Growth |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 343-346
John W. Boyd,
Gerhard W. Kalmus,
Sam N. Pennington,
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摘要:
Retarded fetal brain growth is associated with a high incidence of mental retardation among the offspring of chronic alcoholic mothers. Research using an embryonic chick model suggests that ethanol exposure suppresses fetal development including suppression of brain growth. Total brain cyclic AMP content and endogenous brain protein kinase specific activity are not altered by ethanol; however, ethanol exposure does significantly stimulate kinase catalytic activity measured in the presence of saturating amounts of exogenous cyclic AMP.
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05677.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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2. |
Neuropsychological Differences between Male Familial and Nonfamilial Alcoholics and Nonalcoholics |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 347-351
Kim Walter Schaeffer,
Oscar A. Parsons,
J. Robert Yohman,
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摘要:
The hypothesis was tested that neuropsychological differences exist between males who have an alcoholic parent, sister, or brother (FH+) versus those who do not (FH‐). Neuropsychological tests measuring verbal, learning/memory, abstracting/problem solving, and perceptual‐motor performance were given to four groups of middle‐aged subjects: alcoholic FH+ (n= 41); alcoholic FH‐ (n= 27); nonalcoholic FH+ (n= 19); and nonalcoholic FH‐ (n= 43). FH+ subjects performed significantly poorer than FH‐ subjects on the abstracting/ problem solving and perceptual‐motor tasks, and approached significance on the verbal and teaming/memory measures. Alcoholics performed more poorly than nonalcoholics on abstracting/problem solving and learning/memory tasks. There were no groups by family history significant interactions. From these results we suggest (1) a performance deficit in abstracting/problem solving and possibly learning/memory may antedate the alcoholic stage in FH+ individuals; (2) alcoholism and positive famiry history of alcoholism have independent, additive deleterious effects on cognitive‐perceptual functioning; and (3) future neuropsychological studies of alcoholism should consider the frequency of FH+ and FH‐ individuals in both alcoholic a
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05678.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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3. |
Effects of Elevated Female Sex Steroids on Ethanol and Acetaldehyde Metabolism in Humans |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 352-358
Candace M. Jeavons,
Arthur R. Zeiner,
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摘要:
Two groups (n = 20 each for pill and no pill groups) of young female social drinkers were tested with an acute ethanol dose (0.52 g/kg) as a 20% solution in water. Ethanol pharmacokinetics and acetaldehyde were repeatedly assayed from breath by a gas chromatograph. Cardiovascular indices were concurrently recorded. Groups did not differ on ethanol pharmacokinetics. However, the group on birth control pilts reached a significantly higher acetaldehyde concentration than did the group of normally cycling females not on birth control pills (3.26 ng/ml vs. 1.45 ng/ml). Further, the pill (P) group showed significantly greater vasodilation 20 mm postdrink as indexed by ear lobe plethysmography than did the no pill (NP) group (P = 160.3% vs. NP = 113.9%). Results are consistent with the interpretation that female sex steroids modulate aldehyde dehydrogenase function. Practical implications are that females with elevated steroids (either pregnant or on birth control pills) may be at greater risk for toxic effects 01 ethanol consumption.
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05679.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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4. |
Relationship of Endocrine Status on the Stimulatory Effect of Ethanol on Hepatic Very Low Density Lipoprotein Synthesis |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 359-361
M. R. Lakshmanan,
Michael E. Felver,
Mildred Ezekiel,
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摘要:
The normal stimulatory effect of an acute oral dose of ethanol on hepatic very low density lipoprotein synthetic rate is abolished in thyroidectomized rats but not in adrenalectomized rats. This lack of stimulation by ethanol can be explained in part by the decreased rate of hepatic fatty acid esterification to neutral lipids in thyroidectomized animals.
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05680.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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5. |
Alcoholic Fathering and Its Relation to Child's Intellectual Development: A Pilot Investigation |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 362-365
Cynthia S. Ervin,
Ruth E. Little,
Ann Pytkowicz Streissguth,
Don E. Beck,
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摘要:
In this study, the relationship between being raised by an alcoholic father and intellectual and academic achievement of the child were investigated. One hundred children of non‐alcoholic mothers, 50 of whom had alcohoec fathers and 50 of whom had non‐alcoholic fathers, were administered age‐appropriate IQ, developmental, and achievement tests. Analysis of covariance revealed significant relationships between alcoholic fathering and IQ and achievement scores, independent of a number of possibly confounding variables. When children with alcoholic biological fathers were excluded, a relationship between IQ and alcoholic fathering persisted. Thus children raised by alcoholic fathers are a population at risk, in need of further scientific and clinical atte
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05681.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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6. |
Effects of Ethanol |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 366-374
James R. Wilson,
V. Gene Erwin,
Gerald E. McClea,
Robert Plomin,
Ronald C. Johnson,
Frank M. Ahem,
Robert E. Cole,
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摘要:
Two doses of ethyl alcohol were administered to 48 young male subjects (24 brother‐pairs), and placebo doses were administered, to five brother‐pairs (controls). Dose 1 amount was calculated to result in a peak blood alcohol content (BAC) of 100 mg/100 ml; dose 2 was given when BAC had fallen to one‐half the peak BAC resulting from dose 1, in an attempt to raise BAC back to 100 mg/100 ml. Prior to alcohol dosage, baseHne measurements were made on a number of behavioral tests. Behavioral performances during metabolism of doses 1 and 2 were compared to baseline performance. Sensitivity to ethanol was indicated by performance decrements on nearly all. tests after ethanol dosing. Acute behavioral tolerance to ethanol (ABTE) was indicated for some tests by improved performance after dose 2 compared to performance at a time after dose 1 when BACs were about equivalent A preliminary search for possible genetic components of sensitivity and ABTE was undertaken by comparing the scores of the brothers.SUMMARY1. Sensitivity to ethanol, measured via a mean performance decrement, was found for many of the tests employed in this study, with larger decrements seen on motor tasks.2. Despite the overall picture of average performance decrements, there was striking individual variability in performance, and a few individuals performed better after ethanol dosage.3. Mean scores revealed a consistent trend for improved performance during clearance of the second dose of ethanol. We have termed this phenomenon “acute behavioral tolerance to ethanol.” When the short individual tests were summed to form a “motor” test battery and a “written” test battery, ABTE was clearly a significant effect.4. Even though tests of familiality (via resemblance of brothers) were not definitive, perhaps due to the small sample size, several promising leads for further research on familiality of responses to etha
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05682.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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7. |
Genetic and Biochemical Factors Relevant to Alcoholism |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 375-383
Stephen B. Thacker,
Richard L. Veech,
Andrew A. Vernon,
David D. Rutstein,
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摘要:
Important biochemical clues from animal and human studies as well as epidemiologic studies of twins and adoptees suggest that genetic factors may predispose to alcohol addiction. This paper critically examines the epidemiology and biochemistry literature to assess the strength of the evidence supporting a genetic element in alcohol addiction. Then, a biochemical hypothesis is presented that involves the identification of specific metabolic pathways, pathway controls, and metabolites that may be unique to alcoholics, and which has been tested by experiment.
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05683.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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8. |
Diagnostic Value of Serum Procollagen Peptide Measurements in Alcoholic Liver Disease |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 384-389
Eeva‐ RiittaSavolainen,
Burton Goldberg,
Maria A. Leo,
Maria Velez,
Charles S. Leber,
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摘要:
Procollagen type I carboxyterminal and type III aminoterminal peptide concentrations were measured in sera of 60 patients with alcoholic and 14 with nonalcoholic liver disease to study whether these assays are useful as clinical tests to differentiate various stages of alcoholic liver injury. Both propeptides were markedly elevated in alcoholic hepatitis and cirrhosis: procollagen type III peptide in 90% and type I peptide in 60‐80% of these patients. Moderately increased values were found less frequently in patients with fatty liver. These tests did not differentiate patients with simple fatty liver from those with fatty liver and early fibrosis. There was a significant difference in serum procollagen type III peptide between fatty fiver and both alcoholic hepatitis and cirrhosis (p<0.001), and in type I peptide between fatty liver and alcoholic hepatitis (p<0.005). Although serum peptide values correlated with the degree of liver fibrosis, appreciable overlap of values was found between the various groups. The peptide concentrations also seemed to be related to the degree of hepatic inflammation, and the highest values were observed in a subgroup of patients with alcoholic hepatitis in whom numerous Mallory bodies were found. The data suggest that in alcoholic liver diseases, serum collagen propeptide determination may be useful in diagnosing severe alcoholic hepatiti
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05684.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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9. |
Brain NaK‐ATPases in Mice Differentially Sensitive to Alcohols |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 390-396
Michael J. Marks,
Andrew Smolen,
Allan C. Collins,
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摘要:
The isozymes of NaK‐ATPase were studied in the particulate fraction of homogenates prepared from cortex of LS and SS mice, two lines of mice that have been selectively bred for differential response to ethanol. In addition to a ouabain‐insensitive Mg‐ATPase, ouabain dose‐response curves have suggested the presence, in brain, of two NaK‐ATPase activities with different sensitivities to ouabain. These are designated low K, (4 times 10‐7M) and high K1(2 times 10‐4M). Ethanol differentially inhibited the ATPases: The ouabain‐insensitive activity was less sensitive to ethanol inhibition than were the two ouabain‐inhibitable activities. The low K1(brain specific) NaK‐ATPase was more sensitive than was the high K, activity. However, ethanol inhibited all three components of the ATPase activity in an identical fashion in the two mouse lines. The low K, activity was also more labile to thermal and p‐hydroxymercurobenzoate denaturabon than was the high K1activity. These measures did not differ between the LS and SS lines. SDS‐polyacrylamide electrophoresis of particulate fraction of cortical homogenates obtained from LS and SS mice revealed the presence of two protein bands with similar32P labeling in both lines. Given that etectrophoretic pattern and heat or p‐hydroxymercurobenzoate inhibition were identical, it seems unlikely that differences in ATPase activity, or inhibition by ethanol, are responsible for the different response of
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05685.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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10. |
Alcohol Ingestion Does Not Cause Sleep‐Disordered Breathing in Premenopausal Women |
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Alcoholism: Clinical and Experimental Research,
Volume 8,
Issue 4,
1984,
Page 397-398
A. Jay Block,
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摘要:
Ingestion of 2 ml/kg of 100 proof vodka before bedtime did not cause sleep‐disordered breathing or nocturnal oxygen desaturation in 20 premenopausal women. These findings are opposite to the results of earlier studies of men, in which ingestion of the same amount of alcohol significantly increased these findings. Protection of young women from sleep‐disordered breathing or oxygen desaturation may be related to the respiratory stimulant effects of circulating progester
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1984.tb05686.x
出版商:Blackwell Publishing Ltd
年代:1984
数据来源: WILEY
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