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The dipsogenic effect of alcohol and the loss of control phenomenon /Lawson, David M. January 1977 (has links)
No description available.
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Effect of ethanol and low dietary copper on perinatal and postweanling copper utilization in the ratBaek, Jong Ho 01 November 1988 (has links)
The hypotheses of this research were (1) to test if
the antagonistic effect of ethanol on liver copper could
be seen within a short period when ethanol ingestion,
low dietary copper and high metabolic demand represented
by either pregnancy plus lactation or rapid growth are
simultaneously present and (2) to test if ethanol
ingestion would exaggerate a marginal dietary copper
status to an obvious copper deficiency.
Pregnant rats were fed liquid diets containing
either 0.75 (low) or 3.75 (control) mg copper/L with or
without 30% of kcal from ethanol throughout gestation
and the first 15 days of lactation. Maternal ethanol
intake failed to exaggerate a marginal copper status to
a copper deficient anemia in both dams and pups as
estimated by concentrations of hemoglobin and liver iron
and oxidase activity of the copper-metalloenzyme
ceruloplasmin. However, maternal ethanol intake did depress maternal liver copper concentration when diet
copper was low (interactive effect P<0.05). This effect
was specific for liver because other tissue copper
concentration was unaffected by ethanol. Although
ethanol depressed total pup liver copper concentration
regardless of dietary copper level, the interactive
effect seen in maternal liver was reflected in copper
content of the pup liver metallothionein fraction eluted
from a Sephadex G-75 column. At least part of the
depressive effect of ethanol on pup liver copper can be
explained by elevated pup serum corticosterone (r=-0.61,
P<0.001), a hormone known to enhance loss of neonatal
liver copper by way of biliary excretion. On the other
hand, the copper status of weanling female rats which
were fed liquid diets containing either 0.5 (low) or 2.5
(control) mg copper/L for 5 weeks was unaffected by
ethanol.
Results demonstrate that the depressive effect of
ethanol on liver copper can be seen within a period of
weeks rather than months when ethanol ingestion, low
dietary copper and pregnancy plus lactation are
simultaneously present in contrast to non-pregnancy.
This ethanol and copper interaction during reproduction,
however, can not be detected if only either serum copper
or oxidase activity of ceruloplasmin is used as an
indicator of copper status. / Graduation date: 1989
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Alcohol drinking in the rat as a function of constitution and experience.Kirouac, Gilles, 1943- January 1972 (has links)
No description available.
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Influence of ethanol on copper utilization by pregnant and growing ratsAstell, Rebecca L. 06 December 1988 (has links)
Pregnant and weanling rats were fed liquid diets with
or without 30 percent of total kcal from ethanol and varying
levels of copper in order to determine if ethanol ingestion would
exaggerate a marginal copper status to an obvious copper
deficiency. Pregnant albino rats were fed either 0.75 or 3.75 mg
Cu/L throughout gestation and the first 15 days of lactation while
female weanling rats received 0.5 or 2.5 mg Cu/L for 5 weeks.
Ethanol consumption exaggerated a marginal copper status during
reproduction as evidenced by significant reductions in maternal
liver copper concentration and enzymatic activity of the copper
metalloprotein Copper-Zinc superoxide dismutase in offspring
liver. Ethanol had little or no effect upon copper status in
weanling rats. In addition, serum copper failed to reflect a
developing depletion of liver copper when ethanol was being consumed. Since it is known that the average American diet is
just adequate in copper content, and that copper balance is
difficult to achieve during times of increased metabolic demand,
pregnant subjects may be at a great risk to develop a copper
deficiency when ethanol is being consumed. This ethanol and
copper interaction, however, will likely go undetected if only
serum copper is used as an indicator of copper status. / Graduation date: 1989
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Effects of Long-Term Moderate Ethanol Intake on the Stress Response in RatsWilliams, Judy L. (Judy Lee) 12 1900 (has links)
The effect of ethanol on the stress response in rats was examined. Experimental animals were given 0.25 ml of 28 percent ethanol or 0.25 ml of water orally once a day, five days a week, for a period of twelve months and were then subjected to fifteen minute cold stress. Corticosterone levels in ethanol-treated males following stress were significantly lower (22 percent) than in the sham group. Adrenal weights in sham-treated females were significantly higher (15 percent) than in the ethanol group at the end of twelve months. Mortality in sham-treated males was significantly higher (60 percent) than in ethanol-treated males. The effects observed may be due to the sedative action of ethanol on cortical centers controlling the hypothalmus.
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Biochemical studies on ethanol and denervation induced muscle atrophy.January 1988 (has links)
by Wu Kwok Hang. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1988. / Bibliography: leaves 213-229.
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The Effects of Long Term Modernate Ethanol Intake on Plasma Levels of ACTH, Beta Endorphin, and Corticosterone in RatsBreedlove, Kenneth 12 1900 (has links)
The effects of single injections and daily oral administration of ethanol on plasma levels of ACTH, beta endorphin, and corticosterone in response to cold stress were examined. The long-term experimental animals were given 0.25 ml of 28% ethanol or water orally once a day, five days a week, for fourteen months. Plasma levels of ACTH, beta endorphin, and corticosterone were lower in alcohol-treated rats as compared with water-treated rats when exposed to cold stress. The effects of a single injection of ethanol significantly elevated plasma levels of all three hormones. Mortality in sham-treated males was higher than ethanol-treated.
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Executive cognitive function, alcohol intoxication, and aggressive behaviour in adult men and womenHoaken, Peter Neil Spencer. January 2001 (has links)
No description available.
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Ethanol and retrograde amnesia : can rats have blackouts and does caffeine help?Spinetta, Michael John 06 September 2012 (has links)
The work in this dissertation aims to describe a simple new test for odor-recognition memory in rats that can be readily performed and results in an easily observable and lasting form of memory. This test has allowed for the demonstration of ethanol-induced retrograde memory impairments in rats when ethanol is administered during both the consolidation and reconsolidation phases of memory encoding. The observation that a high-dose of ethanol can cause retrograde memory impairments when administered immediately or within hours after learning has taken place is an original finding that may have implications for understanding human blackouts. Furthermore, the finding that ethanol can disrupt the reconsolidation of a previously consolidated memory has not been previously established. It is also demonstrated that caffeine can prevent ethanol’s memory impairing effects, a result that contributes a new piece of evidence for caffeine’s effects on the learning and memory process. This effect has been further investigated mechanistically and attributed to caffeine’s dual role as a phosphodiesterase type 5 inhibitor and adenosine A2A antagonist. Neither of these mechanisms alone appear to be sufficient enough to prevent the retrograde memory impairments seen with ethanol. It is hoped that this test and our findings will prove useful for future investigations into the effects of ethanol on learning and memory and the human phenomenon of alcohol-induced blackouts. / text
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T-cell activation by ethanol: a possible mechanism for immunosuppressionNaqvi, Hassan Raza, 1976- 29 August 2008 (has links)
Alcohol abuse has been commonly associated with enhanced susceptibility to pathogens. Studies on the effects of ethanol on the immune system are complicated by a lack of consensus on whether ethanol activates, inhibits or has no effect on immune cells. We present data showing that acute exposure of T cells to ethanol elicits responses that broadly parallel responses seen in normally stimulated T cells such as the formation of the immune synapse, polarization of the microtubule organizing center (MTOC) to the synapse and tyrosine phosphorylation of signaling proteins as seen when the T cell Receptor (TcR) engages antigen-MHC. However, incomplete activation of the T cell signaling program leads to unresponsive or anergic T cells. Our data suggests the hypothesis that ethanol can activate T cells in a manner that leads to anergy. We have found that ethanol triggers calcium signaling and this has provided one of the primary tools for analyzing the effects of ethanol on T cells. Ethanol induced calcium transients are dose-dependent and are comparable to those triggered by low doses of anti-TcR antibody. This is important because it allows us to compare ethanol dependent signaling to that normally triggered through stimulation of the T cell receptors. Analysis of the calcium signaling pathway indicates that ethanol-stimulated calcium transients depend on calcium entry and are likely due to opening of CRAC type calcium channels. The observed calcium transients go a long way towards explaining how ethanol may stimulate T cells and provides a mechanism for immune suppression through the observed translocation of NF-AT in ethanol pulsed cells. The translocation of NF-AT is particularly important because of reports that it plays a crucial role in triggering anergy and immunosuppression. Taken together, these data can help explain how ethanol can both activate T cells and cause immunosuppression.
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