Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine and other mediators have been shown to be involved in the ethanol-induced jejunal plasma protein loss. In this study we have investigated whether the histamine (H)-related component of this protein loss is mediated by H1-receptors, H2-receptors or both. Four groups of dogs (n = 12 in each) were studied. They were: untreated, H1 + H2-receptor blockade, H1-receptor blockade and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptors respectively. In all animals, jejunal protein loss was measured over 10 min periods for 90 min. Ethanol increased protein loss in all time periods (p less than 0.001). This protein loss was depressed by H1 + H2-receptors blockade throughout 90 min (p less than 0.01). H1-receptor blockade caused a similar depression of ethanol effect but only during 20 to 40 min (p less than 0.05). In contrast, H2-receptor blockade aggravated the protein losing effect of ethanol throughout 90 min (p less than 0.01). Analyses of data tend to suggest that the ethanol-induced protein loss is mediated principally by H1-receptors, and that a complete inhibition of the histamine-related ethanol-induced protein loss can be achieved only by a simultaneous blockade of both H1 and H2-receptors, and not by H1- or H2-receptor blockade alone.
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PMID:The role of histamine1 and histamine2 receptors in the ethanol-induced jejunal plasma protein loss. 152 91

This study compared the performance of alcoholics (18 male, 16 female) with community controls (15 male, 12 female) on the Adaptive Skills Battery (ASB), a test of interpersonal problem-solving. The ASB consists of 30 situations. Fifteen situations require subjects' typical responses and 15, their optimal responses. Male and female alcoholics were inferior to controls in their typical responses [F(1,57) = 45.22, p = 0.0001], but did not differ on the optimal responses (F less than 1). Further analyses indicated that decreased feelings of self-efficacy could not account for the alcoholic deficit. Females were superior to males in the optimal response condition [(F(1,56) = 9.90, p = 0.003]. No significant group x sex interactions were obtained. Performance on the ASB was not correlated with performance on traditional measures of problem-solving. Post-hoc correlational analyses revealed differential patterns between depression scores and performance for alcoholics and controls. These data suggest that (1) female and male alcoholics exhibit similar interpersonal problem-solving deficits, (2) alcoholic self-efficacy expectancies cannot account for the impairment, (3) the ASB appears to assess aspects of problem-solving not typically examined, and (4) the role of depression in alcoholic performance deserves continued empirical evaluation.
Alcohol Clin Exp Res 1992 Aug
PMID:Interpersonal problem-solving in male and female alcoholics. 153 Jan 30

In previous studies serotonin uptake inhibitors such as citalopram decreased alcohol consumption in alcoholics. The mechanism of the effect is not fully understood. This study tested the hypothesis that it is mediated by changes in desire to drink and alcohol effects. After a 1-week baseline period, subjects (13 men and three women; aged 26 to 69 years; healthy, nondepressed, alcohol-dependent drinkers [mean, 6.6 drinks per day]) were randomized in a double-blind fashion to receive 40 mg/day citalopram and placebo for 1 week each, separated by a 1-week washout period. Daily standard alcoholic drinks (13.6 gm ethanol), nonalcoholic drinks, and tobacco use were recorded; evening urine samples were taken; and interest, desire, craving, and liking for alcohol were rated. Medical status, depression, and anxiety were assessed weekly, but no other treatment or advice was given. Daily alcoholic drinks significantly decreased during citalopram treatment (mean +/- SEM = 4.6 +/- 0.6) compared with placebo (5.7 +/- 0.8; p = 0.01), and the average decrease was 17.5%. Percentage of days abstinent increased during citalopram administration (27.7% +/- 5.7%) compared with placebo (15.5% +/- 3.7%; p less than 0.01). Citalopram decreased interest, desire, craving, and liking for alcohol (all p less than 0.05). There was clear internal validation of these measures in that variations in each correlated with alcohol consumption (all r greater than 0.5, p less than 0.05). Nonalcoholic drinks, self-reports of cigarettes smoked (daily smokers), and body weight did not change significantly. In experimental bar sessions, after the citalopram and placebo periods, subjects were required to consume as many of 18 minidrinks as possible (equivalent to six standard drinks) at 5-minute intervals. Subjects rated their desire for alcohol, intoxication, and mood. Citalopram had no significant effects on the desirability of alcohol or subjective feelings of intoxication. The findings indicate that serotonin uptake inhibitors may act by decreasing the urge to drink and the reinforcing effects of alcohol. Also, a naturalistic outpatient trial is a sensitive, simple, and economic procedure for detecting these drug effects.
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PMID:Citalopram decreases desirability, liking, and consumption of alcohol in alcohol-dependent drinkers. 153 2

Alcohol use was correlated with depression and suicidal behavior in two independent studies of schizophrenic outpatients. Depression alone accounted for over 80% of the explained variance in suicidal behavior in both studies; alcohol use alone and the correlation between depression and alcohol use accounted for only small amounts of variance.
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PMID:Alcohol abuse, depression, and suicidal behavior in schizophrenia. 153 80

Although hydralazine is a commonly prescribed antihypertensive agent, reports of acute human poisoning are uncommon. Most of the literature focuses on chronic toxicity, most notably, the drug-induced systemic lupus erythematosus syndrome. A case of acute hydralazine overdose associated with marked ECG ST segment depression in a young adult is presented. Although the patient also had mild hypotension, acidemia, and ethanol intoxication, the ECG abnormality was alarming and suggestive of myocardial ischemia. The patient was managed conservatively in an ICU setting, and the metabolic and ECG abnormalities resolved. No reports of such marked ECG changes associated with acute hydralazine poisoning in a young adult could be found. Clinical and experimental data on acute hydralazine exposure suggest that the possibility of direct drug effects, including positive inotropic and chronotropic effects and myocardial cell injury, should be considered.
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PMID:Acute hydralazine overdose: marked ECG abnormalities in a young adult. 153 97

Moderate ethanol consumption, associated with cardiac depression, occurs in greater than 50% of trauma. Hemorrhagic shock, a significant component of trauma in the clinical setting, causes intrinsic cardiac contractile dysfunction. In this study, we used an isolated heart model to determine whether acute ethanolism increases the cardiovascular risk associated with hemorrhagic shock. We hypothesized that hemorrhagic shock in the acutely intoxicated subject would cause significantly greater cardiac dysfunction compared with that observed in a nonintoxicated subject. A total of 116 guinea pigs was divided into four groups: control (no ethanol, no shock), ethanol intoxication alone (1 mg/kg iv), hemorrhagic shock alone (mean arterial blood pressure, 30 mmHg for 2 h), and a combination of hemorrhagic shock plus ethanol. Half of the hearts in each group were used for isolated heart studies, and half were used to assess myocardial cell membrane integrity. Ethanol alone reduced peak isovolumic pressure by 36%, maximal rate of left ventricular pressure (LVP) rise by 27%, and maximal rate of LVP fall by 35%; however, contractile depression was significantly greater in the intoxicated, hemorrhaged, group compared with the nonintoxicated, hemorrhaged, group (P less than 0.05). Both ethanol and hemorrhage independently altered myocardial cell volume regulation; however, abnormalities in myocardial cell volume regulation induced by hemorrhage were similar in the intoxicated and nonintoxicated groups. Our data show that hemorrhagic shock causes significantly greater cardiac contractile dysfunction in the intoxicated subject.
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PMID:Cardiac contractile effects of ethanolism and hemorrhagic shock. 156 92

Moderate drinking for the elderly of both genders is no more than one drink per day, where a drink is defined as 12 oz of beer, 5 oz of wine, or 1.5 oz of spirits. Age does not affect the rate of absorption or elimination of alcohol. Lean body mass decreases and adipose tissue increases with age, however, resulting in a corresponding decrease in the volume of total body water. With a smaller volume of distribution, an alcohol dose identical to that administered to a younger individual of the same size and gender will produce a higher blood alcohol concentration in the elderly. Low-dose alcohol stimulates appetite and promoters regular bowel function. In the well-nourished nonalcoholic elderly, the negative impact of alcohol consumption on nutrition is minimal. Alcohol consumption improves mood by increasing feelings of happiness and freedom from care while lessening inhibitions, stress, tension, and depression. Although in the laboratory low-dose alcohol improves certain types of cognitive function in young men, in other types of task performance, alcohol induces impairment, which worsens with age. The effects of alcohol on sleep are primarily detrimental, worsening both insomnia and breathing disturbances during sleep. Although the role of alcohol consumption in mortality from heart disease has not been investigated in the elderly, moderate drinking appears safe. Under some circumstances low-dose alcohol may produce analgesia whereas in others it may worsen pain. The elderly use a significant proportion of both prescription and over-the-counter medication, a large variety of which interact with alcohol. Alcoholic beverage consumption may exacerbate cognitive impairment and dementias of other etiology. Although some studies suggest that moderate use of alcohol by institutionalized senior citizens appears to produce benefits including improved socialization, separation of the effects of the social situation from those specifically attributable to alcohol remains to be accomplished. Older individuals who want to drink, have no medical contraindications, and take no drugs (prescription or over-the-counter) that interact with alcohol, may consider one drink a day to be a prudent level of alcohol consumption. Patients should be counseled to avoid alcohol consumption immediately prior to going to bed in order to avoid sleep disturbances. They also should be cautioned against potential drug-alcohol interactions and told to avoid alcohol ingestion prior to activities such as driving. The decision to recommend a particular level of alcohol consumption in any given patient must, however, be carefully tailored not only to that individual's specific medical needs but to his or her social and environmental circumstances as well.
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PMID:Alcohol and the elderly. 157 71

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

Depression and alcoholism are associated with impaired immune responses. Complement proteins and fragments participate in the induction and modulation of both specific and non-specific immune reactions. This study examined the effect of prolonged ethanol ingestion on complement CH50 levels in two strains of rats, the Flinders Resistant Line (FRL) and the Flinders Sensitive Line (FSL), that differ in cholinergic sensitivity and depressive tendencies. Chronic ethanol exposure given as either the source of drinking fluid or as a liquid diet had a significant inhibition on mean CH50 unit responses in both FSL (41-48%) and FRL (23-24%) rats. The difference in group response to ethanol was confirmed by a significant interaction of ethanol treatment versus group in the two-way ANOVA. The FSL rats appear to be more easily affected than FRLs. Genetic differences in the neurotransmitter systems, therefore, may play a role in susceptibility to immunosuppression resulting from ethanol exposure.
Alcohol Alcohol 1992 Jan
PMID:Ethanol and complement hemolytic activity of selectively bred hypercholinergic rats. 158 Sep 28

Diazepam-sensitive (DS) and -resistant (DR) mice were selectively bred for increased and reduced sensitivity to the ataxic effects of diazepam (40 mg/kg). Other response differences between DS and DR mice may reflect pleiotropic effects of the genes fixed during their selection. These mice were tested for their sensitivity to the locomotor stimulant effects of several doses of diazepam, flunitrazepam, pentobarbital, phenobarbital, and ethanol. DR mice were more sensitive than DS mice to the locomotor stimulant effects of all drugs except phenobarbital. These results largely support the hypothesis that a common biological mechanism mediates sensitivity to the stimulant effects of sedative-hypnotic drugs. Receptor mediation of the benzodiazepine effects was examined by administering the benzodiazepine receptor antagonist, RO15-1788. Locomotor depression produced by diazepam and flunitrazepam in DS mice was blocked by RO15-1788. However, while the locomotor stimulation produced by diazepam in DR mice was antagonized, the stimulant effect of flunitrazepam was not. This suggests that binding of flunitrazepam to the GABAA-benzodiazepine receptor is not necessary for production of locomotor stimulation.
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PMID:Locomotor responses to benzodiazepines, barbiturates and ethanol in diazepam-sensitive (DS) and -resistant (DR) mice. 158 60


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