[Diagnosis of ligament damages of the external ankle].
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Biomedical subjects
Publications and source records attributed to H Adler.
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Ketonuria has been observed in alcoholics. To study the mechanism of this effect, healthy, volunteers were given adequate diets (36% of calories as lipid and 15% as protein) for 18 days, with isocaloric replacement of carbohydrate (46% of calories) by either ethanol or additional fat. The latter resulted in a high fat diet, with 82% of calories as lipid. After about 1 wk of alcohol, massive and persistent ketonuria developed. Compared with the control period, there was a 30-fold increase in fasting blood acetoacetate and beta-hydroxybutyrate (P < 0.001). With the high fat diet, acetoacetate and beta-hydroxybutyrate increased 8- to 10-fold (P < 0.001). In the postprandial state, ethanol also induced hyperketonemia, but less markedly than when ethanol followed an overnight fast. With low fat diets (5% of calories), alcohol (46% of total calories) did not induce ketonuria or hyperketonemia, suggesting that a combination of alcohol and dietary fat is necessary. The addition of alcohol to rat liver slices did not affect ketogenesis. In rats pretreated with alcohol for 3 days, however, ketonemia developed, hepatic glycogen was decreased, and liver slices (incubated with palmitate-(14)C and glucose) had a significant increase in acetoacetate production, when compared to carbohydrate pretreated controls. Alcohol pretreatment or addition of alcohol in vitro had no effect on acetoacetate utilization by rat diaphragms, and decreased only slightly the conversion of beta-hydroxybutyrate-(14)C to (14)CO(2). Thus, the hyperketonemia and ketonuria observed after alcohol consumption cannot be attributed to an immediate effect of alcohol, but is the consequence of a delayed change in intermediary metabolism characterized by increased hepatic ketone production from fatty acids, possibly linked to ethanol-induced glycogen depletion and depression of citric acid cycle activity.
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Fifty-one cases of bovine pyelonephritis were investigated. The annual prevalence rate for 2089 cows was 1.6% in 1987 with a mean interval from calving to onset of cases of 82.9 days. Multipara were at higher risk. Loss from pyelonephritis was 33.3% of all affected cows, and relapse occurred in 9.4% of apparently recovered animals. Serum creatinine and urea concentrations were of high prognostic values. Odds ratios being culled for cows with levels of creatinine above 1.5 mg/dl (132.6 mumol/l) and of urea above 100.0 mg/dl (16.7 mmol/l) were 104.0 and 60.0 respectively compared with those with lower values. Haematological results were of no diagnostic value. Odds ratio for cows with no post-parturient uterine diseases having pyelonephritis was 8.9 compared with infected cows treated at calving with antibiotics.
Three hundred and sixty inseminated Holstein cows were monitored in a controlled trial for low milk progesterone concentration 21-23 days post-breeding. Information about low progesterone cows was given to herdsmen for the experimental group only. Of the cows in the experimental group with milk progesterone of less than or equal to 4.5 ng/ml, 56.0% were inseminated within 2 days of monitoring compared to 28.8% of the control animals. Of the cows reaching the 42-day rectal pregnancy diagnosis, 13.7% and 43.6% were negative for the experimental and the control groups respectively. Inter-service intervals were 34.5 +/- 14.5 days and 44.3 +/- 17.7 days for the experimental and control groups respectively. Pregnancy rates were the same for 264 cows served on routine progesterone monitoring and for 318 cows bred on behavioural oestrus when matched to farm and day of breeding. A gain of US $32.5 (an equivalent of 85 l milk) per lactation for a cow in the monitored herd was established using the data in a model of a 250-cow herd with a total pregnancy goal of 82.4%.
The sulfurtransferases are a group of proteins that catalyze the formation, interconversion and reactions of compounds containing sulfane sulfur atoms. Serum albumin has properties that implicate it as a major potential sulfur carrier/transferase. The relevance of the sulfane pool system as a whole to cyanide detoxication appears clear. The mechanisms of action of the various components at the molecular level are still under investigation.