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Hepatic glutathione content in patients with alcoholic and non alcoholic liver diseases.
No full textReduced and oxidized hepatic glutathione was evaluated during alcoholic and non alcoholic liver injury. We studied 35 chronic alcoholics, 20 patients with non alcoholic liver diseases, 15 control subjects. Hepatic glutathione was measured in liver biopsies and correlated with histology and laboratory tests. Alcoholic and non alcoholic patients exhibited a significant decrease of hepatic glutathione compared to control subjects (controls: 4.14 +/- 0.1 mumol/g liver; alcoholics: 2.55 +/- 0.1, p less than 0.001; non alcoholics 2.77 +/- 0.1, p less than 0.001). Oxidized glutathione was significantly higher in the two groups of patients compared to controls (controls: 4.4 +/- 0.2\% of total; alcoholics 8.2 +/- 0.3, p less than 0.001; non alcoholics: 8.5 +/- 0.8, p less than 0.001). The decreased hepatic glutathione levels in patients with alcoholic and non alcoholic liver diseases may represent a contributing factor of liver injury and may enhance the risk of toxicity in these patients
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Protein-ubiquinone interactions in mitochondrial cytochrome c reductase. Ellis Horwood Publishers, Chichester.
No full text
[2-3 diphosphoglycerate and tissue oxygenation in the cirrhotic].
No full textIncreased 2-3 Diphosphoglycerate levels in cirrhotic patients have been reported. Previous studies did not show significant changes in 2-3 DPG in anaemic cirrhotic patients when compared to non anaemic cirrhotic patients, but the role played by alkalosis and/or hypoxia has not been investigated. To study this question, haematic 2-3 DPG was measured in 8 male patients with liver cirrhosis (histologically diagnosed) together with PO2, PCO2, pH and Hct. 2-3 DPG was also measured in 6 healthy male volunteers. We found a significant increase in blood 2-3 DPG of cirrhotic patients compared to control subjects (5,55 +/- 0,4 vs 2,18 +/- 0,3 mmol/l erythrocytes respectively, p less than 0,001) in agreement with previous studies. PO2 levels and Hct value did not show important changes, whereas PCO2 and pH resulted to be very altered when compared to normal values, even though we could not correlate these values with blood 2-3 DPG. We conclude that the genesis of 2-3 DPG increase is multifactorial, however an alteration in acid-base equilibrium seems to play a more important role than hypoxia
Livelli di ATP nel fegato durante la intossicazione sperimentale da tetracloruro di carbonio.
No full textArch. It. Mal. App. Dig. 1967;34:424-43
[Beta-cell activity during the oral glucose tolerance test in subjects with hepatic cirrhosis].
No full textTo study beta-cells response during liver cirrhosis, OGTT (0.75 g/kg b.w.) was performed in 7 cirrhotic patients (histologically diagnosed). An impaired glucose tolerance was observed in all the subjects: basal plasma glucose was 0.74 g/l +/- 0.05 (M +/- SEM); at 90 min was 1.50 g/l +/- 0.10, and at 180 min was 1.10 g/l +/- 0.17. Plasma insulin peak was delayed at 90 min (78.2 microU/ml +/- 27.7); two patients showed basal hyperinsulinemia. C peptide concentration reached the peak at 120 min (3.6 ng/ml +/- 0.5), in agreement with Gragnoli and coll. Plasma insulin concentration did not correlate with hepatic laboratory findings. All the patients had severe liver disease, including esophageal varices; in 4 patients ascites was observed. The results show that impaired glucose tolerance in patients with liver cirrhosis is not directly related to the degree of the disease and confirm the decreased insulin catabolism and peripheric resistance
Increased plasma levels of glutathione and malondialdehyde after acute ethanol ingestion in humans.
No full textThe effect of acute ethanol consumption on plasma glutathione (GSH) and malondialdehyde (MDA) concentrations was studied in two groups of healthy male subjects. The first group (n = 15) received an acute dose of ethanol (1.5 g/kg p.o. over a period of 3 h); in the control group (n = 15), ethanol was replaced isocalorically with carbohydrates. Blood samples were taken at 0 time (ethanol/carbohydrates ingestion) and every 60 min for 6 h. A significant increase in plasma MDA concentration as well as in plasma GSH values were observed in subjects receiving ethanol compared to controls. The enhancement of plasma GSH was accompanied by a concomitant increase of oxidized glutathione (GSSG). These data support the hypothesis of an increase of lipid peroxidation as a possible mechanism of acute ethanol toxicity. The enhancement of plasma GSH and GSSG may reflect an increased utilization and loss of the tripeptide from the liver induced by ethanol
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