1,721,020 research outputs found
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
Altered biliary excretion of acetaminophen in rats fed ethanol chronically.
No full textTo study the effect of chronic ethanol consumption on biliary excretion of acetaminophen, male Sprague-Dawley rats were pair-fed a nutritionally adequate liquid diet containing either ethanol or isocaloric carbohydrate for 4-6 weeks. One day after bile duct cannulation, acetaminophen (250 mg/kg body weight) was given ip and drug metabolism was studied for 5 hr. Biliary excretion of acetaminophen and its principal metabolites was significantly decreased in rats fed alcohol chronically when compared to pair-fed controls. Although no difference was found in the urinary excretion of the drug, the total elimination (biliary + urinary) was significantly depressed in the alcohol-fed animals. The decreases in hepatic glutathione content and in biliary glutathione concentration (after acetaminophen injection) were significantly greater in ethanol-fed rats than in controls. These data support the possibility that diminished hepatic glutathione and biliary excretion of the drug may contribute to the increased hepatotoxicity of acetaminophen after chronic alcohol feeding
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
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
[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
Oxidation of circulating proteins in alcoholics: role of acetaldehyde and xanthine oxidase.
No full textThis study aimed to evaluate the protein and lipid redox status in plasma erythrocytes and erythrocyte ghosts of alcoholics and of patients with non-alcoholic liver disease; we also investigated the relation to glutathione levels and the role of acetaldehyde and xanthine oxidase activity in plasma.Carbonyl and sulfhydryl proteins, glutathione and malondialdehyde levels and the activity of the circulating xanthine oxidase were determined in: active and abstinent alcoholics, patients with chronic viral hepatitis and healthy controls.Active alcoholics showed a decrease of sulfhydryl protein and glutathione concentrations in plasma, erythrocytes and ghosts compared to the other groups. Also, an increase of the carbonyl protein and malondialdehyde levels and of the activity of circulating xanthine oxidase (9.2 +/- 1.8 nmol.min.ml, p < 0.001) were observed. Significant correlations between carbonyl protein and malondialdehyde concentrations in plasma (r = 0.775, p < 0.001), as well as between daily alcohol intake and carbonyl protein content in plasma (r = 0.879, p < 0.001) and erythrocytes (r = 0.605, p < 0.01) were observed. However, carbonyl protein levels did not correlate with the degree of liver injury. Incubation of plasma with acetaldehyde, but not with ethanol, significantly increased the carbonyl protein formation. Administration of N-Ethylmaleimide, a thiol depletor, or glutathione significantly increased or delayed, respectively, the carbonyl protein formation.Proteins are oxidatively modified in plasma and erythrocytes of active alcoholics, whereas no such alterations are detectable in patients with non-alcoholic liver disease. Protein oxidation in alcoholics does not seem to result directly from ethanol; circulating xanthine oxidase, delivered from injured cells, may play a contributory role and glutathione appears to be directly involved in the protection of plasma proteins against acetaldehyde toxicity
Gastric and intestinal ethanol toxicity in the rat. Effect on glutathione level and role of alcohol and acetaldehyde metabolisms.
No full textThis study investigated the dose- and time-dependent effect of ethanol on gastric and intestinal glutathione and protein oxidative state in the rat.Rats received 1 or 4 g/kg of 25\% ethanol solution orally or isocaloric glucose. Some rats received diethylmaleate, cimetidine or cyanamide before ethanol (1 g/kg). Glutathione, carbonyl proteins and histological damage were evaluated in the gastric and intestinal mucosa 6 hours after treatment.An increase in glutathione was observed 2 to 6 hours after 1 g/kg of ethanol both in the gastric and intestinal mucosa, whereas 4 g/kg decreased glutathione. The rise in glutathione after ethanol was associated with increased levels of its oxidized form; however, the total/oxidized ratio was significantly decreased only in the intestinal tract. Diethylmaleate depleted mucosal glutathione, while the subsequent ingestion of ethanol increased it. Unlike stomach, intestine showed a significant increase in carbonyl proteins and marked histological lesions after ethanol ingestion. Cimetidine and cyanamide inhibited by 50\% the activity of alcohol dehydrogenase and by 80\% aldehyde dehydrogenase, respectively, in the gastric and intestinal mucosa. Cyanamide significantly enhanced ethanol-induced protein oxidation and mucosal injury in the stomach. No such effect was observed in the intestine.The increase of glutathione after ingestion of low amounts of ethanol appears to be an adaptive mechanism against ethanol toxicity. Depletion of glutathione increased protein oxidation and the extent of histological damage in ethanol-treated rats. At gastric level, the effects of ethanol are exaggerated by the inhibition of acetaldehyde metabolism; while intestinal damages appear to be ascribed to ethanol itself
[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
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