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M Ledig

Publications and source records attributed to M Ledig.

86 records · Page 5Linked to original sources

Relationships between 34 HLA-A, HLA-B and HLA-DR antigens and three serological markers of viral infections in alcoholic cirrhosis.

In order to study the genetic risk of alcoholic cirrhosis, the frequency of 26 HLA-A and -B antigens was compared in 184 normal controls, 175 alcoholic cirrhotic patients and 83 alcoholic patients with hepatic steatosis of carefully selected ethnic origin. Eight HLA-DR antigens were also determined in 95 subjects of the normal control group and 63 patients of the alcoholic cirrhosis group. The incidence of hepatitis B virus antibodies (anti-HBc and anti-HBs) was defined in 74 patients of the alcoholic steatosis group, 170 patients of the alcoholic cirrhosis group and 111 normal controls different from the previously mentioned normal control group. The incidence and the titers of cytomegalovirus and rubella antibodies were also determined in 93 patients of the alcoholic cirrhosis group and the 111 normal controls. Serum immunoglobulin concentrations were measured in the same 93 cirrhotic patients. Compared with the controls, the alcoholic cirrhosis group revealed a significantly higher frequency of HLA-B15 (21.7 vs. 9.8%, p less than 0.00025, corrected p less than 0.050) and HLA-DR4 (38.1 vs. 17.9%, p less than 0.005, corrected p less than 0.050) and a significantly lower frequency of HLA-B13 (2.9 vs. 11.4%, p less than 0.025, corrected p less than 0.050). As for the frequency of all other HLA antigens, there was no significant difference between the three groups (normal controls, alcoholic cirrhosis and alcoholic steatosis).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Frequencies of glyoxalase I phenotypes as biological markers in chronic alcoholism.

Biological markers for alcoholism would be a valuable tool for early diagnosis. We have studied the phenotype frequencies of genetically determined erythrocyte enzymes in 397 alcoholics, including two populations with liver disease: steatosis (n = 86) and cirrhosis (n = 128) and a population of alcoholics without apparent liver disease (n = 183) compared to a well selected control population (n = 177). Only for Glyoxalase I (GLO) phenotypes (1,2 and 2-1) were significant differences found between the male controls and the male alcoholics. In the total male alcoholic population the frequency of phenotype 1 was significantly increased (23.2% vs. 11%, p less than 0.02), and the frequency of phenotype 2 was significantly decreased (32.3% vs. 46.3 p less than 0.02) compared to the male control population. For normal women the frequency of phenotype 1 and 2 was significantly different from normal men. (1: +177% p less than 0.001, 2: -45% p less than 0.01), but no significant differences were found between alcoholic and normal women. Our results suggest that in male subjects Glyoxalase I phenotype 1 may provide a marker for predisposition to alcoholism.

Alcoholism↗

Prenatal exposure to alcohol in rat: effect on intestinal enzymes in offspring.

Intestinal hydrolase activities were studied during postnatal development in the offspring of rats exposed to 20% ethanol during gestation; alcohol was withdrawn at birth. Controls received water during gestation. Sucrase, lactase, glucoamylase and aminopeptidase activities were determined 2 and 4 weeks after birth in the proximal jejunum. Offspring prenatally exposed to ethanol showed a deficit in body weight and lower aminopeptidase activity during the suckling period (2 weeks). These effects were reversible by 4 weeks when alcohol was withdrawn at birth. The prenatal exposure to ethanol did not change the pattern of sucrase maturation in the intestine of offsprings. The activities of lactase and glucoamylase were not modified following prenatal exposure to ethanol. In conclusion, exposure to ethanol during gestation caused decreased abilities for the intestine of the offspring to digest protein.

Animals↗

Blood cell superoxide dismutase and enolase activities as markers of alcoholic and nonalcoholic liver diseases.

Monitoring of chronic alcoholism would be facilitated by using sensitive biochemical markers in blood cells, mainly to detect differences between alcoholic subjects with or without liver injury. We propose two types of markers: the first one is superoxide dismutase (SOD) activity involved in the conversion of superoxide radicals (O2-.) formed during acetaldehyde oxidation by xanthine oxidase after chronic alcohol consumption; the second one is enolase activity with both isoenzyme forms: nonneuronal enolase (NNE) and neuron specific enolase (NSE) which has been shown to be modified in many injuries related to the glycolytic pathways. For SOD activity we found a significant increase in alcoholic patients with liver injury and mainly in cirrhotic patients with ascitis. Both enolase activities were also found to be significantly increased in alcoholic patients with liver injury but NNE activity was also increased in alcoholics without apparent liver disease. Our results suggest that increased activity of SOD and NSE in blood cells may be related to liver injury mainly in alcoholism while increased NNE activity may also be a marker of alcohol abuse without liver injury.

Adult↗

Acetaldehyde-induced growth inhibition in cultured rat astroglial cells.

Due to the important role of glial cells in brain maturation and reports on delayed astroglial proliferation following ethanol exposition, it was of great interest to examine the effects of the primary metabolite of ethanol--acetaldehyde--on astroglial cell growth. This was carried out by examining biochemical parameters of astroglial cells cocultured with Chinese hamster ovary cell line (CHO) transfected with alcohol dehydrogenase (ADH), able to generate acetaldehyde from ethanol. Acetaldehyde generated from ethanol by ADH-transfected CHO cells had an inhibitory effect on the growth of astroglial cells as assessed by measuring marker enzyme activities and culture protein levels. Moreover, both acetaldehyde and ethanol altered cell cycle and increased astroglial superoxide dismutase activity. Additionally, acetaldehyde, but not ethanol, increased malondialdehyde levels in cultured astroglia. These results clearly show that acetaldehyde may participate in the development of the Fetal Alcohol Syndrome.

Acetaldehyde↗

Ethanol-induced cell death in cultured rat astroglia.

Because of the important role of glial cells in brain maturation and reports on their delayed proliferation following ethanol exposure, it was considered of interest to investigate the mechanism of ethanol action on these cells. Biochemical parameters related to the apoptotic and necrotic processes in astroglial cells exposed for 1 week to 50 and 100 mM ethanol were examined. Ethanol increased intracellular calcium levels without changing transglutaminase activity and nitrite levels. Moreover, DNA fragmentation was noted with flow cytometry and with the random oligonucleotide primed synthesis assay but neither following agar gel electrophoresis nor in UV microscopy of cell nuclei. The DNA patterns obtained were different from these seen in programmed cell death. Additionally, immunocytochemical analysis showed greater fragility of astrocytes than oligodendrocytes to ethanol. These results support the hypothesis that astroglial cells in vitro exposed to ethanol die due to necrotic but not apoptotic mechanisms.

Animals↗

[Comparative study of phosphopeptides in various animal tissues].

We determined the phosphopeptide (PP) level in several tissues and compared the values to the phosphoprotein and phosphatide level. We studied whole organs and subcellular fractions isolated from these organs. The results showed that the PP were preferentially localised in membranes. Among all the organs analyzed, the electrical organ of "Torpedo marmorata" had the highest PP level. The phosphoprotein distribution was different from the PP one; the highest level of phosphorproteins was found in nuclei. There was also an increase in phosphoprotein level comparing whole tissues and membranes isolated from the same tissue. The preferential localisation of PP in membranes is also suggested by the parallelism between PP and phosphatide level, which is also higher in membranes than in whole organs. The peculiar polyanionic structure, as well as the active metabolism and the membranous localisation of PP support the hypothesis that these compounds might be good intermediates in active transport mechanisms.

Anguilla↗