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M C Lescs

Publications and source records attributed to M C Lescs.

28 records · Page 2Linked to original sources
PubMed1992

[AIDS-related progressive multifocal leukoencephalopathy limited to U fibers, responsible for subacute encephalopathy with normal CT scan findings].

A 41-year-old male homosexual with AIDS was hospitalized for temperature elevation to 40 degrees C with confusion. Neurologic evaluation found psychomotor slowing and temporospatial disorientation with no focal signs. The CD4 count was 100/mm3. CSF analysis and the CT scan were normal. Despite antiviral treatment the patient died fifteen days after admission. Gross appearance of the brain was normal. Histologic examination disclosed multiple, small foci of demyelination characteristic of progressive multifocal leukoencephalopathy. These foci were disseminated among the U fibers. In situ hybridization and immunocytochemical studies demonstrated papovavirus particles in oligodendrocytes and a few astrocytes. This case shows that papovavirus infection in AIDS patients may be responsible for a diffuse febrile encephalopathy with normal CT scan findings and a rapidly progressive course.

AIDS-Related Opportunistic Infections↗
PubMed1990

Mechanism of gamma-glutamyl transpeptidase release in serum during intrahepatic and extrahepatic cholestasis in the rat: a histochemical, biochemical and molecular approach.

The mechanism of the elevation of serum gamma-glutamyl transpeptidase activity in cholestasis is not clear. We therefore analyzed rat gamma-glutamyl transpeptidase activities in liver, bile and serum during intrahepatic cholestasis induced by a single dose of alpha-naphthyl isothiocyanate (20 mg/100 gm body weight) and during extrahepatic cholestasis after bile duct ligation. At days 1 and 2 after alpha-naphthyl isothiocyanate ingestion, we saw a fivefold and a 60-fold increase in serum and bile gamma-glutamyl transpeptidase activities, respectively. These increases were associated with a decrease in hepatic gamma-glutamyl transpeptidase activity and of corresponding mRNA. Simultaneously, necrosis of the biliary epithelium appeared in portal tracts. From day 2 to day 14, gamma-glutamyl transpeptidase activity in bile and serum progressively returned to basal levels; in the liver, cholangiolar proliferation was mild and was associated with moderate elevation of the gamma-glutamyl transpeptidase activity and of its corresponding mRNA. In extrahepatic cholestasis, a 10-fold increase in serum gamma-glutamyl transpeptidase activity was detected between day 0 and day 14. This increase was associated with major cholangiolar proliferation and with a progressive rise in hepatic gamma-glutamyl transpeptidase activity and in specific mRNA; in bile, gamma-glutamyl transpeptidase activity was slightly elevated. In these two models of cholestasis, histochemically detected gamma-glutamyl transpeptidase activity was largely predominant in biliary cells. We found no significant induction of gamma-glutamyl transpeptidase activity in hepatocytes. These results suggest that in these two models of cholestasis, the increase in serum gamma-glutamyl transpeptidase activity is of biliary cell origin and does not originate from hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Naphthylisothiocyanate↗
PubMed1989

Mouse hepatic endothelial cells in culture secrete a growth inhibitor for hepatic lipocytes and Balb/c 3T3 fibroblasts.

Hepatic lipocytes are sinusoidal cells in close contact to endothelial cells. They proliferate, switch to a fibroblastic phenotype and synthetize collagen during hepatic fibrosis. Since it is known that vascular endothelial cells can influence the proliferation of neighboring cells such as smooth muscle cells, we investigated the role of hepatic endothelial cells on the growth of lipocytes and Balb/c 3T3 fibroblasts. Concentrated conditioned medium from endothelial cells inhibited both [3H]thymidine incorporation and actual growth of lipocytes and Balb/c 3T3 fibroblasts. The inhibition was lost when conditioned medium was treated with heat or trypsin, or when medium was conditioned in the presence of cycloheximide. We conclude that hepatic endothelial cells secrete a proteic growth inhibitor for lipocytes and hepatic Balb/c 3T3 fibroblasts. This inhibitor could be of importance in limiting lipocyte proliferation in the liver and possibly in preventing hepatic fibrosis.

Animals↗
PubMed1988

Copper and copper-binding protein in liver tumors.

The presence of copper and copper-binding protein was histochemically investigated in 39 hepatocellular carcinomas, 24 metastatic tumors of the liver, and eight benign hepatic tumors. None of the hepatocellular carcinomas was fibrolamellar. The presence of copper (demonstrated by rhodanine) and of copper-binding protein (demonstrated by modified orcein) was simultaneously observed in 11 of the 39 hepatocellular carcinomas (28%). Deposition was mild in three cases, moderate in two cases, and marked in six cases, and it was significantly related to the presence of bile within the tumor. Copper and copper-binding protein granules were not found in metastatic tumors of the liver, and were observed in two of the eight cases of benign hepatic tumors. These results suggest that the presence of copper and copper-binding protein in tumor cells may be found in all variants of hepatocellular carcinomas and not only in fibrolamellar carcinomas as previously suggested, and might be helpful in differentiating primary from secondary liver tumors.

Adult↗
PubMed1985

Phenotype-karyotype correlations in dup(18q): report of a case and review.

We report on a case of dup(18q) due to de novo translocation 46,XX,-21,t(18;21)(18qter----cen----21qter). The patient had many characteristic signs of full trisomy 18 except for internal organ malformations and early death. We review the phenotype-karyotype correlations between full trisomy 18 and dup(18q) and discuss the possibility of the existence of "critical zone(s)" at the proximal or/and distal region of 18q responsible for most signs of trisomy 18, such as congenital heart defect and early death.

Abnormalities, Multiple↗
PubMed1984

[Ring chromosome 14. I. A case report on homogeneous r(14)].

A ring chromosome derived from a no. 14 was observed, without mosaicism, in a 2-month-old male with craniofacial dysmorphism, retarded psychomotor development, seizures and retinal anomalies. Serum immunoglobulins concentrations were normal.

Abnormalities, Multiple↗
PubMedDate not supplied

In vitro toxicity of polymorphonuclear neutrophils to rat hepatocytes: evidence for a proteinase-mediated mechanism.

Human polymorphonuclear neutrophils, when exposed to soluble or particulate stimuli, can destroy various types of cells. The aim of this study was to investigate their toxicity against hepatocytes. Human polymorphonuclear neutrophils were incubated in basal conditions and after stimulation with 5 mg per ml opsonized zymosan in the presence of rat hepatocytes isolated by collagenase digestion. Cytotoxicity was quantified by the percentage of ALT activity released by hepatocytes in culture medium. Whereas unstimulated neutrophils exhibited only minor effects, opsonized zymosan-stimulated neutrophils induced, after 16 hr incubation, a 24.0 +/- 4.1% (mean +/- 1 S.E.) ALT activity release at a neutrophil/hepatocyte ratio of 5, and a 51.7 +/- 6.8% ALT activity release at a ratio of 20. At this ratio of 20, the ALT activity release was 9.0% at 1 hr and 24.0% at 4 hr. Three proteinase inhibitors (i.e., soybean trypsin inhibitor, alpha 1-proteinase inhibitor and fetal calf serum) decrease cytotoxicity by 78, 76 and 78%, respectively. The protective effect of proteinase inhibitors was not due to a nonspecific effect of proteins, since bovine serum albumin did not decrease the toxicity of stimulated polymorphonuclear cells. The supernatant of stimulated neutrophils was also found to be toxic against hepatocytes, and again, this effect was inhibited by soybean trypsin inhibitor, alpha 1-proteinase inhibitor and fetal calf serum. Finally, the role of proteinases was supported by the demonstration of a cytotoxic effect of two purified proteinases: porcine pancreatic elastase and human neutrophil cathepsin G. The toxicity of these proteinases was also markedly reduced by the specific inhibitors used in the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

In vitro toxicity of hydrogen peroxide against normal vs. tumor rat hepatocytes: role of catalase and of the glutathione redox cycle.

Hydrogen peroxide produced by stimulated phagocytic cells or during the metabolism of drugs, is toxic to various cell types. The aim of this study was to investigate its toxicity against normal vs. tumor rat hepatocytes. Isolated normal hepatocytes and tumor hepatocytes from three hepatocarcinoma cell lines, Fao, C2 (Faof1C2) and HTC, were incubated in the presence of a H2O2-generating system consisting of glucose and varied concentrations of glucose oxidase. The toxicity of H2O2 was quantified by measuring the percentage of lactate dehydrogenase activity released in the culture medium after various times of incubation. By comparison to normal hepatocytes, tumor hepatocytes exhibited an increased susceptibility to lysis by H2O2. At a concentration of 100 mU per ml, glucose oxidase induced a lactate dehydrogenase activity release of only 6.1 +/- 2.2% (mean +/- S.E.) from normal hepatocytes and of 71.0 +/- 2.9, 45.5 +/- 2.5 and 34.7 +/- 3.4% from Fao, C2 and HTC cells, respectively, after an 18-hr incubation. At a concentration of 10 mU per ml, glucose oxidase had no toxic effect to normal hepatocytes or HTC cells, whereas it induced a lactate dehydrogenase activity release of 58.7 +/- 7.6 and 51.2 +/- 5.6% from Fao and C2 cells, respectively. In addition, the time courses of lactate dehydrogenase activity release, studied with 500 mU per ml glucose oxidase, demonstrated that Fao cells, C2 cells and, to a lesser degree, HTC cells were lysed more rapidly than normal hepatocytes. The toxicity of glucose oxidase was suppressed by the addition of catalase, indicating that it was actually mediated by H2O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗