Search PubMed⌕ Search

Biomedical subjects

G Feldmann

Publications and source records attributed to G Feldmann.

At least 271 records · Page 15Linked to original sources
PubMed1977

Hepatocyte giant mitochondria: an almost constant lesion in systemic scleroderma.

Liver electron microscopic studies were performed in 14 patients with systemic scleroderma. In 13 of these patients, giant mitochondria were demonstrated in the hepatocytes. This ultrastructal abnormality was present whatever the type and duration of the disease and was also present even when the liver was histologically normal. The mechanism of formation of giant mitochondria in systemic scleroderma is unknown.

Adult↗
PubMed1977

Proteolytic activation of rat liver adenylate cyclase by a contaminant of crude collagenase from Clostridium histolyticum.

Treatment of rat liver plasma membranes with various commercial preparations of crude collagenase from Clostridium histolyticum at concentrations as low as 1 mug/ml, resulted in activation of the adenylate cyclase system. Maximal activation occurred at 50 to 100 mug/ml of collagenase, and promoted a 2- to 3-fold increase in the basal activity as well as in the activities stimulated by catecholamines, glucagon, fluoride, or GTP. This was due to an increase in the maximal velocity of the cyclizing reaction without any increase in the affinity of the enzyme for its substrate. Treatment of plasma membranes with crude collagenase did not induce gross structural modifications as judged by electron microscopic examination. 5'-Nucleotidase activity was slightly inhibited and ATPase activity remained unaffected. The stimulatory substance was nondialyzable, thermolabile, and inhibited by both EDTA and -SH reagents, thus appearing to be a protein. The following observations suggest the effects observed were due to other protease(s) present in crude collagenase: (a) only crude collagenase was active on liver adenylate cyclase: treatment with purified collagenase from C. histolyticum or from Achromobacter iophagus gave no stimulation; (b) the stimulatory activity was irreversible since washing of the membranes after treatment was without effect; (c) crude collagenase contained no lecithinase or sphingomyelinase activity under our conditions of adenylate cyclase assay; (d) after chromatography on Sephadex G-100, the activator appeared as a peak in the 30,000-dalton region and was clearly separated from the collagenase and clostripain peaks, but coincident with elastolytic and caseinolytic activities; (e) the effect of crude collagenase could be prevented by addition of elastin in vitro and was mimicked by purified elastase from hog pancreas. It remains to be seen whether the effects observed result from an increase in the catalytic constant of adenylate cyclase, or an unmasking of new catalytic sites.

Adenosine Triphosphate↗
PubMed1977

Detection of hepatitis B antigen in circulating immune complexes in acute and chronic hepatitis.

By using polyethylene glycol precipitation at low concentration (PEG test) and the radiolabeled C1q binding test, immune complexes were detected sera from acute (23/28) and chronic (28/32) hepatitis patients, hemodialyzed patients with chronic hepatitis B surface (HBs) antigenemia (7/19), and asymptomatic HBs antigen carriers (2/11). After treatment of PEG precipitates with acidic pH, heating, or proteolytic enzyme (protease), electroimmunodiffusion or radioimmunoassay revealed the presence of HBs antigen or antibody in dissociated immune complexes in sera from several acute and chronic hepatitis patients. Electron microscopy showed immune complexes of HB virus in 9 of 12 PEG precipitates obtained from PEG-test-positive sera; these 9 precipitates were from patients with acute or chronic hepatitis and the other three from chronic HBs Ag carriers. Free HB virus particles were observed after protease digestion of PEG precipitates. Neither immune complexes nor virus particles were seen in precipitates from PEG-test-negative but HBs-Ag-positive sera from chronic carriers.

Acute Disease↗
PubMed1977

Barbiturate-induced choleresis: possible independence from microsomal enzyme induction.

The influence of four barbiturates, phenobarbital, barbital, thiopental, and pentobarbital, on bile secretion and on the hepatic microsomal system was studied in anesthetized rats. The barbiturates were injected intraperitoneally for 4 days and the animals were studied on the 5th day. It was found that: (1) phenobarbital, barbital, and thiopental, but not pentobarbital, significantly increased liver weight, cytochrome P-450 concentration in the liver, decreased pentobarbital sleeping time and induced a hypertrophy of the smooth endoplasmic reticulum in the hepatocytes at electron microscopy; (2) in contrast, the four barbiturates, including pentobarbital, significantly increased bile flow; this increase was attributed to an increase in the bile acid independent bile flow. There was no correlation between the increase in bile flow and the cytochrome P-450 concentration in the liver. It is concluded that the increase in bile flow observed after barbiturate treatment in the rat is possibly independent of the hepatic microsomal enzyme induction produced by these drugs.

Animals↗
PubMed1977

[Acrodermatitis enteropathica; zinc sulfate therapy].

We present the case of two siblings with acrodermatitis enteropathica. Zinc levels were low. Oral administration of 100 mg of zinc sulfate allowed total regression of all signs. When zinc therapy was interrupted, the manifestations reappeared and disappeared again when treatment was resumed. A defect of genetic origin in digestive zinc absorption is suggested. Mohnahan's advocated zinc treatment of acrodermatitis enteropathica in 1973; it is a non-toxic treatment, which is always active and be considered as a diagnostic test.

Acrodermatitis↗
PubMed1976

Bilirubin and paranitrophenol glucuronyl transferase activities and ultrastructural aspect of the liver in patients with chronic hemolytic anemias.

The hepatic ultrastructural aspect and the hepatic bilirubin (Bil-GT) and paranitrophenol (PNP-GT) glucuronyl transferase activities were studied in twenty subjects with a chronic hemolytic anemia (HA) and five subjects with an aplastic anemia. In chronic HA: the hepatic ultrastructural aspect showed mitochondrial abnormalities affecting structure (paracrystalline inclusions), size (giant mitochondria) and shape (irregular mitochondria); there was a decrease of Bil-GT activity in 80 percent of the patients. No connection could be shown between the HA etiology and the degree of the enzymatic activity decrease. The physiopathological mechanism of this enzymatic activity decrease is unknown; no deficiency of PNP-GT was observed; in chronic aplastic anemias there does not seem to be any modification, either of Bil-GT activity, or of hepatic PNP-GT activity. It is concluded that Bil-GT is often decreased in HA and that neither Bil-GT measurement nor the ultrastructural aspect of the liver distinguish chronic HA from Gilbert's syndrome.

Anemia, Aplastic↗
PubMed1976

[Intracellular localization of concanavalin A receptors in rat hepatocytes].

Intracellular binding sites of concanavalin A were studied in rat hepatocytes under electron microscopy with a cytochemical method using peroxidase. The penetration of concanavalin A occurs only in cells previously cut and the binding sites of this lectin are located on the endoplasmic reticulum and the Golgi apparatus. The results suggest that these sites are in relationship, at least in part, with the plasma glycoproteins synthesized and secreted by the hepatocytes.

Age Factors↗
PubMed1976

Effects of anticopper therapy on hepatocellular mitochondria in patients with Wilson's disease: an ultrastructural and stereological study.

Liver biopsy specimens from 7 patients with Wilson's disease (hepatolenticular degeneration), obtained before and after 3 to 5 years of D-penicillamine therapy, were studied by electron microscopy and stereology. The characteristic mitochondrial abnormalities encountered in the hepatocytes of untreated patients were less pronounced or disappeared after treatment in 5 of the 7 patients. Simultaneously, relative mitochondrial volume, surface density of the external mitochondrial membranes, and the number of these profiles per unit area increased, whereas abnormal elevations SGOT and SGPT returned to normal levels.

Adolescent↗
PubMed1975

Heterozygous alpha 1-antitrypsin deficiency and cirrhosis in adults, a fortuitous association.

Pi (protease inhibitor) genotype was determined in 394 healthy blood-donors, 132 adult patients with alcoholic cirrhosis, and 37 adult patients with cryptogenic cirrhosis. The frequency of the heterozygous genotype with a single allele Pi Z (heterozygous alpha 1-antitrypsin deficiency) was not different in blood-donors and in patients with cirrhosis. This finding suggests that the association of this heterozygous genotype with cirrhosis is not causal but fortuitous and that this heterozygous genotype does not increase susceptibility to cirrhosis due to other causes, in particular alcoholism.

Adult↗
PubMed1975

Ultrastructural immunoperoxidase demonstration of autologous albumin in the alveolar capillary membrane and in the alveolar lining material in normal rats.

The location of autologous serum albumin within the alveolar-capillary membrane was studied in the rat under physiological conditions using antialbumin antibodies labeled with peroxidase. Albumin was detected in the lung interstitium, and in numerous pinocytic vesicles within endothelial cells and type I alveolar epithelial cells. The immunoreaction was also positive at the level of plasmalemmal membranes of both cell types and in the alveolar lining material.

Animals↗
PubMed1975

Inhibition by colchicine of fibrinogen translocation in hepatocytes.

In the rat, 8 h after intraperitoneal administration of colchicine, fibrinogen (detected by antirat fibrinogen antibodies labeled with peroxidase) accumulated in the lumina of the rough endoplasmic reticulum of the hepatocytes; 16 and 24 h after colchicine administration, fibrinogen was detected, respectively, in the lumina of the smooth endoplasmic reticulum and in the Golgi apparatus. The effect of colchicine on the cytoplasmic translocation of fibrinogen could be due to a direct action of the drug on the membranes of the endoplasmic reticulum or could be the indirect result of the disruptive action of the drug on the microtubules.

Animals↗
PubMed1975

The ultrastructure of hepatocytes in alpha-1-antitrypsin deficiency with the genotype Pi--.

The ultrastructural appearance of the endoplasmic reticulum of the hepatocytes was found to be normal in a 5-year-old girl with alpha-1-antitrypsin deficiency with the genotype Pi--. The liver ultrastructure of this variant is therefore different from that of alpha-1-antitrypsin deficiency with the genotype PiZZ in which aggregates of an abnormal, unsecreted alpha-1-antitrypsin accumulate in the endoplasmic reticulum of the hepatocytes. The normal appearance of the endoplasmic reticulum in alpha-1-antitrypsin deficiency with the genotype Pi-- is compatible with the hypothesis, in this variant, synthesis of alpha-1-antitrypsin is completely, or nearly completely, absent; an alternative hypothesis would be that an abnormal alpha-1-antitrypsin is produced by the liver and secreted into the plasma, but disappears rapidly from the plasma.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1975

Increased sulfobromophthalein clearance in a patient receiving phenobarbital and other anticonvulsant drugs.

A marked increase in bromosulfophthalein, dibromosulfophthalein, and indocyanine green fractional clearance was found in a patient who had received phenobarbital for 30 years and other anticonvulsant agents for 6 years. This was related to a marked increase in hepatic blood flow, while hepatic extraction remained normal. These changes were associated with signs of hepatic microsomal enzyme induction (in particular a 2-fold increase in liver bilirubin UDP-glucuronyltransferase activity and hypertrophy of the smooth endoplasmic reticulum in the hepatocytes). Drug administration (especially phenobarbital) should be considered as a possible cause of increased bromosulfophthalein clearance in man.

Adult↗
PubMed1975

Immune complex type glomerulonephritis in cirrhosis of the liver.

Glomerular lesions were detected in 9 of 10 patients with liver cirrhosis: these lesions consisted of a) thickening of basement-membrane-like material, b) electron-dense deposits in mesangial areas and in capillary walls, c) round areas of rarefaction in the membrane-like material and in some deposits, and d) presence of IgA, with IgG and/or IgM and/or C3, in the deposits. The association of these four abnormalities seems to be characteristic of "cirrhotic glomerulonephritis." The deposits could be the result of precipitation in the glomeruli of either aggregated immunoglobulins or circulating immune complexes.

Adult↗
PubMed1974

Calcium-binding properties and ATPase activities of rat liver plasma membranes.

Plasma membranes from rat liver purified according to the procedure of Neville bind calcium ions by a concentration-dependent, saturable process with at least two classes of binding sites. The higher affinity sites bind 45 nmol calcium/mg membrane protein with a K(D) of 3 microM. Adrenalectomy increases the number of the higher affinity sites and the corresponding K(D). Plasma membranes exhibit a (Na(+)-K(+))-independent-Mg(2+)-ATPase activity which is not activated by calcium between 0.1 microM and 10 mM CaCl(2). Calcium can, with less efficiency, substitute for magnesium as a cofactor for the (Na(+)-K(+))-independent ATPase. Both Mg(2+)- and Ca(2+)-ATPase activities are identical with respect to pH dependence, nucleotide specificity and sensitivity to inhibitors. But when calcium is substituted for magnesium, there is no detectable membrane phosphorylation from [gamma-(32)P] ATP as it is found in the presence of magnesium. The existence of high affinity binding sites for calcium in liver plasma membranes is compatible with a regulatory role of this ion in membrane enzymic mechanisms or in hormone actions. Plasma membranes obtained by the procedure of Neville are devoid of any Ca(2+)-activated-Mg(2+)-ATPase activity indicating the absence of the classical energy-dependent calcium ion transport. These results would suggest that the overall calcium-extruding activity of the liver cell is mediated by a mechanism involving no direct ATP hydrolysis at the membrane level.

Adenosine Triphosphatases↗