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Biomedical subjects

G Feldmann

Publications and source records attributed to G Feldmann.

At least 235 records · Page 13Linked to original sources
PubMed1982

Immunoperoxidase localization of albumin and fibrinogen in rat liver fixed by perfusion or immersion: effect of saponin on the intracellular penetration of labeled antibodies.

Immunoperoxidase localization of albumin and fibrinogen in rat liver was tested with perfusion or immersion fixation and saponin as a membrane permeabilizing agent. The distribution of albumin- or fibrinogen-containing hepatocytes was examined by light microscopy. Labeled antibody penetration was assessed by electron microscopy on transversely cut cryostat sections. Paraformaldehyde liver fixation by perfusion, followed by incubation of the sections with labeled antibodies together with saponin, demonstrated that albumin and fibrinogen were present in all hepatocytes; mainly in the Golgi apparatus and rarely in the endoplasmic reticulum, the ultrathin sections being labeled throughout their entire thickness. A constant labeling of the endoplasmic reticulum was obtained when saponin was added from the beginning of fixation. In the absence of saponin, albumin was seen in most of the hepatocytes but only at the periphery of the transverse sections, in a few Golgi apparatus, and in some parts of the endoplasmic reticulum; under this condition, fibrinogen was not visualized in the hepatocytes. Paraformaldehyde liver fixation by immersion showed the presence of albumin or fibrinogen in a few hepatocytes only, with irregular labeled antibody penetration. The use of saponin did not improve albumin and fibrinogen localization, except when the liver was poorly fixed. These results show that liver fixation by perfusion gives a homogeneous labeling of all the hepatocytes, whereas fixation by immersion leads to a heterogeneous labeling. Satisfactory results are obtained with saponin, which must be used to improve the penetration of labeled antibodies when the liver is fixed by perfusion. Saponin does not work when immersion is employed, at least under the conditions tested.

Albumins↗
PubMed1982

Ultrastructural localization of concanavalin a surface receptors on brush-border enterocytes in normal children and during coeliac disease.

Concanavalin A surface receptors were detected on brush border enterocytes from child intestinal biopsies by the concanavalin A-peroxidase method. On electron microscopy, these receptors appeared as electron-dense deposits, located on a band running along the innermost part of the brush border membrane glycocalyx. In the five control subjects tested, brush border length was 1.06 +/- 0.18 micrometer, and band thickness, 19 +/- 4 nm. Deposits were regular in shape and evenly spaced out along the entire membrane, reflecting homogeneous glycosylation of the normal brush border. In seven patients with villous atrophy induced by gluten, the brush border was damaged and its length was 1.04 +/- 0.39 micrometer. The thickness of the electron-dense deposit band was 19 +/- 6 nm; deposit shape was irregular and the band ran discontinuously along the membrane. The degree of this abnormality seemed to correspond to the degree of brush border damage. In six treated coeliac patients with normalized mucosa, the brush border was structurally normal but it was significantly longer (1.25 +/- 0.32 micrometer) than in the controls (p less than 0.01). The electron-dense band was significantly thinner (16 +/- 7 nm) than in the controls (p less than 0.01). The distribution of the electron-dense deposits was sporadic in some parts of the band and regular in others. These results suggest abnormal glycosylation of the brush border membrane in coeliac disease, and might be due to the presence of abnormal glycoconjugates. It remains to be established if these changes are induced by gluten toxicity or are the consequences of nonspecific intestinal disorders.

Adolescent↗
PubMed1982

Ultrastructural aspects of the liver perisinusoidal space in diabetic patients with and without microangiopathy.

To determine whether abnormalities of the perisinusoidal space of Disse are present in the liver of diabetic patients with microangiopathy, an ultrastructural stereologic study of the space of Disse was performed in six insulin-treated diabetics with severe performed in six insulin-treated diabetics with severe proliferative retinopathy and six insulin-treated diabetics with normal fluorescein angiography, six patients with familial unconjugated hyperbilirubinemia were studied as controls. No patient had clinical and/or biochemical hepatic abnormalities and none suffered from any of the pathologic conditions known to be associated with collagenization of the perisinusoidal space. In control patients, the space of Disse of liver sinusoids contained occasional small deposits of collagen fibers. The relative volume of these fibers per unit of sinusoid represented 2.63 +/- 0.82%. In all diabetic patients with retinopathy, marked deposition of collagen fibers within the perisinusoidal space was constantly observed, a finding confirmed by ultrastructural stereologic analysis which showed that the relative volume of collagen fibers per unit of sinusoid represented 7.33 +/- 1.44% and differed significantly from control patient values (P less than 0.001). On the contrary, the relative volume of collagen fibers within the space of Disse in diabetic patients without retinopathy (3.95 +/- 2.96%) did not differ significantly from control patient values. These findings demonstrate that collagenization of the space of Disse is positively correlated with the presence of diabetic microangiopathy. Ultrastructural examination of the liver sinusoids might constitute a sensitive and useful approach for detecting the early changes of the microcirculation in diabetic patients.

Adult↗
PubMed1982

A quantitative ultrastructural analysis of the leukocytes in contact with hepatocytes in chronic active hepatitis, with a cytochemical detection of mononuclear phagocytes.

In an attempt to characterize in vivo the immune cells cytotoxic to hepatocytes in patients with chronic active hepatitis (CAH), a quantitative ultrastructural analysis of leukocytes in close contact with hepatocytes was performed in 13 patients with untreated HBsAg-negative CAH. Mononuclear phagocytes were identified by detection of endogenous peroxidase. Of the leukocytes, 8.3-4.1% were mononuclear phagocytes, 12.5-25.8% were large lymphocytes with a prominent secretory apparatus, assumed to represent mostly killer cells (T-cytotoxic cells and/or null cells), 12.2-56.8% were small lymphocytes poor in cytoplasmic organelles, and 0-45.8% were plasma cells. Patients with high serum transaminase levels had significantly more mononuclear phagocytes (P less than 0.001) and significantly fewer plasma cells (P less than 0.001) and small lymphocytes (P less than 0.001) than patients with lower disease activity. The profile of the leukocytes in contact with hepatocytes in these CAH patients suggests that mononuclear phagocyte-mediated mechanisms play an important role in hepatocyte necrosis in vivo.

Adolescent↗
PubMed1981

Hepatocyte localization of hepatitis B core and surface antigens in renal transplant recipients. An ultrastructural prospective study.

A prospective series of 45 liver biopsies taken from 22 renal transplant patients was investigated for the presence of hepatitis B antigen core (HBc) and surface (HBs) components by electron microscopy. At the time of each biopsy serum HBs Ag was sought by radioimmunoassay. Sections were taken for the detection of HBs Ag by immunofluorescence. In seropositive patients, intravesicular tubular structures resembling HBs Ag were found in 61% of biopsies while the intranuclear core HBc was present in 69%. No correlation could be made between the ultrastructural pattern of the viral components and the intensity of the histological liver damage. During the follow up, there was an accumulation of both HBs and HBc Ag even in a period as short as 1 year. The 9 liver specimens examined after three years of transplantation showed a marked accumulation of both antigens. Thus the expression of HB Ag at the hepatocellular level seems to correlate better with the duration of antigenaemia than with the histological pattern. Lastly, on matched semithin and ultrathin sections, the ground glass appearance of cytoplasm appeared to correlate with smooth endoplasmic reticulum distorsion, irrespective of the simultaneous presence or absence of intravesicular tubular structures. The sanded nuclei expressed a rare massive accumulation of core antigen.

Biopsy↗
PubMed1981

Ultrastructural lesions of bile ducts in primary biliary cirrhosis. A comparison with the lesions observed in graft versus host disease.

Intrahepatic bile duct destruction is a characteristic feature of primary biliary cirrhosis and hepatic graft versus host disease. Lymphocytotoxicity against antigens on the surface of biliary cells is one of the cell mediated immune mechanisms debated in the pathogenesis of persistent bile duct destruction during primary biliary cirrhosis. Immune complex injury has also been hypothesized. In graft versus host disease, damage to bile duct cells is also believed to be due to a cytotoxic reaction of the grafted lymphoid cells against the host histocompatibility antigens, and immune complex deposition is likely to occur. The aim in this comparative ultrastructural study of intrahepatic bile ducts in 10 patients with primary biliary cirrhosis and six patients with hepatic graft versus host disease was to investigate whether identical or different ultrastructural lesions were detected in both diseases. Features of conspicuous necrosis of biliary cells, including cytolysosomes, apoptosis, and basement membrane disruption, were observed in both diseases. Numerous lymphocytes established close membrane contacts with biliary cells, especially with the necrotic ones. They had cytoplasmic pseudopods, and some of them displayed a uropod or contained lysosomal vesicles. Abnormalities of the bile duct basement membrane, also observed in both diseases, included thickening or multilayering and numerous lucent areas of rarefaction often containing osmiophilic inclusions. The striking similarity of the ultrastructural lesions in both diseases provides an additional morphological argument to suggest that certain common pathogenic mechanisms might be involved in the destruction of bile ducts in primary biliary cirrhosis as well as in hepatic graft versus host disease.

Adolescent↗
PubMed1981

Hepatocytic PAS-positive diastase-resistance inclusions in the absence of alpha-1-antitrypsin deficiency--high prevalence in alcoholic cirrhosis.

The presence of PAS-positive, diastase-resistant inclusions in the cytoplasm of the hepatocytes is characteristic of alpha-1-antitrypsin deficiency. The purpose of this investigation was to determine whether the presence of these inclusions is a specific feature, permitting the recognition of alpha-1-antitrypsin deficiency in patients with liver disease. We examined the liver specimens from 20 patients suffering from alcoholic cirrhosis with the Pi M phenotype, i.e., in whom alpha-1-antitrypsin deficiency was excluded. In seven of these patients, PAS-positive, diastase-resistant inclusions were seen in the hepatocytes; in two patients, these inclusions contained a material antigenically similar to alpha-1-antitrypsin. These inclusions might represent deposits of glycoproteins poorly excreted by the diseased hepatocytes. It is concluded that, in patients with liver disease, the presence of PAS-positive, diastase-resistant inclusions--even containing alpha-1-antitrypsin--in the cytoplasm of the hepatocytes does not permit the hepatic lesions to be ascribed to alpha-1-antitrypsin deficiency.

Amylases↗
PubMed1981

Chronic active hepatitis and giant multinucleated hepatocytes in adults treated with clometacin.

The authors report the cases of 2 adults who became jaundiced during prolonged administration of clometacin, a new analgesic drug. Jaundice and serum aminotransferase activity progressively increased while the drug administration was continued but quickly decreased when it was eventually interrupted. 1 patient resumed the intake of clometacin and died with jaundice and ascites. In both patients, liver lesions were those of severe chronic active hepatitis with numerous giant multinucleated hepatocytes.

Aged↗
PubMed1981

Synchronous increase of four acute phase proteins synthesized by the same hepatocytes during the inflammatory reaction: a combined biochemical and morphologic kinetics study in the rat.

The hepatic synthesis of four "acute phase reactants" (APR), i.e., fibrinogen, alpha 1-acid glycoprotein, alpha 2-macroglobulin, and haptoglobin has been investigated in rats suffering from turpentine-induced inflammation. To follow the change in the rates of synthesis of the four APR, their concentrations were measured by immunonephelemetry in both the plasma and the hepatic microsomal fraction at various times after injury. A synchronous increase in the concentrations of these four proteins was observed in the liver (maximum 24 hours) as well as in the plasma (maximum 40 hours) of the same animals. In parallel, the site of their synthesis was localized in liver sections by light and electron microscopy using direct immunoperoxidase labeling. Of the liver cells, only the hepatocytes were labeled. In the early period of the inflammatory reaction (10 to 16 hours), synthesizing cells were detected principally in the periportal zone, but later (24 hours), the labeled area was extended to nearly the entire hepatic lobule. When serial sections of liver were examined at that time, the same cells were found to contain simultaneously the four APR. Within the cells examined by electron microscopy, the four proteins were localized in the secretory pathway, i.e., rough and smooth endoplasmic reticulum, Golgi apparatus, and secretory vacuoles. Therefore, we conclude that: (1) the experimental inflammatory reaction induces a synchronous increase in the synthesis of four APR by the liver; (2) this increased synthesis apparently results from an increased number of synthesizing hepatocytes; (3) these cells have a preferential periportal localization; and (4) individual hepatocytes are not specialized in the synthesis of a single plasma protein.

Animals↗
PubMed1980

Hepatitis B antigen-associated periarteritis nodosa in patients undergoing long-term hemodialysis.

Periarteritis nodosa was observed in three of 266 persistent hepatitis B antigen (HBsAg) carriers undergoing long-term hemodialysis; no cases of necrotizing vasculitis occurred among 384 other patients undergoing dialysis having either no or transient antigenemia. Circulating e antigen, but no e antibody, was found in two of these three patients. The serum level of the third component of complement (C3) was normal in two patients and low in the third. Circulating immune complexes were demonstrated in all three patients, using polyethylene-glycol (PEG) precipitation, PEG-C4, and solid phase C1q tests. HBsAg and anti-hepatitis B antibody (HBsAb) were identified in the PEG precipitates using radioimmunoassay and electron microscopy technics. Direct immunofluorescence performed on a muscle biopsy specimen from one patient was positive for HBsAg, but not for immunoglobulin G (IgG), immunoglobulin M (IgM), C3 or C1q. These data support the hypothesis that circulating immune complexes involving HBsAg may be involved in the pathogenesis of periarteritis nodosa.

Antigen-Antibody Complex↗
PubMed1980

Evidence for fibrinogen synthesis and secretion by rat foetal hepatocytes.

Fibrinogen concentration in rat foetal plasma is very low at 18 days of gestation but increases rapidly thereafter. The present study provides evidence that this increase is due to synthesis by the foetus itself. (1) 125I-labelled human fibrinogen, injected intravenously into the pregnant adult, did not reach the foetal circulation; (2) turpentine administration to the adult induced an increased maternal plasma fibrinogen concentration without affecting the foetal one; (3) conversely, in utero administration of turpentine to foetuses increased their plasmas fibrinogen concentration without affecting the maternal one; (4) using sheep anti-rat fibrinogen antibodies labelled with peroxidase, in electron microscopy, fibrinogen was located in foetal hepatocytes within the organelles known to be responsible for the synthesis and the ultimate secretion of the protein.

Animals↗