[Thorotrast-induced hepatic hemangioendothelial sarcoma--extensive radiological examinations (author's transl)].
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Biomedical subjects
Publications and source records attributed to G Ohta.
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A patient who developed pancytopenia and hepatosplenomegaly with portal hypertension is described. Liver wedge biopsy at the time of operation showed typical histology of congenital hepatic fibrosis. Renal surgical biopsy revealed tubular ectasia. A continuous anastomosing network of the biliary tree was observed by reconstruction of serial sections of the liver. Some parts of the network were dilated and no isolated bile ducts were present.
Antibody-dependent cell-mediated cytotoxicity was studied in patients with chronic active hepatitis (CAH) and normal controls (N) using a non-immune allogeneic lymphocytes and cultured rat parenchymal cells (Coon cells). Normal non sheep erythrocyte rosette forming cells (non E-RFC) alone showed a mild cytotoxicity to Coon cells in the absence of human sera (21.5 +/- 1.5) and in the presence of N sera (26.0) +/- 1.5) and in the presence of N sera (29.0) +/- 5.1), however, preincubation of Coon cells with CAH sera significantly augmented the cytotoxic activity of normal non E-RFC (49.4 +/- 8.7). This was blocked by aggregated IgG, anti-IgG and anti-IgG/Fc. CAH sera absorbed with Coon cells or rat hepatocyte-surface membranes failed to induce significant target cell lysis. In the absence of normal non E-RFC, N and CAH sera alone did not provoke cytotoxicity to Coon cells. Using membrane immunofluorescence method membrane-fixed IgG on target Coon cells was demonstrated in 7 of 10 sera from CAH. It seems likely that the IgG.antibody-dependent cell-mediated cytotoxicity may play a role in pathogenesis of CAH.
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Antibodies against non-histone chromosomal proteins for 89Sr-induced osteogenic sarcoma (mouse) were prepared by immunization of rabbits. The immunoreactivity of this antigen was then compared with those of non-histone chromosomal proteins from Ehrlich ascites tumor, normal mouse liver, and calf thymus by the method of quantitative microcomplement fixation. The non-histone chromosomal proteins of 98Sr-induced osteogenic sarcoma, fractionated by hydroxylapatite chromatography, exhibited significant affinity for the antibodies. Similar proteins from Ehrlich ascites tumor, normal mouse liver, or calf thymus were virtually inactive, indicating the tissue-specificity of 89Sr-induced osteogenic sarcoma proteins.
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Patients with chronic liver disease were tested for delayed hypersensitivity to the outer and the inner membranes of mitochondria (OMM and IMM) and the insoluble hepatocyte-surface membranes (IHSM), prepared from rat livers, by means of leucocyte migration inhibition technique. Positive reaction to OMM was found in 37% of patients with chronic persistent hepatitis and 35% of those with chronic active hepatitis and 43% of those with liver cirrhosis (P less than 0-05). That to IMM was 55%, 43% and 36% (P less than 0-05) and to IHSM was 37%, 47% and 45% respectively (P less than 0-05). IHSM was found to contain liver-specific components and patients with positive response to IHSM did not reveal at all a positive reaction to rat renal cell-surface membranes. The incidence of positive response to IHSM was significantly higher (54-2%) in patients with the present or previous infection with HBAg than in HBAg-non-infected patients (21-4%) (P less than 0-05). And there seemed to be a good correlation between a degree of cellular response to purified HBsAg and that to IHSM in these HBAg-infected patients. No correlation, however, was found between that to purified HBsAg and that to OMM or IMM in the same patients. This suggested that the cellular response to either HBsAg or IHSM, both related closely, may play a role in the perpetuation of chronic liver disease.
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