Concanavalin A Reduces Liver Collagen Accumulation in Murine Schistosomiasis

Shizuko Takahashi, Michio Kobayashi – 1 March 1982 – Mice infected with Schistosoma mansoni develop hepatic fibrosis associated with enhanced collagen synthesis that out‐paces induced collagenase activity. Administration of one dose of concanavalin A [Con A (200 jug)] by i.p. injection to mice at 5 or 6 weeks after infection with 50 S. mansoni cercariae decreased liver collagen content by 50% compared to levels in control‐infected mice injected with either homologous immunoglobulin (200 jug) or phosphate‐buffered saline; additional doses of Con A had no further effect.

Hepatic Microvascular Regulatory Mechanisms. II. Cholinergic Mechanisms

Frank D. Reilly, Ruth V. W. Dimlich, Eugene V. Cilento, Robert S. Mccuskey – 1 March 1982 – Several cholinergic agonists and their antagonists were administered topically at various concentrations (10−10 to 10−4 gm per ml) to the livers of anesthetized Sprague‐Dawley rats. Changes in the microvasculature were measured for a period of 15 min using in vivo microscopic methods. The influence of cholinergic agonists on hepatic mast cells was determined by histochemical methods.

Water Content of Gallstones: Location and Contribution to a Hypothesis Concerning Stone Structure

Roger D. Soloway, Eleanor B. Fayusal, Bruce W. Trotman, Norman E. Weston, James F. Ficca – 1 March 1982 – The water content of black pigment and cholesterol gallstones was evaluated with the use of moisture evolution analysis, electron spectroscopy for surface analysis, and X‐ray diffraction. X‐ray diffraction identified complex hydrated hydroxyapatite compounds in two stones. Moisture evolution analysis demonstrated that 18 pigment gallstones contained between 0.83 and 6.87% water; six cholesterol stones contained 0 to 0.27% (p < 0.001).

Inducer and Suppressor T‐Cells in Hepatitis B Virus‐induced Liver Disease

Howard C. Thomas, David Brown, Guitaine Routhier, George Janossy, Patrick C. Kung, Gideon Goldstein, Sheila Sherlock – 1 March 1982 – During acute type B hepatitis, the proportion of inducer to cytotoxic/suppressor T‐cells is decreased due to an increase in the concentration of suppressor cells. Similar changes are seen in chronically infected subjects with evidence of active viral replication (HBeAg positive) and chronic hepatitis of varying severity.

Ultrastructural and Biochemical Liver Analyses in Fabry's Disease

Stephan G. M. Meuwissen, Kurt P. Dingemans, Anneke Strijland, Joseph M. Tager, Bert C. M. Ooms – 1 March 1982 – Ultrastructural and biochemical analyses were made of liver biopsy material from a patient with longstanding Fabry's disease. Both hepatocytes as well as periportal macrophages showed lipid accumulations consisting of amorphous material as well as stacks of lamellar leaflets. Lipid inclusions in periportal macrophages were much larger than in hepatocytes. Furthermore, small round spheres were found exclusively in periportal macrophages.

A Mitochondrial Antigen‐Antibody System in Cholestatic Liver Disease Detected by Radioimmunoassay

Michael Manns, Karl‐Hermann Meyer, Zum Büschenfelde – 1 January 1982 – A radioimmunoassay (RIA) was established for the detection of antimitochondrial autoantibodies (AMAs) in patient sera. AMAs were detected by RIA in 12 of 14 patients with primary biliary cirrhosis and in 3 of 29 patients with chronic active hepatitis. AMAs were detected by indirect immunofluorescence in all sera positive by RIA.

Toxic Doses of Acetaminophen Suppress Hepatic Glutathione Synthesis in Rats

Bernhard H. Lauterburg, Jerry R. Mitchell – 1 January 1982 – The effect of a toxic dose of acetaminophen on hepatic glutathione turnover was studied in fed and fasted rats. Following the administration of 1 gm per kg of acetaminophen, the fractional rate of glutathione turnover increased from 0.19 to 0.28 hr−1 in fed rats and from 0.43 to 0.50 hr−1 in rats fasted for 48 hr. The increase in the fractional rate of turnover was proportionally much less than the decrease in hepatic glutathione concentration resulting from the toxic dose of acetaminophen.

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