[Primary biliary cirrhosis: epidemiological analysis].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
J Hirohara
Publications and source records attributed to J Hirohara.
Prediction of prognosis of primary biliary cirrhosis in Japan.
The clinical profile of primary biliary cirrhosis in Japan was clarified on the basis of data on 1066 patients attending 212 hospitals and institutions in this country. Six hundred and twelve patients (57.4%) were asymptomatic. The majority of the patients were middle-aged women. Pruritus was the most frequent initial symptom of symptomatic primary biliary cirrhosis. Antimitochondrial antibodies were positive in 877 patients (82.5%). Sjögren's syndrome was the most common associated autoimmune disease. Liver biopsy was performed in 753 patients at the time of diagnosis, and histological staging by Scheuer's classification indicated that 307 (43.7%) patients were in stage I and 222 (31.6%) were in stage II. The most frequent causes of death were hepatic failure and/or gastrointestinal bleeding, which affected 166 (78.3%) of the 212 patients who died. Statistical analysis using Cox's regression method revealed that the patient's age and the serum bilirubin, albumin, and total cholesterol concentrations were significant predictors of the prognosis. A prognostic index was also calculated that could be used to predict the duration of survival for patients with primary biliary cirrhosis.
Adult↗
Protothecosis in a patient with systemic lupus erythematosus.
A rare case of protothecosis in a 40-year-old Japanese woman with systemic lupus erythematosus, under long-term prednisolone treatment is presented. The patient developed extensive ulcerative skin lesions after injury. The characteristic histopathological findings and biochemical sugar assimilation tests indicated infection by Prototheca wicherhamii. The lesions improved following treatment with amphotericin B. The immunodeficient state of this patient seemed to contribute to the infection with Prototheca.
Abscess↗
Purification and characterization of phospholipase A2 from rat stomach.
Phospholipase A2, which is localized in the mucosal part of the corpus of rat stomach (Hirohara et al. (1987) Biochim. Biophys. Acta 919, 231-238), was purified 990-fold from the supernatant of a tissue homogenate by heat treatment at acidic pH, ammonium sulfate fractionation, ion-exchange chromatography, gel-filtration and reverse-phase high-performance liquid chromatography (reverse-phase HPLC). The purified enzyme gave a single protein band on sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis with a molecular mass of approx. 17 kDa. The enzyme had a pH optimum of 8.0 and hydrolyzed the 2-arachidonoyl residue of phosphatidylcholine preferentially to the 2-oleoyl residue, the Vmax and Km values for the two being 227 and 29 mumol/min per mg protein and 0.037 and 0.019 mM, respectively. The activity was calcium-dependent and was markedly increased by SDS and dimethyl sulfoxide (DMSO). The enzyme showed typical product inhibition. Free unsaturated fatty acids (oleic, arachidonic and docosahexaenoic acids), which are supposedly the main enzymatic products in vivo, inhibited the activity. Arachidonic acid caused noncompetitive inhibition and its concentration for its maximal inhibition (50% inhibition) was 5 x 10(-5) M. Lysophosphatidylcholine, free saturated fatty acids (palmitic and stearic acids) and arachidonic acid metabolites (leukotrienes and prostaglandins) had no effect on the activity.
Ammonium Sulfate↗
Gastric hemodynamic disturbance induced by hemorrhagic shock in rats. Role of platelet-activating factor.
The role of platelet-activating factor (PAF) in the induction of rat gastric mucosal damage by ischemia-reperfusion was examined with reference to hemodynamic characteristics. Gastric mucosal hemodynamics was measured continuously, using laser-Doppler flowmetry and reflectance spectrophotometry. Not only gastric mucosal damage but also characteristic hemodynamic change--that is, ischemia with congestion--was observed in the PAF infusion and reperfusion periods of the ischemia-reperfusion model. CV-6209, a specific PAF antagonist, significantly alleviated gastric mucosal damage and hemodynamic disturbance induced by ischemia-reperfusion. These results strongly suggest that PAF is a potent mediator of gastric mucosal damage during reperfusion in the ischemia-reperfusion model.
Animals↗
Colchicine-induced inhibition of fat globule development in hepatocytes of rats injected with ethionine.
To examine the effect of colchicine on ethionine-induced fatty liver, adult female rats were starved overnight and then injected i.p. with 1 g/kg ethionine at 11th hour of fasting; then a half of the rats were also injected i.p. with 2.5 mg/kg colchicine twice at 3 and 6 h after the single administration of ethionine. Similarly, fasted control rats were injected i.p. with vehicle alone at the above times. All of the rats were sacrificed after a 20-h fast, and the hepatocytes in periportal areas were observed ultrastructurally. In addition, total lipids in the liver tissue were extracted and determined biochemically. Although similar significant increases of triglyceride were observed in the liver tissue of all ethionine-injected rats, the hepatocytes in the group treated with both chemicals had fewer cytoplasmic fat globules (CFG) than those in the group treated with ethionine only. On the other hand, the diameters of markedly increased membrane-bound lipid particles (MLP) in the double-treated group were distributed mainly in the range 0.2-0.4 micron, compared with those (0.1-0.2 micron) in the other groups. These findings indicate that colchicine inhibits the development of CFG in ethionine-injured hepatocytes.
Animals↗
Gastric mucosal damage induced in rats by intravenous administration of platelet-activating factor.
We examined the time courses for gastric mucosal hemodynamics and lipid peroxides after intravenous infusion of PAF (platelet-activating factor). The gastric mucosal hemodynamics were continuously monitored by laser-Doppler flowmetry and reflectance spectrophotometry during 20 min infusion of PAF and the subsequent 60 min. Gastric mucosal damage was assessed by microscopical scoring and measurement of thiobarbituric acid (TBA) reactants. Intravenous infusion of PAF caused macroscopical gastric mucosal damage, hemodynamic disturbance, a reduction in blood pressure and elevation of TBA reactants. These changes did not recover to control levels, even at 60 min after PAF infusion. The mucosal injury caused by the hemodynamic disturbance (congestion) was related to the elevation of TBA reactants, that reflect lipid peroxidation and oxygen-derived free radicals.
Animals↗
Properties and localization of phospholipase A2 activity in rat stomach.
In the glandular stomach of rat, phospholipase A2 activity was detected and characterized by the use of sonicated 1-acyl-2-[1-14C]oleoyl-sn-glycero-3-phosphocholine (1 mM in 200 mM glycylglycine buffer/2 mM CaCl2) as substrate. The specific activity was 4.9 X 10(-2) mumol/min per mg protein in the whole glandular stomach homogenate (n = 8). It showed individual variation among rats. The optimal pH was 8.0. The activity was relatively heat-resistant and calcium-dependent. More than 90% of phospholipase A2 activity was located in the corpus and less than 10% was in the antrum. In the corpus wall, which consists of mucosa, submucosa, muscularis externa and serosa, the mucosal part (mucosa and submucosa) contained 80-90% of total activity. The effect of some clinical agents (ulcerogenic and anti-ulcer agents) on the phospholipase A2 activity was examined. The activity in the corpus was inhibited by cimetidine (50% inhibition at 5 X 10(-3) M) and stimulated by indomethacin (50% stimulation at 5 X 10(-5) M). Cetraxate hydrochloride (10(-6)-10(-3) M), 16,16-dimethylprostaglandin E2 (10(-7)-10(-4) M) and dexamethasone (10(-7)-10(-3) M) had no effect.
Acyltransferases↗