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Biomedical subjects

Y Mizoguchi

Publications and source records attributed to Y Mizoguchi.

At least 307 records · Page 17Linked to original sources
PubMed1976

Immunological studies on drug-induced allergic hepatitis.

In many cases of drug-induced allergic hepatitis, peripheral lymphocytes were transformed by the stimulation with a given drug in the presence of autologous serum. However, when rat liver microsome fraction of soluble liver specific antigen fraction was added to the culture instead of autologous serum, the drug-induced lymphocyte transformation was more efficiently seen than autologus serum, while rat liver mitochondria fraction was less effective. On the other hand, in the cases of allergic drug eruption which did not show any liver injury, the addition of liver subcellular fractions were much less effective to induce the lymphocyte transformation than autologous serum. These results may suggest that liver subcellular component is involved in pathogenesis of drug-induced allergic hepatitis.

Adult↗
PubMed1975

Detection of hypersensitivity to drugs by lymphocyte cultures in drug-induced allergic hepatitis.

Fifty-three out of 70 patients with drug-induced liver injury showed an immunological response to the drug using either the lymphocyte transformation test or the macrophage migration inhibitory test (MI test) or both. Both the separated lymphocyte culture and the microvolume whole blood culture technique are available as assay methods. The latter method is simpler and the results of both methods are comparable. The administration of a synthetic copolymer of polyadenylic and polyuridylic acid (poly A:U) to the culture medium enhances the lymphocyte response to antigen and is therefore very useful to detect weak responses.

Adolescent↗
PubMed1975

Studies on the subpopulation and function of peripheral lymphocytes, and inhibitor to PHA stimulation existing in the serum of patients with liver disease.

In our recent report we observed the abnormal response to PHA stimulation in the peripheral lymphocytes of patients with chronic liver diseases. The present report concerns extensive studies of this earlier report; analysis of the subpopulation and function of peripheral lymphocytes in patients with liver diseases. PHA responsiveness in acute hepatitis was reduced in the acute phase and improved during the convalescent stage. In chronic liver disease, half of the patients showed a decrease in T-cell population as well as a reduced response to PHA stimulation. These phenomena were observed more frequently in HBs-antigen positive patients than in HBs-antigen negative cases. Furthermore, we found the existence of an inhibitor to PHA response in the serum of 8 cases among 19 patients with various liver diseases. In patients with such a serum inhibitor, the reactivity of the lymphocyte itself to PHA was considerably higher but the T-cell population was much more decreased than that of inhibitor negative cases.

Acute Disease↗
PubMedDate not supplied

The protective effects of prostaglandin E1 in an experimental massive hepatic cell necrosis model.

When a small amount of Gram-negative lipopolysaccharide was intravenously injected into mice which had been injected with heat-killed Propionibacterium acnes 7 days before, massive hepatic cell necrosis was induced and most of the mice died 24 hr later. However, when prostaglandin E1 was administered with lipopolysaccharide, remarkable improvements in the survival rate and in the histological changes of the liver were observed. In order to find out how prostaglandin E1 suppressed the induction of massive hepatic cell necrosis in this experimental model, we studied the effects of prostaglandin E1 on the activation of liver adherent cells, from which the cytotoxic factor is released, and on the protection of hepatocytes from the cytotoxic factor. As a result, prostaglandin E1 not only inhibited the activation of liver adherent cells and suppressed the release of the cytotoxic factor, but it also directly affected the hepatocytes and protected them from the cytotoxic factor.

Alprostadil↗
PubMedDate not supplied

Effects of arachidonic acid metabolites and interleukin-1 on platelet activating factor production by hepatic sinusoidal endothelial cells from mice.

The effects of interleukin-1 (IL-1) and arachidonic acid metabolites, prostaglandin (PG) E1, leukotriene (LT) B4 and LTC4, on the amount of platelet activating factor (PAF) produced and released by mouse hepatic sinusoidal endothelial cells were investigated. When hepatic sinusoidal endothelial cells were incubated with 1 microgram/mL of calcium ionophore (CaI) A23187, PAF production increased until 20 min after the start of incubation, but when the cells were incubated with PGE1 and CaI A23187, PAF production was significantly suppressed. On the other hand, when hepatic sinusoidal endothelial cells were incubated with IL-1 beta, LTB4 or LTC4 alone, PAF production significantly increased compared with that of the cells incubated without these substances. However, when the cells were incubated with PGE1 alone or with IL-1 beta, LTB4 or LTC4 and CaI A23187, these effects were not observed. These results indicated that PAF produced by hepatic sinusoidal endothelial cells is affected by IL-1 and arachidonic acid metabolites, suggesting that immune and inflammatory reactions in these cells may be regulated by chemical mediators produced by the cells themselves.

Alprostadil↗