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Biomedical subjects

Y Mizoguchi

Publications and source records attributed to Y Mizoguchi.

At least 163 records · Page 9Linked to original sources
PubMed1988

[Autotransplantation of nipple-areolar complex in a modified radical mastectomy--indications and three-stage breast reconstruction].

Necessity of breast reconstruction after mastectomy has been increasing in recent years. For better reconstruction, we preserve a nipple-areolar complex (NAC) by transplanting it temporarily onto the lower abdominal wall and retransplant it to the restored breast mound in a subsequent operation. Indications for NAC preservation are as follows: (1) by palpation the tumor is found to be smaller than 3.0cm in diameter without apparent regional and distant metastasis, (2) neither abnormal nipple discharge nor nipple retraction is observed, (3) tumor is remote more than 3.0cm from the areolar margin, (4) no abnormal shadows are seen below the nipple and areola in the mammogram, (5) no microscopic extension of the cancerous cells is detected beneath the resected NAC. We have performed 18 transplantations using this procedure with good cosmetic results. There were no recurrent cases due to NAC preservation. It is concluded that this technique for preserving the NAC by autotransplantation is easy to perform and useful for breast reconstruction because of low risk of recurrence and better cosmetic results.

Adult↗
PubMed1987

Protection of liver cells against experimental damage by extract of cultured Lentinus edodes mycelia (LEM).

Liver cell damage can be induced when isolated liver cells coated with specific antibodies against the liver cell membrane are cultured with peripheral blood mononuclear cells. Although this antibody-dependent cell-mediated cytotoxicity (ADCC) is dependent on the close contact of effector cells with target cells via specific antibodies, a cytotoxic factor or factors causing the inhibition of protein synthesis in liver cells has been detected in the culture supernatant from the ADCC reaction. Similarly, peritoneal exudate macrophages activated by endotoxin lipopolysaccharide also exert cytotoxic effects on isolated liver cells by production of a cytotoxic substance or substances. The liver cell damage caused by either the ADCC or activated macrophage culture supernatants were significantly reduced by pretreating the isolated liver cells with the extract of cultured Lentinus edodes mycelia (LEM). These results suggest that LEM may protect liver cells from immunological damage.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1987

Detection of the cholestatic factor in the liver tissue of patients with acute intrahepatic cholestasis.

A novel lymphokine, which we have designated as cholestatic factor (CF), was produced from peripheral blood lymphocytes of patients with drug-induced allergic intrahepatic cholestasis by stimulation with a causative drug in the presence of the liver soluble fraction containing liver-specific lipoprotein (LSP). Marked reductions in bile flow and bile acid excretion were induced in rats by injecting CF through a mesenteric vein. In order to confirm the presence of CF in the liver tissue of patients, we attempted to detect this lymphokine by using the enzyme-labelled antibody method. As a result, CF was found in the liver tissue of eleven out of thirty-eight patients with acute intrahepatic cholestasis including one with hepatitis A type, one with hepatitis B type, two with hepatitis non-A non-B type, five with drug-induced allergic hepatitis, one with alcoholic hepatitis and one with lupoid hepatitis. In contrast, CF was undetectable in the liver tissue of patients without intrahepatic cholestasis. These results may additionally support our assumption that CF plays an important role in the induction of intrahepatic cholestasis in various liver diseases.

Acute Disease↗
PubMed1987

Effects of extract of cultured Lentinus edodes mycelia (LEM) on polyclonal antibody response induced by pokeweed mitogen.

When polyclonal antibody response induced by pokeweed mitogen (PWM) was estimated by measuring antibody-forming cells produced against trinitrophenylated sheep red blood cells (TNP-SRBC) using hemolytic plaque assay, it was found to be augmented by the extract of cultured Lentinus edodes mycelia (LEM). Since some factor enhancing antibody response was detected in the culture supernatant of LEM-treated macrophages, this was fractionated by gel filtration, which revealed a substance with a molecular weight of about 15,000 daltons. This suggested that interleukin-1 (IL-1) was produced, and that it had caused, at least partially, the enhancement of antibody response. This possibility was confirmed by the direct assay of IL-1 activity, which demonstrated increased DNA synthesis in PHA-stimulated thymocytes.

Animals↗
PubMed1987

The protective effect of cyclosporin A on experimentally-induced acute hepatic injury in mice.

When heat-killed Propionibacterium acnes (P. acnes) and a small amount of endotoxin lipopolysaccharide (LPS) were intravenously injected into mice at a week's interval, most of them died of massive hepatic cell necrosis. This experimentally-induced acute liver injury was significantly inhibited by cyclosporin A (CsA), resulting in a remarkable improvement of the survival rate. This protective effect of CsA on acute liver injury was also histopathologically confirmed. To study the mechanism by which CsA protected the mice from fatal hepatic injury, adherent cells prepared from the murine liver 7 days after P. acnes injection were incubated with LPS in the presence of CsA, and the effect of CsA on the production of the cytotoxic factor from the adherent cells was estimated. As a result, CsA inhibited the activation of liver adherent cells and suppressed the release of the cytotoxic factor.

Animals↗
PubMed1987

Inhibitory effect of TJN-101 ((+)-(6S,7S,R-biar)-5,6,7,8-tetrahydro-1,2,3,12-tetramethoxy -6,7-dimethyl-10,11- methylenedioxy-6-dibenzo[a,c]cyclooctenol) on immunologically induced liver injuries.

TJN-101, which is a lignan component isolated from schisandra fruits, inhibits hepatotoxic chemicals-induced liver injuries. In this study, effects of TJN-101 on immunologically induced liver injuries were investigated in vivo and in vitro. When a small dose of lipopolysaccharide was injected into mice previously injected with heat-killed Propionibacterium acnes, most of the animals died with acute hepatic failure which was produced by cytotoxic factors from activated adherent cells, and liver cells were injured by antibody-dependent cell-mediated cytotoxic (ADCC) reaction or activated macrophages in vitro. TJN-101 reduced the mortality of the mice with acute hepatic failure dose-dependently. Histologically, necrosis was suppressed by the treatment of TJN-101, but infiltration of non-specific inflammatory cells was not. TJN-101 inhibited the isolated liver cell injuries induced by ADCC reaction or activated macrophages in vitro. These results suggest that TJN-101 can be markedly protective against immunological liver injuries.

Alanine Transaminase↗