PubMed Health⌕ Search

Biomedical subjects

Y Sakagami

Publications and source records attributed to Y Sakagami.

At least 109 records · Page 6Linked to original sources
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

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

Conversion of the alpha component of penicillin-binding protein 1b to the beta component in Escherichia coli.

Among components alpha, beta, and gamma of penicillin-binding protein 1b, the alpha and gamma components were confirmed to represent the primary gene products by agreement of their N-terminal amino acid sequences with those predicted from the nucleotide sequence of the ponB (penicillin-binding protein 1b) gene with exclusion of the first methionine in each component. The generation of beta occurred primarily after cell disruption, and the simultaneous loss of alpha suggested the conversion of alpha to beta. The N-terminal amino acid sequence analyzed for beta showed that the conversion was due to the removal of 24 amino acids from the N terminus of alpha.

Amino Acid Sequence↗
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↗
PubMed1987

Serological relationship among ten strains of avian infectious bronchitis virus.

Ten strains of avian infectious bronchitis virus (IBV) were studied serologically by cross-neutralization test using rabbit and chicken immune sera. With the chicken sera all 10 IBV strains were antigenically related. In particular, anti-KH serum neutralized all heterologous strains except of the Ishida strain; Nerima strain was neutralized by all antisera except of anti-Ishida serum. Most cross-reactions were less or more heterologous, thus all 10 IBV strains seemed to belong to one serological type. Using rabbit sera, all strains except of Connecticut A-5968, cross-reacted with certain other strains. Most cross-reactions were partially heterologous showing one-way-relationship; heterologous relations were observed less frequently than with chicken sera.

Animals↗
PubMed1987

Effects of interleukin 2 on estradiol binding capacity of peripheral blood mononuclear cells in asymptomatic HBV carriers.

Peripheral blood mononuclear cells from asymptomatic hepatitis B (HBV) carriers and healthy controls were incubated with or without recombinant interleukin 2 (r-lL2) at 37 degrees C for 24 hours. They were then incubated for another hour with 3H-estradiol and cold estradiol at 37 degrees C, and the estradiol binding capacity was estimated by measuring the radioactivity bound to these cells. As a result, when r-lL2 was not added, the estradiol binding capacity of the mononuclear cells in asymptomatic HBV carriers was lower than that in healthy controls. However, when r-lL2 was added, it increased to about the same level as that in healthy controls. This increase in the estradiol binding capacity of the mononuclear cells in asymptomatic HBV carriers may be due to the differentiation and proliferation of the cells induced by r-lL2.

Carrier State↗