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Biomedical subjects

Y Sakagami

Publications and source records attributed to Y Sakagami.

At least 163 records · Page 9Linked to original sources
PubMed1983

Modulation of cholestatic factor production by serum components.

When lymph node cells from sensitized guinea pigs were stimulated in vitro with a specific antigen and their culture supernatant was injected into the mesenteric vein of rats, a marked decrease in bile flow was demonstrated. The treatment of activated lymphocytes with a higher molecular weight fraction of normal human serum Fr-1 and Fr-2 was shown to decrease the reduction of bile flow. Conversely, a lower molecular weight fraction of serum (Fr-3) was found to augment the reduction of bile flow. These findings suggest that the serum components may regulate the production of a factor (or factors) causing the decrease in bile flow from the activated lymphocytes.

Animals↗
PubMed1982

Participation of the cholestatic factor in the pathogenesis of intrahepatic cholestasis, found in various liver diseases.

The possible involvement of lymphokine, cholestatic factor, in the pathogenesis of intrahepatic cholestasis was investigated in nine patients with different types of liver diseases; two cases with acute viral hepatitis (nonA and nonB type), five patients with alcoholic hepatitis and two cases with liver cirrhosis. All patients showed the typical clinical features of intrahepatic cholestasis. The production of the cholestatic factor from the sensitized lymphocytes was demonstrated by antigenic stimulation in vitro and the existence of the factor was detected in seven out of nine patients in patients' own serum. These results strongly suggest that the cholestatic factor may be partially involved in the induction of intrahepatic cholestasis in various types of liver disease.

Acute Disease↗
PubMed1981

Accelerated mammary cancer development by fetal salivary mesenchyma isografted to adult mouse mammary epithelium.

Transplantation of fetal salivary mesenchyma into adult mammary glands resulted in atypical outgrowths from the mammary duct system. These duct-alveolus nodules (DAN) were distinguishable from hyperplastic alveolar nodules (HAN) that arose from normal mammary duct systems in mice infected with murine mammary tumor virus (MuMTV). DAN displayed a type of ductal branching characteristic of salivary gland rather than of mammary gland, reflecting a tissue-specific perturbation of epithelium-mesenchyma in DAN in milk-transmitted MuMTV-infected C3H/HeN mice and in MuMTV-negative BALB/c mice given 7,12-dimethylbenz[a]anthracene (DMBA) subsequent to transplantation of fetal salivary mesenchyma. Mammary cancers were not increased in milk-transmitted MuMTV-free C3H/HeN and GRS/A mice that received salivary mesenchyma transplants. Salivary mesenchyma accelerated mammary carcinogenesis by increasing the mammary epithelial cell population responsive to MuMTV and DMBA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Earlier appearance of murine mammary tumor virus-associated antigens in duct-alveolus nodules induced by transplantation of fetal salivary mesenchyme into C3H mouse mammary glands.

Mammary epithelium of adult C3H mice in contact with fetal salivary mesenchyme took morphogenetically a salivary gland-like pattern of growth and developed a hyperplastic nodular mass at the site of transplantation. When murine mammary tumor virus-bearing C3H mice were treated in this way, early development and high incidence of mammary cancer were observed from these nodules compared to unstimulated mammary glands of the same host. Since tumor development, the viral antigens in these hyperplastic nodules were examined by means of the immunofluorescence technique. As early as 2 weeks after mesenchyme transplantation, the antigens were observed in the ductular or alveolar structure of these nodules, while surrounding normal tissues were not stained. Positive fluorescence was also observed in the mammary tumors that developed from these stimulated nodules. These results strongly suggested the involvement of murine mammary tumor virus in the early development of mammary cancer induced by fetal mesenchyme transplantation.

Animals↗