|Budget Amount *help
¥2,700,000 (Direct Cost : ¥2,700,000)
Fiscal Year 2001 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 2000 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1999 : ¥600,000 (Direct Cost : ¥600,000)
Fiscal Year 1998 : ¥700,000 (Direct Cost : ¥700,000)
The investigation was performed following last year.
The rat was administrated intraperitoneally thioacetoamide 200mg/kg three times a week for 5 weeks to get chronic liver damage. Postoperative liver failure model was made by additional 84% hepatectomy to these chronically damaged rats Sham operation group was set as control.
[MAP kinase activity] MAP kinase assay of the remnant liver was done in the same manner of Day et al, MAP kinase activity was seemed to be up in the hepatic failure model, however, no significant difference was seen compared with the control group. We judged that no appropriatensess was recognized in further investigation to examine the failure of lower stream of the signal transmission, because of the result that no tendency was seen in the level of MAP kinase of the hepatic failure rats.
[Failure of signal transmission through ho] Another investigation was tried to evaluate existence of failure of lower transmission through ho that affect cell mobility. However, this result was not significant as same as that of MAP kinase in the hepatic failure rats. [Histological examination of the remnant liver] The hepatectomized rats were sacrificed and these remnant liver were examined microscopically. Control group was set as no liver damage rats with 84% hepatectomy. Mitotic index after 48hr. of hepatectomy had no significant difference compared with that of control group. Therefore, rats in hepatic failure after hepatectomy might not have had significantly depressed liver regeneration. In addition to above, the previous results were evaluated and analyzed.