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Biomedical subjects

H Fusamoto

Publications and source records attributed to H Fusamoto.

At least 181 records · Page 10Linked to original sources
PubMed1989

Cellular analysis of c-Ha-ras gene expression in rat liver after CCl4 administration.

Expression of the c-Ha-ras proto-oncogene is specifically enhanced during liver regeneration, in parallel with increased DNA replication, which suggests that c-Ha-ras may play a role in the control of regeneration. In this study, an in situ hybridization technique was applied for analysis of expression of the c-Ha-ras gene at the cellular level during liver regeneration induced by CCl4 administration. The in situ hybridization was compared with the observation for the p21c-Ha-ras protein, the corresponding protein of the c-Ha-ras gene, by immunohistochemistry. In normal rat liver, a few hepatocytes expressed the mRNAs and the corresponding proteins without any preferential localization. Zonal heterogeneity of c-Ha-ras gene expression first became evident at 12 hr after CCl4 administration, a higher number of gene products being detected in the pericentral zone than in the periportal zone. This heterogeneity became maximal at 24 hr after CCl4 administration. Zonal heterogeneity in the level of the p21c-Ha-ras protein paralleled that in the level of gene expression. Furthermore, both hepatocytes and nonparenchymal cells participated in expression of the c-Ha-ras gene during liver regeneration.

Animals↗
PubMed1989

Detection of hepatitis B virus X gene protein and antibody in type B chronic liver disease.

The genome of the hepatitis B virus contains a sequence (X gene) whose role is unclear. The almost complete region of the hepatitis B virus X gene was expressed in Escherichia coli, with the resulting protein being approximately 17 kilodaltons in molecular weight. Sera from 139 subjects were analyzed by Western blot analysis. Of the hepatitis B surface antigen-positive patients, anti-X was not found in 4 patients with acute hepatitis and in 12 healthy carriers, but was present in 41% (21/51) of the patients with chronic hepatitis, 63% (15/24) of those with liver cirrhosis, and 46% (12/26) of those with hepatocellular carcinoma. The expression of the X product in the liver tissues (43 hepatitis B surface antigen-positive patients) was investigated using an indirect immunohistochemical method. The X protein was observed in 64% (21/33) of the patients with chronic hepatitis and 50% (5/10) of those with liver cirrhosis, and was found when the serum was negative for anti-X. Hepatitis B core antigen was frequently expressed together with the X protein in the liver. The conclusions reached were that the frequency of anti-X increases with the length of chronic hepatitis B virus infection, that anti-X may suppress the expression of the X protein in the liver, and that the X protein may be related to hepatitis B virus replication.

Blotting, Western↗
PubMed1989

[Expression of Pre-S2 antigen and antibody in patients with hepatitis B virus infection].

We investigated the expression of Pre-S2 antigen (Ag) and antibody (Ab) in sera quantitatively using ELISA. Four patients with acute hepatitis B and 87 chronic HBV carriers were included in this study. We also investigated the expression of Pre-S2Ag in the liver tissues obtained from 26 chronic HBV carriers by direct fluorescent antibody method. There was a significant correlation between Pre-S2Ag titers and HBsAg titers in sera. Pre-S2Ag titers were higher in sera positive for HBeAg, HBV-related DNA polymerase or HBV-DNA than in sera negative for those markers. The ratio of Pre-S2Ag titers to HBsAg titers, however, was constant irrespective of virus replicative markers. Pre-S2Ag in the liver had almost same intracellular localization with HBsAg in the liver. It was suggested that Pre-S2Ag was expressed with an intimate relation to the expression of HBsAg and was not useful as a virus replicative marker. Pre-S2Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels compared to patients with chronic inactive hepatitis. This may be explained by the release of Pre-S2Ag in the liver. In addition, all patients positive for Pre-S2Ag on the membrane of hepatocytes had chronic active hepatitis. The overproduction of Pre-S2-containing surface proteins in the liver may have some implication related to cell injury via the immune response to Pre-S2Ag etc. Pre-S2Ab was detected only in few cases of chronic HBV infected patients. The lack of immune response to Pre-S2 region may play a role in the persistence of HBV infection.

Enzyme-Linked Immunosorbent Assay↗
PubMed1989

[Expression of pre-S1 antigen and pre-S1 antibody in sera obtained from HBV infected patients].

We investigated the expression of Pre-S1 antigen and Pre-S1 antibody using a synthetic peptide and the monoclonal antibody against it. Four patients with acute hepatitis B and 87 chronic HBsAg carriers were included in this study. There was a significant correlation between Pre-S1 antigen titers and HBsAg titers. Pre-S1 antigen showed higher titers in patients with active viral replication, positive for HBeAg, HBV-DNA or HBV-related DNA polymerase. The ratio of Pre-S1 antigen titers to HBsAg titers, however, had no significant relationship with those replicative markers. It was suggested that Pre-S1 antigen was expressed with an intimate relation to the expression of HBsAg and was not so useful as a new replicative marker. Pre-S1Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels. This may be due to the release of overproduced intracellular Pre-S1 antigen. Pre-S1 antibody was detected only in few cases of chronic HBsAg carriers. This result shows that the immune tolerance to Pre-S1 region may play a role in the persistence of HBV infection.

Carrier State↗
PubMed1988

Hepatic circulation and hepatic oxygen consumption in alcoholic and nonalcoholic fatty liver.

The purpose of this study was to determine the differences in hepatic circulation and oxygen consumption in two groups: those with nonalcoholic obesity-related fatty live and those with alcoholic fatty liver. Although the histological degree of fatty infiltration was equal in the two groups, the delta Er569-650, as an index of the regional liver blood flow estimated by spectrophotometric method, was significantly lower in alcoholic fatty liver than in nonalcoholic fatty liver, and the in vivo hepatic oxygen consumption (VO2), also determined by hepatic reflectance spectrophotometry during peritoneoscopy, tended to be lower in alcoholic fatty liver than in nonalcoholic fatty liver. The oxygen saturation of hemoglobin in local liver blood (SO2) was, however, significantly higher in alcoholic fatty liver than in nonalcoholic fatty liver. These results suggest that an increase in oxygen extraction to maintain oxygen consumption, which was indicated by the lowering of the SO2, was not found in alcoholic fatty liver, in spite of a reduction of oxygen supply to the liver. It is concluded that the impairment of hepatic circulation and hepatic oxygen consumption was more serious in alcoholic fatty liver than in nonalcoholic fatty liver, possibly contributing to a different prognosis for the two forms of fatty liver.

Fatty Liver, Alcoholic↗
PubMed1985

Influence of ranitidine on hepatic blood flow assessed by organ-reflectance spectrophotometer and pulse-Doppler ultrasonic flowmeter.

The influence of the intravenous injection of ranitidine (50 mg) on hepatic hemodynamics was investigated in normal subjects and patients with chronic liver disease. Using the organ-reflectance spectrophotometer, the regional hepatic blood hemoglobin concentration (delta Er569-650), an indicator of the regional hepatic blood flow, and the oxygen saturation of hemoglobin in the regional hepatic tissue (So2) were measured in patients with chronic liver disease after ranitidine injection under peritoneoscopy. With the pulse-Doppler ultrasonic flowmeter, the portal blood flow was measured in patients with chronic liver disease and normal subjects. There were no significant changes in the regional hepatic blood flow, the oxygen saturation of hemoglobin, and the portal blood flow after the intravenous injection of ranitidine. Thus, it is concluded that usual dose of ranitidine has no significant influence on the hepatic blood flow and that it can be prescribed without reducing the hepatic blood flow.

Adult↗
PubMed1985

Oxygen supply to the liver in patients with alcoholic liver disease assessed by organ-reflectance spectrophotometry.

In the present study we have investigated hepatic hemodynamics in patients with alcoholic liver disease using reflectance spectrophotometry and the hydrogen clearance method. Analysis of 38 cases has shown that estimated regional hepatic-tissue hemoglobin concentration, expressed as a difference in absorbance between 569 and 650 nm (delta Er569-650), decreased significantly with progress of fibrosis or fat accumulation in the liver. This suggests that the relative compression of the vascular compartment is due to the progress of alcoholic liver disease. Estimated hepatic hemoglobin concentration also correlated positively with prothrombin time, and negatively with serum gamma-globulin level and 15-min retention rate of indocyanine green. The difference in absorbance between 569 and 650 nm obtained by reflectance spectrophotometry was positively correlated with the regional hepatic blood flow as measured by the hydrogen clearance method. Thus, it is concluded that the estimated regional hepatic-tissue hemoglobin concentration decreases with progress of fibrosis and fat accumulation in the liver, and that this decreased oxygen supply to the liver may have an important role in the progress of alcoholic liver disease.

Absorption↗