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Biomedical subjects

H Koga

Publications and source records attributed to H Koga.

473 records · Page 27Linked to original sources
PubMedDate not supplied

Budd-Chiari syndrome complicated by hepatocellular carcinoma with no evidence of infection with hepatitis virus: a case report.

Hepatocellular carcinoma occurs in patients with Budd-Chiari syndrome. However, the etiology of hepatocellular carcinoma accompanied with Budd-Chiari syndrome has not been elucidated. We report a case of Budd-Chiari syndrome with membranous obstruction of the inferior vena cava complicated by hepatocellular carcinoma in an 80 year-old man. There was no evidence of co-infection with hepatitis A, B, C, D, E, and G virus. Histologically, the non-cancerous liver tissue showed chronic venous congestion with no evidence of hepatitis virus-associated liver cirrhosis. This case suggests that chronic venous congestion of the liver may be one of the pathologic conditions that occurs in hepatocellular carcinoma.

Aged↗
PubMedDate not supplied

Positive and negative oral contrast agents for combined abdominal and pelvic helical CT: first iodinated agent and second water.

Combined abdominal and pelvic helical computed tomography (CT) with intravenous contrast media was performed on 19 patients with 400 mL of diluted iodine solution 60 minutes before and 400 mL of water just before CT. The distal small bowel was opacified by the positive contrast agent, and the stomach by the negative contrast agent in all patients. The gastric contents were homogenous, and the density was a mean +/- standard deviation 2.5+/-7.3 HU. The difference between the densities of the gastric contents and of the gastric wall (mean +/- s.d. 80.8+/-20.9 HU) was statistically significant (p<.05). There were no pseudotumors. Thus our protocol, first diluted iodine solution and second water, can be used as a method for the oral administration of contrast agents for combined abdominal and pelvic helical CT with intravenous contrast media.

Administration, Oral↗
PubMedDate not supplied

Familial multiple system degeneration associated with iron deposition: determination of subcellular localization of elementary iron by energy-dispersive X-ray analysis.

We report an autopsy case characterized by iron deposition associated with multiple system degeneration. Although iron deposition was distributed as in Hallervorden Spatz syndrome, no spheroid was detectable. On the other hand, multiple system degeneration was observed mainly in the pallido-nigral and dentato-rubral systems which resembled pallido-nigro-luysian degeneration. However, the clinical course and manifestations, and the neuropathology of this case were not completely consistent with any previous report. Differential diagnosis and classification of the case are discussed, and the genetic diagnostic procedures are presented. We also investigated the subcellular localization of elemental iron in glial cells using energy-dispersive X-ray spectral analysis. A small amount of elementary iron was clearly demonstrated in some regions of membrane-bound electron-dense material presumably derived from lysosomes. Further accumulation of clinical and neuropathological data in such cases will provide some clues to discover the etiology and classification of multiple system degeneration that occurs in association with iron deposition.

Cytoplasm↗
PubMedDate not supplied

Biliary secretion of endotoxin and pathogenesis of primary biliary cirrhosis.

Previous studies suggested endotoxin, derived from the intestine through the portal blood to the liver, was predominantly metabolized by Kupffer cells. In the present study, fluorescent-labeled endotoxin injected into the rat portal vein was demonstrated not only in Kupffer cells but also in hepatocytes. Furthermore a great amount of labeled endotoxin was recovered in bile. In the livers of patients with primary biliary cirrhosis (PBC), immunohistochemistry demonstrated significant retention of endotoxin in the biliary epithelial cells, and treatment with ursodeoxycholic acid significantly reduced the retention in those cells. The study for detection of apoptosis demonstrated increased rates of apoptosis in hepatocytes and biliary epithelial cells in PBC liver, and the rate of apoptosis in biliary epithelial cells was significantly reduced after treatment with ursodeoxycholic acid. Immunohistochemistry in PBC liver demonstrated significant reduction of fluorescence intensity for a 7H6 antigen in biliary epithelial cells, indicating the increased paracellular permeability of bile ducts, because cellular immunolocalization of that antigen has been shown to be inversely correlated with the paracellular permeability of the tight junction. These results suggest that, in biliary epithelial cells, retention of endotoxin, increased apoptosis, and increased permeability of tight junctions may be involved in the pathogenesis of PBC.

Animals↗