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Biomedical subjects

Y Shimada

Publications and source records attributed to Y Shimada.

At least 775 records · Page 43Linked to original sources
PubMed1982

Differences in urinary monochlorobenzene metabolites between rats and humans.

Differences in urinary excretion of monochlorobenzene between rats and humans were studied. Monochlorobenzene was administered to rats and humans intraperitoneally, orally or by inhalation. Urinary p-chlorophenylmercapturic acid and 4-chlorocatechol, after hydrolysis of its conjugate, were measured. The excretion of p-chlorophenylmercapturic acid was somewhat more than that of 4-chlorocatechol in rats which were administered monochlorobenzene orally or intraperitoneally. The excretion of p-chlorophenylmercapturic acid was markedly less than that of 4-chlorocatechol in humans who received monochlorobenzene orally or by inhalation. The results indicate that the 4-chlorocatechol conjugate is a suitable index of metabolites in the urine of workers exposed to monochlorobenzene.

Animals↗
PubMed1982

Increased excretion of urinary cyclic GMP in primary hepatoma and preneoplastic liver.

Urinary excretion of cyclic GMP (cGMP) and the plasma level of cyclic AMP (cAMP) were determined in patients with liver diseases. The urinary excretion of cGMP, expressed on the basis of creatinine excreted per day, was at significantly higher levels not only in primary hepatoma but also in liver cirrhosis, while the plasma level of cAMP was higher only in liver cirrhosis. Thus, the ratio of urinary cGMP excretion to plasma cAMP level in primary hepatoma was significantly higher than that in liver cirrhosis. In cirrhotic patients studied by catheterization, the level of cGMP in the hepatic vein was significantly lower than that in the superior mesenteric or portal vein, indicating the uptake of cGMP by the liver. Since cGMP excretion correlated with KICG both in liver cirrhosis and primary hepatoma, the increased cGMP excretion appeared to be explained by a reduced uptake of cGMP by the liver.

Adolescent↗
PubMed1982

[Treatment of unresectable liver cancer with intrahepatic arterial infusion chemotherapy].

Intra-arterial infusion chemotherapy was performed in 50 patients with cancer of the liver including 12 primary hepatoma and 38 metastatic cancers, at Kurashiki Central Hospital from December 1977 through December 1981. B.D. Fomocath 5 French catheter was inserted through the lateral femoral circumflex artery and advanced retrogradely to the common hepatic or proper hepatic artery using a loop catheter technique and the catheter was connected to the tube of infusion pump. The dose of 5-Fluorouracil and Mitomycin C was 250 mg per day and 4-10 mg once a week, respectively. The patients had average survival of 8.2 months in hepatoma and 4.8 months in metastatic tumor. The results were unfortunately not encouraging but this regimen occasionally provides excellent results and has no contraindication.

Adult↗
PubMed1981

Fluorescent staining of neuromuscular junctions by using the antibody against acetylcholine receptors of Narke japonica, and double staining with the antibody and erabutoxin b.

The neuromuscular junctions of various vertebrates were visualized by indirect immunofluorescence microscopy using antibody against purified acetylcholine receptors (AChRs) of the electric organ from Narke japonica. Further, by using rhodamine-labeled erabutoxin b (TMR-Eb), we showed that AChRs at the neuromuscular junctions of frog, chick and mouse muscle could not be doubly stained with the antibody and erabutoxin b. AChRs of snake muscle could not be stained with TMR-Eb, while they were stained with the antibody against AChR. Moreover, the antibody did not inhibit the binding of 3H-labeled erabutoxin b to the solubilized AChRs from the mouse muscle. These results indicate that, as far as the antibodies against Narke AChRs are concerned, most antibody-binding sites in the molecules of muscle AChR in situ are different from those responsible for binding of the snake neurotoxin.

Acetylcholine↗
PubMed1981

Kupffer cell hyperplasia in liver diseases. Demonstration by scanning electron microscopy of biopsy samples.

Kupffer cells were observed in liver biopsy tissues of 9 cases of liver diseases by scanning electron microscopy to prove Kupffer cell proliferation numerically. Kupffer cell count per 0.01 mm2 of cracked surface of liver lobule was 1.2 +/- 0.3 in the convalescent stage of a mild acute hepatitis case and 1.2 +/- 0.1 in a chronic persistent hepatitis case with slight inflammation. Whereas it was increased to 2.4-5.5 (P less than 0.01) in the convalescent stage of moderate to severe acute hepatitis cases, 1.8 +/- 0.1 (p less than 0.05) in a chronic active hepatitis case, 2.5 +/- 0.3 (p less than 0.001) in an alcoholic portal fibrosis case and 2.2 +/- 0.4 (p less than 0.001) in a liver cirrhosis case. Kupffer cell count per mm3 of liver lobule was estimated roughly 3,500 in the convalescent stage of a mild acute hepatitis case and in a mild chronic persistent hepatitis case and 7,000 to 16,000 in the convalescent stage of moderate to severe acute hepatitis cases.

Acute Disease↗