[Changes of granulocytes during the recovery period of agranulocytosis, and in vitro CFU assay for the determination of causative drugs].
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Biomedical subjects
Publications and source records attributed to K Kawada.
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Male Sprague-Dawley rats were fed a cube diet containing 2.51 mmol/kg of 3'-methyl-4-(dimethylamino)azobenzene (3'-Me-DAB), 3'-CH2OH-DAB, 3'-CHO-DAB, or 3'-COOH-DAB (at a level equivalent to 0.06% 3'-Me-DAB in the diet) for a period of 1 to 3 months. Almost all the livers of rats given 3'-CH2OH-DAB for a period of 2 to 3 months or 3'-Me-DAB for 3 months showed marked cirrhosis macroscopically. The common histological findings were cholangiofibrosis with or without markedly atypical bile ducts. Moreover, one hepatocellular carcinoma was found in the liver of a rat given 3'-Me-DAB and one in the liver of a rat given 3'-CH2OH-DAB for 3 months. On the other hand, 3'CHO-DAB and 3'-COOH-DAB did not induce these changes (including neoplastic nodules) at all. Consequently, 3'-CH2OH-DAB, like 3'-Me-DAB, was found to be a hepatocarcinogen.
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Male Sprague-Dawley rats were fed a cube diet containing 2.51 mmol/kg 3'-hydroxymethyl-N,N-dimethyl-4-aminoazobenzene (3'-CH2OH-DAB) for a period of 1 or 3 months. (This is the molar equivalent of 0.06% 3'-Me-DAB in the diet). The oral administration of 3'-CH2OH-DAB for 3 months resulted in a high incidence of liver tumors at 6 months and the 1 month feeding also caused the development of liver tumors. Histologically, the tumors were cholangiocellular carcinomas and hepatocellular carcinomas. The development of tumors in other sites was not seen. Consequently, 3'-CH2OH-DAB, a recently identified metabolite of 3'-Me-DAB, is a potent hepatocarcinogen.
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Concentrations of a peroxidation product (malondialdehyde), fluorescent chromophores, lipofuscin-like fluorescent products, superoxide dismutase, catalase, glutathione peroxidase, and vitamin E in the maternal blood and the cord blood were determined and the results obtained were related to the estimation of lipid peroxidation and protective mechanism against uncontrolled oxidative processes in late pregnancy. Serum levels of fluorescent products were higher in the maternal blood than in the cord blood, indicating less frequent lipid peroxidation in the fetus than in the mother. In support of this assumption, the three protective enzymes and vitamin E were present in relatively lower concentrations in the cord blood. Sudden exposure of the newborn infant to a normobaric atmosphere after beginning breathing seems, therefore, to cause oxidation of red blood cell membrane, denaturation of the membrane, inducing hemoglobin breakdown, and consequently hemolysis.
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An infected graft and a mycotic pseudoaneurysm were successfully resected by employing an ascending aortasupraceliac abdominal aorta bypass graft in a 19-year-old man. He had formerly undergone graft replacement surgery for traumatic aneurysm of the descending thoracic aorta, with the aid of a temporary external bypass graft. After this first operation, the patient had suffered from septicemia due to Psudomonas aeruginosa, which resulted in formation of mycotic pseudoaneurysms at the distal anastomotic site of the prosthetic graft and at both stumps of the formerly employed external bypass graft.
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