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Y Tokusashi

Publications and source records attributed to Y Tokusashi.

24 records · Page 2Linked to original sources
PubMed1996

Intrahepatic transplantation of normal hepatocytes prevents Wilson's disease in Long-Evans cinnamon rats.

BACKGROUND & AIMS: Long-Evans cinnamon (LEC) rats are an animal model of Wilson's disease. This study investigated whether intrahepatic transplantation of normal hepatocytes can prevent Wilson's disease in LEC rats. METHODS: Hepatocytes of newborn Long-Evans agouti (LEA) rats were transplanted into the livers of LEC rats before onset of hepatic disease. Expression of normal transcripts from the gene linked to Wilson's disease was investigated at 30 weeks of age by reverse-transcription polymerase chain reaction and in situ hybridization. RESULTS: Eight of 16 (50.0%) untreated LEC rats died of hepatic failure during 20-30 weeks of age. Of the 27 LEC rats with transplanted cells, 2 (7.4%) died of hepatic failure and 4 died of ileus complicated by the surgical treatment. In the recipient livers, the transplanted cells comprised 4%-20% of the hepatocyte populations, expressing normal messenger RNA transcribed from the Wilson's disease gene, and hepatic copper deposition was reduced to approximately 60% of that in untreated LEC rats. CONCLUSIONS: Transplantation of normal hepatocytes prevents Wilson's disease in LEC rats.

Animals↗
PubMed1996

Absence of p53 mutations in methylnitrosourea-induced mammary tumors in rats.

Administration of methylnitrosourea (MNU) to female rats during or before puberty induces a high incidence of mammary tumors, most of which contain a G to A transition at the second base of H-ras codon 12. However, this mutation alone is presumably not sufficient for normal mammary epithelial cells to develop into neoplastic cells, because it can be detected in mammary tissues prior to the appearance of tumors. To clarify whether p53 genetic changes may complement the H-ras mutation in mammary carcinogenesis, we investigated nine MNU-induced mammary tumors of F344 rats by polymerase chain reaction-mediated denaturing gradient gel electrophoresis (DGGE). However, no mutations were identified in p53 exons 5 through 8, which include the known mutational hot spots. Our data thus indicate that p53 mutations are not involved in MNU-induced rat mammary carcinogenesis.

Animals↗
PubMed1994

Absence of p53 mutations and various frequencies of Ki-ras exon 1 mutations in rat hepatic tumors induced by different carcinogens.

Mutations of p53 and Ki-ras exon 1 were investigated in rat hepatic lesions induced by four kinds of hepatocarcinogenic protocols: continuous feeding of 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), daily intraperitoneal injection of aflatoxin B1 (AFB1), and the Solt and Farber regimen (Nature 236:701-703, 1976), in which diethylnitrosamine (DEN) or nitrosomethylurea (NMU) was used as initiating agents. DNA from microdissected tissue sections was amplified by the polymerase chain reaction (PCR) directly using primers for p53 exons 5-8 and Ki-ras exon 1 and analyzed for mutations by denaturing gradient gel electrophoresis (DGGE) or constant denaturant gel electrophoresis (CDGE). One or both of the p53 PCR primers were located within introns to prevent amplifying the p53 processed pseudogenes. In a total of 59 hepatocellular carcinomas (HCCs), no p53 aberrations were detected, indicating that p53 mutations are not very important in rat hepatic carcinogenesis. On the other hand, Ki-ras codon 12 mutations were found at low frequency in HCCs, hyperplastic foci, and cholangiofibroses induced by 3'-Me-DAB and by AFB1 but not in the lesions induced by the Solt and Farber regimen. Although Ki-ras codon 12 mutations are generally infrequent in rat hepatic tumors, their incidence thus appears to vary depending on the carcinogen used for their induction.

Animals↗
PubMed1994

A case of apocrine adenocarcinoma associated with hamartomatous apocrine gland hyperplasia of both axillae.

We report an apocrine adenocarcinoma of the left axilla associated with hamartomatous apocrine gland hyperplasia of both axillae. The patient, a 69-year-old man, presented with no symptoms or complaints other than an oval mass felt in the left axilla. The mass was resected and histopathological examination revealed a papillary apocrine adenocarcinoma located within hyperplastic apocrine glands. Because gallium scintigraphy performed after the operation still showed bilateral abnormal uptakes, skin and subcutaneous tissues of the bilateral axillary areas were resected. Histological examination demonstrated marked multilobular hyperplasia of the apocrine glands. These hyperplastic glands did not show distinct atypia, and there was no evidence of tumor remnants in the left axilla. The patient has shown no signs of local recurrence or metastasis at 20 months' follow-up. To our knowledge, this is the first case of malignant transformation of hamartomatous apocrine gland hyperplasia (apocrine gland organic hamartoma or apocrine nevus).

Adenocarcinoma↗
PubMed1994

[Apolipoprotein E immunoreactivity in normal and abnormal adrenal tissues].

Immunohistochemical study on localization of apo E in normal and abnormal adrenal tissues was performed using polyclonal anti-human apo E antibodies. In normal adrenal glands, the cortex showed intense staining, in particular, in the zona fasciculata and the zona reticularis, while the medulla showed weak staining. In a case of adrenal hyperplasia, apo E immunoreactivity was equivalent to that in the normal cortex. In adenomas (primary aldosteronism, n = 7; Cushing's syndrome, n = 2; others, n = 2), apo E was stained normally or to some extent weakly in comparison with the normal cortex. Adrenocortical carcinoma showed only faint staining. The results indicate that apo E may relate to the functional activity of adrenal cortex, and suggest that immunohistochemical study for apo E may help to distinguish the malignancy from benign adrenal neoplasms.

Adenocarcinoma↗