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M C Yoshida

Publications and source records attributed to M C Yoshida.

At least 109 records · Page 6Linked to original sources

The banding patterns of normal canine chromosomes.

The chromosomal banding patterns of canine normal chromosome were analyzed by G-, Q-, C- and N-banding techniques. The chromosomes of canine normal lymphocytes consisted of 38 acrocentric autosome pairs and X-, Y-metacentric sex chromosomes. Their G- and Q-banding patterns corresponded to the those reported by Manolache et al. in 1976. C-bands of chromosomes were found on the centromeric regions of the 7th, 26th, 34th, 35th, 37th and 38th pairs of chromosomes. In addition, N-bands whose location had not been confirmed until now were recognized on the telomitic regions of the 7th, 9th and 22nd pairs of chromosomes.

Animals↗

Isolation and characterization of new mammalian kinase genes by cross hybridization with a tyrosine kinase probe.

We isolated two novel mammalian kinase genes by weak cross-hybridization with v-ros oncogene. (1) A cDNA of about 7.7 kb obtained from a human placenta cDNA library carried a 4.2 kb open reading frame, and the predicted amino acid sequence of 1338 residues contained extracellular, transmembrane and tyrosine kinase domains. The overall structure including cysteine motifs in its extracellular domain and a long peptide insertion in its tyrosine kinase domain indicates that this new gene is closely related to the fms family. Consequently, the gene was designated as flt(fms-like tyrosine kinase) gene. The expression of the flt gene was examined in normal and transformed cells, and it was mapped to human chromosome 13q12-13. (2) Another new gene was found to be expressed almost exclusively in testis. The cDNA sequence analysis revealed that the predicted product carried protein kinase consensus motifs in its amino-terminal region. Comparison of the deduced amino acid sequence of this gene in the kinase domain with those of other protein kinase genes will be discussed.

Amino Acid Sequence↗

Human M2-type pyruvate kinase: cDNA cloning, chromosomal assignment and expression in hepatoma.

Two overlapping clones, covering the entire coding sequence of human M2-type pyruvate kinase (PK) cDNA, were isolated and sequenced. Nucleotide sequencing results showed that they contained the 109-bp 5'-untranslated region, the 1593-bp coding region and the 585-bp 3'-untranslated region. Nucleotide sequence homology was 90% and 69% with rat M2-type and L-type PK cDNA, respectively. In situ hybridization using the human M2-type PK cDNA probe disclosed that the gene for M2-type PK is located at band q22 on chromosome 15. Northern blot analysis with RNA from human hepatoma demonstrated that M2-type PK was predominantly expressed in hepatoma cells, whereas L-type PK was preferentially expressed in the non-tumor portion of the liver.

Amino Acid Sequence↗

Gene for parathyroid hormone-like peptide is on rat chromosome 2.

Parathyroid hormone-like peptide (PLP) is thought to be a mediator of hypercalcemia in both human and rodent malignancies. A rat PLP cDNA was used as a hybridization probe in Southern blot analysis of DNAs isolated from a panel of rat-mouse somatic cell hybrids. The single-copy gene for PLP was assigned to rat chromosome 2, whereas the rat parathyroid hormone (PTH) gene has previously been assigned to rat chromosome 1. Consequently, despite significant amino-terminal homology between PLP and PTH the genes encoding these peptides in the rat as well as human species have discrete chromosomal localizations.

Animals↗

Hepatoma-associated alterations of serum alpha 1-antitrypsin in hereditary hepatitis LEC rats as a new animal model of liver disease.

1. The LEC rats, a novel animal model of hepatitis and liver tumor, were found to have charge variants of serum alpha 1-antitrypsin (alpha 1AT) at the stage of liver tumor as judged by isoelectric focusing. 2. Treatment of the sera with neuraminidase showed that acidic variants of alpha 1AT in LEC rats seemed to be highly sialylated forms. 3. The concentration and enzymatic activity of serum alpha 1AT in LEC rats were not affected before the onset of hepatitis and even during the development of fulminant hepatitis and hepatocarcinogenesis. This indicates that hereditary hepatitis and subsequent liver tumor in LEC rats do not appear to be associated with alpha 1AT deficiency.

Animals↗

Human HST1 (HSTF1) gene maps to chromosome band 11q13 and coamplifies with the INT2 gene in human cancer.

The human HST1 gene, previously designated the hst gene, and now assigned the name HSTF1 for heparin-binding secretory transforming factor in human gene nomenclature, was originally identified as a transforming gene in DNAs from human stomach cancers by transfection assay with mouse NIH 3T3 cells. The amino acid sequence of the product deduced from DNA sequences of the HST1 cDNA and genomic clones had approximately 40% homology to human basic and acidic fibroblast growth factors and mouse Int-2-encoded protein. We have mapped the human HST1 gene to chromosome 11 at band q13.3 by Southern blot hybridization analysis of a panel of human and mouse somatic cell hybrids and in situ hybridization with an HST1 cDNA probe. The HST1 gene was found to be amplified in DNAs obtained from a stomach cancer and a vulvar carcinoma cell line, A431. In all of these samples of DNA, the INT2 gene, previously mapped to human chromosome 11q13, was also amplified to the same degree as the HST1 gene.

Animals↗

Metabolic predisposition of a novel mutant (LEC rats) to hereditary hepatitis and hepatoma: alterations of the drug metabolizing enzymes.

Previously we established that 'LEC rats' have displayed spontaneous fulminant hepatitis with severe jaundice, which progressed to liver cancer, and a single autosomal recessive gene is responsible for the cause of the diseases. The activities of drug metabolizing enzymes were assayed in livers from LEC and control (LEA) rats at 4 weeks and 3 months before the onset of liver cancer. At 4 weeks the cytochrome P-450 content of the LEC rat livers was 43% of the control (LEA) value. At 3 months the level was 65% of the control. Epoxide hydrolase, gamma-glutamyltranspeptidase and UDP-glucuronyltransferase activities were 2.6-, 6.9- and 2.4-times higher than those in the LEA rats at 4 weeks, respectively, while glutathione S-transferase activity was not significantly different between the two strains. The enzyme changes in the LEC rats are quite similar to those observed in hyperplastic foci and nodules in chemical carcinogenesis of hepatocytes.

Animals↗

Spontaneous occurrence of placental glutathione S-transferase-positive foci in the livers of LEC rats.

Spontaneous occurrence of placental glutathione S-transferase (GST-P)-positive foci was observed in the livers of 5-month-old LEC rats. Quantitative studies revealed that GST-P foci appeared after the onset of hepatitis. The number and size of GST-P foci increased with age and more foci were induced in males than in females. No sex difference, however, was found in the incidence of hepatitis. Although hepatitis is necessary for the induction of GST-P foci, it is insufficient for their further growth. Since hereditary hepatitis first appears at around 4 months of age, leading to a high incidence of hepatocellular carcinomas in later life, the spontaneous occurrence of the foci may be related to the development of hepatocellular carcinoma.

Animals↗

High susceptibility to hepatocellular carcinoma development in LEC rats with hereditary hepatitis.

A remarkably high incidence of hepatocellular carcinomas was observed in long-surviving LEC rats with hereditary hepatitis. Among the 60 LEC rats examined between 12 and 28 months of age from F29 and F30, 55 (92%) developed putative preneoplastic and neoplastic lesions such as hyperplastic foci and nodules, and hepatocellular carcinomas. Of these, hepatocellular carcinomas were observed with a high frequency (46/55; 84%). All rats of advanced age that survived more than 18 months developed hepatocellular carcinomas. These results suggest that the development of liver tumors in LEC rats is an age-associated phenomenon with serial hepatic alterations after the subsidence of acute hepatitis. The long-surviving rats had no normal tissue and showed chronic hepatitis in nontumorous tissues of the liver. Cholangiofibrosis was also found in most rats with hepatic lesions. Metastasis of hepatocellular carcinomas was found in four rats. Histologically, the hepatocellular carcinomas were of a well-differentiated type with a typical trabecular structure. Thus, LEC rats seem to be a promising animal model for studying the pathogenesis of hepatitis and hepatocellular carcinoma.

Age Factors↗

A transplantable cell line derived from spontaneous hepatocellular carcinoma of the hereditary hepatitis LEC rat.

A serially transplantable rat hepatocellular carcinoma (HCC) line was established. The primary spontaneous HCC which developed in a 506-day-old male hereditary hepatitis LEC rat was inoculated into young LEC rats. Only this HCC of 18 primary HCCs was successful in serial transplantation. The established cell line was histologically identical to the primary HCC showing a well-differentiated type with a trabecular structure of tumorous hepatocytes. The characteristic of albumin production was maintained. Chromosome analysis revealed rather widely dispersed polyploid chromosome numbers with a modal value at 96. Every metaphase contained two to five unusually large marker chromosomes.

Animals↗

Nucleotide sequence and chromosomal mapping of the human c-yes-2 gene.

We molecularly characterized the second gene, c-yes-2, of two copies of yes-related genes which we previously found to contain in the human genome. First, nucleotide sequence analysis revealed that the c-yes-2 gene is a pseudogene of the c-yes-1 gene. Second, by using two independent methods, hybridization of both DNAs from sorted chromosomes and metaphase spreads with c-yes-2 DNA, we assigned the c-yes-2 gene to chromosome 22q11.2. This chromosomal localization is consistent with that given in our previous report. The failure of proper mapping in our experiment might have been caused by instability of hybrid cell clones.

Base Sequence↗

Spontaneous hepatitis in Long-Evans rats. A potential animal model for fulminant hepatitis in man.

Spontaneous hepatitis associated with severe jaundice occurred in 90% of an inbred strain of Long-Evans rats. The rapidly progressive syndrome was characterized by abrupt onset, hyperbilirubinemia and increased serum levels of glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, associated with massive and multifocal necrosis of the liver. This strain should provide a useful animal model for analysis of the pathogenesis of fulminant hepatitis in humans.

Alanine Transaminase↗

Evolution, expression, and chromosomal location of a novel receptor tyrosine kinase gene, eph.

Partial sequence analysis of the genomic eph locus revealed that the splicing points of kinase domain-encoding exons were completely distinct from those of the other protein tyrosine kinase members reported, suggesting that this is the earliest evolutionary split within this family. In Northern (RNA) blot analysis, the eph gene was expressed in liver, lung, kidney, and testis of rat, and screening of 25 human cancers of various cell types showed preferential expression in cells of epithelial origin. Overexpression of eph mRNA was found in a hepatoma and a lung cancer without gene amplification. Comparison of cDNA sequences derived from a normal liver and a hepatoma that overproduces eph mRNA demonstrated that two of them were completely identical throughout the transmembrane to the carboxy-terminal portions. Southern blot analysis of DNAs from human-mouse hybrid clones with an eph probe showed that this gene was present on human chromosome 7.

Animals↗