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T Komeda

Publications and source records attributed to T Komeda.

At least 37 records · Page 2Linked to original sources
PubMed1996

Infrequent alterations of the p16INK4A gene in liver cancer.

We examined the genomic status of the p16INK4A (inhibitor of cyclin-dependent kinase 4 A) and cyclin-dependent kinase 4 (CDK4) genes in 62 human hepatocellular carcinomas (HCCs), 5 cholangiocellular carcinomas and 6 cell lines derived from human liver cancers. Although no samples showed the homozygous deletion of the p16INK4A gene, we detected intragenic mutations of the p16INK4A gene in 3 HCCs and one HCC cell line, which led to an amino-acid substitution or a frameshift. In 2 HCC samples with mis-sense mutations of the p16INK4A gene, loss of heterozygosity on 9p22 was also detected, suggesting that the loss of function of p16 was induced during hepatocarcinogenesis. On the other hand, amplification or rearrangement of the CDK4 gene was not detected in any samples examined in this study. These results indicated that the mutations or deletions of the p16INK4A gene are not frequent, but may play a role in a sub-set of human HCC.

Base Sequence↗
PubMed1996

Gene analysis of trehalose-producing enzymes from hyperthermophilic archaea in Sulfolobales.

The genes encoding new trehalose-producing enzymes from S. acidocaldarius ATCC33909 were cloned to analyze the distribution of these genes in Sulfolobales. Comparison of the amino acid sequences with S. solfataricus KM1 showed approximately 50% similarity. Southern analysis suggest that homologues of the trehalose-producing enzyme genes exist widely in sulfolobales and strains in Sulfolobales were classified into three kinds of genotypes.

Amino Acid Sequence↗
PubMed1996

Gene cloning and expression of new trehalose-producing enzymes from the hyperthermophilic archaeum Sulfolobus solfataricus KM1.

The genes encoding for trehalose-producing enzymes, a glycosyl-trehalose-producing enzyme (glycosyltransferase) and a gylcosyl-trehalose-hydrolyzing enzyme (alpha-amylase), from Sulfolobus solfataricus KM1 were cloned and expressed in E. coli. The nucleotide sequence of the glycosyltransferase gene and the alpha-amylase gene indicated proteins with lengths of 728 and 558 amino acids and molecular masses of 86-kDa and 65-kDa, respectively. Regions highly conserved in the alpha-amylase family exist in the amino acid sequences of these enzymes.

Amino Acid Sequence↗
PubMed1995

Sensitive detection of circulating hepatocellular carcinoma cells in peripheral venous blood.

BACKGROUND: This study was performed to develop a sensitive method for the detection of circulating hepatocellular carcinoma (HCC) cells in peripheral blood, in advance of the diagnosis of distant metastasis of HCC by conventional means. METHODS: Peripheral blood (5 ml) samples were obtained from 64 patients with HCC and from 48 control subjects (31 patients with benign liver disease, 8 with metastatic liver cancer, and 9 with normal liver function). To identify HCC cells in peripheral blood, liver-specific human alpha-fetoprotein (hAFP) mRNA was amplified from total RNA extracted from whole blood by reverse transcriptase-polymerase chain reaction. RESULTS: Human alpha-fetoprotein mRNA was detected in 23 blood samples from the HCC patients (23/64, 36%), in 17 patients in whom there was no clinical evidence of distant metastasis. In contrast, there were no control patients whose samples showed detectable hAFP mRNA in the peripheral blood. The presence of hAFP mRNA in blood seemed to be correlated with the stage (by TNM classification) of HCC, the serum hAFP value, and the presence of intrahepatic metastasis, portal vein thrombosis, and/or distant metastasis. CONCLUSIONS: Reverse-transcriptase polymerase chain reaction is a very sensitive method for detecting circulating HCC cells. With this technique, important information for the management of HCC can be acquired, such as the indications for orthotopic liver transplantation in HCC patients. Moreover, use of this detection method may encourage investigation of the mechanism of metastasis in HCC.

Adult↗
PubMed1994

Amplification and overexpression of the cyclin D1 gene in aggressive human hepatocellular carcinoma.

We analyzed the genetic alterations of the cyclin D1 and INT-2 genes in hepatocellular carcinomas (HCCs) from 45 patients. Among these, expression of the cyclin D1 mRNA was also analyzed in 18 of them by Northern blotting. The cyclin D1 gene was amplified 3-16 fold in five HCCs (11%); among these, the INT-2 gene was also amplified 2-10 fold in four HCCs. We analyzed the mRNA of cyclin D1 in four HCCs with gene amplifications, and 6-10 fold overexpressions were detected in all of them. Because the cyclin D1 gene was amplified in patients at an advanced stage of HCC with rapid tumor growth, it appeared to be associated with the aggressive behavior of tumors. Studies on loss of heterozygosity on chromosome 13q, where the retinoblastoma (RB) gene is located, indicated that all HCCs with an amplified cyclin D1 gene retained heterozygosity on chromosome 13q. These results suggest that amplification and overexpression of the cyclin D1 gene result in the rapid growth of a subset of HCC, even though the function of the RB gene is retained.

Carcinoma, Hepatocellular↗
PubMed1992

Echo/Doppler diagnosis of tetralogy of Fallot, ventricular septal defect, pulmonary valve dysplasia, and hypertrophic cardiomyopathy in WKY/NCrj rats.

We examined the hearts of 97 WKY/NCrj rats, a strain which spontaneously develops congenital cardiac malformations, by means of echocardiography with a pulsed Doppler ultrasound, and compared the results with those of 20 WKY/Ta rats and 30 normal Wistar rats. Dissection of these WKY/NCrj rats revealed a ventricular septal defect (VSD) in 20 and pulmonary valve dysplasia (PVD) in 41, both VSD and PVD occurring together in 18. VSD was readily diagnosed in vivo by the jet flow signal derived from the left-to-right shunt near the membranous portion, with a sensitivity of 85% and a specificity of 99%. Ultrasound imaging revealed overriding of the aorta and right ventricular (RV) hypertrophy in 18 of the 20 rats with VSD. Of the 20 rats with VSD, 10 had a systolic high-velocity jet across the RV outflow indicating an infundibular stenosis. PVD was commonly accompanied by a pulmonary regurgitation signal, with severe cases showing intensified echo and low excursion of the cusps. The regurgitation signal showed a good diagnostic value for PVD with a sensitivity of 82% and a specificity of 85%. In the remaining 54 WKY/NCrj rats without VSD or PVD, the ratio of mean left ventricular (LV) wall thickness to cavity dimension, the fractional shortening of the LV dimension, and the septal to LV free wall thickness ratio were all abnormally high, and the motion of the ventricular septum was reduced in most of the cases compared with that of the other two strains. All these features resemble the hypertrophic cardiomyopathy seen in humans, which further promises that the rats should be a useful model for the controversial disease.

Animals↗
PubMed1991

Hereditary transmission of tetralogy of Fallot, cardiac hypertrophy, and anomalies of great vessels in WKY/NCrj rats.

We examined 78 fetuses on d 21 of gestation (G21) and 83 neonates on d 2 after birth (A2), which were first generation offspring of WKY rats mated with normal Wistar rats (F1). In addition, we examined six groups of fetuses on d 19 of gestation (G19): 65 Wistar rats, 111 WKY rats, 85 F1, 100 F1 X F1, 92 F1 X Wistar, and 97 F1 X WKY progeny. In the F1 at G19, G21, and A2, there were abnormalities of the pulmonary valve, pulmonary outflow tract, architecture of muscle bundle, and pulmonary arterial branch, as well as hypoplastic ductus arteriosus and postnatal cardiac hypertrophy, similarly in males and females but at a lower incidence and to a lesser extent than in the WKY rats. Severe pulmonary valve dysplasia and ventricular septal defect with overriding of the aorta (tetralogy of Fallot), usually associated with a markedly small ductus, were not present or were very rare in the F1 and the F1 X Wistar but were present in the F1 X WKY and in the F1 X F1 less prevalently than in the WKY. The size of the ductus showed a continuous distribution in all of the six groups; there was a large skewing toward lower values in the WKY, the F1 X WKY, and the F1 X F1. These results suggest that cardiovascular anomalies of WKY rats are transmitted as autosomal recessive or incomplete autosomal dominant traits with an incomplete penetrance and variable expressivity or as polygenic traits. Chromosomal analysis of 31 WKY fetuses revealed no aberrations specifically related to the development of cardiovascular malformations.

Animals↗
PubMed1990

Role of Bacteroides uniformis in susceptibility of Ta:CF# 1 mice to infection by Treponema hyodysenteriae.

Among the various strains and colonies of mice tested specific-pathogen-free (SPF) Ta:CF#1 mice exhibited the highest susceptibility to Treponema hyodysenteriae infection. Staphylococcus epidermidis 1047, Streptococcus faecalis 2039, Lactobacillus murinus 3010, Escherichia coli 1049, and Bacteroides thetaiotaomicron 3008 were administered to the Ta:CF#1 mice. B. uniformis IK, which appeared to colonize in the breeding facility under SPF conditions, was isolated from the cecal content of a Ta:CF#1 mouse and identified in the mouse flora. Germfree mice were infected with these six bacteria and challenged with T. hyodysenteriae DJ70P3 to elucidate the causal relationship between these bacteria and the sensitivity of mice to T. hyodysenteriae infection. No cecal lesions were observed in gnotobiotic mice either monoassociated with T. hyodysenteriae DJ70P3 or B. uniformis IK or inoculated with T. hyodysenteriae DJ70P3 combined with the 5 a.m. strains. Gross cecal lesions appeared only in mice inoculated with T. hyodysenteriae DJ70P3 combined with B. uniformis IK. A new SPF mouse colony (CF#1/b Ta) established from gnotobiotic mice by inoculation with B. uniformis IK and the 5 laboratory stock cultures was as susceptible to T. hyodysenteriae as the original Ta:CF#1 mice. This suggests that B. uniformis IK plays an important role in the high susceptibility of Ta:CF#1 mice to T.hyodysenteriae.

Animals↗
PubMed1990

Tetralogy of Fallot, pulmonary valve stenosis, ventricular septal defect, and hypertrophic cardiomyopathy in WKY/NCrj rats.

We examined anatomically the hearts of 198 WKY/NCrj rats of 20 litters. There were 51 rats with moderate to severe thickening of the pulmonary valve and 19 rats with a ventricular septal defect; the two lesions occurred together in 16 rats, in 15 of which there were overriding of the aorta, stenosis of the pulmonary outflow tract, and hypertrophy of the right ventricle, fulfilling the criteria for tetralogy of Fallot in man. The papillary muscle of the conus was absent in 65 rats. The heart was abnormally heavy in 18. We analyzed the relationship between cardiac hypertrophy and valvular lesions and septal defects in these rats plus 27 selected WKY rats with abnormally heavy hearts. Of the 151 rats with neither severe valvular lesions nor septal defects, six rats had abnormally heavy hearts and 67 rats had disproportionate ventricular septal thickening. This situation in the rats is similar to hypertrophic cardiomyopathy. The occurrence of these abnormalities, isolated or in association, in rats of an established inbred strain strongly suggests that they are etiologically or genetically linked, and that the rats should be a useful animal model for these diseases in man.

Animals↗
PubMed1990

Tetralogy of Fallot, cardiac hypertrophy, pulmonary hypertension, and anomalies of great vessels in fetuses and neonates of WKY/NCrj rats.

We examined anatomically the hearts, lungs, and great vessels of 269 WKY/NCrj rats at three fetal and three neonatal stages. Severe pulmonary valve thickening was present in 16 and ventricular septal defects with overriding of the aorta in 15 of the 90 near-term fetuses and in 10 and nine, respectively, of the 79 neonates at 2-4 d of age. These abnormalities occurred together (tetralogy of Fallot) in seven of the near-term fetuses and in five of the neonates. A narrow pulmonary outflow tract was present in 55% of the fetuses and in 56% of the neonates. The wall of the pulmonary arterial branch was abnormally thick in 19% of the fetuses and in 26% of the neonates, most of which did not have septal defects. In about 80% of the fetuses, the middle latitudinal muscle bundle of the ventricular septum was not continuous with the left ventricular free wall, but rather with the right; after birth, it was discontinuous with both free walls. The heart was abnormally heavy in 49% of the 79 neonates. In about half of the heavy hearts, there were no septal defects or pulmonary valvular and arterial lesions. There were double aortic arches in four and right aortic arches in six of the total WKY fetuses and neonates; the ductus arteriosus was abnormally small in 47% and the aorta was large in 51% of the near-term fetuses. This constellation of congenital heart disease is genetic in origin, but altered by hemodynamics late in fetal life.

Animals↗