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Biomedical subjects

Y Murakami

Publications and source records attributed to Y Murakami.

At least 307 records · Page 17Linked to original sources
PubMed1999

[Analysis of the long-term survived patients with P-N2 non-small cell lung cancer].

We had 308 patients with P-N2 non-small cell lung cancer who were treated with pulmonary resection therapy from June 1975 to March 1994. We analysed 9 patients who could survive for 5 years and more after the operation. All of them were male and the mean age was 61.1 years. Histologically, 2 patients had adenocarcinoma and 7 patients had squamous cell carcinoma. The clinical staging was T2N1M0 in 2 patients, T1N2M0 in one, T2N2M0 in 2, T3N2M0 in 2, and T4N2M0 in 2 patients. The histopathological staging was T1 in one patient, T2 in 4, T3 in 3, and T4 in one patient. Three patients who had absolute non-curative operation (residual carcinoma on bronchial stump in 2 patients and residual mediastinal lymph nodes in one patient) were treated with radiation therapy after having operation. The one level mediastinal lymph node metastasis was found in 7 patients and multi-level one in 2 patients. Four patients out of nine are still alive and free from the cancer and 2 patients died of other unrelated disease. The patient who even have P-N2 non-small cell lung cancer with mediastinal lymph node involvement will live long after curative operation.

Adenocarcinoma↗
PubMed1999

[Department of microbiosensing system using micromachine techniques].

This paper reviews devices for Point Of Care (POC) testing, especially focusing on current and future biosensors and biosensing fields. POC testing involves on-site diagnosis such as bedside diagnosis and near-patient testing. Biosensors and biosensing devices are a key technology to measure all clinically important parameters. For many reasons such as historical, simplicity, the high stability and activity of the enzyme required, and large demand from diabetics, only glucose sensors are commercially available. Various biosensors are waiting for commercialization. Not only simple biosensors having a biofunctional membrane on a transducer, but more complicated biosensing systems are fabricated on a microchip. Micro-Total Analysis System (mu TAS) is a research field to fabricate miniaturized sensing devices or systems. In these devices or systems, biochemical reactions for detection can be well controlled by running buffers, even though the consumption of reagents and sample is very small. Microarray chip technology, such as the DNA chip, is now receiving much attention in not only genetic research, but other biochemical research and application fields as well. Detection apparatus for the DNA chip is currently bench-top size. According to recent research, however, the size will be reduced as to a portable-size that is suitable for POC testing. Research and development of POC devices are advanced not alternative methods of conventional laboratory test, but as complement technology with advantages such as mobility, speed, and low-cost.

Biosensing Techniques↗
PubMed1999

[Distributions of the numbers of monitoring stations in the surveillance of infectious diseases in Japan].

To describe the characteristics of monitoring stations for the infectious disease surveillance system in Japan, we compared the distributions of the number of monitoring stations in terms of population, region, size of medical institution, and medical specialty. The distributions of annual number of reported cases in terms of the type of diseases, the size of medical institution, and medical specialty were also compared. We conducted a nationwide survey of the pediatrics stations (16 diseases), ophthalmology stations (3 diseases) and the stations of sexually transmitted diseases (STD) (5 diseases) in Japan. In the survey, we collected the data of monitoring stations and the annual reported cases of diseases. We also collected the data on the population, served by the health center where the monitoring stations existed, from the census. First, we compared the difference between the present number of monitoring stations and the current standard established by the Ministry of Health and Welfare (MHW). Second, we compared the distribution of all medical institutions in Japan and the monitoring stations in terms of the size of the medical institution. Third, we compared the average number of annual reported cases of diseases in terms of the size of medical institution and the medical specialty. In most health centers, the number of monitoring stations achieved the current standard of MHW, while a few health centers had no monitoring station, although they had a large population. Most prefectures also achieved the current standard of MHW, but some prefectures were well below the standard. Among pediatric stations, the sampling proportion of large hospitals was higher than other categories. Among the ophthalmology stations, the sampling proportion of hospitals was higher than other categories. Among the STD stations, the sampling proportion of clinics of obstetrics and gynecology was lower than other categories. Except for some diseases, it made little difference in the average number of annual reported cases of diseases in terms of the type of medical institution. Among STD, there was a great difference in the average number of annual reported cases of diseases in terms of medical specialty.

Child↗
PubMed1999

[Determination of the numbers of monitoring medical institutions necessary for estimating incidence rates in the surveillance of infectious diseases in Japan].

Our purpose was to determine the number of monitoring stations (medical institutions) necessary for estimating incidence rates in the surveillance system of infectious diseases in Japan. Infectious diseases were selected by the type of monitoring stations: 15 diseases in pediatrics stations, influenza in influenza stations, 3 diseases in ophthalmology stations and 5 diseases in the stations of sexually transmitted diseases (STD). For each type of monitoring station, 5 cases of the number of monitoring stations in each health center, including the number determined from presently established standards and the actual number in 1997, were given. It was assumed that monitoring stations were randomly selected among medical institutions in health centers. For each infectious disease, each case and each type of monitoring station, standard error rates of estimated numbers of incidence cases in the whole country were calculated in 1993-1997 using the data of the surveillance of infectious diseases. Among 5 cases of monitoring stations, the case satisfied the condition that those standard error rates were lower than the critical values, was selected. The critical values were 5% in pediatrics and influenza stations, and 10% in ophthalmology and STD stations. The numbers of monitoring stations in the selected cases were 3,000 in pediatrics stations, 5,000 in influenza stations (including all pediatrics stations), 605 in ophthalmology stations and 900 in STD stations.

Child↗
PubMed1998

Self-protection of PC12 cells by 6R-tetrahydrobiopterin from nitric oxide toxicity.

Nitric oxide (NO) has cytotoxic effects but NO producing neurons are resistant to NO toxicity. These results suggest the presence of self-protecting factors for NO toxicity. Recently, 6R-tetrahydrobiopterin (6R-BH4), a cofactor for NO synthase (NOS), has been reported to degrade NO raising the possibility that 6R-BH4 acts as a self-protecting factor for NO toxicity. In PC12 cells which have NOS, three-day culture with sodium nitroprusside (SNP) or NOC-12, NO generators, at 10-100 microM increased nitrite and nitrate concentrations in the culture medium and induced death of PC12 cells. Coadministration of 6R-BH4 (10 or 30 microM) with SNP or NOC-12 prevented cell death with reduction of nitrite and nitrate in the medium. Inhibition of 6R-BH4 synthesis by 2,4-diamino-6-hydroxypyrimidine (DAHP), an inhibitor for GTP cyclohydrolase I, decreased cellular 6R-BH4 content and viable cell number. The inhibiting effects of DAHP were restored by exogenous 6R-BH4. NOS activity, as estimated by nitrite concentrations in the medium, was unchanged by DAHP. Hypoxanthine and xanthine oxidase, which produce superoxide, mimicked the cell-protecting effect of 6R-BH4 which is reported to generate superoxide during its autoxidation. These results suggest that 6R-BH4 acts as a self-protecting factor for NO toxicity with generation of superoxide in NO-producing neurons.

Animals↗
PubMed1998

Localization of tumor suppressor activity important in nonsmall cell lung carcinoma on chromosome 11q.

Loss of heterozygosity on chromosome 11q23 is observed at high frequency in human nonsmall cell lung carcinomas (NSCLCs), suggesting the presence of a tumor suppressor gene. Previous analysis of DNA from 79 patients identified a commonly deleted segment of 5 centimorgans. Complementation analysis was used to further localize a putative tumor suppressor gene. Three yeast artificial chromosome (YAC) clones spanning the minimal loss of heterozygosity region were modified, and spheroplast fusion was used to transfer them into human A549 NSCLC or murine Lewis lung carcinoma (LLC) cell lines. The resulting yeast x human hybrid cell lines containing an intact copy of a 1.6-Mb YAC, 939b12, showed reduced growth in vitro. Injection of parental A549 cells into athymic (nu/nu) mice resulted in tumor formation at 27 of 28 injection sites. In contrast, two independent 939b12-containing cell lines formed tumors at only 3 of 20 injection sites. 939b12 also suppressed tumor formation by LLC NSCLC cells in nude mice, but YACs 785e12 and 911f2, which flank 939b12, had no suppressor activity. Further localization of tumor suppression activity on 939b12 was accomplished by introduction of defined fragmentation derivatives into A549 cells and by analysis of YACs that were broken on transfer into LLC cells. This complementation approach localized tumor suppression activity to the central 700 kb of 939b12 and provides a functional assay for positional cloning of this tumor suppressor gene.

Animals↗
PubMed1998

Agmatine suppresses proliferation by frameshift induction of antizyme and attenuation of cellular polyamine levels.

Polyamines are required for entry and progression of the cell cycle. As such, augmentation of polyamine levels is essential for cellular transformation. Polyamines are autoregulated through induction of antizyme, which represses both the rate-limiting polyamine biosynthetic enzyme ornithine decarboxylase and cellular polyamine transport. In the present study we demonstrate that agmatine, a metabolite of arginine via arginine decarboxylase (an arginine pathway distinct from that of the classical polyamines), also serves the dual regulatory functions of suppressing polyamine biosynthesis and cellular polyamine uptake through induction of antizyme. The capacity of agmatine to induce antizyme is demonstrated by: (a) an agmatine-dependent translational frameshift of antizyme mRNA to produce a full-length protein and (b) suppression of agmatine-dependent inhibitory activity by either anti-antizyme IgG or antizyme inhibitor. Furthermore, agmatine administration depletes intracellular polyamine levels to suppress cellular proliferation in a transformed cell line. This suppression is reversible with polyamine supplementation. We propose a novel regulatory pathway in which agmatine acts as an antiproliferative molecule and potential tumor suppressor by restricting the cellular polyamine supply required to support growth.

3T3 Cells↗
PubMed1998

Comparison of the structural characteristics of chromosome VI in Saccharomyces sensu stricto: the divergence, species-dependent features and uniqueness of saké yeasts.

Previous studies have revealed that chromosome VI of saké yeasts is much larger than that of the other strains of Saccharomyces cerevisiae. Southern analysis using segments of chromosome VI of a laboratory strain as probes suggested that the nucleotide sequence of a major portion of this chromosome is conserved, but considerable diversity was found in the distal parts in the other strains. Physical maps also indicated that differences in length of chromosome VI were mainly due to differences in its ends. NotI was found to generate 9 kb and/or 16 kb fragments from the left telomere of chromosome VI in most saké yeasts, but no fragment in the case of AB972. SfiI produced one or two 30-50 kb fragments from the right end of this chromosome in all saké yeasts tested, but produced a 20 kb fragment in the case of AB972. All S. cerevisiae strains not employed in saké brewing were the same as AB972 in these respects. S. paradoxus had one NotI site in chromosome VI, while S. bayanus had two, one of which is possibly common to both species. The SfiI site mentioned above was present in chromosome VI of all species, while that of S. bayanus and S. paradoxus each had a second site distinct from the other. Chromosome VI of S. pastorianus was not distinguishable from that of S. bayanus.

Blotting, Southern↗
PubMed1998

Accumulation of genetic alterations and their significance in each primary human cancer and cell line.

Analyses of multiple genetic alterations accumulated in each cancer cell is expected to provide useful information to elucidate the molecular mechanisms involved in tumorigenesis. Here, we summarized the results of studies on aberrations of oncogenes and tumor suppressor genes by ourselves and other groups. DNAs analyzed were from particular sets of surgical specimens from human tumors and cancer cell lines derived from non-small cell lung cancers, pancreatic cancers, hepatocellular carcinomas and gliomas. Tumors could be grouped into two types based on the genetic alterations detected. Tumors in group 1 had mutations in genes encoding proteins involved in a limited number of signal transduction cascades such as p16-cyclin D1/CDK4-RB or MDM2-p53-p21, where the aberration of one component seems to be sufficient to cause dysfunction of the cascade. Group 2 contained a subset of tumors in which no alteration was detected in the genes analyzed, even in the advanced stage or established cancer cells, indicating the involvement of completely different oncogenic pathways.

Cell Division↗
PubMed1998

Evidence for axial coordination of 5,6-dimethylbenzimidazole to the cobalt atom of adenosylcobalamin bound to diol dehydratase.

It was demonstrated by electron paramagnetic resonance (EPR) spectroscopy that organic radical intermediates disappeared and cob(II)alamin accumulated upon suicide inactivation of diol dehydratase by 2-methyl-1,2-propanediol. The resulting EPR spectra showed that the eight hyperfine lines due to the divalent cobalt atom of cob(II)alamin further split into triplets by the superhyperfine coupling to the 14N nucleus. Essentially the same superhyperfine splitting of the octet into triplets was observed with [14N]- and [15N]apoenzyme. When the adenosyl form of [14N2]- and [15N2]imidazolyl analogues of the coenzyme [Toraya, T., and Ishida, A. (1991) J. Biol. Chem. 266, 5430-5437] was used with unlabeled apoenzyme, the octet showed superhyperfine splitting into triplets and doublets, respectively. Therefore, it was concluded that cobalamin is bound to this enzyme with 5,6-dimethylbenzimidazole coordinating to the cobalt atom. This conclusion is consistent with the fact that the consensus sequence forming part of a cobalamin-binding motif, conserved in methionine synthase and some of the other cobalamin enzymes, was not found in the deduced amino acid sequences of the subunits of diol dehydratase. Adenosylcobinamide methyl phosphate, a coenzyme analogue lacking the nucleotide moiety, underwent cleavage of the cobalt-carbon bond upon binding to the enzyme in the presence of substrate, forming a cob(II)inamide derivative without nitrogenous base coordination, as judged by EPR and optical spectroscopy. Therefore, this analogue may be a useful probe for determining whether the replacement of the 5, 6-dimethylbenzimidazole ligand by a histidine residue takes place upon binding of cobalamin to proteins.

Benzimidazoles↗
PubMed1998

Prognostic values of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 expression in bladder cancer.

BACKGROUND: Matrix metalloproteinase-2 (MMP-2), which degrades the extracellular matrix or the basement membrane, has an essential role in tumor invasion and metastasis. To evaluate the roles of MMP-2, its inhibitor (tissue inhibitor of metalloproteinase-2 [TIMP-2]), and its activator (membrane-type matrix metalloproteinase-1 [MT1-MMP]) in tumor invasion or as a prognostic factor in patients with bladder carcinoma, the authors investigated the expression of MMP-2, TIMP-2, and MT1-MMP in patients with bladder carcinoma. METHODS: Tissues obtained from 41 patients with bladder carcinoma were used for analysis. Expression of MMP-2, TIMP-2, MT1-MMP, and glyceraldehyde-3-phosphate dehydrogenase was examined by reverse transcriptase-polymerase chain reaction analysis. Correlations between the levels of MMP-2, TIMP-2, and MT1-MMP expression and histologic findings or patient outcome were evaluated. RESULTS: Expression of MMP-2 and TIMP-2 was significantly higher in muscle invasive pT2< or = bladder tumors than in pT1a tumors (MMP-2: P < 0.0005; TIMP-2: P < 0.005). Moreover, high levels of MMP-2 and TIMP-2, as well as MT1-MMP expression, all were strongly associated with decreased survival (MMP-2: P < 0.0001; TIMP-2: P < 0.0001; and MT1-MMP: P < 0.005). Even within the radically cystectomized muscle invasive pT2< or = tumor group, patients with a high expression of any of these three genes had a worse prognosis than those with low expression (MMP-2: P < 0.05; TIMP-2: P < 0.05; and MT1-MMP: P = 0.0641). CONCLUSIONS: MMP-2 and TIMP-2 are believed to contribute to the invasive properties of bladder carcinoma. The authors report that expression of MMP-2, TIMP-2, and MT1-MMP are useful prognostic indicators in patients with bladder carcinoma and may be helpful in designing treatment protocols.

Aged↗
PubMed1998

Molecular cloning of membrane cofactor protein (MCP; CD46) on B95a cell, an Epstein-Barr virus-transformed marmoset B cell line: B95a-MCP is susceptible to infection by the CAM, but not the Nagahata strain of the measles virus.

Measles virus (MV) infects not only human beings but also some simian species. The MV receptor on Vero cells (a cell line established from African Green monkey kidney cells) and human cells has been shown to be the membrane cofactor protein MCP/CD46, which is an inhibitor of autologous complement (C) activation. B95a, an Epstein-Barr virus (EBV)-transformed marmoset B cell line, is a simian cell line used for MV selection and is much more susceptible to MV than Vero cells. In the present study, we isolated cDNAs encoding MCP homologues from B95a cDNA library and assessed whether B95a-MCP is responsible for the high susceptibility of B95a to MV. The deduced amino acid sequence of the cDNA of B95a-MCP was 76% identical to that of human-MCP, and the recombinant B95a-MCP exerts C inhibitor activity. Although CAM, a vaccine strain of MV, infected Chinese hamster ovary (CHO) cells expressing B95a-MCP, Nagahata strain, a wild type of MV, failed to infect the CHO transfectants, suggesting that additional membrane molecules of B95a are responsible for the high susceptibility of B95a to the Nagahata strain.

Amino Acid Sequence↗
PubMed1998

Restricted Zn2+ availability affects the antizyme-dependent ornithine decarboxylase degradation pathway in isolated primary cultured rat hepatocytes.

We previously reported that lack of Zn2+ decreased ornithine decarboxylase (ODC) activity without any change in ODC messenger RNA levels and the half-life of ODC activity being about 2-fold more rapid in primary cultured adult rat hepatocytes, suggesting that lack of Zn2+ decreased ODC activity mainly by degrading the enzyme. The present investigations showed that the chelator, diethylenetriamine penta-acetic acid (DTPA), increased the ratio of ODC-antizyme complex to total ODC (about 2-fold) and caused a decrease in antizyme inhibitor, a protein inhibitor of ODC antizyme (about 50%). These results indicate that a restricted Zn2+ availability affects the antizyme-dependent ODC degradation pathway and consequently decreases ODC activity in primary cultured rat hepatocytes.

Animals↗
PubMed1998

Involvement of tetrodoxin-sensitive sodium channels in rat growth hormone secretion induced by pituitary adenylate cyclase-activating polypeptide (PACAP).

Both pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) and growth hormone-releasing hormone (GRH) stimulated growth hormone (GH) release from perfused rat anterior pituitary cells. Tetrodotoxin (TTX) blunted the GH release induced by PACAP-38 but not by GRH. Mefenamic acid, a blocker of non-selective cation channels, unaffected GH release elicited by PACAP-38 and GRH. These results suggest an involvement of TTX-sensitive Na+ channels but not Ca2+-activated nonselective cation channels in PACAP-38-induced GH secretion, and that post-receptor mechanisms for PACAP-38 are different from those activated by GRH.

Animals↗
PubMed1998

Structural and functional evidence for the presence of tumor suppressor genes on the short arm of chromosome 10 in human gliomas.

Loss of heterozygosity (LOH) observed at polymorphic loci on both arms of chromosome 10 in many human gliomas suggests the presence of multiple tumor suppressor genes on this chromosome. Recently, the PTEN/MMAC1 gene on 10q23 was isolated as one of these putative glioma suppressors. To determine the subchromosomal localization of others, we analysed 79 gliomas for LOH using 30 polymorphic microsatellite markers on the short arm and 10 markers on the long arm of chromosome 10. Twenty tumors showed LOH at all the loci examined, while 17 others showed LOH at loci on a portion of chromosome 10. Deletion mapping of the latters demonstrated that two distinct regions, encompassing genetic distances of 5.6 cM on 10p15 and 5.5 cM on 10p14, were lost frequently. Introduction of chromosomal fragments 10p14-p15, which included the entire region on 10p15 and a portion of that on 10p14 assigned by deletion mapping, into the human glioblastoma cell line T98G through microcell-mediated chromosome transfer markedly suppressed colony forming ability in soft agar compared with parental T98G cells. The combined results of structural and functional analyses strongly suggest that aberrations of the tumor suppressor gene(s) within chromosomal region 10p14-p15 are involved in development of human gliomas.

Brain Neoplasms↗