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H Nishimori

Publications and source records attributed to H Nishimori.

At least 19 recordsLinked to original sources

Ubiquitous V-shape density of states in a mixed state of clean limit type II superconductors.

It is demonstrated theoretically and experimentally that the low energy density of states N(E) is described by a singular V-shape form N(E)=N(0)(H)+alpha|E|+O(E2) for all clean superconductors in a vortex state, irrespective of the underlying gap structure. The linear term alpha|E| which has not been recognized so far is obtained by exactly evaluating the vortex contribution. Based on microscopic Eilenberger theory N(E) is evaluated for the isotropic gap, line, and point-node gaps to yield a V-shape N(E). Scanning tunneling spectroscopy-STM experiments on NbSe2 and YNi2B2C give direct evidence for this. We provide arguments on the significance of this finding and on the relevance to other experiments.

Journal Article↗

Antiangiogenic activity of BAI1 in vivo: implications for gene therapy of human glioblastomas.

Glioblastomas are the most common primary brain tumors in adults. These tumors exhibit a high degree of vascularization, and malignant progression from astrocytoma to glioblastoma is often accompanied by increased angiogenesis and the upregulation of vascular endothelial growth factor and its receptors. In this study, we investigated the in vivo antiangiogenic and antitumor effects of brain-specific angiogenesis inhibitor 1 (BAI1) using human glioblastoma cell lines. Glioblastoma cells were transduced with an adenoviral vector encoding BAI1 (AdBAI1), and Northern and Western blot analyses, respectively, demonstrated BAI1 mRNA and protein expression in the transduced tumor cells. Using an in vivo neovascularization assay, we found that angiogenesis surrounding AdBAI1-transduced glioblastoma cells transplanted into transparent skinfold chambers of SCID mice was significantly impaired compared to control treated cells. Additionally, in vivo inoculation with AdBAI1 of established subcutaneous or intracerebral transplanted tumors significantly impaired tumor growth and promoted increased mouse survival. Morphologically, the tumors exhibited signs of impaired angiogenesis, such as extensive necrosis and reduced intratumoral vascular density. Taken together, these data strongly indicate that BAI1 may be an excellent gene therapy candidate for the treatment of brain tumors, especially human glioblastomas.

Adenoviridae↗

Metastases-related genes in the classification of liver and peritoneal metastasis in human gastric cancer.

INTRODUCTION: With the aim of identifying metastases-related genes in gastric cancer, we performed a broad analysis of differential gene expression between low-metastatic parental cell lines and established highly metastatic sublines. MATERIALS AND METHODS: We established novel cell lines, AZ-H5c, NUGC-3H5, and TMK-1H7, with a high potential of liver metastasis, and AZ-P7a, NUGC-3P4T, and TMK-1P4a, with a high potential of peritoneal metastasis. These cell lines were derived from low-metastatic parental AZ-521, NUGC-3, and TMK-1 cell lines, respectively. Furthermore, to investigate different levels of gene expression implicated in metastatic potentials in gastric cancer, we investigated approximately 2000 expressed genes in each cell line using a DNA microarray. RESULTS: Varieties of genes were up-regulated or down-regulated in highly metastatic liver and peritoneal cell lines. Fifty-eight genes, including the transferrin receptor, ras-related rho, and osteopontin, and 22 genes, including apolipoprotein E and inhibin A-submit, were up-regulated and down-regulated in two or three liver metastatic sublines. On the other hand, 19 genes, the transferrin receptor, c-fos, and RANTES, and 26 genes, including MAC25, PISSLRE, and RNA polymerase, were up-regulated and down-regulated in two or three peritoneal metastatic sublines. CONCLUSION: How gene expression is implicated in gastric cancer metastasis has never been thoroughly explained, and further studies are necessary to understand the involvement of genes in cancer metastasis more thoroughly. We hope that our highly metastatic liver and peritoneal experimental models are helpful for further study and gene therapy of human gastric cancer.

Cell Line, Tumor↗

Percutaneous radiofrequency ablation for unresectable large hepatic tumours during hepatic blood flow occlusion in four patients.

AIM: To evaluate percutaneous radiofrequency (RF) ablation therapy for unresectable large hepatic tumours combined with regional interruption of hepatic blood flow, and to assess the safety and efficacy of this procedure. MATERIALS AND METHODS: Four patients with hepatic tumours were enrolled in this study. Patients were treated by a single session of RF ablation during occlusion of both hepatic artery and hepatic vein. Tumour size ranged from 45-57 mm (mean 50.2 mm). Initial therapeutic efficacy was evaluated with helical computed tomography (CT) performed within 9 days after the treatment. CT or magnetic resonance imaging (MRI) was performed every 2-3 months thereafter. RESULTS: The largest axis of coagulated lesions after the ablation was 50-60 mm (mean 56.5 mm) in diameter. The ablation therapy was considered complete in three patients; after a mean follow-up of 12.7 months, CT and MRI revealed complete destruction of their tumours. One patient required further treatment. No severe complications occurred. CONCLUSION: Although further studies are needed, in this limited clinical trial a local ablation area exceeding 50 mm in diameter was achieved safely.

Aged↗

Profiling analysis of differential gene expression between hematogenous and peritoneal metastatic sublines of human pancreatic cancer using a DNA chip.

We established the novel sublines HPC-1H5, HPC-3H4, HPC-4H4, and Panc-1H5, which have a high potential of liver metastasis, and HPC-1P5a, HPC-3P4a, HPC-4P4a, and Panc-1P5a, which have a high potential of peritoneal dissemination, derived from low metastatic HPC-1, HPC-3, HPC-4, and Panc-1cell lines, respectively. To clarify the molecular mechanisms of cancer metastasis and of the different levels of gene expression in a variety of metastatic potentials in pancreatic cancer, we performed a broad analysis of differential gene expression analysis between parental cell lines and metastatic sublines. In comparison with the parental cell lines, 65 and 36 genes were overexpressed and underexpressed in highly liver-metastatic sublines. On the other hand, 43 and 45 genes were overexpressed and underexpressed in highly peritoneal-metastatic sublines. uPAR and Serin protease were overexpressed, and E2A and IGF1R were underexpressed in both metastatic sublines. Hierarchical clustering analysis revealed 22 genes classifying liver, peritoneal metastatic sublines and low-metastatic parental cell lines. These genes might be targeted genes separating those two major metastatic forms after surgery. A greater number of cell line samples and more genes will have to be utilized in future studies in order to understand the involvement of genes in cancer metastasis more thoroughly. However, these results will help to clarify the molecular mechanisms of pancreatic cancer metastasis.

Cell Line, Tumor↗

Differential gene expression screening between parental and highly metastatic pancreatic cancer variants using a DNA microarray.

To clarify the difference in genes expressed in hematogenous metastasis and peritoneal dissemination, a broad analysis of differential gene expression analysis between parental cell lines and established metastatic sublines was performed. Using an oligonucleotide array (Gene Chip, Affymetrix), approximately 2,000 genes involved in cancer were analyzed for each of the cell lines. HPC-4H4 (highly metastatic lines to the liver) compared with HPC-4 (low metastatic parental lines), in which 20 overexpressed genes and 5 underexpressed genes were recognized. HPC-4P4a (highly metastatic to the peritoneum) compared with HPC-4, in which 12 overexpressed genes and 15 underexpressed genes were also recognized. Analysis of HPC-4H4 and HPC-4P4a showed comparative up-regulation of 20 genes and down-regulation of 13 in the former, HPC-4H4. Further studies are needed to validate our hypothesis that some of the resulting differentially expressed genes might be implicated in the development of metastasis in pancreatic cancer. In conclusion, this genome-wide expression analysis will help to clarify the molecular mechanisms of cancer metastasis and of the different levels of gene expression in a variety of metastatic potentials in pancreatic cancer.

Cell Line, Tumor↗

Metastatic-associated biological properties and differential gene expression profiles in established highly liver and peritoneal metastatic cell lines of human pancreatic cancer.

To elucidate metastasis mechanisms, we established a Panc-1H5 subline with a highly liver metastatic cell line and a Panc-1P4a with a highly peritoneal metastatic cell line, which were sequentially selected from the parental pancreatic cancer cell line Panc-1. Using these three cell lines, we investigated several biological properties and mRNA levels of differentially-expressed genes involved in cancer metastasis with a cDNA macroarray. The tumorigenicity, motile activity, adhesive activity and cytokine production of metastatic sublines were higher than those of parental Panc-1 cells. Particularly, in Panc-1H5 cells, adhesive activity to the extracellular matrix and angiogenetic factors increased, whereas in Panc-1P4a cells, motile activity was extremely enhanced compared with Panc-1 cells. Histopathological findings for the three cell lines were the same. In cDNA macroarray analysis of Panc-1H5 cells, 11 genes were up-regulated and 20 genes were down-regulated compared with parental Panc-1 cells. In Panc-1P4a cells, 7 genes were up-regulated and 13 genes were down-regulated compared with parental Panc-1 cells. This study provides a demonstration of global gene expression analysis of pancreatic cancer cells with liver and peritoneal metastasis and these results provide new insight into the study of human pancreatic cancer metastasis.

Animals↗

A new peritoneal dissemination model established from the human pancreatic cancer cell line.

We established a new cell line, HPC-3P4a, with high peritoneal disseminated potential in nude mice. HPC-3P4a was derived from a human pancreatic carcinoma cell line (HPC-3) that had low capacity for peritoneal dissemination. HPC-3P4a developed peritoneal dissemination in 10 of 11 (90.9%) cases, whereas parental HPC-3 developed peritoneal dissemination in one of six (16.7%) cases. The metastatic foci in the peritoneum showed essentially the same histologic appearance of parental involvement. The tumorigenicity, motility, and adhesive activity of HPC-3P4a to the extracellular matrix were stronger than were those of the HPC-3. In FACS analysis, HPC-3P4a significantly increased the expression of alpha6 and alpha(v)beta5 integrins, while it decreased alpha2 integrin, hCD44H, and hCD44v 10, as compared with HPC-3. The VEGF production of HPC-3P4a was significantly lower than that of HPC-3. Analysis of gene macroarrays showed a variety of cytokines, interleukin, and other immunomodulatory, and their receptors were up-regulated and down-regulated on an mRNA level in HPC-3P4a cells, compared with HPC-3 cells. Intrasplenic injection of HPC-3P4a produced no liver metastasis. We named our original highly liver metastatic cell line HPC-3H4 (previously reported). This HPC-3H4 cell was established by repeated intrasplenic injection from parental cell HPC-3; thus, it developed high liver metastasis. Moreover, HPC-3H4 developed peritoneal dissemination by intra-abdominal injection. In contrast, HPC-3P4a did not develop liver metastasis by intrasplenic injection. These findings are very interesting and might suggest that the process of hematogenous metastasis differed from that of peritoneal dissemination. Thus, this cell line may be useful for investigating the mechanism of peritoneal dissemination in human pancreatic cancer.

Adenocarcinoma↗

A novel experimental mouse model of peritoneal dissemination of human gastric cancer cells: analysis of the mechanism of peritoneal dissemination using cDNA macroarrays.

We established a new cell line, NUGC-3P4T, with high peritoneal metastatic disseminating potential in nude mice. NUGC-3P4T cells were derived from the human gastric carcinoma line NUGC-3, which has low capacity for peritoneal dissemination. NUGC-3P4T cells developed peritoneal dissemination in 10 / 10 (100%) mice, whereas the parental NUGC-3 cells developed dissemination in 1 / 5 (20.0%) mice. The metastatic foci in the peritoneum showed essentially the same histological appearance as those induced by parental cells. The tumorigenicity, the motile activity and the adhesive activity to the laminin of NUGC-3P4T cells were stronger than those of NUGC-3 cells. Production of IL-8 was significantly higher in NUGC-3P4T than in NUGC-3. cDNA macroarrays analysis showed that a variety of cytokines, interleukins, and other immunomodulators and their receptors were up- or down-regulated at the mRNA level in NUGC-3P4T cells, compared with NUGC-3 cells. Thus, this unique cell line and in vivo model might be useful to study the biology of peritoneal dissemination of human gastric cancer.

Animals↗

Adenosquamous carcinoma of the colorectum: report of two cases.

Adenosquamous carcinomas of the colorectum are rare neoplasms. Our experience with two cases is presented in this paper. One patient, who complained of bloody stool, was found to have adenocarcinoma in the sigmoid colon. He received a laparoscopy-assisted sigmoidectomy. The histological examination revealed that the tumor was adenosquamous carcinoma. To date, he has survived six months post operatively without evidence of recurrence. The other patient, who complained of anal bleeding, was found to have rectal adenocarcinoma and received a low anterior resection. Histological examination revealed that the tumor was an adenosquamous carcinoma. He remains alive, with no evidence of recurrence, nine years post operatively. Both cases showed paracolic lymph node metastasis. Because of its very low incidence, the histogenesis, malignancy and prognosis of this disease remain unclear. Thus, further clinical and histological study of this disease entity is required.

Carcinoma, Adenosquamous↗

p53AIP1, a potential mediator of p53-dependent apoptosis, and its regulation by Ser-46-phosphorylated p53.

Through direct cloning of p53 binding sequences from human genomic DNA, we have isolated a novel gene, designated p53AIP1 (p53-regulated Apoptosis-Inducing Protein 1), whose expression is inducible by wild-type p53. Ectopically expressed p53AIP1, which is localized within mitochondria, leads to apoptotic cell death through dissipation of mitochondrial A(psi)m. We have found that upon severe DNA damage, Ser-46 on p53 is phosphorylated and apoptosis is induced. In addition, substitution of Ser-46 inhibits the ability of p53 to induce apoptosis and selectively blocks expression of p53AIP1. Our results suggest that p53AIP1 is likely to play an important role in mediating p53-dependent apoptosis, and phosphorylation of Ser-46 regulates the transcriptional activation of this apoptosis-inducing gene.

Adenocarcinoma↗

Tubular adenoma of the breast in a 73-year-old woman.

A 73-year-old woman presenting with a right breast mass is described. The patient underwent lumpectomy under a diagnosis of breast cancer. However, histopathologically the surgical specimen was tubular adenoma of the breast. This is a rare benign tumor that is difficult to differentiate from breast cancer clinically, especially in elderly patients. We describe two reported cases of tubular adenoma in patients older than 65-years in Japan, as well as the present case.

Adenoma↗

Detection of congenital malaria by polymerase-chain-reaction methodology in Dar es Salaam, Tanzania.

The examination of congenital malaria was performed by Giemsa staining and polymerase-chain-reaction (PCR) methodology. We randomly selected 298 neonates who had been admitted to Muhimbili Medical Center (MMC) at Dar es Salaam, Tanzania. One baby among all the enrolled neonates was recognized as having a congenital malaria infection, which gave a prevalence of 0.33%. The present result was 5-fold the clinically recognized prevalence of congenital infection with malaria in the ward. The PCR method identified two cases, one of which was negative as determined by the Giemsa-staining method. Therefore, the PCR method was useful for the detection of scant amounts of malarial parasites in numerous blood samples. The screening of malaria by a sensitive PCR method contributes to reduce the mortality of asymptotic neonates in particular.

Gestational Age↗

Analysis of the p300/CBP-Associated Factor (PCAF) gene in astrocytic tumors.

The PCAF gene encodes the p300/CBP-Associated Factor (PCAF), a histone acetyltransferase, which regulates p53 by acetylation of Lys320 in the C-terminal portion of p53. While the p53 gene is one of the most frequently mutated tumor suppressor genes in human tumors, such mutations occur in only 30% of astrocytic tumors. Since PCAF can regulate p53 activity, abrogation of PCAF function by PCAF gene mutation could be an alternate mechanism to inactivate the p53 pathway in tumors lacking p53 mutations. To test this hypothesis, we determined the nucleotide sequence of the entire PCAF coding region in 37 astrocytic tumors (17 glioblastomas, 10 anaplastic astrocytomas, 7 low-grade astrocytomas, and 3 pilocytic astrocytomas). We detected two single-nucleotide alterations that represented non-deleterious polymorphisms (GAG > GAA Glu103Glu, AAT > AGT Asn386Ser) but no obvious functional mutations. Moreover, the frequency of the Asn386Ser allele that contained Ser386 in glioma patients was not statistically different from its frequency in individuals without disease, and no significant association was observed between the PCAF polymorphisms and the presence or absence of p53 mutations in the tumors. We conclude that the PCAF gene is not mutated during the development of the astrocytic tumors studied here.

Alleles↗

Error-correcting codes and image restoration with multiple stages of dynamics

We consider the problems of error-correcting codes and image restoration with multiple stages of dynamics. Information extracted from the former stage can be used selectively to improve the performance of the latter one. Analytic results were derived for the mean-field systems using the cavity method. We find that it has the advantage of being tolerant to uncertainties in hyperparameter estimation, as confirmed by simulations.

Journal Article↗

A novel experimental mouse model of peritoneal dissemination of human gastric cancer cells: different mechanisms in peritoneal dissemination and hematogenous metastasis.

We established a new cell line, AZ-P7a, with high peritoneal-metastatic potential in nude mice. AZ-P7a cells were derived from the human gastric carcinoma line AZ-521, which has low capacity for peritoneal dissemination. AZ-P7a cells developed peritoneal metastasis in 11 / 14 (78.6%) mice, whereas the parental AZ-521 cells developed metastasis in 2 / 6 (33.3%) mice. The metastatic foci in the peritoneum showed essentially the same histological appearance as those induced by parental cells. The tumorigenicity and the motile activity of AZ-P7a cells were stronger than those of the parental AZ-521 cells; in contrast, adhesion to the extracellular matrix and the production of vascular endothelial growth factor by AZ-P7a cells were decreased. In fluorescence-activated cell sorter (FACS) analysis, AZ-P7a cells expressed significantly greater levels of integrins alpha2, alpha3, alpha5, alpha6 and alphavbeta5, as compared with AZ-521 cells. However, alpha1, alpha4, alphavbeta3, hCD44H, hCD44v3, hCD44v6 and hCD44v10 were not expressed in either cell line. AZ-P7a cells developed no liver metastasis when administered by the intrasplenic injection method, though the highly liver metastatic cell line AZ-H5c showed the same rate of peritoneal dissemination as that exhibited by AZ-P7a cells after intraabdominal injection. These findings suggested that the mechanism of peritoneal dissemination differed from that of hematogenous metastasis. Moreover, the latter appears to be controlled by more complex mechanisms than the former. Thus, this cell line might be useful for investigating the mechanism of peritoneal dissemination of human gastric cancer.

Adenocarcinoma↗

Localization of membrane-associated guanylate kinase (MAGI)-1/BAI-associated protein (BAP) 1 at tight junctions of epithelial cells.

Membrane-associated guanylate kinase (MAGI)-1/BAI-associated protein (BAP) 1 and Synapse-associated protein (SAP) 97/human Discs-large tumor suppressor gene (hDLG) are ubiquitous isoforms of synaptic scaffolding molecule (S-SCAM) and Postsynaptic density (PSD)-95/SAP90, both of which are implicated in the structures of synapses, respectively. SAP97/hDLG is localized at epithelial junctions and may function as a scaffolding protein, but the subcellular localization or the function of MAGI-1/BAP1 has not been clarified. In intestinal epithelial cells, MAGI-1/BAP1 was localized at tight junctions, whereas SAP97/hDLG was localized diffusely at cell - cell junctions. In Madine Darby canine kidney (MDCK) cells, MAGI-1/BAP1 was colocalized with ZO-1, whereas SAP97/hDLG was colocalized with E-cadherin. In MDCK cells, dominant active and negative mutants of Rac1 small G protein changed the amounts of SAP97/hDLG at cell - cell junctions, but not that of MAGI-1/BAP1. When MDCK cells were switched to a low Ca2+ medium, E-cadherin disappeared from the plasma membrane, and cells were dissociated. The phorbol 12-myristate 13-acetate-treatment after the low Ca2+ switch induced a tight junction-like structure. MAGI-1/BAP1 was recruited with ZO-1 to this structure, but SAP97/hDLG or E-cadherin was not. These findings suggest that MAGI-1/BAP1 is a component of tight junctions of epithelial cells, and that its role is different from that of SAP97/hDLG.

Adaptor Proteins, Signal Transducing↗