原発性肺癌におけるインターロイキン8の発現に関する検討

取得学位 : 博士（医学）, 学位授与番号 : 医博乙第1482号, 学位授与年月日：平成11年3月17日,学位授与年：199

Mercury and cadmium immobilization in potassium-activated geopolymer: the effect of mixing design and heavy metals concentration

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Laser-captured microdissection-microarray analysis of the genes involved in endometrial carcinogenesis: stepwise up-regulation of lipocalin2 expression in normal and neoplastic endometria and its functional relevance

Endometrial carcinoma often arises from normal endometrial glandular cells via a precursor, atypical endometrial hyperplasia. However, the genetic changes involved in this carcinogenetic process are not fully understood. Differentially expressed genes were selected from glandular cells of normal proliferative-phase endometria, atypical endometrial hyperplasia, and endometrial carcinoma using laser-captured microdissection and microarray. The microarray analysis revealed a total of 51 genes to be up-regulated and 23 genes to be down-regulated in neoplastic endometrial epithelia. We focused on lipocalin2 (LCN2), which showed the largest magnitude of up-regulation. Immunostaining for lipocalin2 confirmed a stepwise increase in its expression in endometrial hyperplasia and carcinoma. In addition, elevated expression of lipocalin2 was correlated with the poor outcome of endometrial carcinoma patients. The subcellular distribution of lipocalin2 was both cytoplasmic and nuclear, despite reports that lipocalin2 is a secretory protein. Treatment of endometrial carcinoma cells with 5-azacytidine increased the expression of lipocalin2, suggesting the expression to be controlled by methylation of the promoter. The forced expression of lipocalin2 resulted in the enhanced cell proliferation and invasion in vitro. The expression of lipocalin2 increased with the endometrial carcinogenesis, and accumulation of the protein conferred biological aggressiveness to endometrial carcinoma cells. These results suggest lipocalin2 to be a novel target in the treatment of endometrial carcinoma.ArticleHUMAN PATHOLOGY. 42(9):1265-1274 (2011)journal articl

Utilisation of Cs-contaminated Fukushima soil as natural pozzolan for embedding into k-alkali activated materials

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A Case of Vaginal Varices that Caused Massive Bleeding after Vaginal Delivery

Article信州医学雑誌 64(1):35-39 (2016)journal articl

Global distributions of storm-time ionospheric currents as seen in geomagnetic field variations

To investigate temporal and spatial evolution of global geomagnetic field variations from high-latitude to the equator during geomagnetic storms, we analyzed ground geomagnetic field disturbances from high latitudes to the magnetic equator. The daytime ionospheric equivalent current during the storm main phase showed that twin-vortex ionospheric currents driven by the Region 1 field-aligned currents (R1 FACs) are intensified significantly and expand to the low-latitude region of ~30° magnetic latitude. Centers of the currents were located around 70° and 65° in the morning and afternoon, respectively. Corresponding to intensification of the R1 FACs, an enhancement of the eastward/westward equatorial electrojet occurred at the daytime/nighttime dip equator. This signature suggests that the enhanced convection electric field penetrates to both the daytime and nighttime equator. During the recovery phase, the daytime equivalent current showed that two new pairs of twin vortices, which are different from two-cell ionospheric currents driven by the R1 FACs, appear in the polar cap and mid latitude. The former led to enhanced northward Bz (NBZ) FACs driven by lobe reconnection tailward of the cusps, owing to the northward interplanetary magnetic field (IMF). The latter was generated by enhanced Region 2 field-aligned currents (R2 FACs). Associated with these magnetic field variations in the mid-latitudes and polar cap, the equatorial magnetic field variation showed a strongly negative signature, produced by the westward equatorial electrojet current caused by the dusk-to-dawn electric field

FoxO1 Gain of Function in the Pancreas Causes Glucose Intolerance, Polycystic Pancreas, and Islet Hypervascularization

Genetic studies revealed that the ablation of insulin/IGF-1 signaling in the pancreas causes diabetes. FoxO1 is a downstream transcription factor of insulin/IGF-1 signaling. We previously reported that FoxO1 haploinsufficiency restored β cell mass and rescued diabetes in IRS2 knockout mice. However, it is still unclear whether FoxO1 dysregulation in the pancreas could be the cause of diabetes. To test this hypothesis, we generated transgenic mice overexpressing constitutively active FoxO1 specifically in the pancreas (TG). TG mice had impaired glucose tolerance and some of them indeed developed diabetes due to the reduction of β cell mass, which is associated with decreased Pdx1 and MafA in β cells. We also observed increased proliferation of pancreatic duct epithelial cells in TG mice and some mice developed a polycystic pancreas as they aged. Furthermore, TG mice exhibited islet hypervascularities due to increased VEGF-A expression in β cells. We found FoxO1 binds to the VEGF-A promoter and regulates VEGF-A transcription in β cells. We propose that dysregulation of FoxO1 activity in the pancreas could account for the development of diabetes and pancreatic cysts

A Case Control Association Study and Cognitive Function Analysis of Neuropilin and Tolloid-Like 1 Gene and Schizophrenia in the Japanese Population

BACKGROUND: Using a knock-out mouse model, it was shown that NETO1 is a critical component of the NMDAR complex, and that loss of Neto1 leads to impaired hippocampal long term potentiation and hippocampal-dependent learning and memory. Moreover, hemizygosity of NETO1 was shown to be associated with autistic-like behavior in humans. PURPOSE OF THE RESEARCH: We examined the association between schizophrenia and the neuropilin and tolloid-like 1 gene (NETO1). First, we selected eight single nucleotide polymorphisms (SNPs) within the NETO1 locus, based on the Japanese schizophrenia genome wide association study (JGWAS) results and previously conducted association studies. These SNPs were genotyped in the replication sample comprised of 963 schizophrenic patients and 919 healthy controls. We also examined the effect of associated SNPs on scores in the Continuous Performance Test and the Wisconsin Card Sorting Test Keio version (schizophrenic patients 107, healthy controls 104). RESULTS: There were no significant allele-wise and haplotype-wise associations in the replication analysis after Bonferroni correction. However, in meta-analysis (JGWAS and replication dataset) three association signals were observed (rs17795324: p = 0.028, rs8098760: p = 0.017, rs17086492: p = 0.003). These SNPs were followed up but we could not detect the allele-specific effect on cognitive performance measured by the Continuous performance test (CPT) and Wisconsin Card Sorting test (WCST). MAJOR CONCLUSIONS: We did not detect evidence for the association of NETO1 with schizophrenia in the Japanese population. Common variants within the NETO1 locus may not increase the genetic risk for schizophrenia in the Japanese population. Additionally, common variants investigated in the current study did not affect cognitive performance, as measured by the CPT and WCST