61 research outputs found

    Spectroscopic characterization of naturally and chemically oxidized silicon surfaces

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    We have determined the thicknesses of naturally and chemically grown oxides on HF-cleaned silicon surfaces in ambient air and in NH4OH/H2O2/H2O solution, respectively, using spectroscopic ellipsometry. The naturally grown oxide thickness versus air-exposure time plots yield a rate constant of 3.5+-0.5 Å/decade in ambient air. Chemical oxidation occurs immediately upon immersing the sample in the chemical solution and leaves the sample surface terminated with ~6 Å of a chemical oxide. Photoreflectance intensity is found to be strongly dependent on such surface processing, and results are explained by the different degree of surface (interface) states

    A Genome-Wide Association Study of Nephrolithiasis in the Japanese Population Identifies Novel Susceptible Loci at 5q35.3, 7p14.3, and 13q14.1

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    Nephrolithiasis is a common nephrologic disorder with complex etiology. To identify the genetic factor(s) for nephrolithiasis, we conducted a three-stage genome-wide association study (GWAS) using a total of 5,892 nephrolithiasis cases and 17,809 controls of Japanese origin. Here we found three novel loci for nephrolithiasis: RGS14-SLC34A1-PFN3-F12 on 5q35.3 (rs11746443; P = 8.51×10−12, odds ratio (OR) = 1.19), INMT-FAM188B-AQP1 on 7p14.3 (rs1000597; P = 2.16×10−14, OR = 1.22), and DGKH on 13q14.1 (rs4142110; P = 4.62×10−9, OR = 1.14). Subsequent analyses in 21,842 Japanese subjects revealed the association of SNP rs11746443 with the reduction of estimated glomerular filtration rate (eGFR) (P = 6.54×10−8), suggesting a crucial role for this variation in renal function. Our findings elucidated the significance of genetic variations for the pathogenesis of nephrolithiasis

    Hepatitis C Virus Infection Suppresses the Interferon Response in the Liver of the Human Hepatocyte Chimeric Mouse

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    BACKGROUND AND AIMS: Recent studies indicate that hepatitis C virus (HCV) can modulate the expression of various genes including those involved in interferon signaling, and up-regulation of interferon-stimulated genes by HCV was reported to be strongly associated with treatment outcome. To expand our understanding of the molecular mechanism underlying treatment resistance, we analyzed the direct effects of interferon and/or HCV infection under immunodeficient conditions using cDNA microarray analysis of human hepatocyte chimeric mice. METHODS: Human serum containing HCV genotype 1b was injected into human hepatocyte chimeric mice. IFN-α was administered 8 weeks after inoculation, and 6 hours later human hepatocytes in the mouse livers were collected for microarray analysis. RESULTS: HCV infection induced a more than 3-fold change in the expression of 181 genes, especially genes related to Organismal Injury and Abnormalities, such as fibrosis or injury of the liver (P = 5.90E-16∼3.66E-03). IFN administration induced more than 3-fold up-regulation in the expression of 152 genes. Marked induction was observed in the anti-fibrotic chemokines such as CXCL9, suggesting that IFN treatment might lead not only to HCV eradication but also prevention and repair of liver fibrosis. HCV infection appeared to suppress interferon signaling via significant reduction in interferon-induced gene expression in several genes of the IFN signaling pathway, including Mx1, STAT1, and several members of the CXCL and IFI families (P = 6.0E-12). Genes associated with Antimicrobial Response and Inflammatory Response were also significantly repressed (P = 5.22×10(-10)∼1.95×10(-2)). CONCLUSIONS: These results provide molecular insights into possible mechanisms used by HCV to evade innate immune responses, as well as novel therapeutic targets and a potential new indication for interferon therapy

    Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples

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    Funder: NCI U24CA211006Abstract: The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts

    Uncompensated Spin Elements in Ferromagnetic and Antiferromagnetic Bilayer with Non-Collinear Spin Structure

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    The exchange bias in a ferromagnetic (FM) and antiferromagnetic (AFM) bilayer with a -phase disordered structure has been investigated within a framework of Heisenberg model. The magnetic atoms in the AFM layer realize the triple Q structure due to geometrical spin frustrations. This non-collinear spin structure can bring about an exchange bias in the FM/AFM bilayer system. Under the influence of the exchange bias, the uncompensated spin element appears in the AFM layer, accompanied by a shifted loop in magnetization curves, in accord with the measured loop by X-ray magnetic circular dichroism spectroscopy for an AFM layer

    Landslides in the Epicentral Area of the Matsushiro Earthquake Swarm : Their Relation to the Earthquake Fault

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    1965年8月に始まった長野県松代付近の群発地震は,現在もその活動を続けているが,これまでに, 1966年4月を中心とする時期と,同年8月から9月にかけてとの2回の著しい活動期があった.特に2回目の活動期(8月~9月,いわゆる第3活動期)には,皆神山北東部を中心とする地域の地殻変動, (土地の隆起及び南北方向の伸長,地震断層の動きによる地割れの発生・開口など)が著しく, 9月に入ってからは同上地域の山麓各所で地下水が湧出をはじめた.地辷りはこの地域内の数ケ所に,隆起・伸長等の地殻変動が逆向きに転じた後, 9月17日からの約25日間に発生した

    Augmenting DR-ASIP flexibility through multi-mode custom instructions

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