60 research outputs found

    The scaffold protein JLP plays a key role in regulating ultraviolet B-induced apoptosis in mice

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    The ultraviolet B (UVB) component of sunlight can cause severe damage to skin cells and even induce skin cancer. Growing evidence indicates that the UVB-induced signaling network is complex and involves diverse cellular processes. In this study, we investigated the role of c-Jun NH2-terminal kinase-associated leucine zipper protein (JLP), a scaffold protein for mitogen-activated protein kinase (MAPK) signaling cascades, in UVB-induced apoptosis. We found that UVB-induced skin epidermal apoptosis was prevented in Jlp knockout (KO) as well as in keratinocyte-specific Jlp KO mice. Analysis of the repair of UVB-induced DNA damage over time showed no evidence for the involvement of JLP in this process. In contrast, UVB-stimulated p38 MAPK activation in the skin was impaired in both Jlp KO and keratinocyte-specific Jlp KO mice. Moreover, topical treatment of UVB-irradiated mouse skin with a p38 inhibitor significantly suppressed the epidermal apoptosis in wild-type mice, but not in Jlp KO mice. Our findings suggest that JLP in skin basal keratinocytes plays an important role in UVB-induced apoptosis by modulating p38 MAPK signaling pathways. This is the first study to show a critical role for JLP in an in vivo response to environmental stimulation. © 2014 by the Molecular Biology Society of Japan and Wiley Publishing Asia Pty Ltd

    恒久的な平和への取組みと市民社会の可能性 : 核廃絶に向けた70年の軌跡と今後

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    要旨...1 開会の言葉...4 趣旨説明...5 第Ⅰ部 核廃絶に向けた努力の軌跡  The OSCE in the Ukrainian Crisis and Beyond...Ertuğrul Apakan...7  核廃絶から遠ざかる世界 : 「大乱」時代の様相...河東哲夫...12  核軍縮・不拡散問題の現状と我が国の政策...中村吉利...18  核に頼るリスクと廃絶に向けた課題...友次晋介...25 基調講演/Keynote speech  The Challenges to Global Peace And the Hiroshima Legacy...Surakiart Sathirathai...29 第Ⅱ部 市民社会の可能性とグローバルな平和への展望  核兵器廃絶へ向けての市民社会のあり方...櫻井本篤...40  市民社会の可能性はあるか : 女性の視点から...坂東眞理子...48  Empowering Peace in the Twenty-first Century...Brian Finlay...53  グローバルな時代に生き残るために...薬師寺克行...59 閉会の言葉...64 資料1 シンポジウム・ポスター...68 資料2 参加者アンケート結果...702015年度第1回広島大学平和科学研究センター主催国際シンポジウ

    Research Activities in the Department of Medical Engineering

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    The Department of Medical Engineering is dedicated to the research and educational activities to fulfill its mission as educating medical professionals in medical engineering under the diploma policy and curriculum policy, that is, "research and education aiming for fostering professionals competent in comprehensive resolving capacity based upon a wide field of knowledge and vision in clinical engineering, which can be attained by wearing the basic knowledge of medical science and engineering." For this reason, the Faculty of the Department of Medical Engineering is composed of the two areas; PhDs in engineering-based clinical medicine, and mainly MDs in medical sciences and clinical medicine. To summarize the research activities at the Department of Medical Engineering, the authors will describe the overview of research activities being performed in the Department of Medical Engineering Fields, by dividing into 1) Research in Biomedical Engineering Fields, and 2) Research in Medical Science and Clinical Engineering Fields

    Dysregulation of Gene Expression in the Artificial Human Trisomy Cells of Chromosome 8 Associated with Transformed Cell Phenotypes

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    A change in chromosome number, known as aneuploidy, is a common characteristic of cancer. Aneuploidy disrupts gene expression in human cancer cells and immortalized human epithelial cells, but not in normal human cells. However, the relationship between aneuploidy and cancer remains unclear. To study the effects of aneuploidy in normal human cells, we generated artificial cells of human primary fibroblast having three chromosome 8 (trisomy 8 cells) by using microcell-mediated chromosome transfer technique. In addition to decreased proliferation, the trisomy 8 cells lost contact inhibition and reproliferated after exhibiting senescence-like characteristics that are typical of transformed cells. Furthermore, the trisomy 8 cells exhibited chromosome instability, and the overall gene expression profile based on microarray analyses was significantly different from that of diploid human primary fibroblasts. Our data suggest that aneuploidy, even a single chromosome gain, can be introduced into normal human cells and causes, in some cases, a partial cancer phenotype due to a disruption in overall gene expression
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