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      • KCI등재

        Irreversible phase transition characteristic of 0.91Pb(Zn1/3Nb2/3) O3-0.09PbTiO3 single crystals by domain observation

        Rongfeng Zhu,Qihui Zhang,Bijun Fang,Jianning Ding,Xiangyong Zhao,Haosu Luo 한국물리학회 2016 Current Applied Physics Vol.16 No.12

        In situ temperature dependent ferroelectric domains dynamic evolution of the (001)pc oriented 0.91Pb(Zn1/3Nb2/3)O3-0.09PbTiO3 (PZNT91/9) single crystals was observed by polarized light microscopy (PLM) and real time synchrotron-radiation (SR) X-ray white-beam topography. Intricate domain structures including monoclinic phase are distinguished by PLM at room temperature, and irreversible domain configuration dynamic evolution upon thermal cycling is observed by both methods. Such irreversible domain evolution combined with coexistence of multi-phases and polarization rotation may be related to the extraordinary piezoelectric performance in the ferroelectric single crystals with the morphotropic phase boundary (MPB) compositions.

      • SCIESCOPUSKCI등재

        Silencing MR-1 attenuates atherosclerosis in ApoE–/– mice induced by angiotensin II through FAK-Akt –mTOR-NF-kappaB signaling pathway

        Yixi Chen,Jianping Cao,Qihui Zhao,Haiyong Luo,Yiguang Wang,Wenjian Dai 대한생리학회-대한약리학회 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.2

        Myofibrillogenesis regulator-1 (MR-1) is a novel protein involved in cellular proliferation, migration, inflammatory reaction and signal transduction. However,little information is available on the relationship between MR-1 expression and the progression of atherosclerosis. Here we report atheroprotective effects of silencing MR-1 in a model of Ang II-accelerated atherosclerosis, characterized by suppression focal adhesion kinase (FAK) and nuclear factor kappaB (NF-κB) signaling pathway,and atherosclerotic lesion macrophage content. In this model, administration of the siRNA-MR-1 substantially attenuated Ang II-accelerated atherosclerosis with stabilization of atherosclerotic plaques and inhibited FAK, Akt, mammalian target of rapamycin (mTOR) and NF-kB activation, which was associated with suppression of inflammatory factor and atherogenic gene expression in the artery. In vitro studies demonstrated similar changes in Ang II-treated vascular smooth muscle cells (VSMCs) and macrophages: siRNA-MR-1 inhibited the expression levels of proinflammatory factor. These studies uncover crucial proinflammatory mechanisms of Ang II and highlight actions of silencing MR-1 to inhibit Ang II signaling, which is atheroprotective.

      • SCIESCOPUSKCI등재

        Silencing MR-1 attenuates atherosclerosis in ApoE<sup>-/-</sup> mice induced by angiotensin II through FAK-Akt -mTOR-NF-kappaB signaling pathway

        Chen, Yixi,Cao, Jianping,Zhao, Qihui,Luo, Haiyong,Wang, Yiguang,Dai, Wenjian The Korean Society of Pharmacology 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.2

        Myofibrillogenesis regulator-1 (MR-1) is a novel protein involved in cellular proliferation, migration, inflammatory reaction and signal transduction. However, little information is available on the relationship between MR-1 expression and the progression of atherosclerosis. Here we report atheroprotective effects of silencing MR-1 in a model of Ang II-accelerated atherosclerosis, characterized by suppression focal adhesion kinase (FAK) and nuclear factor kappaB ($NF-{\kappa}B$) signaling pathway, and atherosclerotic lesion macrophage content. In this model, administration of the siRNA-MR-1 substantially attenuated Ang II-accelerated atherosclerosis with stabilization of atherosclerotic plaques and inhibited FAK, Akt, mammalian target of rapamycin (mTOR) and NF-kB activation, which was associated with suppression of inflammatory factor and atherogenic gene expression in the artery. In vitro studies demonstrated similar changes in Ang II-treated vascular smooth muscle cells (VSMCs) and macrophages: siRNA-MR-1 inhibited the expression levels of proinflammatory factor. These studies uncover crucial proinflammatory mechanisms of Ang II and highlight actions of silencing MR-1 to inhibit Ang II signaling, which is atheroprotective.

      • KCI등재

        Apoptosis induced in vivo by new type gosling viral enteritis virus

        Shun Chen,Anchun Cheng,Mingshu Wang,Dekang Zhu,Renyong Jia,Qihui Luo,Hengmin Cui,Yi Zhou,Yin Wang,Zhiwen Xu,Zhengli Chen,Xiaoyue Chen,Xiaoyu Wang 대한수의학회 2011 JOURNAL OF VETERINARY SCIENCE Vol.12 No.4

        In this study, apoptosis was induced by new type gosling viral enteritis virus (NGVEV) in experimentally infected goslings is reported in detail for the first time. After 3-day-old goslings were orally inoculated with a NGVEV-CN strain suspension, the time course of NGVEV effects on apoptotic morphological changes of the internal tissues was evaluated. These changes were observed by histological analysis with light microscopy and ultrastructural analysis with transmission electron microscopy. DNA fragmentation was assessed with a terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay and DNA ladder analysis. A series of characteristic apoptotic morphological changes including chromatin condensation and margination, cytoplasmic shrinkage, plasma membrane blebbing, and formation of apoptotic bodies were noted. Apoptosis was readily observed in the lymphoid and gastrointestinal organs, and sporadically occurred in other organs after 3 days post-infection (PI). The presence and quantity of TUNEL-positive cells increased with infection time until 9 days PI. DNA extracted from the NGVEV-infected gosling cells displayed characteristic 180~200 bp ladders. Apoptotic cells were ubiquitously distributed, especially among lymphocytes, macrophages, monocytes, and epithelial and intestinal cells. Necrosis was subsequently detected during the late NGVEV-infection phase, which was characterized by cell swelling, plasma membrane collapse, and rapidly lysis. Our results suggested that apoptosis may play an important role in the pathogenesis of NGVE disease.

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