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RISS 인기검색어
- 검색키워드
- 저자 : Zhixin Deng (검색결과 4 건)
- 무료
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- 유료
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Yan, Qixiang,Li, Binjia,Deng, Zhixin,Li, Bin Techno-Press 2018 Structural Engineering and Mechanics, An Int'l Jou Vol.65 No.6
The aim of this study was to investigate the mechanical responses of a high-speed railway shield tunnel subjected to impact by a derailed train, with emphasis on the protective effect of the secondary lining. To do so, the extended finite element method was used to develop two numerical models of a shield tunnel including joints and joint bolts, one with a cast-in-situ concrete secondary lining and one without such a lining. The dynamic responses of these models upon impact were analyzed, with particular focus on the distribution and propagation of cracks in the lining structures and the mechanical responses of the joint bolts. The numerical results showed that placing a secondary lining significantly constricted the development of cracking in the segmental lining upon the impact load caused by a derailed train, reduced the internal forces on the joint bolts, and enhanced the safety of the segmental lining structure. The outcomes of this study can provide a numerical reference for optimizing the design of shield tunnels under accidental impact loading conditions.
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Qixiang Yan,Binjia Li,Zhixin Deng,Bin Li 국제구조공학회 2018 Structural Engineering and Mechanics, An Int'l Jou Vol.65 No.6
The aim of this study was to investigate the mechanical responses of a high-speed railway shield tunnel subjected to impact by a derailed train, with emphasis on the protective effect of the secondary lining. To do so, the extended finite element method was used to develop two numerical models of a shield tunnel including joints and joint bolts, one with a cast-in-situ concrete secondary lining and one without such a lining. The dynamic responses of these models upon impact were analyzed, with particular focus on the distribution and propagation of cracks in the lining structures and the mechanical responses of the joint bolts. The numerical results showed that placing a secondary lining significantly constricted the development of cracking in the segmental lining upon the impact load caused by a derailed train, reduced the internal forces on the joint bolts, and enhanced the safety of the segmental lining structure. The outcomes of this study can provide a numerical reference for optimizing the design of shield tunnels under accidental impact loading conditions.
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Involvement of Orai1 in tunicamycin-induced endothelial dysfunction
Hui Yang,Yumei Xue,Sujuan Kuang,Mengzhen Zhang,Jinghui Chen,Lin Liu,Zhixin Shan,Qiuxiong Lin,Xiaohong Li,Min Yang,Hui Zhou,Fang Rao,Chunyu Deng 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.2
Endoplasmic reticulum (ER) stress is mediated by disturbance of Ca2+ homeostasis. The store-operated calcium (SOC) channel is the primary Ca2+ channel in non-excitable cells, but its participation in agent-induced ER stress is not clear. In this study, the effects of tunicamycin on Ca2+ influx in human umbilical vein endothelial cells (HUVECs) were observed with the fluorescent probe Fluo-4 AM. The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin induced endothelial dysfunction by activating ER stress. Orai1 expression and the influx of extracellular Ca2+ in HUVECs were both upregulated during ER stress. The SOC channel inhibitor SKF96365 reversed tunicamycin-induced endothelial cell dysfunction by inhibiting ER stress. Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.
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Involvement of Orai1 in tunicamycin-induced endothelial dysfunction
Yang, Hui,Xue, Yumei,Kuang, Sujuan,Zhang, Mengzhen,Chen, Jinghui,Liu, Lin,Shan, Zhixin,Lin, Qiuxiong,Li, Xiaohong,Yang, Min,Zhou, Hui,Rao, Fang,Deng, Chunyu The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.2
Endoplasmic reticulum (ER) stress is mediated by disturbance of $Ca^{2+}$ homeostasis. The store-operated calcium (SOC) channel is the primary $Ca^{2+}$ channel in non-excitable cells, but its participation in agent-induced ER stress is not clear. In this study, the effects of tunicamycin on $Ca^{2+}$ influx in human umbilical vein endothelial cells (HUVECs) were observed with the fluorescent probe Fluo-4 AM. The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin induced endothelial dysfunction by activating ER stress. Orai1 expression and the influx of extracellular $Ca^{2+}$ in HUVECs were both upregulated during ER stress. The SOC channel inhibitor SKF96365 reversed tunicamycin-induced endothelial cell dysfunction by inhibiting ER stress. Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.
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