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RISS 인기검색어
- 검색키워드
- 저자 : Zhixin Shan (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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Influence of Coastal Wind on Surface Ozone and Nitrogen Oxides in Suburban Shanghai
Wenpo Shan,Peng Yang,Haixia Lu,Kefeng Ma,Zhixin Huang 한국기상학회 2016 Asia-Pacific Journal of Atmospheric Sciences Vol.52 No.5
Surface ozone, NO, NO2, and NOx were measured at a coastal site (Shihua) and a nearby inland site (Zhujing) in suburban Shanghai for the whole year of 2009. More days with ozone pollution in a longer time range were observed at the coastal site than the inland site. The diurnal variations of NOx concentrations were obviously higher at Zhujing station, while those of ozone concentrations were higher at Shihua station, indicating their different air pollution conditions. Coastal wind has significant influence on the levels and characteristics of the air pollutants. The ozone concentrations during maritime winds (MW) were much higher than those during continental winds (CW) at each of the site, while the NO and NO2 concentrations were both opposite. The ozone concentrations at Shihua station were much higher than those at Zhujing station, while the NO and NO2 concentrations were both opposite. The ozone concentrations at both of the two sites showed a distinct “weekend effects” and “weekdays effects” patterns during CW and MW, respectively. Correlation analysis of the pollutants showed that, the compounds during MW were more age than those during CW, and the compounds at Shihua were more age than those at Zhujing. The air pollutions at both of the two sites are mainly associated with the pollutants emitted in this region instead of long range transport.
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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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