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RISS 인기검색어
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- 저자 : Yayi Huang (검색결과 2 건)
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Yayi Cheng,Jianfeng Huang,Liyun Cao,Yongfeng Wang,Ying Ma,Shaohua Xi,Bingyao Shi,Hui Xie,Jiayin Li 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2019 NANO Vol.15 No.01
SnSe2 and SnSe nanocrystals were prepared using a simple solvothermal method by changing the molar ratio of SnCl2 · 2H2O and Se powder. When SnSe2 and SnSe are acted as lithium ion battery anodes, the SnSe hybrid structure shows more excellent electrochemical performance than that of SnSe2 interconnected nanosheet. It delivers a reversible capacity of 1023 mA h g -1 at a current density of 200 mA g -1, and maintaining a capacity of 498 mA h g -1 till 120 cycles. According to many present works, SnSe2 with interconnected thin nanosheet should possess more superior property than hybrid structured SnSe due to short charge transfer paths. However, in our research, the result is the opposite. Therefore, we consider that the superior electrochemical performance of SnSe is attributed to its highly reversible conversion reaction mechanism than SnSe2.
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Huaxin Wang,Xuan Peng,Yayi Huang,Yeda Xiao,Zhuo Wang,Liying Zhan 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.12
Purpose: The aim of this study was to investigate whether propofol could attenuate hypoxia/reoxygenation-induced apoptosisand autophagy in human renal proximal tubular cells (HK-2) by inhibiting JNK activation. Materials and Methods: HK-2 cells were treated with or without propofol or JNK inhibitor SP600125 for 1 hour and then subjectedto 15 hours of hypoxia and 2 hours of reoxygenation (H/R). Cell viability and LDH release were measured with commercial kits. Cell apoptosis was evaluated by flow cytometry. The expressions of p-JNK, cleaved-caspase-3, Bcl-2, and autophagy markers LC3and p62 were measured by Western blot or immunofluorescence. Results: HK-2 cells exposed to H/R insult showed higher cell injury (detected by increased LDH release and decreased cell viability),increased cell apoptosis index and expression of cleaved-caspase-3, a decrease in the expression of Bcl-2 accompanied byincreased expression of p-JNK and LC3II, and a decrease in expression of p62. All of these alterations were attenuated by propofoltreatment. Similar effects were provoked upon treatment with the JNK inhibitor SP600125. Moreover, the protective effects weremore obvious with the combination of propofol and SP600125. Conclusion: These results suggest that propofol could attenuate hypoxia/reoxygenation induced apoptosis and autophagy inHK-2 cells, probably through inhibiting JNK activation.
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