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Study of the electrochemical reaction mechanism of nitinol in the methanol-perchloric acid system
Weidong Miao,Xujun Mi,Ming Zhu,Huachu Li 한양대학교 세라믹연구소 2006 Journal of Ceramic Processing Research Vol.7 No.4
Cyclic voltammetry and polarization curves were used for a study of the electrochemical reaction mechanism of the NiTi alloy in the methanol-perchloric acid system. The anodic polarization curves and the Tafel curves were obtained. The dynamic parameters of the anodic NiTi are: a: 5.0805, b: 1.1958, i0: 5.6416×10−5A/cm2, nβ: 0.048. The results of cyclic voltammetry show that NiTi alloy dissolves in the solution as an intermetallic instead of titanium and nickel separately, and that the anodic reaction of the NiTi alloy in the system is an irreversible process, the anodic peak on the CV curve corresponds to an onestep oxidation process involving seven electrons, and the anodic reaction is NiTi - 7e → Ti4++Ni3+ followed by a reduction process Ni3+ + e → Ni2+. Cyclic voltammetry and polarization curves were used for a study of the electrochemical reaction mechanism of the NiTi alloy in the methanol-perchloric acid system. The anodic polarization curves and the Tafel curves were obtained. The dynamic parameters of the anodic NiTi are: a: 5.0805, b: 1.1958, i0: 5.6416×10−5A/cm2, nβ: 0.048. The results of cyclic voltammetry show that NiTi alloy dissolves in the solution as an intermetallic instead of titanium and nickel separately, and that the anodic reaction of the NiTi alloy in the system is an irreversible process, the anodic peak on the CV curve corresponds to an onestep oxidation process involving seven electrons, and the anodic reaction is NiTi - 7e → Ti4++Ni3+ followed by a reduction process Ni3+ + e → Ni2+.
LncRNA taurine up-regulated gene 1 participates in isoflurane induced neurotoxicity
Zhang Faqiang,Chen Guoqing,Wang Long,Feng Zeguo,Mi Weidong 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.3
Background Isoflurane (ISO), with the characteristics of rapid induction and recovery, has become one of the most commonly used inhalation anesthetics in the world. Objective The purpose of this study was to explore the biological mechanism of long non-coding RNA taurine up-regulated gene 1 (TUG1) in isoflurane (ISO) induced neurotoxicity through in vitro cell experiments. Result ISO exposure inhibited cell viability while promoted ROS generation, cell apoptosis and inflammatory cytokines release in HT22 cells via upregulating long noncoding RNA (lncRNA) TUG1. MiR-15a-5p was a direct target of TUG1 and was reversed regulated by TUG1. Overexpression of miR-15a-5p alleviated neurotoxicity induced by ISO exposure, while downregulation of TUG1 alleviated the neurotoxicity induced by ISO exposure via upregulation of miR-15a-5p. Conclusion Downregulation of TUG1 reduced ISO-induced ROS generation, neuron cell apoptosis and inflammatory response. ISO-induced neurotoxicity in HT22 cells was regulated by TUG1/miR-15a-5p axis. Background Isoflurane (ISO), with the characteristics of rapid induction and recovery, has become one of the most commonly used inhalation anesthetics in the world. Objective The purpose of this study was to explore the biological mechanism of long non-coding RNA taurine up-regulated gene 1 (TUG1) in isoflurane (ISO) induced neurotoxicity through in vitro cell experiments. Result ISO exposure inhibited cell viability while promoted ROS generation, cell apoptosis and inflammatory cytokines release in HT22 cells via upregulating long noncoding RNA (lncRNA) TUG1. MiR-15a-5p was a direct target of TUG1 and was reversed regulated by TUG1. Overexpression of miR-15a-5p alleviated neurotoxicity induced by ISO exposure, while downregulation of TUG1 alleviated the neurotoxicity induced by ISO exposure via upregulation of miR-15a-5p. Conclusion Downregulation of TUG1 reduced ISO-induced ROS generation, neuron cell apoptosis and inflammatory response. ISO-induced neurotoxicity in HT22 cells was regulated by TUG1/miR-15a-5p axis.