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RISS 인기검색어
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- 저자 : Huang Haiming (검색결과 4 건)
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Jianle Wang,Majid Nisar,Chongan Huang,Xiangxiang Pan,Dongdong Lin,Gang Zheng,Haiming Jin,Deheng Chen,Naifeng Tian,Qianyu Huang,Yue Duan,Yingzhao Yan,Ke Wang,Congcong Wu,Jianing Hu,Xiaolei Zhang,Xiangy 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Oxidative stress-induced mitochondrial dysfunction is implicated in the pathogenesis of intervertebral disc degeneration (IVDD). Sirtuin 3 (SIRT3), a sirtuin family protein located in mitochondria, is essential for mitochondrial homeostasis; however, the role of SIRT3 in the process of IVDD has remained elusive. Here, we explored the expression of SIRT3 in IVDD in vivo and in vitro; we also explored the role of SIRT3 in senescence, apoptosis, and mitochondrial homeostasis under oxidative stress. We subsequently activated SIRT3 using honokiol to evaluate its therapeutic potential for IVDD. We assessed SIRT3 expression in degenerative nucleus pulposus (NP) tissues and oxidative stressinduced nucleus pulposus cells (NPCs). SIRT3 was knocked down by lentivirus and activated by honokiol to determine its role in oxidative stress-induced NPCs. The mechanism by which honokiol affected SIRT3 regulation was investigated in vitro, and the therapeutic potential of honokiol was assessed in vitro and in vivo. We found that the expression of SIRT3 decreased with IVDD, and SIRT3 knockdown reduced the tolerance of NPCs to oxidative stress. Honokiol (10 μM) improved the viability of NPCs under oxidative stress and promoted their properties of anti-oxidation, mitochondrial dynamics and mitophagy in a SIRT3-dependent manner. Furthermore, honokiol activated SIRT3 through the AMPKPGC- 1α signaling pathway. Moreover, honokiol treatment ameliorated IVDD in rats. Our study indicated that SIRT3 is involved in IVDD and showed the potential of the SIRT3 agonist honokiol for the treatment of IVDD.
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Rapid fabrication of NiFe(OH)x/Fe0.2Co-Se complexes for oxygen evolution reaction electrocatalysis
Kang Gao,Miao Xu,Chuankun Zhang,Haiming Huang,Dongming Cai,Minglei Cao,Jun Wu,Chengrui Wu,Yongjin Hu,Rui Tong 한국공업화학회 2023 Journal of Industrial and Engineering Chemistry Vol.124 No.-
Exploiting the inexpensive and efficient oxygen evolution reaction (OER) electrocatalysts is crucial forimproving the efficiency of electrocatalytic water splitting (EWS), since the slow 4-electron OER processis a rate-limiting step in EWS. Herein, we prepared the NiFe(OH)x/Fe0.2Co-Se complexes on carbon paper(CP) via an easy two-step electrochemical deposition strategy. By varying the doping amount of Fe andthe deposition time of Fe0.2Co-Se, the OER property of NiFe(OH)x/Fe0.2Co-Se/CP was optimized to the best:only requiring low overpotentials of 243 and 277 mV at the current density of 20 and 100 mA/cm2 (j20and j100) and a small Tafel slope of 36.8 mV/dec, along with a terrific long-term durability in 1 M KOH. According to the experimental results, the rich exposed active sites, improved intrinsic site activityand enhanced electrical conductivity lead to the superior OER performance. Our work will provide someinspiration for designing other metal selenide/hydroxide heterostructures for other energy conversion orstorage applications.
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Frequency Response Analysis on Modified Plant of Extended State Observer
Yuqiong Zhang,Yali Xue,Donghai Li,Zhiqiang Gao,Haiming Niu,Huanpao Huang 제어로봇시스템학회 2017 제어로봇시스템학회 국제학술대회 논문집 Vol.2017 No.10
The active disturbance rejection control (ADRC) framework gives birth to a new concept, the modified plant (MP), describing the dynamics after the total disturbance is estimated and cancelled approximately. Ideally the modified plant is in integral form, to greatly simplify and fix the controller design, even though actual plant contains higher-order dynamics or dead time. This paper investigates that when such processes are modified into the integral, how the parameters of the extended state observer (ESO) impact on the dynamic characteristics and stability of the MP. Frequency-domain analyses show that the MP can gradually approach the integral form through parameters tuning. However, it should be cautious that an aggressive set of parameters may lead to an unstable modified plant in the presence of order mismatch.
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The Role of Macrophage Migration Inhibitory Factor (MIF) in Asthmatic Airway Remodeling
Li Ruyi,Wang Feiyun,Wei Jianghong,Lin Yun,Tang Guofang,Rao Lizong,Ma Libing,Xu Qing,Wu Jingjie,Lv Qian,Zhou Rui,Lei Huiren,Zhao Xueqiang,Yao Dong,Xiao Bo,Huang Haiming,Zhang Jiange,Mo Biwen 대한천식알레르기학회 2021 Allergy, Asthma & Immunology Research Vol.13 No.1
Purpose: Recent studies have demonstrated that macrophage migration inhibitory factor (MIF) is of importance in asthmatic inflammation. The role of MIF in modulating airway remodeling has not yet been thoroughly elucidated to date. In the present study, we hypothesized that MIF promoted airway remodeling by intensifying airway smooth muscle cell (ASMC) autophagy and explored the specific mechanisms. Methods: MIF knockdown in the lung tissues of C57BL/6 mice was conducted by instilling intratracheally adeno-associated virus (AAV) vectors (MIF-mutant AAV9) into mouse lung tissues. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) was used to detect the role of autophagy in ovalbumin (OVA)-asthmatic murine models. Moreover, to block the expression of MIF and CD74 in vitro models, inhibitors, antibodies and lentivirus transfection techniques were employed. Results: First, MIF knockdown in the lung tissues of mice showed markedly reduced airway remodeling in OVA murine mice models. Secondly, ASMC autophagy was increased in the OVA-challenged models. Mice genetically deficient in the autophagy marker ATG5 (ATG5+/−) that were primed and challenged with OVA showed lower airway remodeling than genetically wild-type asthmatic mice. Thirdly, MIF can induce ASMC autophagy in vitro. Moreover, the cellular source of MIF which promoted ASMC autophagy was macrophages. Finally, MIF promoted ASMC autophagy in a CD74-dependent manner. Conclusions: MIF can increase asthmatic airway remodeling by enhancing ASMC autophagy. Macrophage-derived MIF can promote ASMC autophagy by targeting CD74.
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