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RISS 인기검색어
- 검색키워드
- 저자 : Luo Zhenhua (검색결과 3 건)
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Thickness-dependent reversible hydrogenation of graphene layers.
Luo, Zhiqiang,Yu, Ting,Kim, Ki-Jeong,Ni, Zhenhua,You, Yumeng,Lim, Sanhua,Shen, Zexiang,Wang, Shanzhong,Lin, Jianyi American Chemical Society 2009 ACS NANO Vol.3 No.7
<P>In this work, graphene layers on SiO(2)/Si substrate have been chemically decorated by radio frequency hydrogen plasma. Hydrogen coverage investigation by Raman spectroscopy and micro-X-ray photoelectron spectroscopy characterization demonstrates that the hydrogenation of single layer graphene on SiO(2)/Si substrate is much less feasible than that of bilayer and multilayer graphene. Both the hydrogenation and dehydrogenation process of the graphene layers are controlled by the corresponding energy barriers, which show significant dependence on the number of layers. The extent of decorated carbon atoms in graphene layers can be manipulated reversibly up to the saturation coverage, which facilitates engineering of chemically decorated graphene with various functional groups via plasma techniques.</P>
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Yanjun Pan,Yang Li,Jinda Luo,Xianyou Wang,Zhenhua Yang 한국물리학회 2019 Current Applied Physics Vol.19 No.10
Tightly and vertically attached graphene nanosheets (GNS) on the surface of FeF3·0.33H2O is extremely desirable to substantially accelerate electron transport, promoting rate capability of FeF3·0.33H2O. Based on present experiment and calculated surface energies, firstly, it has confirmed that F-terminated FeF3·0.33H2O (002) surface (FeF3·0.33H2O (002)-F) is more stable than FeF-terminated FeF3·0.33H2O (002) surface (FeF3·0.33H2O (002)- FeF) when μF varies from −1.92 eV to −0.30 eV. Then, by analysis of the interfacial structure and adsorption energies, it was proposed that GNS is incline to stand vertically on the FeF3·0.33H2O (002) surface via C–F bond. However, structural stability of FeF3·0.33H2O/GNS heterostructure is gradually weakened with increasing the number of GNS layers. Therefore, we further reported the important role of optimal doping element (Hf) in strengthening the vertical adsorption behavior of GNS on FeF3·0.33H2O (002) surface via thorough doping element search. And it turns out interfacial structure with hexa-coordinate polyhedron consists of Hf, F and O atoms is formed by strong hybridization of atomic orbits, which induces the interaction between FeF3·0.33H2O (002) surface and GNS to be profoundly strengthened.
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Huang Guangwei,Bao Hailong,Zhan Peng,Lu Xiyang,Duan Zonggang,Xiong Xinlin,Lin Muzhi,Wang Bing,An Hongxin,Xiahou Luanda,Zhou Haiyan,Luo Zhenhua,Li Wei 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2
Objectives This study aimed at investigating the role of the proprotein convertase subtilisin/Kexin type 9 (PCSK9)-mediated autophagy on myocardial ischemia/reperfusion injury (MIRI). To determine the relationship between autophagy, apoptosis, fibrosis, and inflammation in the myocardium, to provide experience in preventing and treating the myocardial ischemia/reperfusion (I/R) injury. Methods An AC16 hypoxia-reoxygenation model and a rat myocardial ischemia–reperfusion model were established. The concentrations of cardiac troponin T (cTnT) and creatine kinase-MB (CKMB) in plasma were measured by ELISA. To determine the size of the myocardial infarction, TTC/EB staining was performed. In addition to identifying pathological changes in myocardial tissue, Masson’s trichrome stains and H&E stains were used to identify pathological changes. Echocardiography was employed to detect cardiac function. Western blot analysis was then performed to detect the protein expression of Parkin, Pink1, and markers associated with autophagy (Beclin-1, p62, LC3). Results A significant increase in PCSK9 was observed in the myocardium during H/R. In the cardiac-specific PCSK9 knockdown model, cardiac autophagy was significantly inhibited, whereas cardiac-specific PCSK9 overexpression promoted cardiac autophagy. In vivo studies have demonstrated a significant decrease in cardiac autophagy when the PCSK9 inhibitor was administered. Apoptosis induced by I/R was greatly decreased, and myocardial infarction size and function were both improved by PCSK9 inhibitors. Mechanistically, the PCSK9 inhibitor improved the degree of myocardial fibrosis and inhibited the development of inflammation. Conclusions Our results demonstrated that increased PCSK9 via the parkin/pink1 signaling pathway contributes to I/R and H/R by exaggerating excessive autophagy during reperfusion/reoxygenation. In addition, the PCSK9 inhibitor blocked the development of inflammation and improved Infarct size, myocardial function, and myocardial fibrosis.
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