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- 저자 : Tian Haibin (검색결과 3 건)
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Synthesis of the wheat-like CdSe/CdTe thin film heterojunction and their photovoltaic applications
Lecheng Tian,Haibin Yang,Juan Ding,Qian Li,Yannan Mu,Yuhang Zhang 한국물리학회 2014 Current Applied Physics Vol.14 No.6
We report on the fabrication of wheat-like CdSe/CdTe thin film heterojunction solar cells made using a simple electrochemical deposition method and close-spaced sublimation technology on indium tin oxide (ITO) substrates. Structural, optical, and electrical properties of the wheat-like CdSe/CdTe thin film junctions were characterized by X-ray diffraction (XRD), field emission scanning electron microscope (FESEM), energy dispersive spectrometry (EDS), ultravioletevisible (UVevis) absorption spectrum and Keithley 2400 analysis. A significant red-shift of the absorption edge is observed in this heterojunction. The heterostructure is composed of the wheat-like CdSe array and CdTe thin film, showing optical properties typical of type II heterostructures that are suited for photovoltaic applications. A photocurrent density of 8.34 mA/cm2 has been obtained under visible light illumination of 100 mW/cm2. This study demonstrates that the electrochemical deposition and the close-spaced sublimation technology, which are easily adapted to other chemical systems, are promising techniques for large-scale fabrication of lowcost heterojunction solar cells.
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Wang, Shuaifei,Li, Fangyuan,Qiao, Ruirui,Hu, Xi,Liao, Hongwei,Chen, Lumin,Wu, Jiahe,Wu, Haibin,Zhao, Meng,Liu, Jianan,Chen, Rui,Ma, Xibo,Kim, Dokyoon,Sun, Jihong,Davis, Thomas P.,Chen, Chunying,Tian, American Chemical Society 2018 ACS NANO Vol.12 No.12
<P>Ferroptosis, an iron-based cell-death pathway, has recently attracted great attention owing to its effectiveness in killing cancer cells. Previous investigations focused on the development of iron-based nanomaterials to induce ferroptosis in cancer cells by the up-regulation of reactive oxygen species (ROS) generated by the well-known Fenton reaction. Herein, we report a ferroptosis-inducing agent based on arginine-rich manganese silicate nanobubbles (AMSNs) that possess highly efficient glutathione (GSH) depletion ability and thereby induce ferroptosis by the inactivation of glutathione-dependent peroxidases 4 (GPX4). The AMSNs were synthesized <I>via</I> a one-pot reaction with arginine (Arg) as the surface ligand for tumor homing. Subsequently, a significant tumor suppression effect can be achieved by GSH depletion-induced ferroptosis. Moreover, the degradation of AMSNs during the GSH depletion contributed to <I>T</I><SUB>1</SUB>-weighted magnetic resonance imaging (MRI) enhancement as well as on-demand chemotherapeutic drug release for synergistic cancer therapy. We anticipate that the GSH-depletion-induced ferroptosis strategy by using manganese-based nanomaterials would provide insights in designing nanomedicines for tumor-targeted theranostics.</P> [FIG OMISSION]</BR>
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Shi Si,Gu Huijie,Xu Jinyuan,Sun Wan,Liu Caiyin,Zhu Tong,Wang Juan,Gao Furong,Zhang Jieping,Ou Qingjian,Jin Caixia,Xu Jingying,Chen Hao,Li Jiao,Xu Guotong,Tian Haibin,Lu Lixia 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Excessive osteoclast activation, which depends on dramatic changes in actin dynamics, causes osteoporosis (OP). The molecular mechanism of osteoclast activation in OP related to type 1 diabetes (T1D) remains unclear. Glia maturation factor beta (GMFB) is considered a growth and differentiation factor for both glia and neurons. Here, we demonstrated that Gmfb deficiency effectively ameliorated the phenotype of T1D-OP in rats by inhibiting osteoclast hyperactivity. In vitro assays showed that GMFB participated in osteoclast activation rather than proliferation. Gmfb deficiency did not affect osteoclast sealing zone (SZ) formation but effectively decreased the SZ area by decreasing actin depolymerization. When GMFB was overexpressed in Gmfb-deficient osteoclasts, the size of the SZ area was enlarged in a dose-dependent manner. Moreover, decreased actin depolymerization led to a decrease in nuclear G-actin, which activated MKL1/SRF-dependent gene transcription. We found that pro-osteoclastogenic factors (Mmp9 and Mmp14) were downregulated, while anti-osteoclastogenic factors (Cftr and Fhl2) were upregulated in Gmfb KO osteoclasts. A GMFB inhibitor, DS-30, targeting the binding site of GMFB and Arp2/3, was obtained. Biocore analysis revealed a high affinity between DS-30 and GMFB in a dose-dependent manner. As expected, DS-30 strongly suppressed osteoclast hyperactivity in vivo and in vitro. In conclusion, our work identified a new therapeutic strategy for T1D-OP treatment. The discovery of GMFB inhibitors will contribute to translational research on T1D-OP.
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