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The simple and easy way to manufacture counter electrode for dye-sensitized solar cells
Jo-Lin Lan,Yung-Yun Wang,Chi-Chao Wan,Tzu-Chien Wei,Hsien-Ping Feng,Chao Peng,Hai-Peng Cheng,Ya-Huei Chang,Wen-Chi Hsu 한국물리학회 2010 Current Applied Physics Vol.10 No.2
We previously developed poly-N-vinyl-2-pyrrolidone (PVP)-capped Pt nanoclusters on ITO glass via a simple ‘‘2-step dip coating process” as counter electrode for DSSC. This new counter electrode was examined by transmission electron microscopy (TEM), inductively coupled plasma-atomic emission spectroscopy (ICP-AES), electrochemical impedance spectroscopy (EIS), cyclic voltammetry (CV), and current–voltage curve (I–V curve). The TEM results revealed that PVP-capped Pt nanoclusters’ size is about 3 nm, and the amount of Pt deposited on ITO glass is about 5 ㎍/㎠. Comparing with sputtered Pt and Solaronix thermal cluster Pt-catalyst T/SP, the PVP-capped Pt counter electrode has lower amount of Pt deposited on TCO glass,more positive potential of tri-iodide reduction, and better performance for the charge-transfer resistance (RCT) and the cell efficiency (g).
Deubiquitination and Stabilization of PD-L1 by CSN5
Lim, Seung-Oe,Li, Chia-Wei,Xia, Weiya,Cha, Jong-Ho,Chan, Li-Chuan,Wu, Yun,Chang, Shih-Shin,Lin, Wan-Chi,Hsu, Jung-Mao,Hsu, Yi-Hsin,Kim, Taewan,Chang, Wei-Chao,Hsu, Jennifer L.,Yamaguchi, Hirohito,Ding Elsevier 2016 Cancer cell Vol.30 No.6
<P><B>Summary</B></P> <P>Pro-inflammatory cytokines produced in the tumor microenvironment lead to eradication of anti-tumor immunity and enhanced tumor cell survival. In the current study, we identified tumor necrosis factor alpha (TNF-α) as a major factor triggering cancer cell immunosuppression against T cell surveillance via stabilization of programmed cell death-ligand 1 (PD-L1). We demonstrated that COP9 signalosome 5 (CSN5), induced by NF-κB p65, is required for TNF-α-mediated PD-L1 stabilization in cancer cells. CSN5 inhibits the ubiquitination and degradation of PD-L1. Inhibition of CSN5 by curcumin diminished cancer cell PD-L1 expression and sensitized cancer cells to anti-CTLA4 therapy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> TNF-α stabilizes cancer cell PD-L1 in response to chronic inflammation </LI> <LI> Activation of NF-κB by TNF-α induces CSN5 expression leading to PD-L1 stabilization </LI> <LI> CSN5 enzyme activity controls T cell suppression via PD-L1 deubiquitination </LI> <LI> Destabilization of PD-L1 by CSN5 inhibitor curcumin benefits anti-CTLA4 therapy </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>