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RISS 인기검색어
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- 저자 : Wenfeng Ye (검색결과 2 건)
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Back-channel-etched InGaZnO thin-film transistors with Au nanoparticles on the back channel surface
Peng Xiao,Wenfeng Wang,Yingyi Ye,Ting Dong,Shengjin Yuan,Jiaxing Deng,Li Zhang,Jianwen Chen,Jian Yuan 대한금속·재료학회 2020 ELECTRONIC MATERIALS LETTERS Vol.16 No.2
In this paper, Au nanoparticles (NPs) were introduced on the surface of oxide thin fi lm to enhance the etching resistance of thethin fi lm, and back-channel-etched (BCE) InGaZnO (IGZO) thin fi lm transistors (TFTs) with Au NPs on the back channel surfacewere successfully fabricated. Detailed studies showed that the etching resistance of IGZO thin fi lms was enhanced signifi cantly byintroducing Au NPs on IGZO thin fi lms, and the etching resistance was enhanced with the increase of Au NPs thickness. Furthermore,Au NPs deposited by vaccum evaporation were uniformly dispersed on the IGZO surface other than forming a continuousthin fi lm. By introducing the Au NPs on the IGZO surface, we successfully patterned the S/D electrodes on Au NPs/IGZO andfabricated BCE TFTs. The IGZO-TFTs with 5-nm-thick Au NPs on the back channel surface exhibited excellent electrical characteristicwith a μ sat of 9.9 cm 2 /V s, a SS of 0.26 V/decade, a V on of 0.23 V, an I on/off of 10 6 and an off -state current of 10 −11 A. Inaddition, the introduction of Au NPs did not lead to an increase in the off -state current, which was mainly ascribed to the Schottkybarrier between Au NPs and IGZO due to the high work function of Au. It is a universal method to fabricate BCE TFTs with highelectrical performance, because it was not limited to the types of oxide materials and had no special requirements for equipment.
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NUP210 and MicroRNA-22 Modulate Fas to Elicit HeLa Cell Cycle Arrest
Qiao Gu,Wenjie Hou,Huan Liu,Lijuan Shi,Zonghao Zhu,Wenfeng Ye,Xiaoyuan Ni 연세대학교의과대학 2020 Yonsei medical journal Vol.61 No.5
Purpose: Cervical cancer is one of the most fatal diseases among women in under-developed countries. To improve cervical cancer treatment, discovery of new targets is needed. In this study, we investigated the expression of NUP210, miR-22, and Fas in cervical cancer tissues and their functions in cell cycle regulation. Materials and Methods: We detected and compared the expression levels of NUP210, miR-22, and Fas in cervical cancer tissues with paired normal tissues using immunohistochemistry, Western blot, and real-time quantitative polymerase chain reaction. NUP210 was knocked down in HeLa cells via lentivirus, followed by cell cycle and proliferation analysis. Using a luciferase reporter assay, we explored the link between miR-22 and NUP210. We overexpressed miR-22 in HeLa cells and analyzed cell cycle and proliferation function. We then overexpressed miR-22 in NUP210 knockdown cells to explore the connection between Fas and miR-22-NUP210 signaling. Results: We found that NUP210 was overexpressed in cervical cancer patients. Knocking down NUP210 restored cell apoptosis and proliferation. We confirmed miR-22 as a regulator of NUP210 and verified that miR-22 was inhibited in cervical cancer development. We also found that restoring miR-22 expression could induce cell apoptosis. Finally, we found that miR-22-regulated expression of NUP210 could alter Fas expression and, in turn, elicit cell cycle arrest and proliferation. Conclusion: miR-22 in cervical cancer is downregulated, resulting in NUP210 overexpression and inhibition of Fas-induced cell apoptosis.
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