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Jonghwa Kim,Sungju Choi,Jaeman Jang,Jun Tae Jang,Jungmok Kim,Sung-Jin Choi,Dong Myong Kim,Dae Hwan Kim 대한전자공학회 2015 Journal of semiconductor technology and science Vol.15 No.5
We quantitatively investigated instability mechanisms under simultaneous positive gate and drain bias stress (SPGDBS) in self-aligned top-gate amorphous indium-zinc-oxide thin-film transistors. After SPGDBS (VGS=13 V and VDS=13 V), the parallel shift of the transfer curve into a negative VGS direction and the increase of on current were observed. In order to quantitatively analyze mechanisms of the SPGDBS-induced negative shift of threshold voltage (ΔVT), we experimentally extracted the density-of-state, and then analyzed by comparing and combining measurement data and TCAD simulation. As results, 19% and 81% of ΔVT were taken to the donor-state creation and the hole trapping, respectively. This donor-state seems to be doubly ionized oxygen vacancy (V<SUP>o2+</SUP>). In addition, it was also confirmed that the wider channel width corresponds with more negative DVT. It means that both the donor-state creation and hole trapping can be enhanced due to the increase in self-heating as the width becomes wider. Lastly, all analyzed results were verified by reproducing transfer curves through TCAD simulation.
Anomalous Rapid Defect Annihilation in Self-Assembled Nanopatterns by Defect Melting
Kim, Bong Hoon,Park, So Jung,Jin, Hyeong Min,Kim, Ju Young,Son, Seung-Woo,Kim, Myung-Hyun,Koo, Chong Min,Shin, Jonghwa,Kim, Jaeup U.,Kim, Sang Ouk American Chemical Society 2015 NANO LETTERS Vol.15 No.2
<P>Molecular self-assembly commonly suffers from dense structural defect formation. Spontaneous defect annihilation in block copolymer (BCP) self-assembly is particularly retarded due to significant energy barrier for polymer chain diffusion and structural reorganization. Here we present localized defect melting induced by blending short neutral random copolymer chain as an unusual method to promote the defect annihilation in BCP self-assembled nanopatterns. Chemically neutral short random copolymer chains blended with BCPs are specifically localized and induce local disordered states at structural defect sites in the self-assembled nanopatterns. Such localized “defect melting” relieves the energy penalty for polymer diffusion and morphology reorganization such that spontaneous defect annihilation by mutual coupling is anomalously accelerated upon thermal annealing. Interestingly, neutral random copolymer chain blending also causes morphology-healing self-assembly behavior that can generate large-area highly ordered 10 nm scale nanopattern even upon poorly defined defective prepatterns. Underlying mechanisms of the unusual experimental findings are thoroughly investigated by three-dimensional self-consistent field theory calculation.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/nalefd/2015/nalefd.2015.15.issue-2/nl5042935/production/images/medium/nl-2014-042935_0006.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/nl5042935'>ACS Electronic Supporting Info</A></P>
Kim, Jonghwa,Choi, Sungju,Jang, Jaeman,Jang, Jun Tae,Kim, Jungmok,Choi, Sung-Jin,Kim, Dong Myong,Kim, Dae Hwan The Institute of Electronics and Information Engin 2015 Journal of semiconductor technology and science Vol.15 No.5
We quantitatively investigated instability mechanisms under simultaneous positive gate and drain bias stress (SPGDBS) in self-aligned top-gate amorphous indium-zinc-oxide thin-film transistors. After SPGDBS ($V_{GS}=13V$and $V_{DS}=13V$), the parallel shift of the transfer curve into a negative $V_{GS}$ direction and the increase of on current were observed. In order to quantitatively analyze mechanisms of the SPGDBS-induced negative shift of threshold voltage (${\Delta}V_T$), we experimentally extracted the density-of-state, and then analyzed by comparing and combining measurement data and TCAD simulation. As results, 19% and 81% of ${\Delta}V_T$ were taken to the donor-state creation and the hole trapping, respectively. This donor-state seems to be doubly ionized oxygen vacancy ($V{_O}^{2+}$). In addition, it was also confirmed that the wider channel width corresponds with more negative ${\Delta}V_T$. It means that both the donor-state creation and hole trapping can be enhanced due to the increase in self-heating as the width becomes wider. Lastly, all analyzed results were verified by reproducing transfer curves through TCAD simulation.
국내 과일·채소음료시장의 소비활성화를 위한 시장분석 및 마케팅 전략
김정래 ( Kim Jeongrae ),김범수 ( Beom-su Kim ),김성진 ( Seong-jin Kim ),박지훈 ( Ji-hoon Park ),김종화 ( Jonghwa Kim ) 한국식품유통학회 2022 한국식품유통학회 학술대회 Vol.- No.하계
최근 국내 과채류음료 시장의 성장이 크게 둔화되고 있다. 그동안 과채류음료는 국내 가공용 과일, 채소의 대량 수요처로서 그 중요성이 강조되어 왔으나, 탄산음료, 액상커피 등의 대체품이 등장하면서 과채음료 시장이 급속히 위축되고 있다. 이에 본 연구에서는 소비자의 과채류음료에 대한 선택속성(원료, 가격, 첨가물, 포장용기)을 살펴보고, 그에 따른 마케팅전략을 제시하였다. 이를 위하여 마케팅 분야에서 널리 사용되는 컨조인트 분석의 부분가치 함수모형을 이용하였으며, 시장세분화를 위한 군집분석을 실시하였다. 그 결과, 국내 과채류시장은 ‘맛선호그룹’, 원료선호그룹’,‘편의선호그룹’으로 세분될 수 있으며, 그에 따른 그룹별 마케팅전략을 제시하였다.
( Dong-ho Kim ),( Mi-jin Kim ),( Na-young Kim ),( Seunghyeong Lee ),( Jun-kyu Byun ),( Jae Won Yun ),( Jaebon Lee ),( Jonghwa Jin ),( Jina Kim ),( Jungwook Chin ),( Sung Jin Cho ),( In-kyu Lee ),( Yeo 생화학분자생물학회 2022 BMB Reports Vol.55 No.11
Sorafenib, originally identified as an inhibitor of multiple oncogenic kinases, induces ferroptosis in hepatocellular carcinoma (HCC) cells. Several pathways that mitigate sorafenib-induced ferroptosis confer drug resistance; thus strategies that enhance ferroptosis increase sorafenib efficacy. Orphan nuclear receptor estrogen-related receptor γ (ERRγ) is upregulated in human HCC tissues and plays a role in cancer cell proliferation. The aim of this study was to determine whether inhibition of ERRγ with DN200434, an orally available inverse agonist, can overcome resistance to sorafenib through induction of ferroptosis. Sorafenib-resistant HCC cells were less sensitive to sorafenibinduced ferroptosis and showed significantly higher ERRγ levels than sorafenib-sensitive HCC cells. DN200434 induced lipid peroxidation and ferroptosis in sorafenib-resistant HCC cells. Mechanistically, DN200434 increased mitochondrial ROS generation by reducing glutathione/glutathione disulfide levels, which subsequently reduced mTOR activity and GPX4 levels. DN200434- induced amplification of the antitumor effects of sorafenib was confirmed in a tumor xenograft model. The present results indicate that DN200434 may be a novel therapeutic strategy to re-sensitize HCC cells to sorafenib. [BMB Reports 2022; 55(11): 547-552]