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Schottky Barrier Tunnel Field-Effect Transistor using Spacer Technique
Kim, Hyun Woo,Kim, Jong Pil,Kim, Sang Wan,Sun, Min-Chul,Kim, Garam,Kim, Jang Hyun,Park, Euyhwan,Kim, Hyungjin,Park, Byung-Gook The Institute of Electronics and Information Engin 2014 Journal of semiconductor technology and science Vol.14 No.5
In order to overcome small current drivability of a tunneling field-effect transistor (TFET), a TFET using Schottky barrier (SBTFET) is proposed. The proposed device has a metal source region unlike the conventional TFET. In addition, dopant segregation technology between the source and channel region is applied to reduce tunneling resistance. For TFET fabrication, spacer technique is adopted to enable self-aligned process because the SBTFET consists of source and drain with different types. Also the control device which has a doped source region is made to compare the electrical characteristics with those of the SBTFET. From the measured results, the SBTFET shows better on/off switching property than the control device. The observed drive current is larger than those of the previously reported TFET. Also, short-channel effects (SCEs) are investigated through the comparison of electrical characteristics between the long- and short-channel SBTFET.
Schottky Barrier Tunnel Field-Effect Transistor using Spacer Technique
Hyun Woo Kim,Jong Pil Kim,Sang Wan Kim,Min-Chul Sun,Garam Kim,Jang Hyun Kim,Euyhwan Park,Hyungjin Kim,Byung-Gook Park 대한전자공학회 2014 Journal of semiconductor technology and science Vol.14 No.5
In order to overcome small current drivability of a tunneling field-effect transistor (TFET), a TFET using Schottky barrier (SBTFET) is proposed. The proposed device has a metal source region unlike the conventional TFET. In addition, dopant segregation technology between the source and channel region is applied to reduce tunneling resistance. For TFET fabrication, spacer technique is adopted to enable self-aligned process because the SBTFET consists of source and drain with different types. Also the control device which has a doped source region is made to compare the electrical characteristics with those of the SBTFET. From the measured results, the SBTFET shows better on/off switching property than the control device. The observed drive current is larger than those of the previously reported TFET. Also, short-channel effects (SCEs) are investigated through the comparison of electrical characteristics between the long- and shortchannel SBTFET .
Interlayer-state-driven superconductivity inCaC6studied by angle-resolved photoemission spectroscopy
Kyung, Wonshik,Kim, Yeongkwan,Han, Garam,Leem, Choonshik,Kim, Chul,Koh, Yoonyoung,Kim, Beomyoung,Kim, Youngwook,Kim, Jun Sung,Kim, Keun Su,Rotenberg, Eli,Denlinger, Jonathan D.,Kim, Changyoung American Physical Society 2015 Physical review. B, Condensed matter and materials Vol.92 No.22
Kim, Garam,Khanal, Prem,Lim, Sung-Chul,Yun, Hyo Jeong,Ahn, Sang-Gun,Ki, Sung Hwan,Choi, Hong Seok IRL Press] ; Oxford University Press 2013 Carcinogenesis Vol.34 No.2
<P>Inflammatory conditions elicited by extrinsic environmental factors promote malignant transformation, tumor growth and metastasis. Although the role of T cells in cancer promotion has been examined, little is known about the underlying molecular mechanisms of interleukin-17 A (IL-17A), a proinflammatory cytokine produced by activated CD4(+) memory T cells, in carcinogenesis. Here, we report that IL-17A induces neoplastic transformation of JB6 Cl41 cells through activation of tumor progression locus 2 (TPL2). IL-17A dose- and time-dependently increases TPL2 phosphorylation in JB6 Cl41 cells through IL-17A receptor. IL-17A activates mitogen-activated protein kinase/extracellular signal-regulated kinase kinases, c-jun N-terminal kinases and STAT3 signaling pathways, which are inhibited by a TPL2 kinase inhibitor (TKI). Furthermore, IL-17A activates c-fos and c-jun promoter activity, resulting in increased activator protein-1 (AP-1) activity. When small interfering RNA of IL-17A receptor (IL-17R), IL-17A and TPL2 were introduced into JB6 Cl41 cells, respectively, IL-17A-induced AP-1 activity was significantly decreased compared with control cells. Similarly, TPL2 inhibition suppressed AP-1 activity induced by IL-17A. The knockdown of IL-17R and TKI treatment in JB6 Cl41 cells resulted in decreased IL-17A-induced cell transformation. The in vivo chorioallantoic membrane assay also showed that IL-17A increased tumor formation of JB6 Cl41 cells, whereas TKI inhibited the tumorigenesis promoted by IL-17A. Consistent with these observations, knockdown of IL-17A and/or inhibition of TPL2 attenuated tumorigenicity of human breast cancer MCF7 cells. Together, our findings point to a critical role for the IL-17A-induced TPL2 signaling pathway in supporting cancer-associated inflammation in the tumor microenvironment. Therapeutic approaches that target this pathway may, therefore, effectively inhibit carcinogenesis.</P>