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Interface between the Electroplated Copper-cobalt Thin Films and the Substrate
Jin-Gyu Kim,Jungju Lee,Jonghak Bae,Wonbae Bang,Kimin Hong,C. H. Yoon,Derac Son,Keeju Jeong 한국자기학회 2006 Journal of Magnetics Vol.11 No.3
We electroplated copper-cobalt thin films on a silicon substrate, which had 150 nm thick copper seed layer. The adhesion between the two metallic layers could be increased by utilizing a proper organic additive, pulse plating technique, and high temperature annealing. The thin films exhibited columnar growth of the deposits and enhanced adhesion. This is attributed to the grain growth mechanism introduced by the additive and annealing.
Suh, Hoyoung,Noh, Jinseong,Lee, Ji-Hyun,Lee, Seok-Hoon,Myung, Nosang V.,Hong, Kimin,Kim, Jin-Gyu Pergamon Press 2017 Electrochimica Acta Vol. No.
<P><B>Abstract</B></P> <P>Co thin films with different crystalline structures including preferred orientation and grain size were electrodeposited from electrolytes containing an additive N-Dimethyldithiocarbamic acid ester, sodium salt, (DPS). Subsequently, the Co electrodeposits were converted to Te and Bi<SUB>2</SUB>Te<SUB>3</SUB> via galvanic displacement reaction (GDR) processes. The morphologies of the produced Te and Bi<SUB>2</SUB>Te<SUB>3</SUB> exhibited granular structures including whiskers and dendrites. Structural analyses showed that the microstructures strongly depended on the crystalline structure of the original Co thin films, which were also affected by the concentration of DPS. The formation mechanism of the Te whiskers and Bi<SUB>2</SUB>Te<SUB>3</SUB> dendrites were elucidated by various analyses.</P>
Kim, In‐,Gyu,Lee, Jei‐,Ha,Kim, Seo‐,Yeon,Hwang, Hai‐,Min,Kim, Tae‐,Rim,Cho, Eun‐,Wie John Wiley and Sons Inc. 2018 Cancer Science Vol.109 No.11
<P>Microenvironment, such as hypoxia common to cancer, plays a critical role in the epithelial‐to‐mesenchymal transition (EMT) program, which is a major route of cancer metastasis and confers γ‐radiation resistance to cells. Herein, we showed that transgelin 2 (TAGLN2), an actin‐binding protein, is significantly induced in hypoxic lung cancer cells and that Snail1 is simultaneously increased, which induces EMT by downregulating <I>E‐cadherin</I> expression. Forced <I>TAGLN2</I> expression induced severe cell death; however, a small population of cells surviving after forced <I>TAGLN2</I> overexpression showed γ‐radiation resistance, which might promote tumor relapse and recurrence. These surviving cells showed high metastatic activity with an increase of EMT markers including Snail1. In these cells, TAGLN2 activated the insulin‐like growth factor 1 receptor β (IGF1Rβ)/PI3K/AKT pathway by recruitment of focal adhesion kinase to the IGF1R signaling complex. Activation of the IGF1Rβ/PI3K/AKT pathway also induced inactivation of glycogen synthase kinase 3β (GSK3β), which is involved in Snail1 stabilization. Therefore, both the IGF1Rβ inhibitor (AG1024) and the PI3K inhibitor (LY294002) or AKT inactivation with MK2206 lower the cellular level of Snail1. Involvement of GSK3β was also confirmed by treatment with lithium chloride, the inducer of GSK3β phosphorylation, or MG132, the 26S proteasomal inhibitor, which also stabilized Snail1. In conclusion, the present study provides important evidence that hypoxia‐inducible TAGLN2 is involved in the selection of cancer cells with enhanced EMT properties to overcome the detrimental environment of cancer cells.</P>