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RISS 인기검색어
- 검색키워드
- 저자 : Volkert, Michael R. (검색결과 2 건)
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고집적용 구리배선의 electromigration 및 thermal fatigue 연구
김영후,박영배,주영창,Kim Y.H.,Park Y.B,Monig R.,Volkert C.A.,Joo Y.C 한국마이크로전자및패키징학회 2005 마이크로전자 및 패키징학회지 Vol.12 No.1
구리 배선에서의 신뢰성 평가를 위해 직류전류와 교류전류를 각각 인가하였을 때의 파손 발생을 분석해 보았다. 직류 전류에서는 electromigration 현상이 발생하는데, 높은 전류 밀도와 온도에서 더욱 빠르게 파손이 진행되었으며, 실험을 통해 구한 활성화 에너지와 전류밀도 의존지수는 각각 0.96eV와 4의 값을 갖는 것으로 나타났다. 교류 전류에서는 열 피로 현상이 발생하였는데, 높은 주파수와 ${\Delta}$T가 클수록 파손이 심하게 진행되었다. 집합 조직에 따른 failure morphology분석 결과, (100)grains에서는 결함이 넓게 성장하여 facetted grains가 되지만 (111)에서는 배선의 두께 방향으로 성장하여 빠르게 단선을 유발하는 것으로 나타났다. We researched damage formation and failure mechanism under DC(direct current) and AC(alternative current) in order to estimate reliability of Cu interconnects in ULSI. Higher current density and temperature induces more short TTF(time to failure) during interconnects carry DC. Measurement reveals that Cu electromigration has activation energy of 0.96eV and current density exponent value of 4. Thermal fatigue is occurred under DC, and higher frequency and ${\Delta}$T value gives more severe damage during interconnects carry AC Through failure morphology analysis with respect to texture, we observed that damages had grown widely and facetted grains had appeared in (100)grain but damages in (111) had grown thickness direction of line and had induced a failure rapidly.
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Deregulation of DNA Damage Signal Transduction by Herpesvirus Latency-Associated M2
Liang, Xiaozhen,Pickering, Mary T.,Cho, Nam-Hyuk,Chang, Heesoon,Volkert, Michael R.,Kowalik, Timothy F.,Jung, Jae U. American Society for Microbiology 2006 Journal of virology Vol.80 No.12
<B>ABSTRACT</B><P>Infected cells recognize viral replication as a DNA damage stress and elicit a DNA damage response that ultimately induces apoptosis as part of host immune surveillance. Here, we demonstrate a novel mechanism where the murine gamma herpesvirus 68 (γHV68) latency-associated, anti-interferon M2 protein inhibits DNA damage-induced apoptosis by interacting with the DDB1/COP9/cullin repair complex and the ATM DNA damage signal transducer. M2 expression constitutively induced DDB1 nuclear localization and ATM kinase activation in the absence of DNA damage. Activated ATM subsequently induced Chk activation and p53 phosphorylation and stabilization without eliciting H2AX phosphorylation and MRN recruitment to foci upon DNA damage. Consequently, M2 expression inhibited DNA repair, rendered cells resistant to DNA damage-induced apoptosis, and induced a G1 cell cycle arrest. Our results suggest that γHV68 M2 blocks apoptosis-mediated intracellular innate immunity, which might ultimately contribute to its role in latent infection.</P>
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