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Post annealing effect on ultra-thin Hf-based high-k gate oxides on Si
Joo-Hyung Kim,Velislava A. Ignatova,Peter Kücher,Martin Weisheit,Ehrenfried Zschech 한국물리학회 2009 Current Applied Physics Vol.9 No.2
We investigated the effect of post annealing on the electrical and physical properties of atomic-layerdeposited thin HfO2, HfSixOy and HfOyNz gate oxide films on Si. It was found that the main leakage conduction of all Hf-based oxide films was of the Poole–Frenkel (P–F) type in low electric fields and Fowler– Nordheim (F–N) conduction in higher fields. Also, it was observed that the transition from P–F to F–N of the annealed HfOyNz sample occurred earlier than that of the as-grown one. By using spectroscopic ellipsometry, it was found that the annealing process decreased the band gap of HfO2, HfSixOy and HfOyNz films. From depth profile measurements on the HfOyNz film, we conclude that N moves toward the surface and interface during annealing. We investigated the effect of post annealing on the electrical and physical properties of atomic-layerdeposited thin HfO2, HfSixOy and HfOyNz gate oxide films on Si. It was found that the main leakage conduction of all Hf-based oxide films was of the Poole–Frenkel (P–F) type in low electric fields and Fowler– Nordheim (F–N) conduction in higher fields. Also, it was observed that the transition from P–F to F–N of the annealed HfOyNz sample occurred earlier than that of the as-grown one. By using spectroscopic ellipsometry, it was found that the annealing process decreased the band gap of HfO2, HfSixOy and HfOyNz films. From depth profile measurements on the HfOyNz film, we conclude that N moves toward the surface and interface during annealing.
Lee, Young ,Ae,Yun, Byeong ,Hwa,Kim, Seog ,K.,Margolin, Yelena,Dedon, Peter ,C.,Geacintov, Nicholas ,E.,Shafirovich, Vladimir WILEY-VCH Verlag 2007 Chemistry Vol.13 No.16
<P>Peroxynitrite is produced during inflammation and combines rapidly with carbon dioxide to yield the unstable nitrosoperoxycarbonate, which decomposes (in part) to CO<SUB>3</SUB><SUP>.−</SUP> and <SUP>.</SUP>NO<SUB>2</SUB> radicals. The CO<SUB>3</SUB><SUP>.−</SUP> radicals oxidize guanine bases in DNA through a one-electron transfer reaction process that ultimately results in the formation of stable guanine oxidation products. Here we have explored these mechanisms, starting with a spectroscopic study of the kinetics of electron transfer from 20–22mer double-stranded oligonucleotides to CO<SUB>3</SUB><SUP>.−</SUP> radicals, together with the effects of base sequence on the formation of the end-products in runs of one, two, or three contiguous guanines. The distributions of these alkali-labile lesions were determined by gel electrophoresis methods. The cascade of events was initiated through the use of 308 nm XeCl excimer laser pulses to generate CO<SUB>3</SUB><SUP>.−</SUP> radicals by an established method based on the photodissociation of persulfate to sulfate radicals and the oxidation of bicarbonate. Although the Saito model (Saito et al., J. Am. Chem. Soc. 1995, 117, 6406–6407) predicts relative ease of one-electron oxidations in DNA, following the trend 5′-⋅⋅⋅GGG⋅⋅⋅ > 5′-⋅⋅⋅GG⋅⋅⋅ > 5′-⋅⋅⋅G⋅⋅⋅, we found that the rate constants for CO<SUB>3</SUB><SUP>.−</SUP>-mediated oxidation of guanines in these sequence contexts (k<SUB>5</SUB>) showed only small variation within a narrow range [(1.5–3.0)×10<SUP>7</SUP> M<SUP>−1</SUP> s<SUP>−1</SUP>]. In contrast, the distributions of the end-products are dependent on the base sequence context and are higher at the 5′-G in 5′-⋅⋅⋅GG⋅⋅⋅ sequences and at the first two 5′-guanines in the 5′-⋅⋅⋅GGG⋅⋅⋅ sequences. These effects are attributed to a combination of initial hole distributions among the contiguous guanines and the subsequent differences in chemical reaction yields at each guanine. The lack of dependence of k<SUB>5</SUB> on sequence context indicates that the one-electron oxidation of guanine in DNA by CO<SUB>3</SUB><SUP>.−</SUP> radicals occurs by an inner-sphere mechanism.</P> <B>Graphic Abstract</B> <P>Rates of one-electron oxidation of guanine in DNA by carbonate radicals do not depend on sequence context: The sequence-dependent damage at guanine sites (see figure) is attributed to a combination of initial hole distributions among the contiguous guanines and the subsequent differences in chemical reaction yields at each guanine. <img src='wiley_img/09476539-2007-13-16-CHEM200601434-content.gif' alt='wiley_img/09476539-2007-13-16-CHEM200601434-content'> </P>
Regulation of Apoptosis by Nitrosative Stress
Kim, Ki-Mo,Kim, Peter K.M.,Kwon, Young-Guen,Bai, Se-Kyung,Nam, Woo-Dong,Kim, Young-Myeong Korean Society for Biochemistry and Molecular Biol 2002 Journal of biochemistry and molecular biology Vol.35 No.1
Nitrosative stress can prevent or induce apoptosis. It occurs via S-nitrosylation by the interaction of nitric oxide (NO) with the biological thiols of proteins. Cellular redox potential and non-heme iron content determine S-nitrosylation. Apoptotic cell death is inhibited by S-nitrosylation of the redox-sensitive thiol in the catalytic site of caspase family proteases, which play an essential role in the apoptotic signal cascade. Nitrosative stress can also promote apoptosis by the activation of mitochondrial apoptotic pathways, such as the release of cytochrome c, an apoptosis-inducing factor, and endonuclease G from mitochondria, as well as the suppression of NF-${\kappa}B$ activity. In this article we reviewed the mechanisms whereby S-nitrosylation and nitrosative stress regulate the apoptotic signal cascade.
Kim, Seung Tae,Kim, Kyoung‐,Mee,Kim, Nayoung K.D.,Park, Joon Oh,Ahn, Soomin,Yun, Jae‐,Won,Kim, Kyu‐,Tae,Park, Se Hoon,Park, Peter J.,Kim, Hee Cheol,Sohn, Tae Sung,Choi, Dong Il,Cho, AlphaMed Press 2017 The oncologist Vol.22 No.10
<P>Molecular profiling of actionable mutations in refractory cancer patients has the potential to enable 'precision medicine,' wherein individualized therapies are guided based on genomic profiling. The molecular-screening program was intended to route participants to different candidate drugs in trials based on clinical-sequencing reports. In this screening program, we used a custom target-enrichment panel consisting of cancer-related genes to interrogate single-nucleotide variants, insertions and deletions, copy number variants, and a subset of gene fusions. From August 2014 through April 2015, 654 patients consented to participate in the program at Samsung Medical Center. Of these patients, 588 passed the quality control process for the 381-gene cancer-panel test, and 418 patients were included in the final analysis as being eligible for any anticancer treatment (127 gastric cancer, 122 colorectal cancer, 62 pancreatic/biliary tract cancer, 67 sarcoma/other cancer, and 40 genitourinary cancer patients). Of the 418 patients, 55 (12%) harbored a biomarker that guided them to a biomarker-selected clinical trial, and 184 (44%) patients harbored at least one genomic alteration that was potentially targetable. This study demonstrated that the panel-based sequencing program resulted in an increased rate of trial enrollment of metastatic cancer patients into biomarker-selected clinical trials. Given the expanding list of biomarker-selected trials, the guidance percentage to matched trials is anticipated to increase.</P>
Spatiotemporal Evolution of the Primary Glioblastoma Genome
Kim, J.,Lee, I.H.,Cho, H.,Park, C.K.,Jung, Y.S.,Kim, Y.,Nam, S.,Kim, B.,Johnson, Mark D.,Kong, D.S.,Seol, H.,Lee, J.I.,Joo, K.,Yoon, Y.,Park, W.Y.,Lee, J.,Park, Peter J.,Nam, D.H. Cell Press 2015 CANCER CELL Vol. No.
Tumor recurrence following treatment is the major cause of mortality for glioblastoma multiforme (GBM) patients. Thus, insights on the evolutionary process at recurrence are critical for improved patient care. Here, we describe our genomic analyses of the initial and recurrent tumor specimens from each of 38 GBM patients. A substantial divergence in the landscape of driver alterations was associated with distant appearance of a recurrent tumor from the initial tumor, suggesting that the genomic profile of the initial tumor can mislead targeted therapies for the distally recurred tumor. In addition, in contrast to IDH1-mutated gliomas, IDH1-wild-type primary GBMs rarely developed hypermutation following temozolomide (TMZ) treatment, indicating low risk for TMZ-induced hypermutation for these tumors under the standard regimen.
Regulation of Apoptosis by Nitrosative Stress
Kim, Ki Mo,Kim, Young Myeong,Kwon, Young Guen,Kim, Peter K . M .,Bai, Se Kyung,Nam, Woo Dong 생화학분자생물학회 1998 BMB Reports Vol.35 No.1
Nitrosative stress can prevent or induce apoptosis. It occurs via S-nitrosylation by the interaction of nitric oxide (NO) with the biological thiols of proteins. Cellular redox potential and non-heme iron content determine S-nitrosylation. Apoptotic cell death is inhibited by S-nitrosylation of the redox-sensitive thiol in the catalytic site of caspase family proteases, which play an essential role in the apoptotic signal cascade. Nitrosative stress can also promote apoptosis by the activation of mitochondrial apoptotic pathways, such as the release of cytochrome c, an apoptosis-inducing factor, and endonuclease G from mitochondria, as well as the suppression of NF-kB activity. In this article we reviewed the mechanisms whereby S-nitrosylation and nitrosative stress regulate the apoptotic signal cascade.
Jeung, Eui-Bae,Park, Se-Hyung,Leung, Peter C.K.,Yang, Hoe-Saeng,Sim, Jae-Chul,Kim, Kyung-Tai,Choi, Kyung-Chul 대한부인종양 콜포스코피학회 2003 Journal of Gynecologic Oncology Vol.14 No.4
Mitogen-activated protein kinases (MAPKs) are a group of serine/threonine kinases which are activated in response to a diverse array of extracellular stimuli, and mediate signal transduction from the cell surface to the nucleus. The chemotherapeutic agents, growth factors and reproductive hormones have been demonstrated to activate MAPKs, suggesting that the MAPK signaling pathway plays an important role in the regulation of proliferation, apoptosis, survival and differentiation in response to these external stimuli in ovarian cancer. In addition to MAPKs as an oncogenic pathway, phosphatidylinositol 3-kinase (PI3K) plays a role in a various range of important cellular processes associated with malignant characterestics including cell growth, survival and migration, which is a member of lipid kinases subfamily that phosphorylates and dephosphorylates the 3-position of the inositol ring of phosphoinositides in a membrane. In this review, recent results of the MAPK and PI3K signaling cascades by external stimuli, and potential roles of these oncogenic pathways as an oncogenic pathway are summarized in epithelial ovarian cancer.
Rock Mechanics Advances for Underground Construction in Civil Engineering and Mining
Peter K. Kaiser,Bo-Hyun Kim 한국암반공학회 2008 한국암반공학회 학술대회 및 세미나 자료집 Vol.- No.-
The underground construction and mining are facing many geomechanics challenges stemming from, geological complexities and stress-driven rock mass degradation processes. Brittle failing rock at depth poses unique problems as stress-driven failure processes often dominate the tunnel behaviour. Such failure processes can lead to shallow unravelling or strainbursting modes of instability that cause difficult conditions for tunnel contractors. This keynote address focuses on the challenge of anticipating the actual behaviour of brittle rocks in laboratory testing, for empirical rock mass strength estimation, and by back-analysis of field observations. This paper summarizes lessons learned during the construction of deep Alpine tunnels and highlights implications that are of practical importance with respect to constructability. It builds on a recent presentation made at the 1<SUP>st</SUP> Southern Hemisphere International Rock Mechanics Symposium held in Perth, Australia, in September this year, and includes results from recent developments.