• 대한전자공학회논문지TC
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• 제43권12호
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• pp.61-67
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• 2006

본 논문에서는 고속무선통신에 널리 사용되고 있는 직교 주파수 분할 다중화 데이터 전송시스템에서 반송파주파수 옵셋(Offset)에 의한 잔류 위상 오차와 샘플링 주파수 옵셋에 의한 잔류 오차를 추적하고 보상하는 알고리즘을 제안한다. 직교 주파수 분할 다중화 시스템에서는 서로 직교성을 가지는 부반송파들이 디지털 데이터에 의해 변조되어 동시에 전송된다 반송파 주파수 옵셋이 존재하는 경우에는 신호 대 잡음비의 감소 그리고 인접 부반송파의 간섭 등이 발생한다. 또한 송신단과 수신단에서의 샘플링 주파수의 차이로 인한 샘플링 시점의 오차도 직교 주파수 분할 다중화 시스템에서 성능저하의 주요한 요인으로 작용한다. 반송파 주파수의 오차와 샘플링 주파수의 오차는 직교 주파수 분할 다중화 시스템에서 중요한 성질중의 하나인 직교성 상실을 초래하며 이는 성능저하의 원인으로 작용하므로 수신단에서는 지속적으로 잔류 오차를 추적하여 보상해 주는 방식의 적용이 필수적이다. 본 논문에서는 주파수 선택적 페이딩 무선 채널 환경에서 파일롯 데이터뿐만 아니라 채널이득 정보 및 페이로드 데이터를 주파수 오차 추정에 반영하여 추정오차를 줄이고 이 추정 값을 주파수 오차 보상에 반영하여 성능 향상을 달성할 수 있는 방식을 제안한다.

• 한국재료학회:학술대회논문집
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• 한국재료학회 2009년도 춘계학술발표대회
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• pp.38.1-38.1
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• 2009

Plasma etching is an essential process for electronic device industries and the particulate contamination during plasma etching has been interested as a big issue for the yield of productivity. The oxynitride glasses have a merit to prevent particulate contamination due to their amorphous structure and plasma etching resistance. The YSiAlON oxynitride glasses with increasing nitrogen content were manufactured. Each oxynitride glasses were fluorine-plasma etched and their plasma etching rate and surface roughness were compared with reference materials such as sapphire, alumina and quartz. The reinforcement mechanism of plasma etching resistance of the YSiAlON glasses studied by depth profiling at plasma etched surface using electron spectroscopy for chemical analysis. The plasma etching rate decreased with nitrogen content and there was no selective etching at the plasma etched surface of the oxynitride glasses. The concentration of silicon was very low due to the generation of SiF4 very volatile byproduct and the concentration of aluminum and yttrium was relatively constant. The elimination of silicon atoms during plasma etching was reduced with increasing nitrogen content because the content of the nitrogen was constant. And besides, the concentration of oxygen was very low on the plasma etched surface. From the study, the plasma etching resistance of the glasses may be improved by the generation of nitrogen related structural groups and those are proved by chemical composition analysis at plasma etched surface of the YSiAlON oxynitride glasses.

• 한국세라믹학회지
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• 제40권11호
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• pp.1073-1077
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• 2003

Sn $O_2$ 가스센서는 낮은 농도의 가연성 가스 및 유독 가스를 표면 저항의 변화로부터 탐지할 수 있으나, 가스 선택성이 부족하다는 단점을 가지고 있다. 이러한 단점을 보완하기 위해서는 가스반응기구의 규명과 같은 기초이론 연구와 함께 선택성이 우수한 센서재료의 개발 및 적절한 신호처리방법의 적용이 필요하다. 본 논문에서는 Sn $O_2$ 표면에서 일어나는 에탄올 (C$_2$ $H_{5}$OH)과 아세토니트릴($CH_3$CN)의 촉매산화반응을 가스크로마토그래피 분석을 통해 확인하였다. PdCl$_2$가 첨가된 Sn $O_2$ 센서는 에탄올과 아세토니트릴에 대하여 높은 감도를 보였고, 반면에 La$_2$ $O_3$가 첨가된 Sn $O_2$ 센서는 에탄올에 대해서는 높은 감도를, 그리고 아세토니트릴에 대해서는 낮은 감도를 보였다. 이들 두 센서재료 개발 및 패턴인식기법적용을 통하여 아세토니트릴에 대한 선택성을 크게 증가시킬 수 있었다. 아세토니트릴에 대한 최소 탐지농도는, 공기 중에서는 15 ppm이었고, 다른 방해가스와 함께 존재할 경우에는 20 ppm에서 100 ppm 정도로 나타났다.

• The Korean Journal of Physiology and Pharmacology
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• 제2권3호
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• pp.279-286
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• 1998

It has been well documented that transient forebrain global ischemia causes selective neuronal degeneration in hippocampal CA1 pyramidal neurons with a delay of a few days. The mechanism of this delayed hippocampal CA1 pyramidal neuronal death (DND) is still controversial. To delineate the mechanisms of the DND, the effects of treatment with MK-801, an NMDA receptor antagonist, kynurenic acid, a NMDA/non-NMDA receptor antagonist, and/or cycloheximide, a protein synthesis inhibitor, on the DND were investigated in male Wistar rats. To examine the participation of apoptotic neuronal death in the DND, TUNEL staining was performed in ischemic brain section. Global ischemia was induced by 4-vessel occlusion for 20 min. All animals in this study showed the DND 3 and 7 days after the ischemic insult. The DND that occured 3 days and 7 days after the ischemia were not affected by pretreatment with MK-801 (1 mg/kg), but markedly attenuated by the pretreatment with kynurenic acid (500 mg/kg). Treatment with cycloheximide (1 mg/kg) also markedly inhibited the DND. The magnitudes of attenuation by the two drugs were similar. The magnitude of attenuation by co-treatments with kynurenic acid and cycloheximide was not greater than that with any single treatment. TUNEL staining was negative in the sections obtained 1 or 2 days after the ischemic insults, but it was positive at hippocampal CA1 pyramidal cells in sections collected 3 days after the ischemia. These results suggested that the DND should be mediated by the activation of non-NMDA receptor, not by the activation of NMDA receptor and that the activation of AMPA receptor should induce the apoptotic process in the DND.

• The Korean Journal of Physiology and Pharmacology
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• 제19권1호
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• pp.51-57
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• 2015

The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammatory cytokines such as interleukin-8 as part of the inflammatory response; however, the exact mechanism of calcium signaling induced by bacterial toxins when gingival epithelial cells are exposed to pathogens is unclear. Here, we investigate calcium signaling induced by bacteria and expression of inflammatory cytokines in human gingival epithelial cells. We found that peptidoglycan, a constituent of grampositive bacteria and an agonist of toll-like receptor 2, increases intracellular calcium in a concentration-dependent manner. Peptidoglycan-induced calcium signaling was abolished by treatment with blockers of phospholipase C (U73122), inositol 1,4,5-trisphosphate receptors, indicating the release of calcium from intracellular calcium stores. Peptidoglycan-mediated interleukin-8 expression was blocked by U73122 and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester). Moreover, interleukin-8 expression was induced by thapsigargin, a selective inhibitor of the sarco/endoplasmic reticulum calcium ATPase, when thapsigargin was treated alone or co-treated with peptidoglycan. These results suggest that the gram-positive bacterial toxin peptidoglycan induces calcium signaling via the phospholipase C/inositol 1,4,5-trisphosphate pathway, and that increased interleukin-8 expression is mediated by intracellular calcium levels in human gingival epithelial cells.

• Biomolecules & Therapeutics
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• 제28권5호
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• pp.423-430
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• 2020

Telmisartan is an angiotensin-II receptor blocker and acts as a selective modulator of peroxisome proliferator-activated receptor gamma (PPARγ). Several studies have demonstrated that telmisartan ameliorates depression and memory dysfunction and reduces brain inflammation. We hypothesized that the beneficial effects of telmisartan on brain could be due to modulation of the blood-brain barrier (BBB) function. Here, we examined the effect of telmisartan on tumor necrosis factor alpha (TNF-α)-induced expression of intercellular adhesion molecule 1 (ICAM-1) which plays an important role in leukocyte transcytosis through the BBB. Telmisartan blocked TNF-α-induced ICAM-1 expression and leukocyte adhesion in U87MG human glioma cells but showed no effect on human brain microvascular endothelial cells. In U87MG cells, a PPAR antagonist, GW9662 did not block the effect of telmisartan on ICAM1 expression but rather potentiated. Moreover, GW9662 caused no change in TNF-α-induced ICAM-1 expression, suggesting no implication of PPARγ in the telmisartan effect. Further studies showed that telmisartan blocked TNF-α-induced activation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), p38, and nuclear factorkappa B (NF-κB). In contrast, inhibitors of JNK, ERK1/2 and NF-κB but not p38, blocked ICAM-1 expression induced by TNF-α. Thus, our findings suggest that the beneficial effect of telmisartan is likely due to the reduction of astrocytic ICAM1 expression and leukocytes adhesion to astrocytes, and that this response was mediated by the inhibition of JNK/ERK1/2/NF-κB activation and in the PPAR-independent manner. In conclusion, this study enhances our understanding of the mechanism by which telmisartan exerts the beneficial brain function.

• Tribology and Lubricants
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• 제35권5호
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• pp.274-285
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• 2019

Chemical mechanical polishing (CMP), which is a material removal process involving chemical surface reactions and mechanical abrasive action, is an essential manufacturing process for obtaining high-quality semiconductor surfaces with ultrahigh precision features. Recent rapid growth in the industries of digital devices and semiconductors has accelerated the demands for processing of various substrate and film materials. In addition, to solve many issues and challenges related to high integration such as micro-defects, non-uniformity, and post-process cleaning, it has become increasingly necessary to approach and understand the processing mechanisms for various substrate materials and abrasive particle behaviors from a tribological point of view. Based on these backgrounds, we review recent CMP R&D trends in this study. We examine experimental and analytical studies with a focus on substrate materials and abrasive particles. For the reduction of micro-scratch generation, understanding the correlation between friction and the generation mechanism by abrasive particle behaviors is critical. Furthermore, the contact stiffness at the wafer-particle (slurry)-pad interface should be carefully considered. Regarding substrate materials, recent research trends and technologies have been introduced that focus on sapphire (${\alpha}$-alumina, $Al_2O_3$), silicon carbide (SiC), and gallium nitride (GaN), which are used for organic light emitting devices. High-speed processing technology that does not generate surface defects should be developed for low-cost production of various substrates. For this purpose, effective methods for reducing and removing surface residues and deformed layers should be explored through tribological approaches. Finally, we present future challenges and issues related to the CMP process from a tribological perspective.

• 약학회지
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• 제42권1호
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• pp.101-107
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• 1998

The antiparkinsonian agent l-deprenyl, a selective monoamine oxidase (MAO)-B inhibitor, is metabolized in part to l-methamphetamine and l-amphetamine. l< /I>-Deprenyl was evaluated for amphetamine and methamphetamine-like discriminative stimulus effects in rats and its mechanism of action was investigated. Rats were trained under a 5-response, fixed ratio schedule of stimulus-shock termination or a 10-response. Fixed-ratio schedule of food-presentation which discriminate between d-amphetamine (1mg/kg, i.p.) and saline or d-methamphetamine (1mg/kg, i.p.) and saline in a two-lever, operant conditioning procedure. Full generalization was obtained to d-amphetamine (1~3mg/kg). d-methamphetamine (1~3mg/kg) and l-deprenyl (17~30mg/kg) under both the food presentation and stimulus shock termination schedule. l-Deprenyl has dose-dependent amphetamine-and methamphetamine-like discriminative stimulus properties in rats only at doses of 17 and 30mg/kg. Reversible MAO-B inhibitor, RO 16-6491 didn`t show any amphetamine-like discriminative properties. Aromatic amino acid decarboxylase inhibitor, NSD 1015 decreased % responding of l-deprenyl in the methamphetamine-trained rats under the stimulus-shock termination schedule. SKF-525A produced partial inhibition of methamphetamine-like discriminative effects of l-deprenyl under the food presentation schedule. These results suggest that l-deprenyl has no abuse liability at the therapeutic range but there needs some caution at high doses and furthermore, drug discrimination studies under the food presentation and shock termination schedule are useful for the assessment of abuse liability of psychostimulants.

• Molecules and Cells
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• 제42권4호
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• pp.321-332
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• 2019

The brain is the most common metastatic site of lung adenocarcinoma; however, the mechanism of this selective metastasis remains unclear. We aimed to verify the hypothesis that exposure of tumor cells to the brain microenvironment leads to changes in their gene expression, which promotes their oriented transfer to the brain. A549 and H1299 lung adenocarcinoma cells were exposed to human astrocyte-conditioned medium to simulate the brain microenvironment. Microarray analysis was used to identify differentially expressed genes, which were confirmed by quantitative real-time PCR and western blotting. Knockdown experiments using microRNAs and the overexpression of genes by cell transfection were performed in addition to migration and invasion assays. In vitro findings were confirmed in clinical specimens using immunohistochemistry. We found and confirmed a significant increase in insulin-like growth factor binding protein-3 (IGFBP3) levels. Our results also showed that the up-regulation of IGFBP3 promoted A549 cell epithelial-mesenchymal transition, migration, and invasion, while the knockdown of IGFBP3 resulted in decreased cell motility. We also found that Transforming growth factor-${\beta}$ (TGF-${\beta}$)/Mothers against decapentaplegic homolog 4 (Smad4)-induced epithelial-mesenchymal transition was likely IGFBP3-dependent in A549 cells. Finally, expression of IGFBP3 was significantly elevated in pulmonary cancer tissues and intracranial metastatic tissues. Our data indicate that up-regulation of IGFBP3 might mediate brain metastasis in lung adenocarcinoma, which makes it a potential therapeutic target.

• The Korean Journal of Physiology and Pharmacology
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• 제23권3호
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• pp.219-227
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• 2019

Polycystic kidney disease 2-like-1 (PKD2L1), polycystin-L or transient receptor potential polycystin 3 (TRPP3) is a TRP superfamily member. It is a calcium-permeable non-selective cation channel that regulates intracellular calcium concentration and thereby calcium signaling. Although the calmodulin (CaM) inhibitor, calmidazolium, is an activator of the PKD2L1 channel, the activating mechanism remains unclear. The purpose of this study is to clarify whether CaM takes part in the regulation of the PKD2L1 channel, and if so, how. With patch clamp techniques, we observed the current amplitudes of PKD2L1 significantly reduced when co-expressed with CaM and $CaM{\triangle}N$. This result suggests that the N-lobe of CaM carries a more crucial role in regulating PKD2L1 and guides us into our next question on the different functions of two lobes of CaM. We also identified the predicted CaM binding site, and generated deletion and truncation mutants. The mutants showed significant reduction in currents losing PKD2L1 current-voltage curve, suggesting that the C-terminal region from 590 to 600 is crucial for maintaining the functionality of the PKD2L1 channel. With PKD2L1608Stop mutant showing increased current amplitudes, we further examined the functional importance of EF-hand domain. Along with co-expression of CaM, ${\triangle}EF$-hand mutant also showed significant changes in current amplitudes and potentiation time. Our findings suggest that there is a constitutive inhibition of EF-hand and binding of CaM C-lobe on the channel in low calcium concentration. At higher calcium concentration, calcium ions occupy the N-lobe as well as the EF-hand domain, allowing the two to compete to bind to the channel.