• Proceedings of the Korean Vacuum Society Conference
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• 1999.07a
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• pp.223-223
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• 1999

PZT(PbZr1-xTixO3) 박막은 고유전율과 같은 remanent polarization을 가져서 고집적 소자의 커패시터 유전율층 또는 비휘발성 메모리 소자의 제조에 이용되고 있으나, fatigue 와 aging 문제로 인하여 새로운 물질의 개발이 필요한데, 그 대표적으로 연구되고 있는 것이 PMN-PT(Pb(Mg1/3Nb2/3)O-PbTiO3) 이다. 본 실험에서는 sol-gel 법에 의하여 제조된 PMN-PT막을 ICP(Inductively coupled plasma)에 의하여 식각하였고 mask층으로는 PR을 사용하였다. 식각 가스로는 Ar, Cl, BCl를 단독 또는 혼합하여 사용하였으며, 식각 특성을 보기 위하여 RF Power, Substrate bias, Operation pressure, Substrate temperature를 변화시켰다. 식각속도는 stylus profiler를 이용하여 측정하였고, 단면 profile은 scanning electron microscopy (SEM)를 이용하여 관찰하였다. 식각 메커니즘을 규명하고자 식각된 박막의 표면을 X-ray photoelectron spectroscopy (XPS)로 관찰하였고, optical emission spectroscopy (OES)로 플라즈마 특성을 규명하고자 하였다. 식각속도는 Ar 또는 Cl2 플라즈마에 BCl3 가스를 혼합하였을 경우 증가되었고, BCl3 가스를 단독으로 사용하여도 높은 식각속도를 나타내었으며, BCl3의 첨가량이 늘어날수록 PR의 식각속도는 감소하여 높은 선택비를 보였다. 90% BCl3/10%Cl2 플라즈마에서 2800$\AA$/min의 식각속도 그리고 1.37:1의 PR 선택비를 얻을 수 있었다. Power나 기판 bias 증가에 따라 식각속도는 증가하였으나 기판 온도변화에는 민감하지 않았다. BCl3 rich에서의 식각속도 증가와 선택비 증가는 B2O3의 형성에 의한 것으로 생각된다.

• Molecules and Cells
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• v.37 no.1
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• pp.17-23
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• 2014

We already had reported that Bcl-w promotes invasion or migration in gastric cancer cells and glioblastoma multiforme (GBM) by activating matrix metalloproteinase-2 (MMP-2) via specificity protein 1 (Sp1) or ${\beta}$-cateinin, respectively. High expression of Bcl-w also has been reported in GBM which is the most common malignant brain tumor and exhibits aggressive and invasive behavior. These reports propose that Bcl-w-induced signaling is strongly associated with aggressive characteristic of GBM. We demonstrated that Sp1 protein or mRNA expression is induced by Bcl-w using Western blotting or RT-PCR, respectively, and markedly elevated in high-grade glioma specimens compared with low-grade glioma tissues using tissue array. However, relationship between Bcl-w-related signaling and aggressive characteristic of GBM is poorly characterized. This study suggested that Bcl-w-induced Sp1 activation promoted expression of glioma stem-like cell markers, such as Musashi, Nanog, Oct4 and sox-2, as well as neurosphere formation and invasiveness, using western blotting, neurosphere formation assay, or invasion assay, culminating in their aggressive behavior. Therefore, Bcl-w-induced Sp1 activation is proposed as a putative marker for aggressiveness of GBM.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2008.11a
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• pp.363-363
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• 2008

The development of dry etching process for sapphire wafer with plasma has been key issues for the opto-electric devices. The challenges are increasing control and obtaining low plasma induced-damage because an unwanted scattering of radiation is caused by the spatial disorder of pattern and variation of surface roughness. The plasma-induced damages during plasma etching process can be classified as impurity contamination of residual etch products or bonding disruption in lattice due to charged particle bombardment. Therefor, fine pattern technology with low damaged etching process and high etch rate are urgently needed. Until now, there are a lot of reports on the etching of sapphire wafer with using $Cl_2$/Ar, $BCl_3$/Ar, HBr/Ar and so on [1]. However, the etch behavior of sapphire wafer have investigated with variation of only one parameter while other parameters are fixed. In this study, we investigated the effect of pressure and other parameters on the etch rate and the selectivity. We selected $BCl_3$ as an etch ant because $BCl_3$ plasmas are widely used in etching process of oxide materials. In plasma, the $BCl_3$ molecule can be dissociated into B radical, $B^+$ ion, Cl radical and $Cl^+$ ion. However, the $BCl_3$ molecule can be dissociated into B radical or $B^+$ ion easier than Cl radical or $Cl^+$ ion. First, we evaluated the etch behaviors of sapphire wafer in $BCl_3$/additive gases (Ar, $N_2,Cl_2$) gases. The behavior of etch rate of sapphire substrate was monitored as a function of additive gas ratio to $BCl_3$ based plasma, total flow rate, r.f. power, d.c. bias under different pressures of 5 mTorr, 10 mTorr, 20 mTorr and 30 mTorr. The etch rates of sapphire wafer, $SiO_2$ and PR were measured with using alpha step surface profiler. In order to understand the changes of radicals, volume density of Cl, B radical and BCl molecule were investigated with optical emission spectroscopy (OES). The chemical states of $Al_2O_3$ thin films were studied with energy dispersive X-ray (EDX) and depth profile anlysis of auger electron spectroscopy (AES). The enhancement of sapphire substrate can be explained by the reactive ion etching mechanism with the competition of the formation of volatile $AlCl_3$, $Al_2Cl_6$ or $BOCl_3$ and the sputter effect by energetic ions.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2008.06a
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• pp.477-477
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• 2008

For more than three decades, the gate dielectrics in CMOS devices are $SiO_2$ because of its blocking properties of current in insulated gate FET channels. As the dimensions of feature size have been scaled down (width and the thickness is reduced down to 50 urn and 2 urn or less), gate leakage current is increased and reliability of $SiO_2$ is reduced. Many metal oxides such as $TiO_2$, $Ta_2O_4$, $SrTiO_3$, $Al_2O_3$, $HfO_2$ and $ZrO_2$ have been challenged for memory devices. These materials posses relatively high dielectric constant, but $HfO_2$ and $Al_2O_3$ did not provide sufficient advantages over $SiO_2$ or $Si_3N_4$ because of reaction with Si substrate. Recently, $HfO_2$ have been attracted attention because Hf forms the most stable oxide with the highest heat of formation. In addition, Hf can reduce the native oxide layer by creating $HfO_2$. However, new gate oxide candidates must satisfy a standard CMOS process. In order to fabricate high density memories with small feature size, the plasma etch process should be developed by well understanding and optimizing plasma behaviors. Therefore, it is necessary that the etch behavior of $HfO_2$ and plasma parameters are systematically investigated as functions of process parameters including gas mixing ratio, rf power, pressure and temperature to determine the mechanism of plasma induced damage. However, there is few studies on the the etch mechanism and the surface reactions in $BCl_3$ based plasma to etch $HfO_2$ thin films. In this work, the samples of $HfO_2$ were prepared on Si wafer with using atomic layer deposition. In our previous work, the maximum etch rate of $BCl_3$/Ar were obtained 20% $BCl_3$/ 80% Ar. Over 20% $BCl_3$ addition, the etch rate of $HfO_2$ decreased. The etching rate of $HfO_2$ and selectivity of $HfO_2$ to Si were investigated with using in inductively coupled plasma etching system (ICP) and $BCl_3/Cl_2$/Ar plasma. The change of volume densities of radical and atoms were monitored with using optical emission spectroscopy analysis (OES). The variations of components of etched surfaces for $HfO_2$ was investigated with using x-ray photo electron spectroscopy (XPS). In order to investigate the accumulation of etch by products during etch process, the exposed surface of $HfO_2$ in $BCl_3/Cl_2$/Ar plasma was compared with surface of as-doped $HfO_2$ and all the surfaces of samples were examined with field emission scanning electron microscopy and atomic force microscope (AFM).

• Journal of Life Science
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• v.23 no.9
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• pp.1118-1125
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• 2013

Naringenin, a naturally occurring citrus flavonone, is a potentially valuable candidate for cancer chemotherapy. However, the cellular and molecular mechanisms responsible for its anticancer activity are largely unknown. In the present study, we attempted to elucidate the mechanisms responsible for naringenin-induced apoptosis in human leukemic U937 cells. We found that naringenin markedly inhibited the growth of U937 cells by decreasing cell proliferation and inducing apoptosis, which was associated with the activation of caspases. A pan-caspase inhibitor, z-VAD-fmk, significantly inhibited naringenin-induced U937 cell apoptosis, indicating that caspases are key regulators of apoptosis in response to naringenin in U937 cells. Although the levels of antiapoptotic Bcl-2 and proapoptotic Bax proteins remained unchanged in naringenin-treated U937 cells, Bcl-2 overexpression attenuated naringenin-induced apoptosis. Furthermore, combined treatment with naringenin and HA14-1, a small-molecule Bcl-2 inhibitor, effectively increased the apoptosis through enhancement of XIAP down-regulation, Bid cleavage, and caspase activation, suggesting that the synergistic effect was at least partially mediated through the death receptor-mediated apoptosis pathway.

• Journal of the East Asian Society of Dietary Life
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• v.24 no.6
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• pp.739-747
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• 2014

The aim of the study was to determine the effects of Ixeris dentata extract (IDE) on anticancer activity in human breast cancer MDA-MB-231 cells at both cellular and molecular levels. The cells were cultured in the presence of 0, 20, 30 and $40{\mu}g/mL$ Ixeris dentata extract for 24 hours, respectively. At the end of culture, cytochemical analyses for MTT activity, trypan blue dye exclusion, Annexin V-FITC Apoptosis, and radical oxygen species (ROS) were conducted. RT-PCR was also performed to determine whether or not alterations in cell viability affect the Bax/Bcl-2 ratio. MTT assay showed that relative cell viability decreased in a dose-dependent manner (p<0.05). Reduction of cell viability matched well with increased cell membrane permeability as determined by trypan blue dye exclusion test (p<0.05). The rates of intracellular ROS also increased in a similar manner to those of TB-stained cells. There was an associated shift of apoptotic cells from early to late apoptosis between the 30 and $40{\mu}g/mL$. Bax/Bcl-2 ratio significantly increased along with significant decreases in Bcl-2 expression between 30 and $40{\mu}g/mL$ groups (p<0.05). In conclusion, anticancer activity of Ixeris dentata extract is modulated by a reduction in cell viability along with increased membrane permeability, leading to ROS accumulation within cells, and subsequently cell death through an apoptotic pathway that involves Bax and Bcl-2 in human breast cancer MDA-MB-231 cells.

• Proceedings of the KIEE Conference
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• 1999.11d
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• pp.863-866
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• 1999

(Ba,Sr)$TiO_3$ thin films have attracted groat interest as new dielectric materials of capacitors for ultra-large-scale integrated dynamic random access memories (ULSI-DRAMs) such as 1 Gbit or 4 Gbit. In this study, inductively coupled $BCl_3/Cl_2$/Ar plasmas was used to etch (Ba,Sr)$TiO_3$ thin films. RF power/dc bias voltage = 600 W/-250 V and chamber pressure was 10 mTorr. The $Cl_2/(Cl_2+Ar)$ was fixed at 0.2, the (Ba,Sr)$TiO_3$ thin films were etched adding $BCl_3$. The highest (Ba,Sr)$TiO_3$ etch rate is 480$\AA/min$ at 10 % $BCl_3$ adding to $Cl_2$/Ar. The characteristics of the plasmas were estimated using optical emission spectroscopy (OES). The change of Cl, B radical density measured by OES as a function of $BCl_3$ percentage in $Cl_2$/Ar. The highest Cl radical density was shown at the addition of 10% $BCl_3$ to $Cl_2$/Ar. To study on the surface reaction of (Ba,Sr)$TiO_3$ thin films was investigated by XPS analysis. Ion enhancement etching is necessary to break Ba-O bond and to remove $BaCl_2$. There is a little chemical reaction between Sr and Cl, but Sr is removed by physical sputtering. There is a chemical reaction between Ti and Cl, and Tic14 is removed with ease. The cross-sectional of (Ba,Sr)$TiO_3$ thin film was investigated by scanning electron microscopy (SEM), the etch slope is about $65\;{\sim}\;70$.

• BMB Reports
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• v.49 no.1
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• pp.51-56
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• 2016

Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine protein kinase that is known to mediate cancer cell death. Here, we show that B-cell lymphoma 2 (Bcl-2), an anti-apoptotic protein, is regulated by GSK-3β and that GSK-3β-mediated regulation of Bcl-2 is crucial for mitochondrial-dependent cell death in paclitaxel-stimulated cells. We demonstrate that MCF7 GSK-3β siRNA cells are more sensitive to cell death than MCF7 GFP control cells and that in the absence of GSK-3β, Bcl-2 levels are reduced, a result enhanced by paclitaxel. Paclitaxel-induced JNK (c-Jun N-terminal kinase) activation is critical for Bcl-2 modulation. In the absence of GSK-3β, Bcl-2 was unstable in an ubiquitination-dependent manner in both basal- and paclitaxel-treated cells. Furthermore, we demonstrate that GSK-3β-mediated regulation of Bcl-2 influences cytochrome C release and mitochondrial membrane potential. Taken together, our data suggest that GSK-3β-dependent regulation of Bcl-2 is crucial for mitochondria-dependent cell death in paclitaxel-mediated breast cancer therapy. [BMB Reports 2016; 49(1): 51-56]

• Biomedical Science Letters
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• v.18 no.4
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• pp.420-427
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• 2012

Sprague-Dawley (SD) rats were orally administered with NG-nitro-L-arginine methyl ester (L-NAME), which inhibits or blocks the production of nitric oxide from L-arginine in vascular endothelial cells and vessel tissue. We examined the effects of nitric oxide on some physiological changes such as blood pressure and heart rate, and confirms the apoptosis induced by the suppressed nitric oxide activity in the kidney. This study was performed to investigate correlation between the activities of nitric oxide and apoptosis by immunohistochemical changes of apoptotic control proteins with regulated chronic inhibition of nitric oxide. In the kidney from L-NAME-treated group, immunohistochemical reaction to the antigens of apoptosis inhibiting proteins such as bcl-2 and bcl-xL, exhibited a time-dependent reduction. The expression of apoptosis-inhibiting proteins such as bax and p53 increased expression in proportion to the duration of treatment. The most sensitive apoptosis regulating proteins to L-NAME were p53 in stimulation and bcl-2 in inhibition, respectively.

• Clinical and Experimental Reproductive Medicine
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• v.24 no.2
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• pp.267-271
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• 1997

Apoptosis, programmed cell death, is posulated to occur in granulosa cells in ovarian follicular atresia. bcl-2 gene serves as protector from apoptosis and, thus, is associated with increased cell survival. TRPM-2 gene expression has been implicated as a trigger of apoptosis in rat prostate, uterus and mammary gland. Our objective was to determine if bcl-2 and TRPM-2 are expressed in luteinized human GC and, therefore, have regulatory functions for apoptosis in GC. Human GC were obtained via oocyte retrival from the infertile patients stimulated with exogeneous gonadotropins while undergoing IVF. GC were isolated from follicular fluid using Percoll gradient centrifugation. The GC were further purified with anti-CD45 magnetic beads to remove contaminating WBC's. RT-PCR were performed to analyze the mRNA expression of bcl-2 and TRPM-2 in the GC. The PCR primers were designed to amplify a 195 bp fragment of bcl-2 and a 174 bp fragment of TRPM-2. The PCR products were electrophoresed on 4% agarose gel. Three separate experiments indicated that both bcl-2 and TRPM-2 are concurrently expressed in human GC. We cultured granulosa cells with FSH (1 ng/ml) for 1 day to investigate the relative changes of TRPM-2 mRNA level with RNAse protection assay. When we cultured GC with serum free medium for 1 day TRPM-2 mRNA level increased with 1.3 fold, however it was decreased 0.64 fold with FSH. Therefore we conclude that bcl-2 and TRPM-2 are concurrently expressed and that the interaction of their products may be involved in GC apoptosis. And TRPM-2 may be regulated with FSH.