• Journal of the Korean Institute of Electrical and Electronic Material Engineers
• /
• v.25 no.9
• /
• pp.681-685
• /
• 2012

We investigated the dry etching characteristics of TiN in $TiN/Al_2O_3$ gate stack using a inductively coupled plasma system. TiN thin film is etched by BCl3/He plasma. The etching parameters are the gas mixing ratio, the RF power, the DC-bias voltages and process pressures. The highest etch rate is in $BCl_3/He$ (25%:75%) plasma. The selectivity of TiN thin film to $Al_2O_3$ is pretty similar with $BCl_3/He$ plasma. The chemical reactions of the etched TiN thin films are investigated by X-ray photoelectron spectroscopy. The intensities of the Ti 2p and the N 1s peaks are modified by $BCl_3$ plasma. Intensity and binding energy of Ti and N could be changed due to a chemical reaction on the surface of TiN thin films. Also we investigated that the non-volatile byproducts such as $TiCl_x$ formed by chemical reaction with Cl radicals on the surface of TiN thin films.

• Proceedings of the Materials Research Society of Korea Conference
• /
• 2009.05a
• /
• pp.26.2-26.2
• /
• 2009

이 논문은 반응성 $BCl_3$ 플라즈마로 GaAs의 건식 식각을 진행한 후 그 결과에 대하여 연구 분석 한 것이다. 이 때 사용한 식각 공정 변수는 $BCl_3$ 플라즈마에서의 가스유량, 공정 압력과 RIE 척 파워의 변화이다. 먼저 공정 압력을 75 mTorr 고정시킨 후 $BCl_3$ 유량을 변화 (2.5~10 sccm)해서 실험하였다. 또한 BCl3의 유량을 5 sccm으로 고정시킨 후 공정압력을 변화(47~180 mTorr)해서 식각 실험을 실시하였다. 마지막으로 47 mTorr와 100 mTorr 의 각각의 공정압력에서 RF 척 파워를 변화시켜 (50~200 W) 실험하였다. GaAs 플라즈마 식각이 끝난 후 표면단차 측정기 (Surface profiler)를 사용하여 표면의 단차와 거칠기를 분석하였다. 그 후 그 결과를 이용하여 식각율 (Etch rate), 식각 표면 거칠기 (RMS roughness), 식각 선택비 (Selectivity) 등의 식각 특성평가를 하였다. 또한 식각 공정 중에 샘플 척에 발생하는 자기 바이어스와 $BCl_3$ 플라즈마 가스를 광학 발광 분석기 (Optical Emission Spectroscopy)를 이용하여 플라즈마의 상태를 실시간으로 분석하였다. 이 실험 결과에 따르면 공정 압력의 증가는 샘플 척의 자기 바이어스의 값을 감소시켰다. $BCl_3$ 압력 변화에 의한 GaAs의 식각 결과를 정리하면 5 sccm의 $BCl_3$ 가스유량과 RF 척 파워를 100 W로 고정시켰을 때 식각율은 47 mTorr에서 가장 높았으며, 그 값은 $0.42{\mu}m/min$ 이었다. GaAs의 식각 속도는 공정압력이 증가할수록 감소하였으며 180 mTorr에서는 식각율이 $0.03{\mu}m/min$로 거의 식각되지 않았다. 또한 공정압력을 75 mTorr, RF 척 파워를 100 W로 고정시키고, $BCl_3$ 가스유량을 2.5 sccm에서 10 sccm까지 변화시켰을 때, 10 sccm 의 $BCl_3$ 가스유량에서 가장 높은 식각율인 $0.87{\mu}m/min$이 측정되었다. 압력에 따른 GaAs의 식각 후 표면 거칠기는 최대 2 nm 정도로 비교적 매끈하였으며, 거의 식각되지 않은 180mTorr의 조건에서는 약 1 nm로 낮아졌다. 본 실험 조건에서 GaAs의 감광제에 대한 식각 선택비는 최대 약 3:1 이내였다.

• Molecules and Cells
• /
• v.38 no.6
• /
• pp.535-539
• /
• 2015

Olfactory stimulation activates multiple signaling cascades in order to mediate activity-driven changes in gene expression that promote neuronal survival. To date, the mechanisms involved in activity-dependent olfactory neuronal survival have yet to be fully elucidated. In the current study, we observed that olfactory sensory stimulation, which caused neuronal activation, promoted activation of the phosphatidylinositol 3'-kinase (PI3K)/Akt pathway and the expression of Bcl-2, which were responsible for olfactory receptor neuron (ORN) survival. We demonstrated that Bcl-2 expression increased after odorant stimulation both in vivo and in vitro. We also showed that odorant stimulation activated Akt, and that Akt activation was completely blocked by incubation with both a PI3K inhibitor (LY294002) and Akt1 small interfering RNA. Moreover, blocking the PI3K/Akt pathway diminished the odorantinduced Bcl-2 expression, as well as the effects on odorant-induced ORN survival. A temporal difference was noted between the activation of Akt1 and the expression of Bcl-2 following odorant stimulation. Blocking the PI3K/Akt pathway did not affect ORN survival in the time range prior to the increase in Bcl-2 expression, implying that these two events, activation of the PI3K pathway and Bcl-2 induction, were tightly connected to promote post-translational ORN survival. Collectively, our results indicated that olfactory activity activated PI3K/Akt, induced Bcl-2, and promoted long term ORN survival as a result.

• Proceedings of the Materials Research Society of Korea Conference
• /
• 2003.03a
• /
• pp.88-88
• /
• 2003

Optical Emission Spectroscopy(OES) is a very important technology for real-time monitoring of plasma in a reactor during dry etching process. OES technology is non-invasive to the plasma process. It can be used to collect information on excitation and recombination between electrons and ions in the plasma. It also helps easily diagnose plasma intensity and monitor end-point during plasma etch processing. We studied high density planar inductively coupled BCl$_3$ and BCl$_3$/Ar plasma with an OES as a function of processing pressure, RIE chuck power, ICP source power and gas composition. The scan range of wavelength used was from 400 nm to 1000 nm. It was found that OES peak Intensity was a strong function of ICP source power and processing pressure, while it was almost independent on RIE chuck power in BCl$_3$-based planar ICP processes. It was also worthwhile to note that increase of processing pressure reduced negatively self-induced dc bias. The case was reverse for RIE chuck power. ICP power and gas composition hardly had influence on do bias. We will report OES results of high density planar inductively coupled BCl$_3$ and BCl$_3$/Ar Plasma in detail in this presentation.

• BMB Reports
• /
• v.51 no.2
• /
• pp.92-97
• /
• 2018

B cell leukemia/lymphoma 3 (Bcl3) plays a pivotal role in immune homeostasis, cellular proliferation, and cell survival, as a co-activator or co-repressor of transcription of the $NF-{\kappa}B$ family. Recently, it was reported that Bcl3 positively regulates pluripotency genes, including Oct4, in mouse embryonic stem cells (mESCs). However, the role of Bcl3 in the maintenance of pluripotency and self-renewal activity is not fully established. Here, we report the dynamic regulation of the proliferation, pluripotency, and self-renewal of mESCs by Bcl3 via an influence on Nanog transcriptional activity. Bcl3 expression is predominantly observed in immature mESCs, but significantly decreased during cell differentiation by LIF depletion and in mESC-derived EBs. Importantly, the knockdown of Bcl3 resulted in the loss of self-renewal ability and decreased cell proliferation. Similarly, the ectopic expression of Bcl3 also resulted in a significant reduction of proliferation, and the self-renewal of mESCs was demonstrated by alkaline phosphatase staining and clonogenic single cell-derived colony assay. We further examined that Bcl3-mediated regulation of Nanog transcriptional activity in mESCs, which indicated that Bcl3 acts as a transcriptional repressor of Nanog expression in mESCs. In conclusion, we demonstrated that a sufficient concentration of Bcl3 in mESCs plays a critical role in the maintenance of pluripotency and the self-renewal of mESCs via the regulation of Nanog transcriptional activity.

• Journal of Chest Surgery
• /
• v.31 no.10
• /
• pp.924-927
• /
• 1998

Background: Myocardial cell death after myocardial infarction or reperfusion is classified into necrosis and apoptosis. Bcl-2 protein is a cytoplasmic protein, which inhibits apoptosis and is expressed in acute stage of myocardial infarction but not in normal heart. This study was performed to investigate whether Bcl-2 protein was expressed respectively to the reperfusion time. Materials and methods: Thirty nine New Zealand white rabbits weighing 1.5-4.8 kg (mean, 2.9kg) were alloted into 7 groups (n=5 in each group) which underwent left anterior descending coronary artery(LAD) occlusion for 30 minutes, followed by reperfusion. The animals were sacrificed at 1, 4, 8, 12, 24 hours, and 3, 7 days after occlusion. Ventricle was excised immediately after intervention. Tissues were fixed in 10% buffured formalin and embedded in paraffin. Bcl-2 protein was detected by immunohistochemical stain with using monoclonal antibody against Bcl-2 protein. Results: The positive immunohistochemical reactivity for Bcl-2 protein was observed in 12, 24 hours, and 3 days reperfusion groups. Bcl-2 protein was detected in salvaged myocytes surrounding the infarcted area. Conclusions: Bcl-2 protein is expressed at the late acute stage of infarct. Therefore, the expression of Bcl-2 protein may not protect acute cell death, but may play a role in the prevention of late cell death after myocardial is chemia-reperfusion.

• Reproductive and Developmental Biology
• /
• v.36 no.3
• /
• pp.167-172
• /
• 2012

The key regulators of apoptosis are the interacting protein of the Bcl-2 family. Bcl-2, an important member of this family, blocks cytochrome C release by sequestering pro-apoptotic BH3-only proteins such as Bid, Bad, Bax and Bim. The pro-survival family members (Bcl-2, Bcl-XL, Bcl-W) are critical for cell survival, since loss of any of them causes cell death in certain cell type. However, its role during early porcine embryonic development is not sufficient. In this study, we traced the effects of Bcl-2 inhibitor, ABT-737, on early porcine embryonic development. We also investigated several indicators of developmental potential, including gene expression (apoptosis-related genes) and apoptosis, which are affected by ABT-737. Porcine embryos were cultured in the PZM-3 medium with or without ABT-737 for 6 days. In result, significant differences in developmental potential were detected between the embryos that were cultured with or without ABT-737 ($14.7{\pm}3.0$ vs $30.3{\pm}4.8%$, p<0.05). TUNEL assay showed that the number of containing fragmented DNA at the blastocyst stage increased in the ABT-737 treated group compared with control (4.7 vs 3.7, p<0.05). The mRNA expression of the pro-apoptotic gene Bax increased in ABT-737 treated group (p<0.05), whereas expressions of the anti-apoptotic Bcl-2 family members (Bcl-2, Bcl-XL, Bcl-W) decreased (p<0.05). Also, expressions of the ER stress indicator genes (GRP78, XBP-1 and sXBP-1) increased in ABT-737 treated group (p<0.05). In conclusion, Bcl-2 is closely associated with of apoptosis- and ER stress-related genes expressions and developmental potential in pig embryos.

• Molecules and Cells
• /
• v.41 no.7
• /
• pp.684-694
• /
• 2018

Upregulation of human telomerase reverse transcriptase (hTERT) expression is an important factor in the cellular survival and cancer. Although growing evidence suggests that hTERT inhibits cellular apoptosis by telomere-independent functions, the mechanisms involved are not fully understood. Here, we show that hTERT contains a BH3-like motif, a short peptide sequence found in BCL-2 family proteins, and interacts with anti-apoptotic BCL-2 family proteins MCL-1 and BCL-xL, suggesting a functional link between hTERT and the mitochondrial pathway of apoptosis. Additionally, we propose that hTERT can be categorized into the atypical BH3-only proteins that promote cellular survival, possibly due to the non-canonical interaction between hTERT and antiapoptotic proteins. Although the detailed mechanisms underlying the hTERT BH3-like motif functions and interactions between hTERT and BCL-2 family proteins have not been elucidated, this work proposes a possible connection between hTERT and BCL-2 family members and reconsiders the role of the BH3-like motif as an interaction motif.

• Molecules and Cells
• /
• v.24 no.3
• /
• pp.378-387
• /
• 2007

The Bcl-2 family of proteins interacts at the mitochondria to regulate apoptosis. However, the anti-apoptotic Bcl-2 and $Bcl-X_L$ are not completely localized to the mitochondria. In an attempt to generate Bcl-2 and $Bcl-X_L$ chimeras that are constitutively localized to the mitochondria, we substituted their C-terminal transmembrane tail or both the C-terminal transmembrane tail and the adjacent loop with the equivalent regions from Bak or Bax mutant (BaxS184V) as these regions determine the mitochondrial localization of Bak and Bax. The effects of these substitutions on subcellular localization and their activities were assessed following expression in HeLa and CHO K1 cells. The substitution of the C-terminal tail or the C-terminal tail and the adjacent loop of Bcl-2 with the equivalent regions from Bak or the Bax mutant resulted in its association with the mitochondria. This change in subcellular localization of Bcl-2 chimeras triggered cells to undergo apoptotic-like cell death. The localization of this Bcl-2 chimera to the mitochondria may be associated with the disruption of mitochondrial membrane potential. Unlike Bcl-2, the loop structure adjacent to the C-terminal tail in $Bcl-X_L$ is crucial for its localization. To localize the $Bcl-X_L$ chimeras to the mitochondria, the loop structure next to the C-terminal tail in $Bcl-X_L$ protein must remain intact and cannot be substituted by the loop from Bax or Bak. The chimeric $Bcl-X_L$ with both its C-terminal tail and the loop structure replaced by the equivalent regions of Bak or Bax mutant localized throughout the entire cytosol. The $Bcl-X_L$ chimeras that are targeted to the mitochondria and the wild type $Bcl-X_L$ provided same protection against cell death under several death inducing conditions.

• Journal of Chest Surgery
• /
• v.32 no.8
• /
• pp.726-731
• /
• 1999

Background: The distinction between non-invasive and invasive or thymic carcinoma has been severely compromised by lack of objective morphological criteria. A reliable biological marker of tumor aggressiveness is, therefore, mandatory for predicting tumor behavior. Material and Method: Thirty thymic epithelial tumors, including 7 non-invasive thymoma, 10 invasive thymoma, and 13 thymic carcinoma of the Rosai's classification; and 5 stage I, 7 stage II, 2 stage III, and 3 stage IVa of the Masaoka stage of thymoma were investigated for expression of bcl-2 and p53 proteins by immunohistochemistry. Result: The thymic epithelial cells showed positive immunostain for bcl-2 in 0 (0%), 3 (30%), 8 (61.5%) of categories in the Rosai's classification respectively and in 0 (0%), 1 (14.3%), 2 (100%), 0 (0%) of stage I, II, III, IVa of the Masaoka stage respectively. Thymic carcinoma, and high stage thymoma had significantly higher proportion of bcl-2 expression than thymoma (p=0.021) and low stage thymoma (p=0.011). However, p53 showed no correlation with the histological subtypes nor with clinical aggressiveness. Bcl-2 expression appeared to be positively correlated with p53 immunoactivity (p=0.007, kappa=0.525). Conclusion: These date indicate that bcl-2 expression correlates with aggressiveness in thymic epithelial tumors, but further studies on mutation of p53 protein is necessary because bcl-2 expression appeared to be positively correlated with p53 immunoactivity.