• 한국진공학회:학술대회논문집
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• 한국진공학회 2016년도 제50회 동계 정기학술대회 초록집
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• pp.406-406
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• 2016

To get high efficiency n-type crystalline silicon solar cells, passivation is one of the key factor. Tunnel oxide (SiO2) reduce surface recombination as a passivation layer and it does not constrict the majority carrier flow. In this work, the passivation quality enhanced by different chemical solution such as HNO3, H2SO4:H2O2 and DI-water to make thin tunnel oxide layer on n-type crystalline silicon wafer and changes of characteristics by subsequent annealing process and firing process after phosphorus doped amorphous silicon (a-Si:H) deposition. The tunneling of carrier through oxide layer is checked through I-V measurement when the voltage is from -1 V to 1 V and interface state density also be calculated about $1{\times}1012cm-2eV-1$ using MIS (Metal-Insulator-Semiconductor) structure . Tunnel oxide produced by 68 wt% HNO3 for 5 min on $100^{\circ}C$, H2SO4:H2O2 for 5 min on $100^{\circ}C$ and DI-water for 60 min on $95^{\circ}C$. The oxide layer is measured thickness about 1.4~2.2 nm by spectral ellipsometry (SE) and properties as passivation layer by QSSPC (Quasi-Steady-state Photo Conductance). Tunnel oxide layer is capped with phosphorus doped amorphous silicon on both sides and additional annealing process improve lifetime from $3.25{\mu}s$ to $397{\mu}s$ and implied Voc from 544 mV to 690 mV after P-doped a-Si deposition, respectively. It will be expected that amorphous silicon is changed to poly silicon phase. Furthermore, lifetime and implied Voc were recovered by forming gas annealing (FGA) after firing process from $192{\mu}s$ to $786{\mu}s$. It is shown that the tunnel oxide layer is thermally stable.

• 한국식품영양과학회지
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• 제35권5호
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• pp.516-523
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• 2006

차가버섯(Inonotus obliquus)은 한랭한 삼림지대에서 자라는 자작나무에 자생하는 버섯으로, 항종양 및 항돌연변이 활성이 있는 것으로 보고되고 있으나, 차가버섯의 항암기전에 대해 밝혀진 바가 없어, 본 연구에서는 인체의 대장암에서 유래한 HT-29 세포를 사용하여 차가버섯 물추출물의 대장암세포 증식 억제기전을 밝히고자 하였다. 차가버섯을 열수추출하여 냉동 건조하여 얻은 물추출물을 HT-29 세포 배양액에 여러 농도($0{\sim}100{\mu}g/mL$)로 첨가하여 세포의 증식에 미치는 영향을 조사하였다. 세포의 증식은 차가버섯 추출물 농도가 증가할수록 현저히 감소하였다. 차가버섯 물추출물 처리 농도에 비례하여 세포의 DNA합성은 감소하였고, apoptotic cell의 수는 현저히 증가하였다. Apoptosis의 주요한 조절 인자인 Bcl-2 family 단백질 수준은 차가버섯에 의해 변화하지 않았으나, cleaved caspase-8, -9, -3의 단백질 수준은 차가버섯에 의해 증가하였다. Caspase-8, -9, -3의 활성도 모두 차가버섯에 의해 유의적으로 증가하였다. Caspase-3의 표적 단백질로 세포의 생존에 결정적인 역할을 하는 PARP단백질의 분해도 차가버섯에 의해 현저히 증가하였다. 이 결과로부터 차가버섯 물추출물이 DNA합성을 억제하고 apoptosis를 유도하여 대장암 세포의 증식을 억제하고, caspase 경로의 활성을 증가하므로써 apoptosis를 유도한다는 결론을 내릴 수 있다. 또한 이 결과는 차가버섯 물추출물을 대장암의 예방이나 치료에 사용할 수 있는 가능성을 제시한다.

• Biomolecules & Therapeutics
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• 제28권6호
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• pp.561-568
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• 2020

We examined the anticancer effects of a novel sirtuin inhibitor, MHY2256, on HCT116 human colorectal cancer cells to investigate its underlying molecular mechanisms. MHY2256 significantly suppressed the activity of sirtuin 1 and expression levels of sirtuin 1/2 and stimulated acetylation of forkhead box O1, which is a target protein of sirtuin 1. Treatment with MHY2256 inhibited the growth of the HCT116 (TP53 wild-type), HT-29 (TP53 mutant), and DLD-1 (TP53 mutant) human colorectal cancer cell lines. In addition, MHY2256 induced G0/G1 phase arrest of the cell cycle progression, which was accompanied by the reduction of cyclin D1 and cyclin E and the decrease of cyclin-dependent kinase 2, cyclin-dependent kinase 4, cyclin-dependent kinase 6, phosphorylated retinoblastoma protein, and E2F transcription factor 1. Apoptosis induction was shown by DNA fragmentation and increase in late apoptosis, which were detected using flow cytometric analysis. MHY2256 downregulated expression levels of procaspase-8, -9, and -3 and led to subsequent poly(ADP-ribose) polymerase cleavage. MHY2256-induced apoptosis was involved in the activation of caspase-8, -9, and -3 and was prevented by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor. Furthermore, the autophagic effects of MHY2256 were observed as cytoplasmic vacuolation, green fluorescent protein-light-chain 3 punctate dots, accumulation of acidic vesicular organelles, and upregulated expression level of light-chain 3-II. Taken together, these results suggest that MHY2256 could be a potential novel sirtuin inhibitor for the chemoprevention or treatment of colorectal cancer or both.

• Journal of Microbiology and Biotechnology
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• 제14권5호
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• pp.978-984
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• 2004

In the course of screening for a novel inhibitor of CDC2, HY558-1 was isolated from a culture broth of Penicillium minioluteum F558. Moreover, it was found that HY558-1 had an effect on both the cell cycle regulation and apoptosis of human cervical adenocarcinoma HeLa cells. A flow cytometric analysis of HeLa cells revealed appreciable cell cycle arrest at the G1 and G2/M phases following treatment with HY558-1. Furthermore, DNA fragmentation due to apoptosis was observed in HeLa cells treated with HY558-1. To obtain further information on the cell cycle arrest and apoptotic induction induced by HY558-1, the expression of certain cell cycle and apoptosis-associated proteins was examined using a Western blot analysis. The results revealed that HY558-1 inhibited the phosphorylation of pRb and decreased the expression levels of CDK2, CDC2, and cyclin A in the cell cycle progression. It was also shown that the level of $p21^{WAF1/CIP1}$ was increased in HeLa cells treated with 0.52 mM of HY558-1. Accordingly, HY558-1 was found to inhibit the proliferation of HeLa cells through the induction of G1 phase arrest by inhibiting pRb phosphorylation via an upregulation of $p21^{WAF1/CIP1}$, and G2/M phase arrest by directly inhibiting CDC2 and cyclin A. Moreover, HeLa cells treated with 0.52 mM of HY558-1 exhibited apoptotic induction associated with the cleavage of Bid and release of cytochrome c from mitochondria into the cytosol. Subsequent investigation of the activation of caspase-3 and cleavage of poly (ADP-ribose) polymerase (PARP) suggested that the mitochondrial pathway was primarily involved in the HY558-1-induced apoptosis in HeLa cells.

• 한국산학기술학회논문지
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• 제17권12호
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• pp.327-332
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• 2016

스팅은 1985년 첫 솔로앨범인 를 필두로 세련된 감각과 폭넓은 음악적 스펙트럼을 선보이며 1억 장 이상의 앨범 판매고를 올린 영국을 대표하는 아티스트다. 본 논문에서는 스팅이 솔로 아티스트로서 폴리스 해체 이 후 30년이 넘도록 다양하고 폭넓은 자신만의 음악적 색채를 인정받는데 큰 발판이 되었던 음반에 수록되어 있는 곡들 중 'Straight To My Heart'와 'Be Still My Beating Heart'의 리듬 편곡에 대해 중점적으로 분석 할 것이다. 음반에 있는 곡들은 전체적으로 드럼파트는 기본적인 연주를 벗어나지 않고 전체적인 리듬분할의 역할을 여러 가지 퍼커션을 통해 하거나 신디사이저를 코드악기로서의 역할보다는 리듬악기로서의 역할에 더 비중을 둔 곡들이 많은 것을 볼 수 있다. 솔로 초기 스팅 만의 독특한 악기별 리듬구성과 역할배분은 다른 뮤지션들의 음반과는 사뭇 다른 그 만의 독특한 사운드를 창출해낸다. 이에 본 논문에서는 이 시기의 음반에 두드러지게 나타난 편곡적인 특징과 리듬적 특성, 즉 드럼비트를 쪼개서 리듬을 분할하는 통상적인 방식에서 벗어나 퍼커션을 포함한 다른 악기들의 리듬분할을 통해 곡의 기본적인 흐름을 이끌어가는 방법에 대해 설명 하고자 한다.

• Tuberculosis and Respiratory Diseases
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• 제75권1호
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• pp.9-17
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• 2013

Background: In cancer cells, autophagy is generally induced as a pro-survival mechanism in response to treatment-associated genotoxic and metabolic stress. Thus, concurrent autophagy inhibition can be expected to have a synergistic effect with chemotherapy on cancer cell death. Monensin, a polyether antibiotic, is known as an autophagy inhibitor, which interferes with the fusion of autophagosome and lysosome. There have been a few reports of its effect in combination with anticancer drugs. We performed this study to investigate whether erlotinib, an epidermal growth factor receptor inhibitor, or rapamycin, an mammalian target of rapamycin (mTOR) inhibitor, is effective in combination therapy with monensin in non-small cell lung cancer cells. Methods: NCI-H1299 cells were treated with rapamycin or erlotinib, with or without monensin pretreatment, and then subjected to growth inhibition assay, apoptosis analysis by flow cytometry, and cell cycle analysis on the basis of the DNA contents histogram. Finally, a Western blot analysis was done to examine the changes of proteins related to apoptosis and cell cycle control. Results: Monensin synergistically increases growth inhibition and apoptosis induced by rapamycin or erlotinib. The number of cells in the sub-$G_1$ phase increases noticeably after the combination treatment. Increase of proapoptotic proteins, including bax, cleaved caspase 3, and cleaved poly(ADP-ribose) polymerase, and decrease of anti-apoptotic proteins, bcl-2 and bcl-xL, are augmented by the combination treatment with monensin. The promoters of cell cycle progression, notch3 and skp2, decrease and p21, a cyclin-dependent kinase inhibitor, accumulates within the cell during this process. Conclusion: Our findings suggest that concurrent autophagy inhibition could have a role in lung cancer treatment.

• Journal of Chest Surgery
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• 제33권6호
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• pp.494-501
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• 2000

Background: Transmyocardial laser revascularization(TMLR) for revascularizing ischemic myocardium in patients was originally based on the assumption that laser channels remain their patency much longer. But recent studies show that laser channels did not remain open and that TMLR could achieve treatment benefits without long-term channel patency. The angiongencesis is currently thought to be induced by non-specific inflammatory response to mechanical tissue injury. This study is to evaluate hypothesis that various transmyocaridal mechanical revascularization(TMMR) may induce the angiogenic responses similar to that seen with TMLR, and transmyocaridal polymer stent revascularization(TMSR), the polymer stent in the myocardial tissue is hydrolyzed in 2 weeks, may enhance the non-specific inflammatory reaction resulting angiogenesis. Furthermore, polymer myocaridal stent channels remain long-term patency. Material and Method: Eight domestic pigs underwent ligation of the proximal circumflex artery, and 2 weeks later they were randomized to undergo transmycardial acupunctural revascularization (TMPR, Group I) of the left lateral wall with 18-G needle(n=2), to undergo transmyocardial (TMDR, Group II) with industrial 2mm steel drill(n=2), to undergo transmyocardial polymer stent revascularization (TMSR, Group III) after drilling the infarcted myocardium(n=2), the stent is poly(lactic acid-co-glycolic acid), which is self-degradated in the myocardium, and to a control group the ischemic zone was unterated(n=2). All the pigs were sacrificed after 4 weeks TMMR. Sections from the ischemic zone were submitted for vascular endothelial growth factor (VEGF) ELISA and histology. Result: There were makedly increase in the VEGF immunoassay in the ischemic zone of the TMMR group compared to the ischemic zone of the control group(control: each 30.85 and 43.15pg/mg protein, TMPR: each 44.14 and 68.61 pg/mg protein, TMDR: each 65.92 and 78.65 pg/mg protein, TMSR: each 177.39 and 168.87 pg/mg protein). TMSR channels caused greatest VEGF expression than channels made by other group and the polymer stent channels remained vacuole after 4 weeks. Conclusion: Transmyocardial polymer stent revascularization promoted the most angiogenci response by the VEGF immunoassay, although our study did not show the statistical significancy. The channels remained but the flow patency was not verified. Transmyocardial polymer stent revascularization (TMSR) is desirable in future experimental trials and in view of the significant cost implications comparable to that of laser.

• Asian Pacific Journal of Cancer Prevention
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• 제16권10호
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• pp.4369-4376
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• 2015

Background: To investigate in-vitro antagonistic effect of low-dose liquiritigenin on gemcitabine-induced capillary leak syndrome (CLS) in pancreatic adenocarcinoma via inhibiting reactive oxygen species (ROS)-mediated signalling pathways. Materials and Methods: Human pancreatic adenocarcinoma Panc-1 cells and human umbilical vein endothelial cells (HUVECs) were pre-treated using low-dose liquiritigenin for 24 h, then added into gemcitabine and incubated for 48 h. Cell viability, apoptosis rate and ROS levels of Panc-1 cells and HUVECs were respectively detected through methylthiazolyldiphenyl-tetrazoliumbromide (MTT) and flow cytometry. For HUVECs, transendothelial electrical resistance (TEER) and transcellular and paracellular leak were measured using transwell assays, then poly (ADP-ribose) polymerase 1 (PARP-1) and metal matrix proteinase-9 (MMP9) activity were assayed via kits, mRNA expressions of p53 and Rac-1 were determined through quantitative polymerase chain reaction (qPCR); The expressions of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and PARP-1 were measured via western blotting. Results: Low-dose liquiritigenin exerted no effect on gemcitabine-induced changes of cell viability, apoptosis rate and ROS levels in Panc-1 cells, but for HUVECs, liquiritigenin ($3{\mu}M$) could remarkably elevate gemcitabine-induced decrease of cell viability, transepithelial electrical resistance (TEER), pro-MMP9 level and expression of ICAM-1 and VCAM-1 (p<0.01). Meanwhile, it could also significantly decrease gemcitabine-induced increase of transcellular and paracellular leak, ROS level, PARP-1 activity, Act-MMP9 level, mRNA expressions of p53 and Rac-1, expression of PARP-1 and apoptosis rate (p<0.01). Conclusions: Low-dose liquiritigenin exerts an antagonistic effect on gemcitabine-induced leak across HUVECs via inhibiting ROS-mediated signalling pathways, but without affecting gemcitabine-induced Panc-1 cell apoptosis. Therefore, low-dose liquiritigenin might be beneficial to prevent the occurrence of gemcitabine-induced CLS in pancreatic adenocarcinoma.

• 동의생리병리학회지
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• 제17권2호
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• pp.394-402
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• 2003

This study was designed to investigate the protective effect of Bojungmyunyuk-dan(BJMY-Dan) on the cisplatin-induced cytotoxicity of primary rat astrocytes. BJMY-Dan is an oriental herbal prescription for its ability to recover protective effects against anti-cancer chemotherapies. After astrocytes were treated cisplatin, MTT assay was performed for cell viability test. To explore the mechanism of cytotoxicity, I used the several measures of apoptosis to determine whether this processes was involved in cisplatin-induced cell damage in astrocytes. Also, astrocytes were treated with BJMY-Dan and then, followed by the addition of cisplatin. Cisplatin decreased the viability of astrocytes in a dose and time-dependent manner. BJMY-Dan increased the viability of astrocytes treated cisplatin. Astrocytes treated cisplatin were revealed as apoptosis characterized by nuclear staining and flow cytometry. BJMY-Dan protected astrocytes from cisplatin-induced nuclear fragmentation and chromatin condensation. Also, caspase-3 and caspase-9 proteases were activated in astrocytes by cisplatin. BJMY-Dan inhibited the activation of caspase proteases in cisplatin-treated astrocytes. Cleavage of [poly(ADP-ribose) polymerase](PARP) was occurred at 12hr after treatment of cisplatin in astrocytes. BJMY-Dan recovered the cleavage of PARP in cisplatin-treated astrocytes. Also, BJMY-Dan inhibited the activation of pro-apoptotic factor, Bak by cisplatin. Lastly, astrocytes stained with JC-1 and Rhodamine 123 were photographed by fluorescence microscope to visualize changes of mitochondrial membrane permeability transition(MPT) during treatment with cisplatin for 24hr. BJMY-Dan recovered the change of MPT by cisplatin in astrocytes. According to above results, BJMY-Dan may protect astrocytes from cytotoxicity induced by chemotherapeutic agents, including cisplatin.

• 생명과학회지
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• 제18권6호
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• pp.804-813
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• 2008

본 연구에서는 전통 민간의학에서 많이 사용되는 동충하초(C. militaris)의 항암 작용에 관한 근거 자료의 제시를 위하여 동충하초 열수 추출물(WECM)의 항암 기전 해석을 시도하였다. 이를 위하여 HepG2 인체 간암세포를 사용하였으며, WECM의 처리에 의하여 HepG2 세포의 증식은 처리 농도의 증가에 따라 매우 억제되었다. WECM 처리에 의한 HepG2 세포의 증식 억제는 암세포의 심한 형태적 변형을 수반하였고, 이는 apoptosis 유도와 연관성이 있음을 DAPI 염색을 통한 apoptotic body 출현의 증가 및 flow cytometry 분석에 의한 sub-G1 기에 속하는 세포 빈도의 증가로 확인하였다. WECM 처리에 의한 HepG2 세포의 증식 억제는 또한 종양 억제 유전자 p53 및 CDKI p21의 발현 증가와도 연관성이 있음을 알 수 있었다. WECM 처리에 의한 apopotosis 유도에서 pro-apoptotic 인자인 Bax의 발현이 전사 및 번역 수준에서 매우 증가하였으며, caspase-3의 활성이 매우 높게 증가되었다. 특히 caspase-3 특이적 억제제인 z-DEVD-fmk로 caspase-3의 활성을 인위적으로 차단시켰을 경우, WECM에 의한 HepG2 세포의 apoptosis 유발에 caspase-3이 중심적인 역할을 하고 있음을 알 수 있었다. 본 연구 결과는 WECM의 생화학적 항암기전 해석을 이해하고 향후 수행될 추가 실험을 위한 기초 자료로서 그 가치가 매우 높은 것으로 생각된다.