• 한국정보과학회논문지:정보통신
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• 제30권5호
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• pp.668-675
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• 2003

본 논문은 WDM(Wavelength Division Multiplexing) 망에서 서비스 품질에 따른 제약조건을 고려하였을 때 장애 복구에 적용될 수 있도록 개선된 p-cycle(preconfigured protection cycle) 기법을 제안한다. 기존의 p-cycle에서는 양방향으로 동일한 대역폭을 가지는 연결만을 고려하기 때문에 단방향 멀티캐스팅이나 양방향으로 서로 다른 대역폭을 사용하는 경우에는 적용하기 어려운 문제점이 있다. 또한 대체 경로의 서비스 품질은 고려하지 않으므로 장애 발생 시 대체 경로에서 서비스 품질을 만족시킬 수 없을 수 있다는 문제점이 있다. 본 논문에서는 단방향 멀티캐스팅이나 양방향 비대칭 대역폭을 사용하는 광대역 멀티미디어 통신에서 사용되는 단방향 연결의 장애복구를 효율적으로 구현할 수 있도록 P-cycle 기법을 개선하였다. 또한 장애복구를 위한 대체 경로의 P-Cycle에서 서비스 품질을 보장할 수 있도록 하기 위해서 P-cycle 선정을 위한 새로운 절차를 제안한다. 단방향 연결 개념을 사용한 P-cycle을 적용함으로서 비대칭적인 대역폭을 사용하는 통신환경에서 장애 복구를 위해 요구되는 대역폭을 줄일 수 있었으며, 제안된 p-cycle 선정 절차에 의해 구성된 대체 경로가 서비스 품질을 보장할 수 있는지의 여부를 시험하기 위해서 미국 시험망에 적용하고 그 결과를 분석하였다.

• 한국컴퓨터정보학회논문지
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• 제22권3호
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• pp.69-79
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• 2017

In this paper, we propose our four-phase life cycle of P2P botnet with corresponding detection methods and the future direction for more effective P2P botnet detection. Our proposals are based on the intensive analysis that compares existing P2P botnet detection schemes in different points of view such as life cycle of P2P botnet, machine learning methods for data mining based detection, composition of data sets, and performance matrix. Our proposed life cycle model composed of linear sequence stages suggests to utilize features in the vulnerable phase rather than the entire life cycle. In addition, we suggest the hybrid detection scheme with data mining based method and our proposed life cycle, and present the improved composition of experimental data sets through analysing the limitations of previous works.

• 대한의생명과학회지
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• 제29권4호
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• pp.287-295
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• 2023

Amifostine was developed to protect cells, but it is known to induce cytotoxicity and apoptosis, and the exact mechanism is unknown. In this study, we investigated how the DNA mismatch repair (MMR) system interacts with p53 to prevent apoptosis, cell cycle arrest, and cytoprotective effects induced by amifostine. HCT116 colon cancer cells sublines HCT116/p53+,HCT116/p53+, HCT116/p53-, HCT116/E6 and HCT116+ch3/E6 cells were used for evaluation. Amifostine induced G1 arrest and increased toxicity two-fold in p53- cells regardless of MMR expression. Both G1 cell cycle arrest and induction of p53 protein peaked at 24 h after the start of amifostine exposure. Both G1 cell cycle arrest and induction of p53 protein peaked at 24 h after the start of amifostine exposure. Amifostine induced the expression of p21 protein in both p53+ and p53- cells. As for apoptosis, compared to p53- cells, p53+ cells showed 3.5~4.2 times resistance to amifostine-induced apoptosis. HCT116+E6 with both p53 and MMR loss showed maximum apoptosis at 48 h, and HCT116+ch3/E6HCT116+ch3/E6 with p53 loss showed maximum apoptosis at 24 h. As a result, it was confirmed through in vitro experiments that amifostine-induced G1 cell cycle arrest and apoptosis are mediated through a pathway dependent on MMR and p53 protein.

• 한국통신학회논문지
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• 제28권3B호
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• pp.200-208
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• 2003

본 논문은 제한된 범위의 광 파장 변환기능을 가진 WDM (Wavelength Division Multiplexing) 망에서의 신속한 장애 복구에 적용될 수 있도록 개선된 p-cycle (preconfigured protection cycle) 기법을 제안한다. 개선된 p-cycle 기법은 단방향 멀티캐스팅이나 양방향으로 연결성을 가지지만 비대칭적인 대역폭을 사용하는 광대역 멀티미디어 통신에서 사용되는 단방향 연결을 수용할 수 있도록 수정하였다. 본 논문에서는 개선된 p-cycle 기법을 광 파장 변환기능이 제한적인 WDM 망에서 적용하고 그 결과를 분석하였다. 개선된 p-cycle 알고리즘은 광 파장 변환 기능이 제한적인 WDM망에서 기존의 방안보다 우수한 성능을 보여준다.

• Biomolecules & Therapeutics
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• 제16권1호
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• pp.21-27
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• 2008

Clotrimazole (CLT), a potent antifungal drug, is known to inhibit tumor cell proliferation. In the present study, we examined the role of intracellular $Ca^{2+}$ in CLT-induced cell cycle arrest of colon adenocarcinoma HT29 cells. CLT inhibited growth of HT29 cells in a concentration-dependent manner, which was associated with inhibition of cell cycle progression at the G(1)-S phase transition and an increase in the expression of cell cycle inhibitor proteins p27 and p53. CLT also suppressed the $Ca^{2+}$ overload by A23187, a calcium ionophore, suggesting its role in modulation of intracellular $Ca^{2+}$ concentration in HT29 cells. The simultaneous application of CLT and A23187 with addition of $CaCl_2$ (1mM) to the medium significantly reversed CLT-induced p27 and p53 protein level increase and growth suppression. Our results suggest that CLT induces cell cycle arrest of colon adenocarcinoma HT29 cells via induction of p27 and p53, which may, at least in part, be mediated by alteration of intracellular $Ca^{2+}$ level.

• International Journal of Oral Biology
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• 제37권3호
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• pp.115-120
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• 2012

Retinoic acid plays an important role in the regulation of cell growth and differentiation. In our present study, we evaluated the effects of all-trans retinoic acid (RA) on cell proliferation and on the cell cycle regulation of human gingival fibroblasts (HGFs). Cell proliferation was assessed using the MTT assay. Cell cycle analysis was performed by flow cytometry, and cell cycle regulatory proteins were determined by western blot. Cell proliferation was increased in the presence of a 0.1 nM to 1 ${\mu}M$ RA dose range, and maximal growth stimulation was observed in cells exposed to 1 nM of RA. Exposure of HGFs to 1 nM of RA resulted in an augmented cell cycle progression. To elucidate the molecular mechanisms underlying cell cycle regulation by RA, we measured the intracellular levels of major cell cycle regulatory proteins. The levels of cyclin E and cyclin-dependent kinase (CDK) 2 were found to be increased in HGFs following 1 nM of RA treatment. However, the levels of cyclin D, CDK 4, and CDK 6 were unchanged under these conditions. Also after exposure to 1 nM of RA, the protein levels of $p21^{WAF1/CIP1}$ and $p16^{INK4A}$ were decreased in HGFs compared with the control group, but the levels of p53 and pRb were similar between treated and untreated cells. These results suggest that RA increases cell proliferation and cell cycle progression in HGFs via increased cellular levels of cyclin E and CDK 2, and decreased cellular levels of $p21^{WAF1/CIP1}$ and $p16^{INK4A}$.

• 생명과학회지
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• 제17권6호통권86호
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• pp.778-782
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• 2007

Diphenyleneiodonium (DPI)는 NADPH oxidase 같은 flavoenzymes의 저해제로써 널리 사용되고 있다. 본 연구에서는 인간 대장암 세포주 HCT-116 (wild-type p53)와 HT-29 (p53 mutant) 및 인간 유방암 세포주인 MCF-7(wild-type p53)의 세포성장 과정에서의 DPI의 효과를 살펴보았다. DPI는 농도 및 시간 의존적으로 암세포주의성장을 막았으며 G2/M phase에서 cell cycle arrest를 일으켰다. Cell cycle arrest의 가장 높은 값은 DPI 처리후 12 시간에서 관찰할 수 있었다. 한편 DPI는 아폽토시스 그리고 cell cycle arres 에 관여하는 유전자 발현에 관여하는 p53의 표현을 크게 증가시켰으며, 이는 DPI처리 후 6시간 후 부터 관찰할 수 있었다. 그러나 NADPH oxidase의 조합을 억제하는 catechol 계인 apocynin은 p53의 발현을 유도하지 못하였다. 이것은 DPI에 의해 유도되는 p53의 발현증가는 NADPH oxidase활성의 저해와 관련되어 있지 않다는 것을 의미한다. 결론적으로 DPI는 HCT-116, HCT-15 및 MCF-7 암세포주에서 ROS에 비 의존적으로 wild-type p53 발현의 증가를 유도하며, 이 증가된 p53은 DPI에 의해 유도되는 성장 억제 및 C2/M phase에서의 cell cycle arrset과정의 조절기전에 관여한다는 것을 시사한다.

• KSBB Journal
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• 제30권4호
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• pp.175-181
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• 2015

Cells proliferate via repeating process that growth and division. This process is G1, S, G2 and M four phases consists. Monitoring the progression of the cell cycle is a specific step that to be a continuous process is repeated to adjust the start of the next step. At this time, this process is called a Checkpoint. Currently, there are three known checkpoints that G1-S phase, G2-M phase, and the M phase. In this study, we confirmed that cell cycle arrest effects by ethanol extracts of Artemisia annua Linne (AAE) in Hep3B liver cancer cells. AAE was regulated proteins which involved in cell cycle such as pAkt, pMDM2, p53, p21, pCDK2 (T14/Y15). AAE induced cell cycle arrest in G1 checkpoint through phosphorylation of CDK2. Akt and p53 upstream is inhibited by AAE and p53 activated by non-activated pMDM2, p53 inhibitor. Thereby, activated p53 is transcript to p21 and activated p21 protein is combined with Cyclin E-pCDK2 complex. Therefore, we confirmed that AAE-induced cell cycle arrest was occurred by p21-Cyclin E-pCDK2 complex by inhibition of pAkt signal. Because of this cell cycle can't pass to S phase from G1 phase.

• Korean Journal of Mathematics
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• 제27권2호
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• pp.525-534
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• 2019

Let $P(G,{\lambda})$ denote the number of proper vertex colorings of G with ${\lambda}$ colors. The chromatic polynomial $P(C_n,{\lambda})$ for the cycle graph $C_n$ is well-known as $$P(C_n,{\lambda})=({\lambda}-1)^n+(-1)^n({\lambda}-1)$$ for all positive integers $n{\geq}1$. Also its inductive proof is widely well-known by the deletion-contraction recurrence. In this paper, we give this inductive proof again and three other proofs of this formula of the chromatic polynomial for the cycle graph $C_n$.

• KSII Transactions on Internet and Information Systems (TIIS)
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• 제7권12호
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• pp.3118-3134
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• 2013

This paper deliberates for a multimedia transmission scheme combining multiple description coding (MDC) and network coding (NC). Our goal is to take advantage from the property of MDC to provide quantized and compressed independent and identically distributed (iid) descriptions and also from the benefit of network coding, which uses network resources efficiently to recover lost data in the network. Recently, p-cycle NC has been introduced to recover and protect any lost or distorted descriptions at the receiver part exactly without need of retransmission. So far, MDC have not been explored using this type of NC. Compressed and coded descriptions are transmitted through the network where p-cycle NC is applied. P-cycle based algorithm is proposed for single and multiple descriptions lost. Results show that in the fixed bit rate, the PSNR (Peak Signal to Noise Ratio) of our reconstructed image and also subjective evaluation is improved significantly compared to previous work which is averaging method joint with MDC in order to conceal lost descriptions.