• Journal of KIISE:Software and Applications
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• v.26 no.5
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• pp.621-638
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• 1999

재시작 회복시 수행해야 할 작업략을 줄이기 위하여 주기적으로 수행되는 검사점 중 퍼지 검사점은 정상적인 트랜잭션들의 수행과 병행하여 수행된다. 트랜잭션들과 퍼지 검사점의 수행시, 로그 레코드 기록의 순서화를 위한 로그 래취를 획득한 상태에서 로그 레코드를 기록할수있으며, 트랜잭션 엔트리의 무결성을 보장하기 위한 트랜잭션 래취를 획득한 상태에서 트랜잭션은 로그 레코드의 기록과 관련된 트랜잭션 상태를 변경할수 있으며 검사점 프로세스는 트랜잭션의 상태를 검사할 수 있다. 퍼지 검사점과 트랜잭션들이 수행이 비동기로 수행되는 상황에서 로그래취와 트랜잭션 래취의 획득 및 해제 방법이 적절하지 못한 경우, 퍼지 검사점이 어떤 트랜잭션의 트랜잭션 상태를 검사하기 전에 그 트랜잭션에 의하여 기록된 로그 레코드이지만 그 퍼지 검사점이 그 트랜잭션 상태를 검사할때까지 그 로그 레코드의 기록상황이 그 트랜잭션의 트랜잭션 상태에 반영되지 않은 경우가 발생할수 있다. 이 경우, 기록 상황이 트랜잭션 상태에 반영되지 않은 그 로그 레코드를 그 퍼지 검사점에 대한 그 트랜잭션의 상태미방영 로그 레코드라고 한다. 본 논문은 상태미반영 로그 레코드를 발생시키는 상황들을 분석하고, 상태미반영 로그 레코드의 발생에 따른 문제점들을 기술하며, 상태미반영 로그 레코드의 발생에 대하여 전면 방지 기법, 일부 방지 기법 그리고 전면 허용하지만 회복시 이를 해결하는 기법등 세가지 해결책을 제시한다.

• The Transactions of the Korea Information Processing Society
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• v.3 no.2
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• pp.327-338
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• 1996

In this paper, we present a new checkpointing algorithm to preserve the consistency of resources in distributed transaction processing systems, and the error recovery algorithms to recover form the failure. In comparison with the existed algorithms, the checkpointing algorithm proposed in this paper can minimize the interference of the distributed transaction and the stroage cost during checkpointing, and does not need the extra message to make th checkpoint. Also we show that the error recovery algorithms prevent the distributed transaction with a partial fault from spreading the fault, which calls domnio-effect and prevent them from restarting cyclically. And we describe the correctness and the performane of the proposed algorithms.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.10
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• pp.4245-4250
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• 2014

Emerging evidence has suggested that glycolysis is enhanced in cancer-associated fibroblasts (CAF), and miR-186 is downregulated during the CAF formation. However, it is not clear whether miR-186 is involved in the regulation of glycolysis and what the role of miR-186 plays during the CAF formation. In this study, quantitative PCR analysises show miR-186 is downregulated during the CAF formation. Moreover, miR-186 targets the 3' UTR of Glut1, and its overexpression results in the degradation of Glut1 mRNA, which eventually reduces the level of Glut1 protein. On the other hand, knockdown of miR-186 increased the expression of Glut1. Both time course and dose response experiments also demonstrated that the protein and mRNA levels of Glut1 increase during CAF formation, according to Western blot and quantitative PCR analyses, respectively. Most importantly, besides the regulation on cell cycle progression, miR-186 regulates glucose uptake and lactate production which is mediated by Glut1. These observations suggest that miR-186 plays important roles in glycolysis regulation as well as cell cycle checkpoint activation.

• IMMUNE NETWORK
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• v.12 no.6
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• pp.240-246
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• 2012

Natural killer (NK) cells play a pivotal role in early surveillance against virus infection and cellular transformation, and are also implicated in the control of inflammatory response through their effector functions of direct lysis of target cells and cytokine secretion. NK cell activation toward target cell is determined by the net balance of signals transmitted from diverse activating and inhibitory receptors. A distinct feature of NK cell activation is that stimulation of resting NK cells with single activating receptor on its own cannot mount natural cytotoxicity. Instead, specific pairs of co-activation receptors are required to unleash NK cell activation via synergy- dependent mechanism. Because each co-activation receptor uses distinct signaling modules, NK cell synergy relies on the integration of such disparate signals. This explains why the study of the mechanism underlying NK cell synergy is important and necessary. Recent studies revealed that NK cell synergy depends on the integration of complementary signals converged at a critical checkpoint element but not on simple amplification of the individual signaling to overcome intrinsic activation threshold. This review focuses on the signaling events during NK cells activation and recent advances in the study of NK cell synergy.

• Proceedings of the Korean Society for Bioinformatics Conference
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• 2001.10a
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• pp.29-44
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• 2001

DNA damage by physical insult including UV and g-radiation might provoke genetic alterations in cells, which is followed by either acute cell death or tumorigenesis. The responsiveness to g-radiation depends on cellular context of target cells. To understand the mechanisms of checkpoint control, repair and cell death following genotoxic stimu]i, cDNA microarray can provide the gene expression profile. To make a profile of gene expression in irradiated Jurkat T cells, we hybridized the cDNA microarray using cDNA from g-irradiated Jurkat T cells. Jurkat T cells were exposed to 4Gy to 16Gy, and total RNA were extracted at 4 to 24 hrs after irradiation. The hybridization of the microarray to fluorescence-labeled cDNA from treated and untreated cells was analyzed by bioinformatic analysis to address relative changes in expression levels of the genes present in the array. Responses varied widely in different time points, suggesting acute stress response and chronic restoration or cell death. From these results we could select 384 genes related to radiation response in Tcells, and radiation response might be different in various types of cells. Using Radchip, we could separate "the exposed" from control PBMCs. We propose that Radchip might be useful to check the radiation research as well as radiation carcinogenesis.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.9
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• pp.3779-3783
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• 2015

Dietary prevention has been known to reduce breast cancer risk. Sesamin is one of the major components in sesame seeds and has been widely studied and proven to have anti-proliferation and anti-angiogenic effects on cancer cells. In this study, the influence of sesamin was tested in the human breast cancer MCF-7 cell line for cell viability (MTT assay) and cell cycling (flow cytometry). Results showed that sesamin dose-dependently (1, 10 and $50{\mu}M$) reduced the cell viability and increased LDH release and apoptosis (TUNEL assay). In addition, there was a significant increase of sub-G1 phase arrest in the cell cycle after sesamin treatment. Furthermore, sesamin increased the expression of apoptotic markers of Bax, caspase-3, and cell cycle control proteins, p53 and checkpoint kinase 2. Taken together, these results suggested that sesamin might be used as a dietary supplement f or prevention of breast cancer by modulating apoptotic signal pathways and inhibiting tumor cell growth.

• Journal of Gastric Cancer
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• v.18 no.1
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• pp.1-19
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• 2018

Gastric cancer (GC) is the second leading cause of cancer mortality and the fourth most commonly diagnosed malignant diseases. While continued efforts have been focused on GC treatment, the introduction of trastuzumab marked the beginning of a new era of target-specific treatments. Considering the diversity of mutations in GC, satisfactory results obtained from various target-specific therapies were expected, yet most of them were unsuccessful in controlled clinical trials. There are several possible reasons underlying the failures, including the absence of patient selection depending on validated predictive biomarkers, the inappropriate combination of drugs, and tumor heterogeneity. In contrast to targeted agents, immuno-oncologic agents are designed to regulate and boost immunity, are not target-specific, and may overcome tumor heterogeneity. With the successful establishment of predictive biomarkers, including Epstein-Barr virus pattern, microsatellite instability status, and programmed death-ligand 1 (PD-L1) expression, as well as ideal combination regimens, a new frontier in the immuno-oncology of GC treatment is on the horizon. Since the field of immuno-oncology has witnessed innovative, practice-changing successes in other cancer types, several trials on GC are ongoing. Among immuno-oncologic therapies, immune checkpoint inhibitors are the mainstay of clinical trials performed on GC. In this article, we review target-specific agents currently used in clinics or are undergoing clinical trials, and highlight the future clinical application of immuno-oncologic agents in inoperable GC.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.2051-2055
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• 2012

Background: The cell cycle checkpoint kinase 2 (CHEK2) gene I157T variant may be associated with an increased risk of colorectal cancer, but it is unclear whether the evidence is sufficient to recommend testing for the mutation in clinical practice. Materials and Methods: We systematically searched PubMed, EMBASES, Elsevier and Springer for relevant articles before Apr 2012. Summary odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using a fixed-effects or random-effects models with Review Manager 5.0 software. Results: A total of seven studies including 4,029 cases and 13,844 controls based on the search criteria were included for analysis. A significant association of the CHEK2 I157T C variant with unselected CRC was found (OR = 1.61, 95% CI = 1.40-1.87, P < 0.001). We also found a significant association with sporadic CRC (OR = 1.48, 95% CI = 1.23-1.77, P < 0.001) and separately with familial CRC (OR = 1.97, 95% CI = 1.41-2.74, P < 0.001). Conclusion: This meta-analysis demonstrates that the CHEK2 I157T variant may be another important CRC-predisposing gene, which increases CRC risk, especially in familial CRC.

• Development and Reproduction
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• v.18 no.1
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• pp.65-71
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• 2014

Cell cycle process is regulated by a number of protein kinases and among them, serine/threonine kinases carry phosphate group from ATP to substrates. The most important three kinase families are Cyclin-dependent kinase (Cdk), Polo-like kinase (Plk), and Aurora kinase. Polo-like kinase family consists of 5 members (Plk1-Plk5) and they are involved in multiple functions in eukaryotic cell division. It regulates a variety of aspects such as, centrosome maturation, checkpoint recovery, spindle assembly, cytokinesis, apoptosis and many other features. Recently, it has been reported that Plks are related to tumor development and over-expressed in many kinds of tumor cells. When injected the anti-Plk antibody into human cells, the cells show aneuploidy, and if inhibit Plks, most of the mitotic cell division does not proceed properly. For that reasons, many inhibitors of Plk have been recently emerged as new target for remedy of the cancer therapeutic research. In this paper, we reviewed briefly the characteristics of Plk families and how Plks work in regulating cell cycles and cancer formation, and the possibilities of Plks as target for cancer therapy.

• Molecules and Cells
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• v.39 no.9
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• pp.699-704
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• 2016

Developmentally regulated GTP-binding protein 2 (DRG2) plays an important role in cell growth. Here we explored the linkage between DRG2 and G2/M phase checkpoint function in cell cycle progression. We observed that knockdown of DRG2 in HeLa cells affected growth in a wound-healing assay, and tumorigenicity in nude mice xenografts. Flow cytometry assays and [$^3H$] incorporation assays indicated that G2/M phase arrest was responsible for the decreased proliferation of these cells. Knockdown of DRG2 elicited down-regulation of the major mitotic promoting factor, the cyclin B1/Cdk1 complex, but upregulation of the cell cycle arresting proteins, Wee1, Myt1, and p21. These findings identify a novel role of DRG2 in G2/M progression.