• 융합보안논문지
• /
• 제1권1호
• /
• pp.69-81
• /
• 2001

우리 군도 하루 속히 사이버전에 대비한 정보보호 요원들을 양성하여 우리 사이버 국토가 외국 사이버 전사들에 의한 경유지로 활용되는 것을 차단하고, 유사시 적절히 군을 보호할 수 있는 역량을 강화하여야 할 필요성이 절실해지고 있어서 향후 국방 정보보호 인력 양성을 위하여 고려되어야 할 사항들을 제시한다.

• BMB Reports
• /
• 제50권6호
• /
• pp.283-284
• /
• 2017

Single cell transcriptome analysis is a powerful tool for defining cell types or sub-populations within a heterogeneous bulk population. Tumor-associated microenvironment is a complex ecosystem consisting of numerous cell types that support tumor growth, angiogenesis, immune evasion, and metastasis. With the success of checkpoint inhibitors targeting the immune cell compartment, tumor microenvironment is emerging as a potential anti-cancer target, and understanding it has become an imminent subject in cancer biology.

• Journal of Radiation Protection and Research
• /
• 제34권1호
• /
• pp.15-24
• /
• 2009

The effect of low doses of ultraviolet (UV) irradiation on morphology changes of cell has been studied based on the observation of the cell length. It was shown that UV-irradiated cell has different behavior in comparison with non-irradiated cell. From the histogram of cell-length distribution, it was confirmed that cell cycle of non irradiated cell was 28 hours, and that cell cycle of irradiated cell with dose of $20\;Jm^{-2}$ was delayed (39 hours), while irradiated cell with $40\;Jm^{-2}$ and $60\;Jm^{-2}$ did not divide and kept growing continuously. It was supposed that in case of $20\;Jm^{-2}$ of irradiation dose, the cell cycle was delayed because the checkpoint worked in order to repair DNA damage induced by generation of pyrimidine dimer, reactive oxygen species and so on. It was also supposed that in case of $40\;Jm^{-2}$ and $60\;Jm^{-2}$ of irradiation dose, overgrowth was induced because the checkpoint was not worked well. The morphology of overgrown cell was similar to that of normally senescent cell. Therefore, it was considered that cell senescence was accelerated by UV irradiation with irradiation doses of $40\;Jm^{-2}$ and $60\;Jm^{-2}$.

• Molecules and Cells
• /
• 제37권2호
• /
• pp.126-132
• /
• 2014

As a tumor suppressor homologue during mitosis, Chk2 is involved in replication checkpoints, DNA repair, and cell cycle arrest, although its functions during mouse oocyte meiosis and early embryo development remain uncertain. We investigated the functions of Chk2 during mouse oocyte maturation and early embryo development. Chk2 exhibited a dynamic localization pattern; Chk2 expression was restricted to germinal vesicles at the germinal vesicle (GV) stage, was associated with centromeres at pro-metaphase I (Pro-MI), and localized to spindle poles at metaphase I (MI). Disrupting Chk2 activity resulted in cell cycle progression defects. First, inhibitor-treated oocytes were arrested at the GV stage and failed to undergo germinal vesicle breakdown (GVBD); this could be rescued after Chk2 inhibition release. Second, Chk2 inhibition after oocyte GVBD caused MI arrest. Third, the first cleavage of early embryo development was disrupted by Chk2 inhibition. Additionally, in inhibitor-treated oocytes, checkpoint protein Bub3 expression was consistently localized at centromeres at the MI stage, which indicated that the spindle assembly checkpoint (SAC) was activated. Moreover, disrupting Chk2 activity in oocytes caused severe chromosome misalignments and spindle disruption. In inhibitor-treated oocytes, centrosome protein ${\gamma}$-tubulin and Polo-like kinase 1 (Plk1) were dissociated from spindle poles. These results indicated that Chk2 regulated cell cycle progression and spindle assembly during mouse oocyte maturation and early embryo development.

• 대한공간정보학회지
• /
• 제21권2호
• /
• pp.45-51
• /
• 2013

정보의 바다에 살고 있는 지금 사람들은 더 신속하고, 정확한 정보에 대한 욕구가 강하게 나타나고 있다. 오래전부터 사람들은 내가 있는 곳과 내가 가야될 곳에 대한 정보를 알고 싶어 했으며, 이러한 위치정보에 대한 욕구를 충족시키기 위한 방법은 다양하게 존재한다. 그 중 가장 많이 사용하고 있는 장비가 디지털 카메라이다. 이에 본 연구에서는 UltraCamX 카메라를 이용하여 다양한 지역적 특색을 가진 연구대상지 3곳을 선정하여 각각에 대한 블록조정을 실시 한 후 지역적 특성과 지상기준점의 분포에 대한 외부표정요소, 지상기준점과 검사점의 정확도를 비교분석하였다. 분석 결과, 산악지역이 포함된 지역은 기준점의 수가 감소함에 따라 외부표정요소의 정확도가 급격히 감소하였으며, 고층건물이 밀집해 있는 지역에서는 검사점의 수직 정확도가 낮아짐을 알 수 있었다. 연구를 통하여 AT분석 시 정확도에 영향을 미치는 지역적 인자들에 대한 분석이 수행되었다.

• 정보처리학회논문지A
• /
• 제13A권7호
• /
• pp.607-614
• /
• 2006

검사점 저장 기법을 사용하여 주기적으로 클러스터 노드들의 프로세스 수행 정보를 전역 저장 장치에 저장하는 분산 클러스터 시스템에서 결함 허용 성능을 유지하는 데 드는 비용을 줄이고 전체 프로세스의 수행 성능을 증가시키기 위해서는 검사점 정보를 저장할 때에 네트워크로 전달되는 부하를 각 노드에 최대한 적절하게 분산하여 데이터 저장 시간을 줄임으로써 검사점 정보를 저장하는 동안 전체 클러스터 시스템의 프로세스가 지연되는 시간을 줄이도록 하여야 한다. 이를 위하여 분산 RAID 기반의 단일 입출력 공간을 사용하는. 클러스터 시스템에서는 여러가지 검사점 저장 기법을 사용하며, 검사점 정보의 저장 기법에 따라서 저장 성능과 결함 회복 성능이 달라진다. 본 연구에서는 분할된 검사점 저장 기법을 개선하여 검사점 데이터를 분산 RAID 기반의 단일 입출력 공간에 저장할 때에 그룹별로 분할되는 분할 그룹 크기를 검사점 정보가 저장될 때의 네트워크의 트래픽에 따라서 동적으로 결정하여 네트워크를 통한 분산 RAID에 저장함으로써 네트워크 병목현상을 최소화하는 다중 분할된 검사점 저장 구조를 제안하였다. 제안된 구조의 성능을 분석하기 위하여 최대 512개의 가상 노드로 구성된 클러스터 시스템을 대상으로 하여 MPI 와 Linpack HPC 벤치마크를 통한 성능 평가를 수행하였으며, 성능 평가 결과는 검사점 정보의 크기와 클러스터의 크기가 증가할수록 제안된 기법이 검사점 정보의 저장과 결함 회복 능력에 대하여 기존의 검사점 저장 기법에 비하여 우수한 성능을 보인다.

• 정보처리학회논문지A
• /
• 제15A권2호
• /
• pp.111-118
• /
• 2008

이동 통신 시스템의 발전과 함께 여러 대의 이동 기기에서 동작하는 분산 응용의 필요성이 점차 커지고 있다. 모바일 기기의 고장이나 통신망 단절이 기존 고정 통신망에 비해 자주 발생하는 환경을 고려할 때 모바일 응용을 위한 복구 기법이 매우 중요하며, 중단된 응용의 재시작을위해 체크포인팅이 널리 사용되고 있다. 본 논문에서도 이런 분산 응용의 복구를 위한 효율적 체크포인팅 기법을 제안한다. 제안된 기법에서는 MSS(Mobile Support Station)에서 동작하는 체크포인팅 에이전트라는 소프트웨어 에이전트를 사용한다. 이 에이전트는 R-distance(rollback-distance) 개념을 지원하며, 이를 통해 복귀되는 지역 체크포인트의 최대 개수를 한정할 수 있다. 제안된 방식은 기존의 문제점이었던 도미노 현상이나 체크포인트 유지에 필요한 추가 비용을 크게 줄이면서도 매우 유연한 방식의 체크포인트 생성을 지원할 수 있다.

• Journal of Ginseng Research
• /
• 제44권1호
• /
• pp.79-85
• /
• 2020

Background: Helicobacter pylori increases reactive oxygen species (ROS) and induces oxidative DNA damage and apoptosis in gastric epithelial cells. DNA damage activates DNA damage response (DDR) which includes ataxia-telangiectasia-mutated (ATM) activation. ATM increases alternative reading frame (ARF) but decreases mouse double minute 2 (Mdm2). Because p53 interacts with Mdm2, H. pylori-induced loss of Mdm2 stabilizes p53 and induces apoptosis. Previous study showed that Korean Red Ginseng extract (KRG) reduces ROS and prevents cell death in H. pylori-infected gastric epithelial cells. Methods: We determined whether KRG inhibits apoptosis by suppressing DDRs and apoptotic indices in H. pylori-infected gastric epithelial AGS cells. The infected cells were treated with or without KRG or an ATM kinase inhibitor KU-55933. ROS levels, apoptotic indices (cell death, DNA fragmentation, Bax/Bcl-2 ratio, caspase-3 activity) and DDRs (activation and levels of ATM, checkpoint kinase 2, Mdm2, ARF, and p53) were determined. Results: H. pylori induced apoptosis by increasing apoptotic indices and ROS levels. H. pylori activated DDRs (increased p-ATM, p-checkpoint kinase 2, ARF, p-p53, and p53, but decreased Mdm2) in gastric epithelial cells. KRG reduced ROS and inhibited increase in apoptotic indices and DDRs in H. pylori-infected gastric epithelial cells. KU-55933 suppressed DDRs and apoptosis in H. pylori-infected gastric epithelial cells, similar to KRG. Conclusion: KRG suppressed ATM-mediated DDRs and apoptosis by reducing ROS in H. pylori-infected gastric epithelial cells. Supplementation with KRG may prevent the oxidative stress-mediated gastric impairment associated with H. pylori infection.

• Molecules and Cells
• /
• 제21권2호
• /
• pp.251-260
• /
• 2006

During mitosis, genomic integrity is maintained by the proper coordination of anaphase entry and mitotic exit via mitotic checkpoints. In budding yeast, mitotic exit is controlled by a regulatory cascade called the mitotic exit network (MEN). The MEN is regulated by a small GTPase, Tem1p, which in turn is controlled by a two-component GAP, Bfa1p-Bub2p. Recent results suggested that phosphorylation of Bfa1p by the polorelated kinase Cdc5p is also required for triggering mitotic exit, since it decreases the GAP activity of Bfa1p-Bub2p. However, the dispensability of GEF Lte1p for mitotic exit has raised questions about regulation of the MEN by the GTPase activity of Tem1p. We isolated a Bfa1p mutant, $Bfa1p^{E438K}$, whose overexpression only partially induced anaphase arrest. The molecular and biochemical functions of $Bfa1p^{E438K}$ are similar to those of wild type Bfa1p, except for decreased GAP activity. Interestingly, in $BFA1^{E438K}$ cells, the MEN could be regulated with nearly wild type kinetics at physiological temperature, as well as in response to various checkpoint-activating signals, but the cells were more sensitive to spindle damage than wild type. These results suggest that the GAP activity of Bfa1p-Bub2p is responsible for the mitotic arrest caused by spindle damage and Bfa1p overproduction. In addition, the viability of cdc5-2 ${\Delta}bfa1 $ cells was not reduced by $BFA1^{E438K}$, suggesting that Cdc5p also regulates Bfa1p to activate mitotic exit by other mechanism(s), besides phosphorylation.

• Journal of Gastric Cancer
• /
• 제23권1호
• /
• pp.207-223
• /
• 2023

Gastric cancer (GC) is the fourth leading cause of cancer-related deaths worldwide. Under the standard of care, patients with advanced GC (AGC) have a median survival time of approximately 12-15 months. With the emergence of immunotherapy as a key therapeutic strategy in medical oncology, relevant changes are expected in the systemic treatment of GC. In the phase III ATTRACTION-2 trial, nivolumab, a monoclonal anti-programmed cell death 1 (PD-1) antibody, as a third- or later-line treatment improved overall survival (OS) compared with placebo in patients with AGC. Furthermore, nivolumab in combination with 5-fluorouracil and platinum as a first-line treatment improved OS in patients with human epidermal growth factor receptor-2 (HER2)-negative AGC in the global phase III CheckMate-649 study. Another anti-PD-1 antibody, pembrolizumab, in combination with trastuzumab and cytotoxic chemotherapy as a first-line treatment, significantly improved the overall response rate in patients with HER2-positive AGC. Therefore, immune checkpoint inhibitors (ICIs) are essential components of the current treatment of GC. Subsequent treatments after ICI combination therapy, such as ICI rechallenge or combination therapy with agents having other modes of action, are being actively investigated to date. On the basis of the success of immunotherapy in the treatment of AGC, various clinical trials are underway to apply this therapeutic strategy in the perioperative and postoperative settings for patients with early GC. This review describes recent progress in immunotherapy and potential immunotherapy biomarkers for GC.