• 한국통신학회논문지
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• 제29권10A호
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• pp.1139-1146
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• 2004

셀룰러 CDMA 시스템에서 특정 셀 영역에 트래픽 부하가 급증할 경우 기지국에서 할당할 수 있는 무선자원 부족으로 인하여 통화품질과 무선자원 사용효율이 급격하게 저하되는 문제가 발생한다. 본 논문에서는 이와 같은 문제를 개선하기 위하여 기지국 송신전력을 제어하는 대신 핸드오버 파라미터를 조정하여 과부하가 발생한 홈셀의 커버리지는 가상적으로 줄이고 인접셀의 커버리지는 가상적으로 확대시켜 과부하 트래픽을 고속으로 핸드오버 시킴으로써 통화품질을 개선할수 있을 뿐만 아니라, 핸드오버 발생 확률에 기반하여 무선자원을 할당함으로써 불필요한 핸드오버에 의한 무선자원 남비를 개선할수 있는 커버리지와 무선자원의 결합형 관리 기법을 제안한다. 특히 제안하는 기법은 기존 CDMA 시스템에 직접 적용이 가능할 뿐만 아니라 차세대 이동통신시스템에서 요구하는 적응형 무선자원 및 커버리지 관리방안을 설계하는데 활용할 수 있을 것으로 기대된다.

• 한국정보통신학회논문지
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• 제19권9호
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• pp.2014-2021
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• 2015

다중 셀 랜덤 액세스 네트워크에서 제안된 기회적 간섭정렬 기법은 인접한 랜덤 액세스 네트워크로 미치는 간섭의 영향을 최소화하는 기술로서 간섭이 극심한 환경에서 기존의 기술들 보다 우수한 성능을 보인다. 랜덤액세스 네트워크용 기회적 간섭정렬 기술은 물리계층과 매체접근제어계층을 동시에 고려한다. 본 논문에서는 기존의 기회적 간섭정렬 기술과 반대로 각 사용자들이 인접 셀 간섭과 상관없이 자신의 전송 신호를 최대화하는 기법을 고려한다. 또한 기존의 기회적 간섭정렬 기술에서 사용한 간섭 최소화 기법과 전송 신호 최대화 기법을 서로 다른 환경에 따라 비교 분석하고 두 기술 사이에 트레이드오프가 일어남을 관찰한다.

• 대한기계학회논문집B
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• 제37권3호
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• pp.259-266
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• 2013

광학 현미경을 통해 일정한 시간 간격으로 얻은 세포 이미지로부터 세포 변화를 자동적으로 추적 및 분석하는 것이 세포 트래킹이라고 한다. 세포 변화 과정에서 이웃에 있는 세포들이 겹쳐져 있는 상태를 클러스터라고 하며 세포트래킹에서 클러스터를 다시 세포로 분리하는 작업은 매우 중요하다. 본 논문에서는 타원 근사법을 기반으로 클러스터를 분리하기 위한 알고리즘을 제안한다. 클러스터의 외곽선을 추출한 후 외곽선의 오목정점을 이용하여 클러스터를 라인 세그먼트들로 분리한 다음 휴리스틱을 이용하여 라인 세그먼트들을 결합해 가며 근사 타원을 생성한다. 실험 결과 두 개의 세포가 겹쳐진 클러스터의 경우 평균적으로 91%, 세 개의 세포가 겹쳐진 경우 평균적으로 84% 그리고 겹쳐진 세포의 개수가 네 개 이상인 경우 약 73%의 정확도로 클러스터를 분리해 주었다.

• Archives of Pharmacal Research
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• 제23권6호
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• pp.633-636
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• 2000

Translationally controlled tumor protein (TCTP), also known as IgE-dependent histamine-releasing factor, is a growth-related tumor protein. Although the primary sequence of rat TCTP does not reveal any recognizable $Ca^{2+}$ -binding motif, previous studies have demonstrated that rat TCTP consisting of 172 amino acids is a $Ca^{2+}$ -binding protein. However. the region of TCTP required for $Ca^{2+}$ interaction has not been mapped to the molecule. Here, we reported that the $Ca^{2+}$ binding region of TCTP which was mapped by using a combination of deletion constructs of rat TCTP and $^{45}Ca^{2+}$-overlay assay. was confined to amino acid residues 81-112. This binding domain did not show any peculiar loop of calcium- binding motif such as CaLB domain and EF hand motif and it seems to be constituted of random coil regions neighboring the a helix. Thus, our data confirm that TCTP is a novel family of $Ca^{2+}$ -binding protein.

• BMB Reports
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• 제51권5호
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• pp.219-224
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• 2018

Necroptosis is an emerging form of programmed cell death occurring via active and well-regulated necrosis, distinct from apoptosis morphologically, and biochemically. Necroptosis is mainly unmasked when apoptosis is compromised in response to tumor necrosis factor alpha. Unlike apoptotic cells, which are cleared by macrophages or neighboring cells, necrotic cells release danger signals, triggering inflammation, and exacerbating tissue damage. Evidence increasingly suggests that programmed necrosis is not only associated with pathophysiology of disease, but also induces innate immune response to viral infection. Therefore, necroptotic cell death plays both physiological and pathological roles. Physiologically, necroptosis induce an innate immune response as well as premature assembly of viral particles in cells infected with virus that abrogates host apoptotic machinery. On the other hand, necroptosis per se is detrimental, causing various diseases such as sepsis, neurodegenerative diseases and ischemic reperfusion injury. This review discusses the signaling pathways leading to necroptosis, associated necroptotic proteins with target-specific inhibitors and diseases involved. Several studies currently focus on protective approaches to inhibiting necroptotic cell death. In cancer biology, however, anticancer drug resistance severely hampers the efficacy of chemotherapy based on apoptosis. Pharmacological switch of cell death finds therapeutic application in drug- resistant cancers. Therefore, the possible clinical role of necroptosis in cancer control will be discussed in brief.

• BMB Reports
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• 제47권2호
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• pp.51-59
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• 2014

Cellular senescence is a physiological process of irreversible cell-cycle arrest that contributes to various physiological and pathological processes of aging. Whereas replicative senescence is associated with telomere attrition after repeated cell division, stress-induced premature senescence occurs in response to aberrant oncogenic signaling, oxidative stress, and DNA damage which is independent of telomere dysfunction. Recent evidence indicates that cellular senescence provides a barrier to tumorigenesis and is a determinant of the outcome of cancer treatment. However, the senescence-associated secretory phenotype, which contributes to multiple facets of senescent cancer cells, may influence both cancer-inhibitory and cancer-promoting mechanisms of neighboring cells. Conventional treatments, such as chemo- and radiotherapies, preferentially induce premature senescence instead of apoptosis in the appropriate cellular context. In addition, treatment-induced premature senescence could compensate for resistance to apoptosis via alternative signaling pathways. Therefore, we believe that an intensive effort to understand cancer cell senescence could facilitate the development of novel therapeutic strategies for improving the efficacy of anticancer therapies. This review summarizes the current understanding of molecular mechanisms, functions, and clinical applications of cellular senescence for anticancer therapy.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제35권4호
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• pp.199-204
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• 2009

Purpose: The purpose of this study is to investigate the epithelial-mesenchymal transition (EMT) induced by Snail transcription factor and Snail-transfected in vivo tumors with histopathological features. Materials and methods: We induced in vivo xenografted tumorigenesis in the oral vestibules of nude mice by a Snail transfected HaCaT cell line and investigated morphological and immunohistochemical features in Snail expressive tumors. Results: We identified tumor masses in 14 out of 15 nude mice in the HaCaT-Snail cell inoculation group, but no tumors were present in any of the HaCaT cell inoculation group. Induced tumors showed features of poorly differentiated carcinoma with invasion to neighboring muscles and bones. The HaCaT-Snail tumors showed decreased expressions of E-cadherin and cytokeratin, but showed increased expressions of vimentin and N-cadherin. Discussion: The Snail transfected xenograft can improve productivity of malignant tumors, show various histopathological features including invasive growth, and aid in the investigation of tumor progression and the interaction with surrounding tissues.

• Journal of Magnetics
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• 제6권4호
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• pp.132-141
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• 2001

The switching characteristics and the magnetization-flop behavior in magnetic tunnel junctions exchange biased by synthetic antiferromagnets (SyAFs) are investigated by using a computer simulations based on a single-domain multilayer model. The bias field acting on the free layer is found to be sensitive to the thickness of neighboring layers, and the thickness dependence of the bias field is greater at smaller cell dimensions due to larger magnetostatic interactions. The resistance to magnetization flop increases with decreasing cell size due to increased shape anisotropy. When the cell dimensions are small and the synthetic antiferromagnet is weakly, or not pinned, the magnetization directions of the two layers sandwiching the insulating layer are aligned antiparallel due to a strong magnetostatic interaction, resulting in an abnormal magneto resistance (MR) change from the high-MR state to zero, irrespective of the direction of the free-layer switching. The threshold field for magnetization-flop is found to increase linearly with increasing antiferromagnetic exchange coupling in the synthetic antiferromagnet. Irrespective of the magnetic parameters and cell sizes, magnetization flop does not exist near zero applied field, indicating that magnetization flop is driven by the Zeeman energy.

• 한국통신학회논문지
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• 제31권6A호
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• pp.586-592
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• 2006

대역확산 시스템에서 나머지 도플러 주파수 오프셋이 (residual Doppler frequency offset, RDFO) 있으면 부호 동기가 정확히 맞을 때에도 표본화된 최고 상관값은 실제 상관값의 꼭지값보다 낮다. 이로 말미암아 기존 단일 주파수 셀 (single frequency cell, SFC) 검파기법의 성능은 떨어진다. 이 논문에서는 RDFO가 있을 때 실제 꼭지값 근처에 상관값이 큰 여러 표본이 존재하는 것에 착안하여 새로운 탐색기법을 제안한다. 이를 위해 먼저 대역 확산 시스템에서 RDFO가 성능을 떨어뜨리는지 분석한다. 그 뒤, 기존 기법과 제안한 기법의 검파확률과 오경보확률을 얻고, 모의실험을 수행하여 RDFO가 있을 때 제안한 기법이 기존 기법보다 성능이 뛰어남을 보인다.

• Experimental and Molecular Medicine
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• 제50권12호
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• pp.7.1-7.14
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• 2018

Dysregulation of long noncoding RNA (lncRNA) expression is linked to the development of various diseases. Recently, an emerging body of evidence has indicated that lncRNAs play important roles in the pathogenesis of inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative Colitis (UC). In IBD, lncRNAs have been shown to be involved in diverse processes, including the regulation of intestinal epithelial cell apoptosis, association with lipid metabolism, and cell-cell interactions, thereby enhancing inflammation and the functional regulation of regulatory T cells. In this review, we aim to summarize the current knowledge regarding the role of lncRNAs in IBD and highlight potential avenues for future investigation. We also collate potentially immune-relevant, IBD-associated lncRNAs identified through a built-by association analysis with respect to their neighboring protein-coding genes within IBD-susceptible loci. We further underscore their importance by highlighting their enrichment for various aspects of immune system regulation, including antigen processing/presentation, immune cell proliferation and differentiation, and chronic inflammatory responses. Finally, we summarize the potential of lncRNAs as diagnostic biomarkers in IBD.