• The Journal of Korean Institute of Communications and Information Sciences
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• v.29 no.10A
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• pp.1139-1146
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• 2004

An abrupt increase of traffic-load in cellular CDMA systems can cause overload, as a result, degrade the quality of service (QoS) and the spectrum utilization due to lacking radio resources in base stations. In this paper, we propose a joint coverage and resource management (JCRM) scheme which can improve the QoS degradation and the spectrum utilization. The JCRM scheme hands over the overloaded traffic to neighboring cells by virtually reducing overloaded cell coverage and extending neighboring cell coverage, as well the scheme allocates radio resources based on the necessary handover probability. The proposed scheme can be applied to the existing cellular CDMA systems as well as adaptive coverage management schemes for next generation mobile communication systems.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.19 no.9
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• pp.2014-2021
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• 2015

Opportunistic interference alignment (OIA) has been proposed for multi-cell random access networks (RAN), which minimizes the generating interference to neighboring RANs and yields better performance compared with the conventional techniques. The OIA for RANs considers both physical (PHY) and medium access control (MAC) layers. In this paper, we introduce a protocol of which each user maximizes the transmit signal regardless of the generating interference to neighboring RANs, contrary to the OIA technique. In addition, we compare the performance of the signal-maximization technique with the OIA technique.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.37 no.3
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• pp.259-266
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• 2013

An automated cell tracking system is used to automatically analyze and track the changes in cell behavior in time-lapse cell images acquired using a microscope with a cell culture. Clustering is the partial overlapping of neighboring cells in the process of cell change. Separating clusters into individual cells is very important for cell tracking. In this study, we proposed an algorithm for separating clusters by using ellipse fitting based on a direct least square method. We extracted the contours of clusters, divided them into line segments, and then produced their fitted ellipses using a direct least square method for each line segment. All of the fitted ellipses could be used to separate their corresponding clusters. In experiments, our algorithm separated clusters with average precisions of 91% for two overlapping cells, 84% for three overlapping cells, and about 73% for four overlapping cells.

• Archives of Pharmacal Research
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• v.23 no.6
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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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• v.51 no.5
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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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• v.47 no.2
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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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• v.35 no.4
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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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• v.6 no.4
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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.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.31 no.6A
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• pp.586-592
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• 2006

In this paper, a novel detection method called the joint multiple frequency cell (JMFC) detection is addressed for spread spectrum code acquisition in the presence of residual Doppler frequency offset (RDFO). When the RDFO exists, the correlation peak used for detection during the acquisition process is split into several lower neighboring peaks, resulting in severe degradation in the detection performance, and consequently, in the overall acquisition performance. In the JMFC detection, a decision variable for detection is formed by combining several consecutive correlator outputs, so that the reduction in the correlation value due to the RDFO can be alleviated. Numerical results show that the proposed scheme can offer better detection performance over the conventional scheme based on the cell-by-cell detection.

• Experimental and Molecular Medicine
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• v.50 no.12
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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.