• The Journal of Korean Institute of Communications and Information Sciences
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• v.40 no.7
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• pp.1424-1432
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• 2015

As the wireless communication technologies are being studied for application to maritime communication networks in a fusion of marine industries and IT technology, interference coordination techniques have been studied in the maritime heterogeneous networks. In this paper, we develop a simulator for measuring, verifying and evaluating performance of a maritime heterogeneous network. Unlike other previous simulators, the developed simulator applies enhanced inter-cell interference coordination (eICIC) that are being introduced in the 3GPP Release 10 for mitigating the cross-tier interference between ships. Furthermore, we investigate the effects of almost blank subframes (ABS) and cell range expansion (CRE) on the throughput of small cells in maritime heterogeneous networks by using the developed simulator.

• Korean Journal of Agricultural Science
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• v.47 no.2
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• pp.361-373
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• 2020

Integrins such as lymphocyte function-associated antigen -1 (LFA-1) have an essential role in T cell immunity. Integrin activation, namely, the transition from the inactive conformation to the active one, takes place when an intracellular signal is generated by specific receptors such as T cell receptors (TCRs) and chemokine receptors in T cells. In an effort to explore the molecular mechanisms underlying the TCR-mediated LFA-1 activation, we had previously established a high-throughput cell-based assay and screened a chemical library deposited in the National Institute of Health in the United States. As a result, several hits had been isolated including HIKS-1 (Benzo[b]thiophene-3-carboxylic acid, 2-[3-[(2-carboxyphenyl) thio]-2,5-dioxo-1-pyrrolinyl]-4,5,6,7-tetrahydro-,3-ethyl ester). In an attempt to reveal the mode of action of HIKS-1, in this study, we did drug affinity responsive target stability (DARTS) assay finding that HIKS-1 interacted with the IQ motif containing GTPase activating protein 1 (IQGAP1), a 189 kDa multidomain scaffold protein critically involved in various signaling mechanisms. Furthermore, the cellular thermal shift assay (CETSA) provided compelling evidence that HIKS-1 also interacted with IQGAP1 in vivo. Taken together, it can be concluded that HIKS-1 interferes with the TCR-mediated LFA-1 activation by interacting with IQGAP1 and thereby disrupting the signaling pathway for LFA-1 activation.

• Journal of Nutrition and Health
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• v.35 no.10
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• pp.1053-1059
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• 2002

In post-genome period, the technique for identifying gene expression has been changed to high throughput screening. In the field of molecular nutrition, the need for this technique to clarify molecular function of the specific nutrient is essential. In this study, we have tested the zinc-regulated gene expression in zinc-deficient U937 cells, using cDNA microarray which is the cutting-edge technique to screen large numbers of gene expression simultaneously. The study result can be used for the preliminary gene screening data for clarifying, using monocyte U937 cell line, molecular Zn aspect in atherosclerosis. U937 cells were cultured in Zn-adequate (control, 12 $\mu$M Zn) or Zn-deficient (experimental, 0 $\mu$M Zn) ESMI media during 2 days, respectively. Cells were harvested and RNA was extracted. Total RNA was reverse-transcriptinized and synthesized cDNA probe labeled with Cy-3. fluorescent labeled cDNA probe was applied to microarray slide for hybridization slide, and after then, the slide was scanned using fluorescence scanner. ‘Highly expressed genes’ in Zn-deficient U937 cells, comparing to Zn-adequate group, are mainly about the genes for motility protein, immune system protein, oncogene and tumor suppressor and ‘Less highly expressed genes’ are about the genes for transcription, apoptosis associated protein, cell cycle, and several basic transcription factors. The results of this preliminary study imply the effectiveness of cDNA microarray for expression profiling of a singly nutrient deficiency, specially Zn. Furthur study, using tailored-cDNA array and capillary endothelial cell lines, would be beneficial to clarify molecular Zn function, more in detail.

• Molecules and Cells
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• v.42 no.6
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• pp.480-494
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• 2019

Aggregates of disease-causing proteins dysregulate cellular functions, thereby causing neuronal cell loss in diverse neurodegenerative diseases. Although many in vitro or in vivo studies of protein aggregate inhibitors have been performed, a therapeutic strategy to control aggregate toxicity has not been earnestly pursued, partly due to the limitations of available aggregate models. In this study, we established a tetracycline (Tet)-inducible nuclear aggregate (${\beta}23$) expression model to screen potential lead compounds inhibiting ${\beta}23$-induced toxicity. High-throughput screening identified several natural compounds as nuclear ${\beta}23$ inhibitors, including peucedanocoumarin III (PCIII). Interestingly, PCIII accelerates disaggregation and proteasomal clearance of both nuclear and cytosolic ${\beta}23$ aggregates and protects SH-SY5Y cells from toxicity induced by ${\beta}23$ expression. Of translational relevance, PCIII disassembled fibrils and enhanced clearance of cytosolic and nuclear protein aggregates in cellular models of huntingtin and ${\alpha}$-synuclein aggregation. Moreover, cellular toxicity was diminished with PCIII treatment for polyglutamine (PolyQ)-huntingtin expression and ${\alpha}$-synuclein expression in conjunction with 6-hydroxydopamine (6-OHDA) treatment. Importantly, PCIII not only inhibited ${\alpha}$-synuclein aggregation but also disaggregated preformed ${\alpha}$-synuclein fibrils in vitro. Taken together, our results suggest that a Tet-Off ${\beta}23$ cell model could serve as a robust platform for screening effective lead compounds inhibiting nuclear or cytosolic protein aggregates. Brain-permeable PCIII or its derivatives could be beneficial for eliminating established protein aggregates.

• Journal of Acupuncture Research
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• v.19 no.6
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• pp.111-124
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• 2002

A line of study reported that electroacupuncture(EA) modulate natural killer cell(NK Cell) activities. One report suggested that EA enhanced splenic interferon-gamma($IFN-{\gamma}$), interleukin-2(IL-2), and NK cell activity in Sprague-Dawley rats. Another study suggested that $IFN-{\gamma}$ mediates the up-regulation of NK cell activity, and endogenous ${\beta}$-endorphin secretion also play a role in the up-regulation of NK cell activity induced by EA stimulation. In order to better understand the molecular regulation underlying the activation of NK cell induced by EA, we have utilized cDNA microarray to elucidate how EA alters program of gene expression of spleen in rats. First, we divided three groups, group I was EA group treated with EA in restriction holder, group II was sham group with only holder stress, and last group III was control group with no treatment. We measured NK cell activity after EA stimulation three times for 2 days using $^{51}Cr$ release assay. Second, Biotin-labeled cDNA probes synthesized from EA group and sham group, were competitively hybridized to the microarray that contained variable genes. Such high-throughput screening has identified a number of EA-responsive gene candidates. Of these, we found that EA induced a subset of genes of genes that functionally could modulatory effects on NK cell activity. Genes(vascular cell adhesion molecule-1, protein-tyrosine kinase, CD94 mRNA) related to boost NK cell activity, were increased by EA And, genes(protein-tyrosine-phospatase mRNA, protein-tyrosine phosphatase(SHP-1) mRNA) related to inhibit NK cell activity, were decreased by EA. These EA-responsive genes may provide key insights from which to understand mechanisms of activation of NK cell induced by EA.

• The Transactions of the Korea Information Processing Society
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• v.3 no.4
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• pp.947-960
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• 1996

The primary goal for developing high performance ATM switching systems is to minimized the probability of cell loss, cell delay and deterioration of throughput. ATM switching element that is the most suitable for this purpose is the shared buffer memory switch executed by common random access memory and control logic. Since it is difficult to manufacture VLIS(Very Large Scale Integrated circuit) as the number of input ports increased, the used of switching module method the realizes 32$\times$32, 150 Mb/s switch utilizing 8$\times$8, 600Mb/s os 16$\times$16, 150Mb/s unit switch is latest ATM switching technology for small and large scale. In this paper, buffer capacity satisfying total-memory-reduction effect by buffer sharing in a shared buffer memory switch are analytically evalu ated and simulated by computer with cell loss level at traffic conditions, and also features of switching network utilizing the switching module methods in small and large-capacity ATM switching system is analized. Based on this results, the structure in outline of 32$\times$32(4.9Gb/s throughput), 150Mb/s switches under research in many countries is proposed, and eventually, switching-network structure for ATM switching system of small and large and capacity satisfying with above primary goals is suggested.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.25 no.4B
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• pp.683-691
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• 2000

In this paper, we proposed the cell multiplexer using Hopfield neural network and the bandwidth predictor using the backpropagation neural network in order to make an accurate call setup decision. The cell multiplexer controls heterogeneous traffic and the bandwidth predictor estimates minimum bandwidth which satisfies traffic's QoS and maximizes throughput in network. Also, a novel connection admission controller decides on connection setup using the predicted bandwidth from bandwidth predictor and available bandwidth in networks. And then, we proposed a fuzzy traffic policer, when traffic sources violate the contract, takes an appropriate action and aim proved traffic shaper, which controls burstness which is one of key characteristics in multimedia traffic. We simulated the proposed controller. Simulation results show that the proposed controller outperforms existing controller.

• ETRI Journal
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• v.40 no.3
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• pp.318-329
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• 2018

Femtocell (FC) technology envisaged as a cost-effective approach to attain better indoor coverage of mobile voice and data service. Deployment of FCs over macrocell forms a heterogeneous network. In urban areas, the key factor limits the successful deployment of FCs is inter-cell interference (ICI), which severely affects the performance of victim users. Autonomous FC transmission power setting is one straightforward way for coordinating ICI in the downlink. Application of intelligent control using soft computing techniques has not yet explored well for wireless networks. In this work, autonomous FC transmission power setting strategy using Adaptive Neuro Fuzzy Inference System is proposed. The main advantage of the proposed method is zero signaling overhead, reduced computational complexity and bare minimum delay in performing power setting of FC base station because only the periodic channel measurement reports fed back by the user equipment are needed. System level simulation results validate the effectiveness of the proposed method by providing much better throughput, even under high interference activation scenario and cell edge users can be prevented from going outage.

• 한국정보디스플레이학회:학술대회논문집
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• 2006.08a
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• pp.1533-1536
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• 2006

A novel single cell gap transflective liquid crystal display was developed. By using the ink jet printing technology, we fabricated a transflective liquid crystal display with the hybrid alignment in the reflective region and the homogeneous alignment in the transmission region. Compared with the traditional technologies, our technology provided the advantages of easy process, high yield, fast throughput, and less material usage. We also applied this technology to the 2.4 inch prototype. This panel could be implemented in the handheld product applications.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3681-3685
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• 2012

Background: In breast cancer, estrogen receptors have been demonstrated to interact with transcription factors to regulate target gene expression. However, high-throughput identification of the transcription regulation relationship between transcription factors and their target genes in response to estradiol is still in its infancy. Purpose: Thus, the objective of our study was to interpret the transcription regulation network of MCF7 breast cancer cells exposed to estradiol. Methods: In this work, GSE11352 microarray data were used to identify differentially expressed genes (DEGs). Results: Our results showed that the MYB (v-myb myeloblastosis viral oncogene homolog [avian]), PGR (progesterone receptor), and MYC (v-myc myelocytomatosis viral oncogene homolog [avian]) were hub nodes in our transcriptome network, which may interact with ER and, in turn, regulate target gene expression. MYB can up-regulate MCM3 (minichromosome maintenance 3) and MCM7 expression; PGR can suppress BCL2 (B-cell lymphoma 2) expression; MYC can inhibit TGFB2 (transforming growth factor, beta 2) expression. These genes are associated with breast cancer progression via cell cycling and the $TGF{\beta}$ signaling pathway. Conclusion: Analysis of transcriptional regulation may provide a better understanding of molecular mechanisms and clues to potential therapeutic targets in the treatment of breast cancer.