• The KIPS Transactions:PartC
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• v.9C no.1
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• pp.89-96
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• 2002

Handoff is one of the most important factors that ma? degrade the performance of TCP connections in wireless data networks. In this paper, we present a lossless and duplication free handoff scheme called LPM (Last Packet Marking) for improving Cellular If semisoft handoff. LPM signals the safe handoff cue by sending a specially marked packet to mobile hosts. SPM (Semisoft rePly Message) is the only newly introduced control packet. Our performance study shows that LPM achieves lossless packet delivery without duplication and increases TCP throughput significantly.

• Proceedings of the Korean Institute of Communication Sciences Conference
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• 2004.11a
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• pp.467-467
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• 2004

• KSII Transactions on Internet and Information Systems (TIIS)
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• v.13 no.3
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• pp.1311-1324
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• 2019

In the traditional cellular network communication, the cellular user and the base station exchange information through the uplink channel and downlink channel. Meanwhile, device-to-device (D2D) users access the cellular network by reusing the channel resources of the cellular users. However, when cellular user channel conditions are poor, not only D2D user cannot reuse its channel resources to access the network, but also cellular user's communication needs cannot be met. To solve this problem, we introduced a novelty D2D communication mechanism in the downlink, which D2D transmitter users as half-duplex (HD) relays to assist the downlink transmission of cellular users with reusing corresponding spectrum. The optimization goal of the system is to make the cellular users in the bad channel state meet the minimum transmission rate requirement and at the same time maximize the throughput of the D2D users. In addition, i for the purpose of improving the efficiency of relay transmission, we use two-antenna architecture of D2D relay to enable receive and transmit signals at the same time. Then we optimized power of base station and D2D relay separately with consideration of backhaul interference caused by two-antenna architectures. The simulation results show that the proposed HD relay strategyis superior to existing HD and full-duplex (FD) models in the aspects of system throughput and power efficiency.

• Proceedings of the Zoological Society Korea Conference
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• 1998.10b
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• pp.75-75
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• 1998

No Abstract, See Full Text

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.4
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• pp.297-305
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• 2021

Luteolin, a sort of flavonoid, has been reported to be involved in neuroprotective function via suppression of neuroinflammation. In this study, we investigated the protective effect of luteolin against oxidative stress-induced cellular senescence and its molecular mechanism using hydrogen peroxide (H₂O₂)-induced cellular senescence model in House Ear Institute-Organ of Corti 1 cells (HEI-OC1). Our results showed that luteolin attenuated senescent phenotypes including alterations of morphology, cell proliferation, senescence-associated 𝛽-galactosidase expression, DNA damage, as well as related molecules expression such as p53 and p21 in the oxidant challenged model. Interestingly, we found that luteolin induces expression of sirtuin 1 in dose- and time-dependent manners and it has protective role against H₂O₂-induced cellular senescence by upregulation of sirtuin 1 (SIRT1). In contrast, the inhibitory effect of luteolin on cellular senescence under oxidative stress was abolished by silencing of SIRT1. This study indicates that luteolin effectively protects against oxidative stress-induced cellular senescence through p53 and SIRT1. These results suggest that luteolin possesses therapeutic potentials against age-related hearing loss that are induced by oxidative stress.

• BMB Reports
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• v.56 no.12
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• pp.651-656
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• 2023

Senescence, a cellular process through which damaged or dysfunctional cells suppress the cell cycle, contributes to aging or age-related functional decline. Cell metabolism has been closely correlated with aging processes, and it has been widely recognized that metabolic changes underlie the cellular alterations that occur with aging. Here, we report that fatty acid oxidation (FAO) serves as a critical regulator of cellular senescence and uncover the underlying mechanism by which FAO inhibition induces senescence. Pharmacological or genetic ablation of FAO results in a p53-dependent induction of cellular senescence in human fibroblasts, whereas enhancing FAO suppresses replicative senescence. We found that FAO inhibition promotes cellular senescence through acetyl-CoA, independent of energy depletion. Mechanistically, increased formation of autophagosomes following FAO inhibition leads to a reduction in SIRT1 protein levels, thereby contributing to senescence induction. Finally, we found that inhibition of autophagy or enforced expression of SIRT1 can rescue the induction of senescence as a result of FAO inhibition. Collectively, our study reveals a distinctive role for the FAO-autophagy-SIRT1 axis in the regulation of cellular senescence.

• Molecular & Cellular Toxicology
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• v.1 no.1
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• pp.52-61
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• 2005

Transcript profiling is a particularly valuable tool in the field of steroid receptor biology, as these receptors are ligand-activated transcription factors and therefore exert their initial effects through altering gene expression in responsive cells. Also, an awareness of endocrine disrupting chemicals (EDCs) and their potential screening methods to identify endocrine activity have been increased. Here we developed an in-house cDNA microarray, named KISTCHIP-400 ver. 1.0, with 416 clones, based on public database and research papers. These clones contained estrogen, androgen, thyroid hormone & receptors, sex hormone signal transduction & regulation, c-fos, c-myc, ps2 gene, metabolism related genes etc. Also, to validate the KISTCHIP-400 ver. 1.0, we investigated gene expression profiles with reference hormones, $10^{8}\;M\;17{\beta}-estradiol,\;10^{-7}\;M\;testosterone\;and\;10^{-7}\;M$ progesterone in MCF-7 cell line. As the results, gene expression profiles of three reference hormones were distinguished from each other with significant and identified 33 $17{\beta}-estradiol$ responsive genes. This study is in first step of validation for KISTCHIP-400 ver. 1.0, as following step transcriptional profile analysis on not only low concentrations of EDCs but suspected EDCs using KISTCHIP-400 ver. 1.0 is processing. Our results indicate that the developed microarray may be a useful laboratory tool for screening EDCs and elucidating endocrine disrupting mechanism.

• BMB Reports
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• v.48 no.7
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• pp.371-372
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• 2015

MicroRNAs (miRNAs) can regulate the expression of genes that are involved in multiple cellular pathways. However, their targets and mechanism of action associated with the autophagy pathway are not fully investigated yet. EWSR1 (EWS RNA-Binding Protein 1/Ewing Sarcoma Break Point Region 1) gene encodes a RNA/DNA binding protein that is ubiquitously expressed and plays roles in numerous cellular processes. Recently, our group has shown that EWSR1 deficiency leads to developmental failure and accelerated senescence via processing of miRNAs, but its role in the regulation of autophagy remains elusive. In this context, we further investigated and found that EWSR1 deficiency triggers the activation of the DROSHA-mediated microprocessor complex and increases the levels of miR125a and miR351, which directly target Uvrag. Interestingly, the miR125a- and miR351-targeted reduction of Uvrag led to the inhibition of autophagy in both ewsr1 knockout (KO) MEFs and ewsr1 KO mice. In summary, our study demonstrates that EWSR1 is associated with the posttranscriptional regulation of Uvrag via miRNA processing. The regulation of autophagy pathway in miRNAs-Uvrag-dependent manner provides a novel mechanism of EWSR1 deficiency-related cellular dysfunction. [BMB Reports 2015; 48(7): 371-372]

• Journal of Communications and Networks
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• v.8 no.4
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• pp.422-431
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• 2006

This paper proposes an adaptive routing protocol called ARCA for converged ad-hoc and cellular network (CACN). Due to the limitation of both bandwidth and transmission range in a cell, a mobile host (MH) may not be able to make a call during busy time. CACN offers a flexible traffic diversion mechanism that allows a MH to use the bandwidth in another cell to ease the congestion problem and increase the throughput in a cellular network. Based on the presentation of CACN's physical characteristics, the paper details the design issues and operation of the adaptive routing protocol for CACN (ARCA). Detailed numerical analysis is presented in terms of both route request rejection rate and routing overhead, which, along with the simulation results, have indicated the effectiveness and efficiency of the ARCA protocol.

• Proceedings of the Materials Research Society of Korea Conference
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• 2010.05a
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• pp.45.2-45.2
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• 2010

Possessing of carbon nanotubes in biopolymer intrigued much interest due to their mechanical and unique nanoscale surface properties. Surface stiffness can be controlled by the amount of carbon nanotubes in polymer and surface wettability can be altered by the order of nanoscale surface roughness. Protein adsorption mechanism on nanostructured carbon nanotube/polymer thin film will be discussed in this study. In addition, we identified that mechanical stimuli also contribute the messenchymal stem cell and bone cell interactions. Importantly, live cell analysis system also showed altered morphology and cellular functions. Thus, embedding of carbon nanostructures simultaneously contribute to protein adsorption and cellular interactions. In conclusion, this study demonstrated the evidence that nanoscale surface features determine the subsequent biological interactions, such as protein adsorption and cellular interactions.