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      • A study on Driving of 35W(T5) fluorescent lamp by the electronic ballast using piezoelectric transformer

        L H Hwang,J H Yoo,H S Song,S K Na,H S Kim,H S Oh,S H Lee,K H Choi,M T Cho 전력전자학회 2007 ICPE(ISPE)논문집 Vol.- No.-

        Recently, 35W class Fluorescent lamps with 32㎜ tube diameter are replaced with 32W one with 26 ㎜ in diameter to conserve lamp materials and to increase luminance efficiency. Moreover, 35, 28 and 14 W fluorescent lamps with 16㎜ (T5) in diameter, which are nowadays developed, also may replace 32 W lamps again. Application of slim lamps, however, requires small sized electronic ballast to full fill the design philosophy of miniaturizing. However, the traditional magnetic ballasts operated at 50-60㎐ have been suffered from noticeable flicker, high loss, large crest factor and heavy weight. In this study, in order to solve these problems, a new type of electronic ballast, which is composed of rectifier, active power factor corrector, series resonant half bridge inverter and piezoelectric transformer, was proposed for driving T5 fluorescent lamp. Driving of piezoelectric transformer was carried out with input region for the ring electrode and output region for the dot electrode. A 35W (T5) fluorescent lamp is successfully driven by the fabricated ballast with piezoelectric transformer. After driving the lamp using the proposed electronic ballast for 20 min, the input power factor and efficiency of ballast shown 0.95 and 86%, respectively, at operating frequency of 81 k㎐. And also, the output power and temperature rise of piezoelectric transformer showed 35.07W and 20.5 , respectively.

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        Interaction of hepatitis B virus X protein with PARP1 results in inhibition of DNA repair in hepatocellular carcinoma

        Na, T-Y,Ka, N-L,Rhee, H,Kyeong, D,Kim, M-H,Seong, J K,Park, Y N,Lee, M-O Nature Publishing Group 2016 Oncogene Vol.35 No.41

        <P>Hepatitis B virus X protein (HBx) contributes to the development of hepatocellular carcinoma (HCC), probably by regulating activities of many host or viral proteins through protein-protein interactions. In this study, we identified poly(ADP-ribose) polymerase (PARP1), a crucial factor in DNA repair, as an HBx-interacting protein using a proteomics approach. Coimmunoprecipitation and proximity ligation assays confirmed the binding and colocalization of HBx and PARP1 in the nucleus. The carboxyl-terminus of HBx protein bound to the catalytic domain of PARP1, and this binding reduced the enzymatic activity of PARP1 in both in vitro and in vivo assays. HBx interrupted the binding of PARP1 to Sirt6, which catalyzes the mono-ADP-ribosylation required for DNA repair. Consistently, overexpression of HBx inhibited the clearance of gamma H2AX DNA repair foci generated under oxidative stress in Chang liver cells. Recruitment of the DNA repair complex to the site-specific double-strand breaks was inhibited in the presence of HBx, when measured by laser microirradiation assay and damage-specific chromatin immunoprecipitation assays. Consequently, HBx increased signs of DNA damage such as accumulation of 8-hydroxy-2'-deoxyguanosine and comet formation, which were reversed by overexpression of PARP1 and/or Sirt6. Finally, the interaction between PARP1 and Sirt6 was markedly lower in the livers of HBx-transgenic mice and specimens obtained from HCC patients to compare with the corresponding control. Our data suggest that the physical interaction of HBx and PARP1 accelerates DNA damage by inhibiting recruitment of the DNA repair complex to the damaged DNA sites, which may lead to the onset of hepatocarcinogenesis.</P>

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        Feasibility experiment of physics-based global electron temperature profile control in KSTAR

        Kim, H.-S.,Kim, S.H.,Jeon, Y.M.,Na, Y.-S.,Bae, Y.S.,Hahn, S.H.,Joung, M.,Lee, K.D.,Han, H.S.,Woo, M.H.,Lee, T.G.,Yun, S.W.,Yoon, S.W. Elsevier 2018 Fusion engineering and design Vol.135 No.1

        <P><B>Abstract</B></P> <P>KSTAR experiments have been conducted aiming at establishing a real-time control system that uses multiple actuators (NBI and ECH) to control the plasma profiles (T<SUB>e</SUB> and q profiles) and validating an applied physics-based plasma profile response model. Toward establishing the multiple plasma profile control system, the control experiment of the electron temperature profile has been performed in KSTAR as a first step. Although the plasma profile control system was in the commissioning phase, the electron temperature was feedback controlled successfully in real-time while the normalized radial profile of electron temperature remained nearly constant. In the circumstance, the implemented physics-based response model was successfully validated against control experiments with a step variation on the control target and an application of multiple actuators. The robustness of the controller is examined against an external disturbance in which a static version of the control matrix was used.</P>

      • Sliding wear of silicon carbide modified by etching with chlorine at various temperatures

        Choi, H.-J.,Bae, H.-T.,Lee, J.-K.,Na, B.- C.,McNallan, M.J.,Lim, D.-S. Elsevier 2009 Wear: An international journal on the science and Vol.266 No.1

        <P><B>Abstract</B></P><P>The effect of reaction temperature on the formation of a carbon layer on the surface of SiC has been investigated. Subsequently, the tribological properties of the formed carbon layers were studied. The experimental procedure involved exposing reaction-bonded SiC balls to a flowing gas mixture of 5% Cl<SUB>2</SUB>, 2.5% H<SUB>2</SUB>, and Ar at a high temperature of 800, 1000, or 1200°C. A ball-on disk tribometer was used to investigate the friction and wear behavior of the treated specimens. While partially unreacted SiC phases were observed in the layer modified at 800°C, rhombohedral graphite crystals were formed in the layer modified at 1200°C. Compared to untreated SiC, the treated SiC materials were found to have relatively low friction coefficients and better wear resistance. Increasing the treatment temperature was found to improve the tribological performance of the resulting surface-modified SiC balls. A possible reason for this tribological improvement has been discussed based on the observed carbon phases.</P>

      • Sucrose-induced anthocyanin accumulation in vegetative tissue of Petunia plants requires anthocyanin regulatory transcription factors

        Ai, T.N.,Naing, A.H.,Arun, M.,Lim, S.H.,Kim, C.K. Elsevier Scientific Publishers Ireland Ltd 2016 Plant science Vol.252 No.-

        <P>The effects of three different sucrose concentrations on plant growth and anthocyanin accumulation were examined in non-transgenic (NT) and transgenic (T-2) specimens of the Petunia hybrida cultivar 'Mirage rose' that carried the anthocyanin regulatory transcription factors B-Peru + mPAP1 or RsMYB1. Anthocyanin accumulation was not observed in NT plants in any treatments, whereas a range of anthocyanin accumulation was observed in transgenic plants. The anthocyanin content detected in transgenic plants expressing the anthocyanin regulatory transcription factors (B-Peru + mPAP1 or RsMYB1) was higher than that in NT plants. In addition, increasing sucrose concentration strongly enhanced anthocyanin content as shown by quantitative real-time polymerase chain reaction (qRT-PCR) analysis, wherein increased concentrations of sucrose enhanced transcript levels of the transcription factors that are responsible for the induction of biosynthetic genes involved in anthocyanin synthesis; this pattern was not observed in NT plants. In addition, sucrose affected plant growth, although the effects were different between NT and transgenic plants. Taken together, the application of sucrose could enhance anthocyanin production in vegetative tissue of transgenic Petunia carrying anthocyanin regulatory transcription factors, and this study provides insights about interactive effects of sucrose and transcription factors in anthocyanin biosynthesis in the transgenic plant. (C) 2016 Elsevier Ireland Ltd. All rights reserved.</P>

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        Enhanced delivery of liposomes to lung tumor through targeting interleukin-4 receptor on both tumor cells and tumor endothelial cells

        Chi, L.,Na, M.H.,Jung, H.K.,Vadevoo, S.M.P.,Kim, C.W.,Padmanaban, G.,Park, T.I.,Park, J.Y.,Hwang, I.,Park, K.U.,Liang, F.,Lu, M.,Park, J.,Kim, I.S.,Lee, B.H. Elsevier Science Publishers 2015 Journal of controlled release Vol.209 No.-

        A growing body of evidence suggests that pathological lesions express tissue-specific molecular targets or biomarkers within the tissue. Interleukin-4 receptor (IL-4R) is overexpressed in many types of cancer cells, including lung cancer. Here we investigated the properties of IL-4R-binding peptide-1 (IL4RPep-1), a CRKRLDRNC peptide, and its ability to target the delivery of liposomes to lung tumor. IL4RPep-1 preferentially bound to H226 lung tumor cells which express higher levers of IL-4R compared to H460 lung tumor cells which express less IL-4R. Mutational analysis revealed that C1, R2, and R4 residues of IL4RPep-1 were the key binding determinants. IL4RPep-1-labeled liposomes containing doxorubicin were more efficiently internalized in H226 cells and effectively delivered doxorubicin into the cells compared to unlabeled liposomes. In vivo fluorescence imaging of nude mice subcutaneously xenotransplanted with H226 tumor cells indicated that IL4RPep-1-labeled liposomes accumulate more efficiently in the tumor and inhibit tumor growth more effectively compared to unlabeled liposomes. Interestingly, expression of IL-4R was high in vascular endothelial cells of tumor, while little was detected in vascular endothelial cells of control organs including the liver. IL-4R expression in cultured human vascular endothelial cells was also up-regulated when activated by a pro-inflammatory cytokine tumor necrosis factor-α. Moreover, the up-regulation of IL-4R expression was observed in primary human lung cancer tissues. These results indicate that IL-4R-targeting nanocarriers may be a useful strategy to enhance drug delivery through the recognition of IL-4R in both tumor cells and tumor endothelial cells.

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        15-Deoxy-Δ<sup>12,14</sup>-prostaglandin J<sub>2</sub> induces p53 expression through Nrf2-mediated upregulation of heme oxygenase-1 in human breast cancer cells

        Kim, D. H.,Song, N. Y.,Kim, E. H.,Na, H. K.,Joe, Y.,Chung, H. T.,Surh, Y. J. Informa Healthcare 2014 Free radical research Vol.48 No.9

        <P>Heme oxygenase-1 (HO-1) is a stress-responsive enzyme that has antioxidant and cytoprotective functions. However, HO-1 has oncogenic functions in cancerous or transformed cells. In the present work, we investigated the effects of HO-1 on the expression of p53 induced by 15-deoxy-Δ<SUP>12,14</SUP>-prostaglandin J<SUB>2</SUB> (15d-PGJ<SUB>2</SUB>) in human breast cancer (MCF-7) cells. Treatment of MCF-7 cells with 15d-PGJ<SUB>2</SUB> led to time-dependent increases in the expression of p53 as well as HO-1. Upregulation of p53 expression by 15d-PGJ<SUB>2</SUB> was abrogated by si-RNA knock-down of HO-1. In MCF-7 cells transfected with HO-1 si-RNA, 15d-PGJ<SUB>2</SUB> failed to induce expression of p53 as well as HO-1. In addition, HO-1 inducers enhanced the p53 expression. We speculated that iron, a by-product of HO-1-catalyzed reactions, could mediate 15d-PGJ<SUB>2</SUB>-induced p53 expression. Upregulation of p53 expression by 15d-PGJ<SUB>2</SUB> was abrogated by the iron chelator desferrioxamine in MCF-7 cells. Iron released from heme by HO-1 activity is mostly in the Fe<SUP>2+</SUP> form. When MCF-7 cells were treated with the Fe<SUP>2+</SUP>-specific chelator phenanthroline, 15d-PGJ<SUB>2</SUB>-induced p53 expression was attenuated. In addition, levels of the Fe-sequestering protein H-ferritin were elevated in 15d-PGJ<SUB>2</SUB>-treated MCF-7 cells. In conclusion, upregulation of p53 and p21 via HO-1 induction and subsequent release of iron with accumulation of H-ferritin may confer resistance to oxidative damage in cancer cells frequently challenged by redox-cycling anticancer drugs.</P>

      • 압전 변압기를 이용한 35W(T5)급 형광등 안정기 구동 시스템 특성에 관한 연구

        황락훈(L. H. Hwang),장진혁(J. H. Jang),나승권(S. K. Na),김영수(Y. S. Kim),안익수(I. S. Ahn),조문택(M. T. Cho),송호빈(H. B. Song) 대한전기학회 2006 대한전기학회 학술대회 논문집 Vol.2006 No.7

        In this study, in order to solve these problems, a new type of electronic ballast, which is composed of rectifier, active power factor corrector, series resonant half bridge inverter and piezoelectric transformer, was proposed for driving T5 fluorescent lamp. Driving of piezoelectric transformer was carried out with input region for the ring electrode and output region for the dot electrode. A 35W (T5) fluorescent lamp was successfully driven by the fabricated ballast with piezoelectric transformer.

      • SCISCIESCOPUS

        Jmjd3 mediates blood-spinal cord barrier disruption after spinal cord injury by regulating MMP-3 and MMP-9 expressions

        Lee, J.Y.,Na, W.H.,Choi, H.Y.,Lee, K.H.,Ju, B.G.,Yune, T.Y. Academic Press Inc 2016 Neurobiology of disease Vol.95 No.-

        <P>The disruption of the blood-spinal cord barrier (BSCB) by matrix metalloprotease (MMP) activation is a detrimental event that leads to blood cell infiltration, inflammation, and apoptosis, thereby contributing to permanent neurological disability after spinal cord injury (SCI). However, the molecular mechanisms underlying Mmp gene regulation have not been fully elucidated. Here, we demonstrated the critical role of histone H3K27 demethylase Jmjd3 in the regulation of Mmp gene expression and BSCB disruption using in vitro cellular and in vivo animal models. We found that Jmjd3 up-regulation, in cooperation with NF-kappa B, after SCI is required for Mmp-3 and Mmp-9 gene expressions in injured vascular endothelial cells. In addition, Jmjd3 mRNA depletion inhibited Mmp-3 and Mmp-9 gene expressions and significantly attenuated BSCB permeability and the loss of tight junction proteins. These events further led to improved functional recovery, along with decreased hemorrhage, blood cell infiltration, inflammation, and cell death of neurons and oligodendrocytes after SCI. Thus, our findings suggest that Jmjd3 regulation may serve as a potential therapeutic intervention for preserving BSCB integrity following SCI. (C) 2016 Elsevier Inc. All rights reserved.</P>

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        Perturbative studies of toroidal momentum transport in KSTAR H-mode and the effect of ion temperature perturbation

        Yang, S.M.,Na, Yong-Su,Na, D.H.,Park, J.-K.,Shi, Y.J.,Ko, W.H.,Lee, S.G.,Hahm, T.S. International Atomic Energy Agency 2018 Nuclear fusion Vol.58 No.6

        <P>Perturbative experiments have been carried out using tangential neutral beam injection (NBI) and non-resonant magnetic perturbation (NRMP) to analyze the momentum transport properties in KSTAR H-modes. Diffusive and non-diffusive terms of momentum transport are evaluated from the transient analysis. Although the operating conditions and methodologies applied in the two cases are similar, the momentum transport properties obtained show clear differences. The estimated momentum diffusivity and pinch obtained in the NBI modulation experiments is larger than that in the NRMP modulation experiments. We found that this discrepancy could be a result of uncertainties in the assumption for the analysis. By introducing time varying momentum transport coefficients depending on the temperature gradient, the linearized equation shows that if the temperature perturbation exists, the evolution of toroidal rotation perturbation could be faster than the transport rate of mean quantity, since the evolution of toroidal rotation perturbation is related to <img ALIGN='MIDDLE' ALT='' SRC='http://ej.iop.org/images/0029-5515/58/6/066008/nfaab90eieqn001.gif'/>, a momentum diffusivity from perturbative analysis. This could explain the estimated higher momentum diffusivity using time independent transport coefficients in NBI experiments with higher ion temperature perturbation compared to that in NRMP modulation experiments. The differences in the momentum transport coefficient with NRMP and NBI are much reduced by considering time varying momentum transport coefficients in the time dependent transport simulation.</P>

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