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      • Field emission from carbon nanotubes for display

        Choi,WonBong,Lee,NaeSung,Lee,Young Hee,Kim,JongMin 국립경상대학교 공과대학 부설 첨단소재연구소 1999 尖端素材 Vol.9 No.-

        Carbon nanotube (CNT)-based field emission displays (FEDs) have been fabricated using well-aligned nanotubes on a glass substrate by paste squeeze and surface rubbing techniques. The fabricated displays were fully scalable at 415℃ and show a high brightness of 1800 cd/m²at 3.7 V/㎛ from the green phosphor. The turn-on fields of 1 V/㎛ and field emission current of 1.5 mA at 3 V/㎛(J=90㎂/cm²) were observed. The fluctuation of the current was found to be about 7 % over a 4.5-inch cathode area. Large field enhancement factors (17000-33000) and low turn-on field(1V/㎛) were attributed to well-aligned carbon nanotubes and a large number of carbon nanotobes of 5-10/㎛².

      • Ultraviolet-C-Induced Apoptosis Protected by 635-nm Laser Irradiation in Human Gingival Fibroblasts

        Lim, Wonbong,Ko, Mikyung,Lee, Sungga,Kim, Inae,Jung, Mina,Kim, Okjoon,Cho, Seonghoun,Yang, Kyuho,Choi, Namki,Kim, Sunmi,Choi, Hongran Mary Ann Liebert 2008 Photomedicine and laser surgery Vol.26 No.3

        <P>OBJECTIVE: The purpose of this study was to examine the protection afforded by 635-nm irradiation against ultraviolet (UV)-C-induced apoptosis in primary human gingival fibroblasts (hGFs). BACKGROUND DATA: UV irradiation is known to cause photoaging and cellular apoptosis of skin cells and is considered to be one of the leading causes of skin carcinogenesis. MATERIALS AND METHODS: To induce apoptosis, UV-C (100 mJ/cm2) was used to irradiate hGFs. To protect them from apoptosis, pretreatment with 635-nm irradiation was performed for 1 h immediately after cell plating 36 or 48 h before UV-C irradiation. The light source used for irradiation was a continuous-wave 635-nm LED laser emitting at 1 mW/cm2. Experimental samples were selected 24 h after UV-C irradiation. To measure the numbers of apoptotic cells, MTT assay and flow cytometric analyses were performed. For histomorphologic findings, Diff-Quick staining was carried out. Also, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were measured. RESULTS: In the present study, the number of apoptotic cells declined in the cells that were pretreated with 635-nm light irradiation in a time-dependent manner. In addition, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were significantly recovered by pretreatment with 635-nm irradiation. CONCLUSION: These results suggest that 635-nm visible light irradiation may be used as a protective tool to prevent UV-C-induced apoptosis.</P>

      • Cell Death and Intracellular Distribution of Hematoporphyrin in a KB Cell Line

        Choi, Hongran,Lim, Wonbong,Kim, Ji-Eun,Kim, Inae,Jeong, Jinan,Ko, Youngjong,Song, Jongwoon,You, Sunyeol,Kim, Doman,Kim, Misook,Kim, Byung-Kuk,Kim, Okjoon Mary Ann Liebert 2009 Photomedicine and laser surgery Vol.27 No.3

        <P>OBJECTIVE: The objective of this study is to investigate the effect of intracellular photosensitizer distribution on tumor cell death after photodynamic therapy (PDT). BACKGROUND DATA: The photosensitizer accumulates in tumor tissue during PDT, and generates intracellular reactive oxygen species (ROS), resulting in tumor cell death. MATERIALS AND METHODS: This study was carried out to elucidate the effects of PDT in a KB oral cancer cell line using hematoporphyrin with irradiation at 635 nm and 5 mW/cm(2). After irradiation, the MTT reduction method, agarose gel electrophoresis, flow cytometry, and Diff-Quick staining were performed. The intracellular ROS level was measured by DCF-DA. Intracellular hematoporphyrin was monitored with a confocal microscope, and Western blot and caspase activity assays were performed. RESULTS: In our study, cell survival was reduced by about 50% after 3 h of hematoporphyrin incubation time. In DNA fragmentation, flow cytometry, and Diff-Quick assay, necrosis was identified within 12 h and apoptosis soon thereafter. Confocal microscopy revealed that hematoporphyrin was localized in the cell membrane, cytoplasm, and nucleus as time passed. The quantities of intracellular ROS correlated with the time of hematoporphyrin accumulation. Additionally, Western blot analysis of Bcl-2/Bax, the release of cytochrome C, and activity of caspase-3 and caspase-9 showed that apoptosis followed the mitochondria-dependent pathway. CONCLUSION: PDT with hematoporphyrin in the KB cell line showed morphological changes of cell necrosis and apoptosis, which were associated with the time of distribution and localization of hematoporphyrin. Also, the apoptosis evoked followed the mitochondria-dependent pathway.</P>

      • SCISCIESCOPUS

        Inflammatory cytokines are suppressed by light-emitting diode irradiation of P. gingivalis LPS-treated human gingival fibroblasts: inflammatory cytokine changes by LED irradiation.

        Choi, HongRan,Lim, WonBong,Kim, InAe,Kim, JiSun,Ko, YoungJong,Kwon, Hyukil,Kim, SangWoo,Kabir, K M Ahsan,Li, Xiaojie,Kim, Oksu,Lee, YoungJoon,Kim, SeoYune,Kim, OkJoon Baillière Tindall ; Springer London 2012 LASERS IN MEDICAL SCIENCE Vol.27 No.2

        <P>Human gingival fibroblasts (hGFs) play an important role in the inflammatory reaction to lipopolysaccharide (LPS) from P. gingivalis, which infects periodontal connective tissue. In addition, although light-emitting diode (LED) irradiation has been reported to have biostimulatory effects, including anti-inflammatory activity, the pathological mechanisms of these effects are unclear. This study examined the effects of 635-nm irradiation of P. gingivalis LPS-treated human gingival fibroblasts on inflammatory cytokine profiles and the mitogen-activated protein kinase (MAPK) pathway, which is involved in cytokine production. Gingival fibroblasts treated or not treated with P. gingivalis LPS were irradiated with 635-nm LED light, and cytokine profiles in the supernatant were assessed using a human inflammation antibody array. Expression of cyclooxyginase-2 (COX-2) protein and phosphorylation of extracellular signal-regulated kinase (ERK 1/2), p38, and c-Jun-N-terminal kinase (JNK) were assessed by Western-blot analysis to determine the effects on the MAPK pathway, and prostaglandin E(2) (PGE(2)) in the supernatant was measured using an enzyme-linked immunoassay. COX-2 protein expression and PGE(2) production were significantly increased in the LPS-treated group and decreased by LED irradiation. LPS treatment of gingival fibroblasts led to the increased release of the pro-inflammatory-related cytokines interleukin-6 (IL-6) and IL-8, whereas LED irradiation inhibited their release. Analysis of MAPK signal transduction revealed a considerable decrease in p38 phosphorylation in response to 635-nm radiation either in the presence or absence of LPS. In addition, 635-nm LED irradiation significantly promoted JNK phosphorylation in the presence of LPS. LED irradiation can inhibit activation of pro-inflammatory cytokines, mediate the MAPK signaling pathway, and may be clinically useful as an anti-inflammatory tool.</P>

      • KCI등재

        광 감응성 물질의 세포내 위치에 따른 Photodynamic therapy(PDT) 의 세포사멸 경로에 관한 연구

        WonBong Lim,SungGa Lee,InAe Kim,MinA Jung,OkJoon Kim,HongRan Choi 대한구강악안면병리학회 2007 대한구강악안면병리학회지 Vol.31 No.5

        Photodynamic therapy(PDT) 는 특정 광 감응 물질 에 광 조사를 수행하여 세 포내애서 활성 산소종(ROS) 의 증가를 통한 암세 포의 사띨을 유도하는 방법이다 광 감응 물질은 암세 포에 선택 적으로 흡수되어 특정 파장의 빛을 홉수하여 다량의 ROS를 발생하여 암세 포의 사멸을 유도한다, 그러나 PDT 수행 시 ROS의 세 포내 작용에 따른 사띨 기전 이 영확히 알려지 지 않았고, 비 선 택 성으로 인한 정 상 세포애서의 피해 도 유발될 수 있다고 보고되었다 본 연 구애서 는 굉 감웅제인 He ma to por p h y rin을 이 용하여 구깅암 세포주인 He p2에서 광조사를 통한 세포 사멸 에 관한 연 구를 수행하였다 Confocal mi crosco py를 통한 분석에서 Hemato po r phyrin은 홉수 시 간에 따라 세포막에서 세 포질 핵 으로의 위치함을 관찰 할 수 있었고. 전기 영 동에 따른 DNA 분절 분석에서 24 시간이상 홉수된 상태 에서 ladder 패턴을 보임으로써 세 포 자띨사에 이 르는 만웅을 보였다 DCF - DA에 의힌 세 포내 ROS 분석 을 수행힌 결과 Hema to po rphyrin의 흡수 시간이 증가할수록 세포 내부에서의 ROS 발생이 증가함을 획 인 할 수 있었 다 이와 같은 결과에 따르면 Hematoporphyrin을 이용한 PDT에서 h ematoporphy ri n의 홉수 시 간에 따라 세 포 자띨사가 유도되었고. 특히 Hematoporphyrin은 흡수 시 간이 증가하여 세 포 내 부까지 충분히 Hematoporphyri n 이 작용된 경우에 서 ‘ ROS 발생애 따른 미 토콘드리아 의존적 경 로를 통해 세 포 자멸사가 유도되 었음을 확인 할 수 있었다-

      • The anti-inflammatory mechanism of 635 nm light-emitting-diode irradiation compared with existing COX inhibitors

        Lim, Wonbong,Lee, SungGa,Kim, Inae,Chung, Mina,Kim, Misook,Lim, Hoisoon,Park, Jinsoo,Kim, Okjoon,Choi, Hongran Wiley Subscription Services, Inc., A Wiley Company 2007 Lasers in surgery and medicine Vol.39 No.7

        <B>Background and Objectives</B><P>Inhibition of cyclooxygenase (COX) and prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>) protects cells against cell injury in specific pathophysiological situations: inflammation and oxidative stress. Although the anti-inflammatory effects have been reported in clinical fields for specific wavelength irradiation during wound healing, the physiological mechanism has not been clarified yet. The aim of the present study is to investigate the anti-inflammatory mechanism of 635 nm light-emitting-diode (LED) irradiation compared with existing COX inhibitors.</P><B>Study Design/Materials and Methods</B><P>The present study investigated anti-inflammatory effects of 635 nm irradiation on PGE<SUB>2</SUB> release, COX and phospholipase A<SUB>2</SUB> (PLA<SUB>2</SUB>) expression, and reactive oxygen species (ROS) dissociation in arachidonic acid (AA)-treated human gingival fibroblast (hGF). These results were compared with their existing COX inhibitors: indomethacin and ibuprofen. The PGE<SUB>2</SUB> release was measured by enzyme immunoassay, the COX expression was measured by western blot and reverse transcriptase polymerase chain reaction (RT-PCR), and ROS level was measured by flow cytometry, laser scanning confocal microscope and RT-PCR.</P><B>Results</B><P>Results showed that 635 nm irradiation and existing COX inhibitors inhibit expression of COX and PGE<SUB>2</SUB> release. Unlike indomethacin and ibuprofen, 635 nm irradiation leads to a decrease of ROS levels and mRNA expression of cytosolic phospholipase A<SUB>2</SUB> (cPLA<SUB>2</SUB>) and secretary phospholipase A<SUB>2</SUB> (sPLA<SUB>2</SUB>).</P><B>Conclusion</B><P>Taken together, 635 nm irradiation, unlike indomethacin and ibuprofen, can directly dissociate the ROS. This inhibits cPLA<SUB>2</SUB>, sPLA<SUB>2</SUB>, and COX expression, and results in the inhibition of PGE<SUB>2</SUB> release. Thus, we suggest that 635 nm irradiation inhibits PGE<SUB>2</SUB> synthesis like COX inhibitor and appears to be useful as an anti-inflammatory tool. Lesers Surg. Med. 39:614–621, 2007. © 2007 Wiley-Liss, Inc.</P>

      • Synthesis and characterization of sulfonated polyimides containing aliphatic linkages in the main chain

        Jang, Wonbong,Kim, Dowan,Choi, Seunghyuk,Shul, Yong Gun,Han, Haksoo John Wiley Sons, Ltd. 2006 Polymer international Vol.55 No.11

        <P>A series of six-membered sulfonated polyimides with aliphatic linkages (SPIAs) was successfully synthesized using 1,4,5,8-naphthalenetetracarboxylic dianhydride (NTDA), 4,4′-diaminobiphenyl 2,2′-disulfonic acid (BDSA) as the sulfonated diamine, and aliphatic diamines H<SUB>2</SUB>N(CH<SUB>2</SUB>)<SUB>n</SUB>NH<SUB>2</SUB> where n = 6, 8, 10, 12. These SPIAs were evaluated for thermal stability, ion exchange capacity (IEC), water uptake, proton conductivity, and hydrolytic stability. Proton conductivity and hydrolytic stability of the SPIAs were compared with the fully aromatic polyimide (MDA-SPI) prepared from 4,4′-methylenedianiline (MDA), BDSA, and NTDA. All the SPIAs exhibited high thermal stability. As the chain length of the aliphatic diamine decreased, the IEC and water uptake of the SPIAs increased. The SPIAs showed higher proton conductivity than commercially available membranes such as Nafion 117 at high temperatures and higher proton conductivity than MDA-SPI at all temperatures. All SPIAs exhibited a hydrolytic stability more than twice as high as that of MDA-SPI. Copyright © 2006 Society of Chemical Industry</P>

      • SCIESCOPUS

        Dichloromethane fraction from <i>Gardenia jasminoides</i>: DNA topoisomerase 1 inhibition and oral cancer cell death induction

        Lim, WonBong,Kim, OkSu,Jung, JinAn,Ko, YoungJong,Ha, JooWon,Oh, HeeKyun,Lim, HoiSoon,Kwon, HyukIl,Kim, InAe,Kim, Jisun,Kim, MiSook,Kim, SeoYune,Kim, Byung-kuk,Kim, SunMi,Kang, Byung-Cheol,Choi, HongRa Informa Healthcare 2010 PHARMACEUTICAL BIOLOGY Vol.48 No.12

        <P><I>Context:</I> A growing body of evidence shows that compounds of plant origin have the ability to prevent cancer. The fruit of gardenia, <I>Gardenia jasminoides</I> Ellis (Rubiaceae), has long been used as a food additive and herbal medicine, and its pharmacological actions, such as protective activity against oxidative damage, cytotoxic effect, and anti-inflammatory and anti-tumor activity, have already been reported.</P><P><I>Objective:</I> The purpose of the present study was to investigate the presence of DNA topoisomerase 1 inhibitor in various solvent fractions of <I>Gardenia</I> extract and examine the induction of oral cancer cell death upon treatment with <I>Gardenia</I> extract.</P><P><I>Materials and methods:</I> The methanol extract of <I>Gardenia</I> was partitioned with <I>n-</I>hexane, dichloromethane, ethyl acetate, <I>n-</I>butanol, and water.</P><P><I>Results:</I> In the DNA topoisomerase 1 assay, <I>n-</I>hexane and dichloromethane fractions inhibited topoisomerase 1 and led to a decrease in the cell viability of KB cells. The dichloromethane fraction (0.1 mg/mL) also showed 77% inhibition of cell viability in KB cells compared with HaCaT cells. Treatment with dichloromethane fraction led to apoptotic cell death as evidenced by flow cytometric analysis and morphological changes. In addition, treatment with <I>Gardenia</I> extract dichloromethane fraction led to the partial increase of caspase-3, caspase-8 and caspase-9 activities and the cleavage of poly (ADP-ribose) polymerase.</P><P><I>Conclusion:</I> Taken together, these results suggest that the dichloromethane fraction from <I>Gardenia</I> extract induces apoptotic cell death by DNA topoisomerase 1 inhibition in KB cells. These findings suggest the possibility that <I>Gardenia</I> extract could be developed as an anticancer modality.</P>

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