天뢰 李廷稷 詩 硏究

이현일 ( Hyunil Lee ) 한국한시학회 2015 韓國漢詩硏究 Vol.23 No.-

天뢰 李廷稷(1781~1816)은 19세기 한시사의 중요한 시인인 藕船 李尙迪(1804~1865)의 生父로, 길지 않은 생애를 살았으면서도 시인으로서의 뚜렷한 자의식을 가지고 일정한 성취를 이룬 인물이었다고 판단된다. 그러나 그동안 학계에서 전혀 주목받지 못했는데, 이는 무엇보다 그의 시집이 아직까지 영인되어 보급되지 않아 연구자들이 널리 접할 수 없었던 탓이 크다. 그의 시집인 『天뢰詩稿』는 이상적이 燕行하였을 때 그곳에서 印刊하여 조선으로 가지고 들어 왔다. 이 책에는 모두 312수의 시가 실려 있는 바, 이정직은 서문에서 자신의 유일한 嗜好가 시를 짓는 것임을 밝히고 있다. 이정직에 대한 첫 번째 연구로서, 이 논문에서는 이 논문에서는 그의 시들을 대략 네 갈래로 나누어 살펴보았다. 우선 시인과 지식인으로서의 自意識이 譯官이라는 현실의 신분과 일으키는 갈등을 볼 수 있는 작품들을 살펴 보았고, 이어서 연행 도중의 풍광과 객수를 읊은 작품들을 읽어 보았다. 그 다음에는 어렸을 때 세상을 떠난 아버지를 그리워하고 어린 아들에 대한 사랑을 읊은 작품들을, 마지막으로 擬古風의 艶情詩 중에서 단순한 擬古作을 넘어서 그 나름의 新意를 보여주는 작품들을 고찰하였다. 이상의 독해를 통해서 그의 시인으로서의 역량을 가늠해 보고, 李尙迪 詩學의 연원을 더듬어 실마리를 찾아 보려고 하였다. 그리고 補論으로 『天뢰詩稿』를 두고 지은 序 3首를 모두 번역하여 싣고, 그 의미에 대해서 살펴보았다. Lee Jeong Jik(李廷稷, 1781~1816), father of Lee Sang Jeok(李尙迪, 1804~1865), who was one of the important official interpreter-poet, was short-lived, and yet a man of achievement as a poet. But he was completely unattracted scholastic attention, owing to his poetical work`s alienation to the scholars. When Lee Sang Jeok went to YanJing(燕京), the Capital of Qing Dynasty, as a member of Chosun Dynasty`s diplomatic delegation, he printed his father`s poetical works, The Poems of Natural Sound(天뢰詩稿), and came back to Chosun with it. It was composed of 312 poems. In Lee Jeong Jik`s preface to these poems, he expressed that composing poetry was his only taste. This paper classified his poems into four kinds and surveyed them. First, we read the poems of self-consciousness, expressed as a poet and a man of intelligence. Second, we read and surveyed the poems which were composed when he was as an interpreter of diplomatic delegation to Qing Dynasty. Third, we read and surveyed the poems of missing father, who died early and the poems of loving his child. Last, we read and surveyed the poems which modelled after old Chinese ballads. After reading his poetical works, we tried to verify him as an excellent poet, and as a perfect ideal to be followed by his son, Lee Sang Jeok.

5-Lipoxygenase mediates RANKL-induced osteoclast formation via the cysteinyl leukotriene receptor 1.

Lee, Jung-Min,Park, Hyojung,Noh, A Long Sae Mi,Kang, Ju-Hee,Chen, Ling,Zheng, Ting,Lee, Juhyun,Ji, Sun-Young,Jang, Chang-Young,Shin, Chan Soo,Ha, Hyunil,Lee, Zang Hee,Park, Hea-Young,Lee, Dong-Seok,Yi American Association of Immunologists 2012 Journal of Immunology Vol. No.

<P>5-Lipoxygenase (5-LO) catalyzes the formation of two major groups of leukotrienes, leukotriene B4 and cysteinyl leukotrienes (CysLTs), and it has been implicated as a promising drug target to treat various inflammatory diseases. However, its role in osteoclastogenesis has not been investigated. In this study, we used mouse bone marrow-derived macrophages (BMMs) to show that 5-LO inhibitor suppresses RANKL-induced osteoclast formation. Inhibition of 5-LO was associated with impaired activation of multiple signaling events downstream of RANK, including ERK and p38 phosphorylation, and IκB degradation, followed by a decrease in NFATc1 expression. Ectopic overexpression of a constitutively active form of NFATc1 partly rescued the antiosteoclastogenic effect of 5-LO inhibitor. The knockdown of 5-LO in BMMs also resulted in a significant reduction in RANKL-induced osteoclast formation, accompanied by decreased expression of NFATc1. Similar effects were shown with CysLT receptor (CysLTR)1/2 antagonist and small RNA for CysLTR1 in BMMs, indicating the involvement of CysLT and CysLTR1 in 5-LO-mediated osteoclastogenesis. Finally, 5-LO inhibitor suppressed LPS-induced osteoclast formation and bone loss in the in vivo mouse experiments, suggesting a potential therapeutic strategy for treating diseases involving bone destruction. Taken together, the results of this study demonstrate that 5-LO is a key mediator of RANKL-induced osteoclast formation and possibly a novel therapeutic target for bone-resorption diseases.</P>

Trolox Prevents Osteoclastogenesis by Suppressing RANKL Expression and Signaling

Lee, Jong-Ho,Kim, Ha-Neui,Yang, Daum,Jung, Kyoungsuk,Kim, Hyun-Man,Kim, Hong-Hee,Ha, Hyunil,Lee, Zang Hee American Society for Biochemistry and Molecular Bi 2009 The Journal of biological chemistry Vol.284 No.20

<P>Excessive receptor activator of NF-kappaB ligand (RANKL) signaling causes enhanced osteoclast formation and bone resorption. Thus, down-regulation of RANKL expression or its downstream signals may be a therapeutic approach to the treatment of pathological bone loss. In this study, we investigated the effects of Trolox, a water-soluble vitamin E analogue, on osteoclastogenesis and RANKL signaling. Trolox potently inhibited interleukin-1-induced osteoclast formation in bone marrow cell-osteoblast coculture by abrogating RANKL induction in osteoblasts. This RANKL reduction was attributed to the reduced production of prostaglandin E(2) via a down-regulation of cyclooxygenase-2 activity. We also found that Trolox inhibited osteoclast formation from bone marrow macrophages induced by macrophage colony-stimulating factor plus RANKL in a reversible manner. Trolox was effective only when present during the early stage of culture, which implies that it targets early osteoclast precursors. Pretreatment with Trolox did not affect RANKL-induced early signaling pathways, including MAPKs, NF-kappaB, and Akt. We found that Trolox down-regulated the induction by RANKL of c-Fos protein by suppressing its translation. Ectopic overexpression of c-Fos rescued the inhibition of osteoclastogenesis by Trolox in bone marrow macrophages. Trolox also suppressed interleukin-1-induced osteoclast formation and bone loss in mouse calvarial bone. Taken together, our findings indicate that Trolox prevents osteoclast formation and bone loss by inhibiting both RANKL induction in osteoblasts and c-Fos expression in osteoclast precursors.</P>

Characterization of In-Sn-Zn-O for Transpaarent Conductive Oxides

Hyunil Jo(조현일),Joung-Joo Kim(김종주),Joon-Hyung Lee(이준형),Sangwook Lee(이상욱),Young-woo Heo(허영우) 한국표면공학회 2019 한국표면공학회 학술발표회 초록집 Vol.2019 No.5

Synthetic anion transporters that bear a terminal ethynyl group

Lee, Eun-Bee,Ryu, Hyunil,Lee, Insu,Choi, Sangbaek,Hong, Jung-Ho,Kim, Sun Min,Jeon, Tae-Joon,Cho, Dong-Gyu The Royal Society of Chemistry 2015 Chemical communications Vol.51 No.45

<P>Cl<SUP>−</SUP> transporters that bear a terminal ethynyl group were synthesized; they consist of non-pyrrolic hydrogen bond motifs such as phenolic OH, amide NH, and triazole CH. The ethynyl group of these non-pyrrolic analogs plays an important role in chloride efflux and they exhibit no significant cytotoxic activity.</P> <P>Graphic Abstract</P><P>Non-pyrrolic synthetic anion transporters without cytotoxicity are capable of transporting the chloride anion through membranes. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c5cc01903f'> </P>

Arthroscopic removal of plica in radiocapitellar joint

Hyunil Lee(이현일),Sang Hoon Chae(채상훈),Min Jong Park(박민종) 대한견주관절의학회 2013 대한견주관절학회 학술대회논문집 Vol.2013 No.3

Influence of Deposition Pressure on the Properties of Round Pyramid Textured a-Si:H Solar Cells for Maglev

Lee, Jaehyeong,Choi, Wonseok,Lee, Kyuil,Lee, Daedong,Kang, Hyunil American Scientific Publishers 2016 Journal of Nanoscience and Nanotechnology Vol.16 No.5

<P>HIT (Heterojunction with Intrinsic Thin-layer) photovoltaic cells is one of the highest efficiencies in the commercial solar cells. The pyramid texturization for reducing surface reflectance of HIT solar cells silicon wafers is widely used. For the low leakage current and high shunt of solar cells, the intrinsic amorphous silicon (a-Si:H) on substrate must be uniformly thick of pyramid structure. However, it is difficult to control the thickness in the traditional pyramid texturing process. Thus, we textured the intrinsic a-Si: H thin films with the round pyramidal structure by using HNO3, HF, and CH3COOH solution. The characteristics of round pyramid a-Si: H solar cells deposited at pressure of 500, 1000, 1500, and 2000 mTorr by PECVD (Plasma Enhanced Chemical Vapor Deposition) was investigated. The lifetime, open circuit voltage, fill factor and efficiency of a-Si: H solar cells were investigated with respect to various deposition pressure.</P>

Electrical and optical properties of InSnZnO prepared by RF magnetron sputtering

Hyunil Jo,Jung-woo Han,Yoo-jin Nam,Joung-Joo Kim,Joon-hyung Lee,Sang-wook Lee,Young-woo Heo 한국진공학회 2019 한국진공학회 학술발표회초록집 Vol.2019 No.2

Synthesis and characteristic study of Amorphous Oxide Transparent Electrode materials for Flexible Display

Hyunil Jo,Yujin Nam,Joon-Hyung Lee,Sang-Wook Lee,Young-Woo Heo 한국진공학회 2020 한국진공학회 학술발표회초록집 Vol.2020 No.8

Pathogenic roles of CXCL10 signaling through CXCR3 and TLR4 in macrophages and T cells: relevance for arthritis

Lee, Jong-Ho,Kim, Bongjun,Jin, Won Jong,Kim, Hong-Hee,Ha, Hyunil,Lee, Zang Hee BioMed Central 2017 Arthritis research & therapy Vol.19 No.-

<P><B>Background</B></P><P>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by uncontrolled joint inflammation and destruction of bone and cartilage. We previously reported that C-X-C motif chemokine 10 (CXCL10; also called IP-10) has important roles in joint inflammation and bone destruction in arthritis. However, the specific mechanisms by which CXCL10 regulates the recruitment of inflammatory cells and the production of osteoclastogenic cytokines in RA progression are not fully understood.</P><P><B>Methods</B></P><P>Bone marrow-derived macrophages and CD4<SUP>+</SUP> T cells were isolated from wild-type (WT), <I>Cxcl10</I><SUP>–/–</SUP>, and <I>Cxcr3</I><SUP>–/–</SUP> mice. CXCL10-induced migration was performed using a Boyden chamber, and CXCL10-stimulated production of osteoclastogenic cytokines was measured by quantitative real-time PCR and ELISA. Collagen antibody-induced arthritis (CAIA) was induced by administration of collagen type II antibodies and lipopolysaccharide to the mice. Clinical scores were analyzed and hind paws were collected for high-resolution micro-CT, and histomorphometry. Serum was used to assess bone turnover and levels of osteoclastogenic cytokines.</P><P><B>Results</B></P><P>CXCL10 increased the migration of inflammatory cells through C-X-C chemokine receptor 3 (CXCR3)-mediated, but not toll-like receptor 4 (TLR4)-mediated, ERK activation. Interestingly, both receptors CXCR3 and TLR4 were simultaneously required for CXCL10-stimulated production of osteoclastogenic cytokines in CD4<SUP>+</SUP> T cells. Furthermore, calcineurin-dependent NFATc1 activation was essential for CXCL10-induced RANKL expression. In vivo, F4/80<SUP>+</SUP> macrophages and CD4<SUP>+</SUP> T cells robustly infiltrated into synovium of WT mice with CAIA but were significantly reduced in both <I>Cxcl10</I><SUP><I>–/–</I></SUP> and <I>Cxcr3</I><SUP><I>–/–</I></SUP> mice. Serum concentrations of osteoclastogenic cytokines and bone destruction were also reduced in the knockout mice, leading to attenuated progression of arthritis.</P><P><B>Conclusion</B></P><P>These findings highlight the importance of CXCL10 signaling in the pathogenesis of RA and provide previously unidentified details of the mechanisms by which CXCL10 promotes the development of arthritis.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/s13075-017-1353-6) contains supplementary material, which is available to authorized users.</P>