http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Macrophages express membrane bound form of APRIL that can generate immunomodulatory signals
Lee, Sang-Min,Jeon, Sung-Tak,Suk, Kyoungho,Lee, Won-Ha Blackwell Publishing Ltd 2010 Immunology Vol.131 No.3
<P>Summary</P><P>Members of the tumour necrosis factor superfamily play an essential role in inducing various biological responses including proliferation, differentiation, survival and cell death. A proliferation-inducing ligand (APRIL), first identified as a stimulant of tumour proliferation, is now known as a regulator of B-cell-mediated immune responses through the modulation of B-cell survival and activation. However, the role of APRIL in macrophage function has not been explored. High level expression of APRIL was detected on the surface of cells of the monocytic lineage including the human macrophage-like cell line, THP-1. To identify the role of APRIL in macrophage functions, THP-1 cells were stimulated with either its counterpart (TACI : Fc fusion protein) or a monoclonal antibody that is specific to APRIL. Stimulation of APRIL resulted in the expression of pro-inflammatory mediators such as interleukin-8 and matrix metalloproteinase-9 through the activation of mitogen-activated protein kinase and nuclear factor-&kgr;B. In contrast, stimulation of APRIL had an inhibitory effect on processes that require cytoskeletal movement such as phagocytosis of opsonized zymosan and chemotaxis through an inhibition of phosphatidylinositol 3-kinase activity. These observations demonstrate that macrophages express a membrane-bound form of APRIL which, upon stimulation, modulates the activities of macrophages through stimulation or inhibition of processes associated with inflammation.</P>
Lee, Min-Young,Kim, Won-Jung,Kang, Yoon-Joong,Jung, Young-Mi,Kang, Young-Mo,Suk, Kyoungho,Park, Jeong-Euy,Choi, Eun-Mi,Choi, Beom-Kyu,Kwon, Byoung S.,Lee, Won-Ha Federation of American Societies for Experimental 2006 Journal of Leukocyte Biology Vol.80 No.4
<P>Z39Ig is a transmembrane protein containing two Ig homology domains with unknown functions. Immunohistochemical analyses of human carotid atherosclerotic plaques detected Z39Ig staining in areas rich in foamy macrophages. Z39Ig staining was also observed in macrophages in the lining layers and sublining areas of rheumatoid arthritis synovium. Z39Ig staining in the osteoarthritis synovium was restricted to macrophages in the lining layers. To identify the role(s) of Z39Ig in the function of macrophages, we used human monocytic cell lines TF-1A (Z39Ig-negative) and THP-1 (Z39Ig-positive). The expression of Z39Ig was induced in TF-1A cells ,when they were differentiated into macrophages by treatment with PMA. The stimulation of PMA-treated TF-1A or THP-1 cells with immobilized anti-Z39Ig mAb induced the secretion of IL-8 and matrix metalloproteinase (MMP)-9, which was dependent on NF-kappaB activation. These data indicate that the macrophage Z39Ig is involved in the pathogenesis of inflammatory diseases through chemokine induction, which will promote the migration of inflammatory cells into the lesion area, and MMP-9 induction, which will contribute to cartilage destruction or extracellular matrix degradation.</P>
Serpentine Microstrip Lines With Zero Far-End Crosstalk for Parallel High-Speed DRAM Interfaces
Kyoungho Lee,Hae-Kang Jung,Hyung-Joon Chi,Hye-Jung Kwon,Jae-Yoon Sim,Hong-June Park IEEE 2010 IEEE TRANSACTIONS ON ADVANCED PACKAGING Vol.33 No.2
<P>Serpentine microstrip lines are proposed to eliminate the far-end crosstalk in parallel high-speed interfaces by increasing the capacitive coupling ratio to equal the inductive coupling ratio. Zero far-end crosstalk voltage waveform and zero crosstalk-induced jitter (CIJ) were achieved on an FR4 printed circuit board, by adjusting the unit section length of the serpentine structure. Application of the proposed serpentine microstrip lines to the 2-drop stub series terminated logic DRAM channel increased the maximum data rate from 0.9 to 1.4 Gb/s and reduced CIJ by ~ 78 ps at 3.3 Gb/s.</P>
Lee, Sang-Min,Kim, Eun-Ju,Suk, Kyoungho,Lee, Won-Ha Kluwer Academic/Plenum Publishers 2012 INFLAMMATION Vol.35 No.1
<P>FasL is a member of the tumor necrosis factor (TNF) superfamily involved in the various immune reactions such as activation-induced cell death, cytotoxic effector function, and establishment of immune privileged sites through its interaction with Fas. On the other hand, FasL is known to transmit a reverse signal that serves as a T cell co-stimulatory signal. However, the role of FasL-mediated reverse signaling in macrophage function has not been investigated. In order to investigate the presence of FasL-mediated signaling in macrophages, the human macrophage-like cell line THP-1 was analyzed after treatment with FasL ligating agents such as recombinant Fas:Fc fusion protein or anti-FasL monoclonal antibody. Stimulation of FasL induced the expression of proinflammatory mediators such as matrix metalloproteinase-9, TNF-α, and IL-8. The specificity of the reaction was confirmed by the transfection of the FasL-specific siRNAs, which suppressed FasL expression as well as the production of proinflammatory mediators. Utilization of various inhibitors of signaling adaptors and ELISA-base nuclear factor (NF)-κB binding assay demonstrated that the signaling initiated from FasL is mediated by mitogen-activated protein kinases including extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase which induce subsequent activation of NF-κB. These data indicate that membrane expression of FasL and its interaction with its counterpart may contribute to the inflammatory activation of macrophages during immune reactions or pathogenesis of chronic inflammatory diseases.</P>
Kyoungho Lee,Hyun-Bae Lee,Hae-Kang Jung,Jae-Yoon Sim,Hong-June Park IEEE 2008 IEEE TRANSACTIONS ON ADVANCED PACKAGING Vol.31 No.4
<P>A serpentine guard trace is proposed to reduce the peak far-end crosstalk voltage and the crosstalk induced timing jitter of parallel microstrip lines on printed circuit boards. The vertical sections of the serpentine guard increase the mutual capacitance without much changing the mutual inductance between the aggressor and victim lines. This reduces the difference between the capacitive and inductive couplings and hence the far-end crosstalk. Comparison with the no guard, the conventional guard, and the via-stitch guard shows that the serpentine guard gives the smallest values in both the peak far-end crosstalk voltage and the timing jitter. The time domain reflectometer (TDR) measurement shows that the peak far-end crosstalk voltage of serpentine guard is reduced to 44% of that of no guard. The eye diagram measurement of pseudo random binary sequence (PRBS) data shows that the timing jitter is also reduced to 40% of that of no guard.</P>
Regulation by lipocalin‐2 of neuronal cell death, migration, and morphology
Lee, Shinrye,Lee, Won‐,Ha,Lee, Myung‐,Shik,Mori, Kiyoshi,Suk, Kyoungho Wiley Subscription Services, Inc., A Wiley Company 2012 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.90 No.3
<P><B>Abstract</B></P><P>A secreted protein, lipocalin‐2 (LCN2), has been previously shown to regulate a variety of cellular phenotypes such as cell death, migration, and morphology. The role of LCN2, however, appears to be different depending on the cellular context. Here, we investigated how LCN2 influences neuronal phenotypes by using primary cortical neuronal cell cultures and neuroblastoma cell lines as a model. When exposed to LCN2 protein, neurons and neuroblastoma cells were sensitized to cell death evoked by nitric oxide, oxidative stress, and tumor necrosis factor‐α (TNF‐α). A forced expression of <I>lcn2</I> in glia enhanced neuronal cell death in cocultures of glia and neurons, indicating that both exogenous protein addition and endogenous expression of <I>lcn2</I> give rise to similar results. Iron and BCL2‐interacting mediator of cell death (BIM) protein were involved in LCN2‐induced cell death sensitization, based on the studies using iron donor, chelator, siderophore, and short hairpin RNA (shRNA)‐mediated knockdown of <I>bim</I> expression. Furthermore, cell migration assay and immunofluorescence microscopic observation revealed that LCN2 accelerated neuronal motility and process extension, suggesting multiple roles for LCN2 in the regulation of neuronal cell death, migration, and morphology. © 2011 Wiley Periodicals, Inc.</P>