• Title/Summary/Keyword: RasU

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A study on remote monitoring & diagnosis system for tower parting facility (기계식 주차설비 원격 고장감시 및 진단 시스템 구현)

  • Lee, W.T.;Cha, J.S.;Lee, J.J.;Kim, K.H.;Kim, B.U.
    • Proceedings of the KIEE Conference
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    • 2000.07d
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    • pp.3184-3186
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    • 2000
  • This paper describes the remote monitoring & diagnosis system of tower parking facilities. This system consists of central station, monitoring equipments and parking system control panel. The central station is developed under client/server architecture, and the monitoring systems are connected to central station by LAN using RAS constructed PSTN. This system offers real-time fault detection and data acquisition of tower parking system.

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The Phospholipase-Protein Kinase C-MEK-ERK Pathway is Essential in Mycobacteria-induced CCL3 and CCL4 Expression in Human Monocytes (사람 단핵구에서 결핵균에 의해 유도되는 CCL3 및 CCL4 발현에 대한 Phospholipase-Protein Kinase C-MEK-ERK 경로의 역할 분석)

  • Yang, Chul-Su;Song, Chang-Hwa;Jung, Saet-Byel;Lee, Kil-Soo;Kim, Su-Young;Lee, Ji-Sook;Shin, A-Rum;Oh, Jae-Hee;Kwon, Yu-Mi;Kim, Hwa-Jung;Park, Jeong-Kyu;Paik, Tae-Hyun;Jo, Eun-Kyeong
    • IMMUNE NETWORK
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    • v.5 no.4
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    • pp.237-246
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    • 2005
  • Background: Little information is available on the identification and characterization of the upstream regulators of the signal transduction cascades for Mycobacterium tuberculosis (M. tbc)-induced ERK 1/2 activation and chemokine expression. We investigated the signaling mechanisms involved in expression of CCL3 /MIP-1 and CCL4/MIP-1 in human primary monocytes infected with M. tbc. Methods: MAP kinase phosphorylation was determined using western blot analysis with specific primary antibodies (ERK 1/2, and phospho-ERK1/2), and the upstream signaling pathways were further investigated using specific inhibitors. Results: An avirulent strain, M. tbc H37Ra, induced greater and more sustained ERK 1/2 phosphorylation, and higher CCL3 and CCL4 production, than did M. tbc H37Rv. Specific inhibitors for mitogen-activated protein kinase (MAPK) kinase (MEK; U0126 and PD98059) significantly inhibited the expression of CCL3 and CCL4 in human monocytes. Mycobactetia-mediated expression of CCL3 and CCL4 was not inhibited by the Ras inhibitor manumycin A or the Raf-1 inhibitor GW 5074. On the other hand, phospholipase C (PLC) inhibitor (U73122) and protein kinase C (PKC)specific inhibitors ($G\ddot{o}6976$ and Ro31-8220) significantly reduced M. tbc-induced activation of ERK 1/2 and chemokine synthesis. Conclusion: These results are the first to demonstrate that the PLC-PKC-MEK-ERK, not the Ras-Raf-MEK-ERK, pathway is the major signaling pathway inducing M. tbc-mediated CCL3 and CCL4 expression in human primary monocytes.

Identification of Differentially Expressed Genes by TCDD in Human Bronchial Cells: Toxicogenomic Markers for Dioxin Exposure

  • Park, Chung-Mu;Jin, Kyong-Suk;Lee, Yong-Woo
    • Biomedical Science Letters
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    • v.18 no.1
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    • pp.1-9
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    • 2012
  • Differentially expressed genes by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were identified in order to evaluate them as dioxin-sensitive markers and crucial signaling molecules to understand dioxin-induced toxic mechanisms in human bronchial cells. Gene expression profiling was analyzed by cDNA microarray and ten genes were selected for further study. They were cytochrome P450, family 1, subfamily B, polypeptide 1 (CYP1B1), S100 calcium binding protein A8 (calgranulin A), S100 calcium binding protein A9 (calgranulin B), aldehyde dehydrogenase 1 family, member A3 (ALDH6) and peroxiredoxin 5 (PRDX5) in up-regulated group. Among them, CYP1B1 was used as a hallmark for dioxin and sharply increased by TCDD exposure. Down-regulated genes were IK cytokine, interferon-induced protein with tetratricopeptide repeats 1 (IFIT1), nuclease sensitive element binding protein 1 (NSEP1), protein tyrosine phosphatase type VI A, member 1 (PTP4A1), ras oncogene family 32 (RAB32). Although up-regulated 4 genes in microarray were coincided with northern hybridization, down-regulated 5 genes showed U-shaped expression pattern which is sharply decreased at lower doses and gradually increased at higher doses. These results introduce some of TCDD-responsive genes can be sensitive markers against TCDD exposure and used as signaling cues to understand toxicity initiated by TCDD inhalation in pulmonary tissues.

Lysophosphatidic acid increases mesangial cell proliferation in models of diabetic nephropathy via Rac1/MAPK/KLF5 signaling

  • Kim, Donghee;Li, Hui Ying;Lee, Jong Han;Oh, Yoon Sin;Jun, Hee-Sook
    • Experimental and Molecular Medicine
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    • v.51 no.2
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    • pp.9.1-9.10
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    • 2019
  • Mesangial cell proliferation has been identified as a major factor contributing to glomerulosclerosis, which is a typical symptom of diabetic nephropathy (DN). Lysophosphatidic acid (LPA) levels are increased in the glomerulus of the kidney in diabetic mice. LPA is a critical regulator that induces mesangial cell proliferation; however, its effect and molecular mechanisms remain unknown. The proportion of ${\alpha}-SMA^+/PCNA^+$ cells was increased in the kidney cortex of db/db mice compared with control mice. Treatment with LPA concomitantly increased the proliferation of mouse mesangial cells (SV40 MES13) and the expression of cyclin D1 and CDK4. On the other hand, the expression of $p27^{Kip1}$ was decreased. The expression of $Kr{\ddot{u}}ppel$-like factor 5 (KLF5) was upregulated in the kidney cortex of db/db mice and LPA-treated SV40 MES13 cells. RNAi-mediated silencing of KLF5 reversed these effects and inhibited the proliferation of LPA-treated cells. Mitogen-activated protein kinases (MAPKs) were activated, and the expression of early growth response 1 (Egr1) was subsequently increased in LPA-treated SV40 MES13 cells and the kidney cortex of db/db mice. Moreover, LPA significantly increased the activity of the Ras-related C3 botulinum toxin substrate (Rac1) GTPase in SV40 MES13 cells, and the dominant-negative form of Rac1 partially inhibited the phosphorylation of p38 and upregulation of Egr1 and KLF5 induced by LPA. LPA-induced hyperproliferation was attenuated by the inhibition of Rac1 activity. Based on these results, the Rac1/MAPK/KLF5 signaling pathway was one of the mechanisms by which LPA induced mesangial cell proliferation in DN models.

Effects of Baicalin on Gene Expression Profiles during Adipogenesis of 3T3-L1 Cells (3T3-L1 세포의 지방세포형성과정에서 Baicalin에 의한 유전자 발현 프로파일 분석)

  • Lee, Hae-Yong;Kang, Ryun-Hwa;Chung, Sang-In;Cho, Soo-Hyun;Yoon, Yoo-Sik
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.39 no.1
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    • pp.54-63
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    • 2010
  • Baicalin, a flavonoid, was shown to have diverse effects such as anti-inflammatory, anti-cancer, anti-viral, anti-bacterial and others. Recently, we found that the baicalin inhibits adipogenesis through the modulations of anti-adipogenic and pro-adipogenic factors of the adipogenesis pathway. In the present study, we further characterized the molecular mechanism of the anti-adipogenic effect of baicalin using microarray technology. Microarray analyses were conducted to analyze the gene expression profiles during the differentiation time course (0 day, 2 day, 4 day and 7 day) in 3T3-L1 cells with or without baicalin treatment. We identified a total of 3972 genes of which expressions were changed more than 2 fold. These 3972 genes were further analyzed using hierarchical clustering analysis, resulting in 20 clusters. Four clusters among 20 showed clearly up-regulated expression patterns (cluster 8 and cluster 10) or clearly down-regulated expression patterns (cluster 12 and cluster 14) by baicalin treatment for over-all differentiation period. The cluster 8 and cluster 10 included many genes which enhance cell proliferation or inhibit adipogenesis. On the other hand, the cluster 12 and cluster 14 included many genes which are related with proliferation inhibition, cell cycle arrest, cell growth suppression or adipogenesis induction. In conclusion, these data provide detailed information on the molecular mechanism of baicalin-induced inhibition of adipogenesis.

An Analysis of the Economic Effects for the Immersive Media Industry (실감미디어 산업의 경제적 파급효과 분석)

  • Lee, Kyoung-Jae;Jeong, Woo-Soo
    • The Journal of Korean Institute of Communications and Information Sciences
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    • v.36 no.7B
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    • pp.795-805
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    • 2011
  • The research on the immersive media technology is actively being done with the emergence of immersive services using immersive media, especially in the broadcasting industry and with the increased market demand for it. The industry which produces, transmits, processes and services the immersive contents is commonly called Immersive Media Industry. Immersive Media Industry has recently received attention as next-generation strategic industry with its high marketability and its high possibility of market expansion through convergence with other industry such as education, health, advertisement, travel and public service industry. As other advanccd country such as the U.S., Japan and Europe buckle down to take the innitiative in the immersive media industry, Korea government also begins to make plan to promote the immersive media industry. As above, immersive media industry is a cutting-edge convergence industry which embraces broadcasting, telecommunication and contents industry and it is rising as core growth engine industry. This article analyses the economic effects of immersive media industry through quantatitive method and evaluates the relations between the immersive media industry and the other related industries. As a result, the effect on production inducement of immersive media industry is 610.9 billion Korean Won; the effect on value-added inducement is 468.7 billion Korean Won; and it is measured that 3,258 job will be created by the immersive media industry.