• Title/Summary/Keyword: Up-Regulation

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국내 상호접속료 산정방식의 문제점 분석

  • Yang, Won-Seok;Jeong, Ji-Hyeong
    • Proceedings of the Korea Database Society Conference
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    • 2010.06a
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    • pp.181-185
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    • 2010
  • The current method for accessing interconnection charges in Korea, called a hybrid model in this paper, mixes a top-down with a bottom-up LRIC model. The method has given stable charges so far. However, according to the fundamental changes of the market, policy, and network technology in the telecommunications industry, it requires analyzing the validity of the method. We investigate the problems of the top-clown, bottom-up, and hybrid model used in Korea and analyze their effect on regulation policy.

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The Effect of Gongjin-dan on Gliosis in Middle Cerebral Artery Occlusion (MCAO) Rats (공진단이 MCAO모델 흰쥐에서 gliosis 억제에 마치는 영향)

  • Seong, Kee-Moon;Hae, Rae-Kyong;Song, Bong-Keun
    • The Journal of Internal Korean Medicine
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    • v.30 no.4
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    • pp.674-684
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    • 2009
  • Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes a physical and a mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. This study was undertaken to examine the effect of the Gongjin-dan (GJD) on CD81 and GFAP expression and its pathway in the rat brain following middle cerebral artery occlusion (MCAO). Methods : In order to study ischemic injuries on the brain, infarction was induced by MCAO using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Also, c-Fos and ERK expression were measured to investigate the signaling pathway after GJD administration in MCAO rats. Results : Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size had decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GF AP expression in the MCAO rat. GJD administration decreased CD81 expression in the MCAO rat. GJD administration induced up-regulation of c-FOS expression compared with MCAO. GJD administration induced down-regulation of ERK expression compared with MCAO. Conclusion : We observed that GJD could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of a rat with cerebral infarction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the regulation of c-Fos and ERK. These results suggest that GJD can be a candidate to regenerate CNS injury.

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Effect of Duloxetine in Functional Gastrointestinal Disorder : In the Perspective of 'Brain-Gut Axis' (기능성 위장관 장애에서 Duloxetine의 효과 : '뇌-장관 축' 모델을 중심으로)

  • Lee, Sang-Shin;Park, Si-Sung
    • Korean Journal of Psychosomatic Medicine
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    • v.20 no.2
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    • pp.135-138
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    • 2012
  • The pathophysiology of functional gastrointestinal disorder(FGID) is not completely understood, but the importance of the 'Brain-Gut Axis(BGA)' model in FGID is being increasingly recognized. The BGA model is a bidirectional, hard-wired and homeostatic relationship between the central nervous system(CNS) and the enteric nervous system(ENS) via neural, neurohormonal and neuroimmunological pathways. In addition, the BGA model would provide a rationale for the use of psychotropics on FGID. The authors experienced two cases in which duloxetine, a serotonin-norepinephrine reuptake inhibitor, was effective in relieving FGID symptoms as well as psychiatric symptoms such as depression and hypochondriacal anxiety. Therefore we discuss the vignettes from the perspective of BGA theory. Duloxetine showed efficacy in these two patients by reducing visceral hypersensivity (bottom-up regulation) and by relieving depression and anxiety(top-down regulation).

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HY253, a Novel Decahydrofluorene Analog, Induces Apoptosis via Intrinsic Pathway and Cell Cycle Arrest in Liver Cancer HepG2 Cells

  • Choi, Ko-woon;Suh, Hyewon;Jang, Seunghun;Kim, Dongsik;Lee, Chul-Hoon
    • Journal of Microbiology and Biotechnology
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    • v.25 no.3
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    • pp.413-417
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    • 2015
  • Recently, we isolated HY253, a novel decahydrofluorene analog with a molecular structure of 7,8a-divinyl-2,4a,4b,5,6,7,8,8a,9,9a-decahydro-1H-fluorene-2,4a,4b,9a-tetraol from the roots of Aralia continentalis, which is known as Dokwhal (獨活), a traditional medicinal herb. Moreover, we previously reported its cytotoxic activity on cancer cell proliferation in human lung cancer A549 and cervical cancer HeLa cells. The current study aimed to evaluate its detailed molecular mechanisms in cell cycle arrest and apoptotic induction in human hepatocellular carcinoma HepG2 cells. Flow cytometric analysis of HepG2 cells treated with $60{\mu}M$ HY253 revealed appreciable cell cycle arrest at the G1 phase via inhibition of Rb phosphorylation and down-regulation of cyclin D1. Furthermore, using western blots, we found that up-regulation of cyclin-dependent kinase inhibitors, such as p21CIP1 and p27KIP1, was associated with this G1 phase arrest. Moreover, TUNEL assay and immunoblottings revealed apoptotic induction in HepG2 cells treated with $60{\mu}M$ HY253 for 24 h, which is associated with cytochrome c release from mitochondria, via down-regulation of anti-apoptotic Bcl-2 protein, which in turn resulted in activation of caspase-9 and -3, and proteolytic cleavage of poly(ADP-ribose) polymerase (PARP). Accordingly, we suggest that HY253 may be a potent chemotherapeutic hit compound for treating human liver cancer cells via up-regulation and activation of the p53 gene.

Transcriptional Alteration of p53 Related Processes As a Key Factor for Skeletal Muscle Characteristics in Sus scrofa

  • Kim, Seung-Soo;Kim, Jung-Rok;Moon, Jin-Kyoo;Choi, Bong-Hwan;Kim, Tae-Hun;Kim, Kwan-Suk;Kim, Jong-Joo;Lee, Cheol-Koo
    • Molecules and Cells
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    • v.28 no.6
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    • pp.565-573
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    • 2009
  • The pig could be a useful model to characterize molecular aspects determining several delicate phenotypes because they have been bred for those characteristics. The Korean native pig (KNP) is a regional breed in Korea that was characterized by relatively high intramuscular fat content and reddish meat color compared to other western breeds such as Yorkshire (YS). YS grew faster and contained more lean muscle than KNP. We compared the KNP to Yorksire to find molecular clues determining muscle characteristics. The comparison of skeletal gene expression profiles between these two breeds showed molecular differences in muscle. We found 82 differentially expressed genes (DEGs) defined by fold change (more than 1.5 fold difference) and statistical significance (within 5% of false discovery rate). Functional analyses of these DEGs indicated up-regulation of most genes involved in cell cycle arrest, down-regulation of most genes involved in cellular differentiation and its inhibition, down-regulation of most genes encoding component of muscular-structural system, and up-regulation of most genes involved in diverse metabolism in KNP. Especially, DEGs in above-mentioned categories included a large number of genes encoding proteins directly or indirectly involved in p53 pathway. Our results indicated a possible role of p53 to determine muscle characteristics between these two breeds.

In vivo anti-metastatic action of Ginseng Saponins is based on their intestinal bacterial metabolites after oral administration

  • Saiki, Ikuo
    • Journal of Ginseng Research
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    • v.31 no.1
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    • pp.1-13
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    • 2007
  • We found that the main bacterial metabolite M1 is an active component of orally administered protopanxadiol-type ginsenosides, and that the anti-metastatic effect by oral administration of ginsenosides may be primarily mediated through the inhibition of tumor invasion, migration and growth of tumor cells by their metabolite M1. Pharmacokinetic study after oral administration of ginsenoside Rb1 revealed that M1 was detected in serum for 24 h by HPLC analysis but Rb1 was not detected. M1, with anti-metastatic property, inhibited the proliferation of murine and human tumor cells in a time- and concentration-dependent manner in vitro, and also induced apoptotic cell death (the ladder fragmentation of the extracted DNA). The induction of apoptosis by M1 involved the up-regulation of the cyclin-dependent kinase(CDK) inhibitor $p27^{Kip1}$ as well as the down-regulation of a proto-oncogene product c-Myc and cyclin D1 in a time-dependent manner. Thus, M1 might cause the cell-cycle arrest (G1 phase arrest) in honor cells through the up/down-regulation of these cell-growth related molecules, and consequently induce apoptosis. The nucleosomal distribution of fluorescence-labeled M1 suggests that the modification of these molecules is induced by transcriptional regulation. Tumor-induced angiogenesis (neovascularization) is one of the most important events concerning tumor growth and metastasis. Neovascularization toward and into tumor is a crucial step for the delivery of nutrition and oxygen to tumors, and also functions as the metastatic pathway to distant organs. M1 inhibited the tube-like formation of hepatic sinusoidal endothelial (HSE) cells induced by the conditioned medium of colon 26-L5 cells in a concentration-dependent manner. However, M1 at the concentrations used in this study did not affect the growth of HSE cells in vitro.

Estragole Exhibits Anti-inflammatory Activity with the Regulation of NF-κB and Nrf-2 Signaling Pathways in LPS-induced RAW 264.7 cells

  • Roy, Anupom;Park, Hee-Juhn;Jung, Hyun Ah;Choi, Jae Sue
    • Natural Product Sciences
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    • v.24 no.1
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    • pp.13-20
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    • 2018
  • Estragole is a naturally occurring phenylpropanoid obtained from essential oils found in a broad diversity of plants. Although the phenylpropanoids show many biological activities, clear regulation of the inflammatory signaling pathways has not yet been determined. Here, we scrutinized the anti-inflammatory effect of estragole. The anti-inflammatory effect of estragole was determined through the inhibitory mechanisms of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), nuclear factor kappa B ($NF-{\kappa}B$), and mitogen-activated protein kinases (MAPK) pathways and the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2)/heme oxygenase (HO)-1 pathways in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Estragole significantly inhibited NO production, iNOS and COX-2 expression as well as LPS-induced $NF-{\kappa}B$ and MAPK activation. Furthermore, estragole suppressed LPS-induced intracellular ROS production but up-regulated the stress response gene HO-1 via the activation of transcription factor Nrf-2. These findings demonstrate that estragole inhibits the LPS-induced expression of inflammatory mediators via the down-regulation of iNOS, COX-2, $NF-{\kappa}B$, and MAPK pathways, as well as the up-regulation of the Nrf-2/HO-1 pathway, indicating that this phenylpropanoid has potential therapeutic and preventive applications in various inflammatory diseases.