• IMMUNE NETWORK
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• v.4 no.2
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• pp.116-122
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• 2004

Background: LIGHT (TNFSF14) is a member of tumor necrosis factor superfamily and is the ligand for TR2 (TNFRSF14/HVEM). LIGHT is known to have proinflammatory roles in atherosclerosis. Methods: To find out the expression pattern of LIGHT in atherosclerotic plaques, immunohistochemical analysis was performed on human carotid atherosclerotic plaque specimens. LIGHT induced atherogenic events using human monocytic cell line THP-1 were also investigated. Results: Immunohistochemical analysis revealed expression of LIGHT and TR2 in foam cell rich regions in the atherosclerotic plaques. Double immunohistochemical analysis further confirmed the expression of LIGHT in foam cells. Stimulation of THP-1 cells, which express TR2, with either recombinant LIGHT or immobilized anti-TR2 monoclonal antibody induced interleukin-8 and matrix metalloproteinase(MMP)-9. Electrophoretic mobility shift assay demonstrated that LIGHT induces nuclear localization of transcription factor, nuclear factor $(NF)-{\kappa}B$. LIGHT induced activation of MMP-9 is mediated by $NF-{\kappa}B$, since treatment of THP-1 cells with the $NF-{\kappa}B$ inhibitor PDTC (pyrrolidine dithiocarbamate) completely blocked the activation of MMP-9. Conclusion: These data indicate that LIGHT is expressed in foam cells in atherosclerotic plaques and is involved in atherogenesis through activation of pro-atherogenic cytokine IL-8 and destabilization of plaque by inducing matrix degrading enzyme.

• World Technopolis Review
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• v.4 no.3
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• pp.144-156
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• 2015

Globalization and knowledge-based economy have increased the importance of local areas as the units of global competition. Therefore, the meaning of localities has been emphasized as the core value of economic activities. In this context, innovation cluster has been recognised and emphasized as effective policy measure for innovation. Therefore, most countries have been trying to develop innovation clusters with their expectation for a rapid growth of economy. Nevertheless, there have been minimal empirical researches on innovation cluster. Therefore, for suggesting implications that activation factors of innovation cluster are to have an effect on tenant's business activities, this study conducted a literature review for the theories of regional innovation system(RIS) and innovation cluster. As a result, the activation factors of innovation cluster were classified into institutional, physicals, and social factor. The case of Gyeonggi province's innovation cluster policy was examined for an empirical analysis. Data were analyzed using ordered logistic regression. The results were as follows:First, Institutional and Infra factors had a positive influence on firms' business activities in every empirical test, so they were the most important activation factors of innovation cluster. Second, regarding the interactive effects of financial support, the interactive effects between financial support and Infra factor had a positive influence on the firms' business activities, according to the result of the empirical test.

• Animal cells and systems
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• v.7 no.3
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• pp.173-186
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• 2003

The transition metal cadmium is a serious occupational and environmental toxin. To inhibit cadmium-induced damage, cells respond by increasing the expression of genes that encode stress-responsive proteins. The metal-regulatory transcription factor 1 (MTF-1) is a key regulator of heavy-metal induced transcription of metallothionein-I and II and other genes in mammals and other metazoans. Transcriptional activation of genes by MTF-1 is mediated through binding to metal-responsive elements in the target gene promoters. Phosphorylation of MTF-1 plays a critical role in the cadmium-inducible transcriptional activation of metallothionein and other responses. Studies using inhibitors indicate that multiple kinases and signal transduction cascades, including those mediated by protein kinase C, tyrosine kinase and casein kinase II, are essential for cadmium-mediated transcriptional activation. In addition, calcium signaling is also involved in regulating metal-activated transcription. In several species, cadmium induces heat shock genes. Recently much progress has been made in elucidating the cellular machinery that regulates this metal-inducible gene expression. This review summarizes these recent advances in understanding the role of some known cadmium-responsive genes and the molecular mechanisms that activate metal-responsive transcription factor, MTF-1.

• Korean Journal of Plant Resources
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• v.33 no.6
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• pp.659-665
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• 2020

Adenophorae Radix (AR) has been used as a traditional medicine for various diseases. However, the regulatory mechanisms of AR in allergic inflammation are not yet understood. The present study was conducted to investigate the effect and mechanisms of AR on the mast cell-mediated allergic response. To determine the pharmacological mechanisms of AR in allergic inflammation, we evaluated the effects of AR on the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-8 as well as the activation of nuclear factor-κB (NF-κB) and caspase-1 in phorbol 12-myristate 13-acetate plus calcium ionophore A23187 (PMACI)-stimulated human mast cells (HMC-1). Our results demonstrated that AR effectively attenuated the PMACI-induced production of TNF-α, IL-6, IL-1β and IL-8 in stimulated HMC-1. Additionally, we showed that the inhibitory effect of AR on inflammatory cytokines in PMACI-stimulated HMC-1 cells involved the suppression of the activation NF-kB/caspase-1 in PMACI-stimulated HMC-1. Collectively, these findings provide experimental evidence that AR may be a useful candidate for the treatment of allergic inflammation.

• Molecules and Cells
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• v.28 no.5
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• pp.495-499
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• 2009

Although insulin-like growth factor-I (IGF-I) and androgen receptor (AR) are well known effectors of skeletal muscle, the molecular mechanism by which signaling pathways integrating AR and IGF-I in skeletal muscle cells has not been previously examined. In this study, the role of PI3K/Akt on IGF-I-induced gene expression and activation of AR in skeletal muscle cells was investigated. C2C12 cells were treated with IGF-I in the absence or presence of inhibitors of PI3K/Akt pathway (LY294002 and Wortmannin). Inhibition of the PI3K/Akt pathway with LY294002 or Wortmannin led to a significant decrease in IGF-I-induced AR phosphorylation and total AR protein expression. Furthermore, IGF-I-induced AR mRNA and skeletal ${\alpha}-actin$ mRNA were blocked by LY294002 or Wortmannin. Confocal images showed that IGF-I-induced AR translocation from cytosol to nucleus was inhibited significantly in response to treatment with LY294002 or Wortmannin. The present results suggest that modulating effect of IGF-I on AR gene expression and activation in C2C12 mouse skeletal muscle cells is mediated at least in part by the PI3K/Akt pathway.

• Journal of Industrial Convergence
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• v.13 no.2
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• pp.1-9
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• 2015

This Study aims to present the guidelines for the activation of the domestic GS certification market through the assessment of the characteristics of the demands of the domestic SW companies pursuing to acquire GS certification. As the results of the factor analysis of the guidelines for the activation of the domestic GS certification market, (1) strictness of the certification standards, (2) level of satisfaction on the certification services and (3) certification effects were deduced as the specific variables. This study is highly significant in that the fact that the certification market is more effectively activated when the 3 factors, namely, strictness of the certification standards, level of satisfaction on the certification services and certification effects, have been intensively reinforced although there exist countless number of specific variables including certification system, certification cost, certification expertise and certification marketing, etc. in order to activate GS certification market has been statistically verified.

• Biomedical Science Letters
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• v.27 no.4
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• pp.248-254
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• 2021

Ulcerative colitis (UC), chronic inflammatory bowel disease, is characterized by severe inflammation in the colon. Tea is one of the most popular beverages consumed worldwide. Pu-erh tea, a unique Chinese tea produced by microbial activities, possesses a broad range of health-promoting effects, including anti-aging, anti-Alzheimer's disease, antioxidation and anti-obesity. However, the inhibitory effect of Pu-erh tea on intestinal inflammation and the underlying mechanism remain unclear. The present study was designed to evaluate the regulatory effect of Pu-erh tea extract (PTE) on dextran sulfate sodium (DSS)-induced colitis clinical signs by analyzing the weight loss and colon length in mice. The inhibitory effects of PTE on inflammatory mediators, such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α, and the activation of nuclear factor-κB (NF-κB) were also determined in DSS-treated colitis tissue. We observed that PTE treatment significantly inhibited the DSS-induced clinical symptoms of weight loss, decrease,in colon length, and colon tissue damage in mice. Moreover, PTE attenuated the DSS-induced levels of IL-6 and TNF-α in colon tissue. We also demonstrated the anti-inflammatory mechanism of PTE by suppressing the activation of NF-κB in DSS-treated colon tissues. Collectively, the findings provide experimental evidence that PTE may be effective in preventing and treatment of intestinal inflammatory disorders, including UC.

• Molecules and Cells
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• v.28 no.3
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• pp.189-194
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• 2009

The modulating effect of IGF-I on the regulation of AR gene expression and activation in skeletal muscle cells remains poorly understood. In this study, the effects of IGF-I treatment on AR induction and activation in the absence of AR ligands were examined. Differentiating C2C12 cells were treated with different concentrations (0-250 ng/ml) of IGF-I or for various periods of time (0-60 min) of 250 ng/ml IGF-I. Treatment of C2C12 cells with IGF-I resulted in a dose- and time-dependent increase in total AR and phosphorylated AR (Ser 213). IGF-I treatment also led to significantly increased AR mRNA expression when compared with the control. The levels of skeletal ${\alpha}-actin$ and myogenin mRNA, known target genes of AR, were also significantly upregulated after 5 or 10 min of treatment with IGF-I. Confocal images revealed that IGF-I stimulated nuclear localization of AR in the absence of ligands. In addition, an electrophoretic mobility shift assay indicated that IGF-I stimulated the AR DNA binding activity in a time-dependent manner. The present results suggest that IGF-I stimulates the expression and activation of AR by ligand-independent mechanism in differentiating C2C12 mouse skeletal muscle cells.

• Applied Chemistry for Engineering
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• v.7 no.2
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• pp.356-361
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• 1996

Cure kinetics of diglycidyl ether of bisphenol A(DGEBA)/4,4'-methylene dianiline(MDA) with hydroquinone-phenyl glycidyl ether(HQ-PGE) as a reactive additive, which was preliminarily synthesized, was investigated by DSC and FT-IR analyses. Kissinger equation and Arrhenius' equation were used to calculate activation energy and pre-exponential factor. When HQ-PGE was added to DGEBA/MDA system, it reduced activation energy of system. When the 5 phr of HQ-PGE was added to DGEBA/MDA system, activation energy was 7.8 kcal/mol by FT-IR analysis and 11.3 kcal/mol by DSC, in comparison with the system without HQ-PGE, activation energy decreased about 30% and 9%, respectively. According to these results, HQ-PGE, introducing agent of this system, acted as a catalyst.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.5
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• pp.237-243
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• 2004

Glial cells are activated in neuropathy and play a key role in hyperalgesia and allodynia. This study was performed to determine whether minocycline could attenuate heat hyperalgesia and mechanical allodynia, and how glial cell activation and nuclear factor kappa B (NF-kappaB) were regulated by minocycline in a model of chronic constriction of sciatic nerve (CCl). When minocycline (50 mg/kg, oral) was daily administered from 1 day before to 9 days after ligation, heat hyperalgesia and mechanical allodynia were attenuated. Furthermore, when minocycline treatment was initiated 1 or 3 days after ligation, attenuation of the hypersensitive behavior was still robust. However, the effect of attenuation was less when minocycline was started from day 5. In order to elucidate the mechanism of pain attenuation by minocycline, we examined the changes of glia and NF-kappaB, and found that attenuated hyperalgesia and allodynia by minocycline was accompanied by reduced microglial activation. Furthermore, the number of NF-kappaB immunoreactive cells increased after CCI treatment and this increase was attenuated by minocycline. We also observed translocation of NF-kappaB into the nuclei of activated glial cells. These results suggest that minocycline inhibits activation of glial cells and NF-kappaB, thereby attenuating the development of behavioral hypersensitivity to stimuli.