http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
탁한호,이병로,김병철,전중창,황석순,정민우 진주산업대학교 산업과학기술연구소 2003 산업과학기술연구소보 Vol.- No.10
In this paper, applications of adaptive fuzzy controller to position control of flexible beam are considered. When a flexible beam is rotated by a motor through the fixed end, transverse vibration may occur. The architecture and learning underlying adaptive networks based fuzzy inference system (ANFIS) is presented, which is a fuzzy inference system implemented in the framework of adaptive networks. By using a hybrid learning procedure, the proposed ANFIS can construct an input-output mapping based on both human knowledge and stipulated input-output data pairs. Therefor, a dynamic model for a flexible beam is derived, and then a comparative analysis was made with before learning and after learning adaptive fuzzy controller through an simulation. The results are presented to illustrate the advantages and improved performance of the proposed position control cver the after learning adaptive fuzzy controller.
Effects of <i> Cymbidium</i> Root Ethanol Extract on Atopic Dermatitis
Kim, Wan-Joong,Cha, Hae-Sim,Lee, Myung-Hun,Kim, Sun-Young,Kim, Seo Ho,Kim, Tack-Joong Hindawi Publishing Corporation 2016 Evidence-based Complementary and Alternative Medic Vol.2016 No.-
<P><I>Cymbidium</I> has known antibacterial and antiedema activity and has been used as an ingredient in cosmetics and fragrances. The effects of<I> Cymbidium</I> ethanol extract (CYM) on allergic response and the underlying mechanisms of action have not been reported. Therefore, the purpose of this study was to determine the effect of CYM on allergic responses. Topical application of CYM was effective against immunoglobulin E (IgE)/dinitrophenyl-conjugated bovine serum albumin- (DNP-BSA-) induced degranulation of RBL-2H3 cells and anaphylaxis in ICR mice. An allergic dermatitis-like mouse model was used to evaluate the therapeutic potential of CYM<I> in vivo. </I>Continuous application of 2,4-dinitrochlorobenzene (DNCB) not only induced dermatitis in ICR mice but also aggravated the skin lesioning. However, the application of CYM decreased skin lesion severity, scratching behavior, and IgE levels. In addition, CYM downregulated the expression of the proinflammatory cytokines interleukin- (IL-) 4, IL-13, and tumor necrosis factor- (TNF-) <I>α</I>. Studies of signal transduction pathways showed that CYM suppressed the phosphorylation of spleen tyrosine kinase (Syk), an upstream molecule. It also inhibited the phosphorylation of Akt, phospholipase C- (PLC-) <I>γ</I>, and mitogen-activated protein kinase kinase kinase (MEKK). These results indicate that CYM may be effective in preventing and reducing allergic response and may have therapeutic potential as an antiallergic agent in disorders such as atopic dermatitis.</P>
Kim, Seo Ho,Kim, Eok-Cheon,Kim, Wan-Joong,Lee, Myung-Hun,Kim, Sun-Young,Kim, Tack-Joong Taylor & Francis 2016 Bioscience, Biotechnology, and Biochemistry Vol. No.
<P>Angiogenesis, neovascularization from pre-existing vessels, is a key step in tumor growth and metastasis, and anti-angiogenic agents that can interfere with these essential steps of cancer development are a promising strategy for human cancer treatment. In this study, we characterized the anti-angiogenic effects of Coptis japonica Makino extract (CJME) and its mechanism of action. CJME significantly inhibited the proliferation, migration, and invasion of vascular endothelial growth factor (VEGF)-stimulated HUVECs. Furthermore, CJME suppressed VEGF-induced tube formation in vitro and VEGF-induced microvessel sprouting ex vivo. According to our study, CJME blocked VEGF-induced cell cycle transition in G1. CJME decreased expression of cell cycle-regulated proteins, including Cyclin D, Cyclin E, Cdk2, and Cdk4 in response to VEGF. Taken together, the results of our study indicate that CJME suppresses VEGF-induced angiogenic events such as proliferation, migration, and tube formation via cell cycle arrest in G1.</P>
Kim, Heejin,Kim, So Young,Kim, Yoon-Joong,Ko, Jae-mun,Park, Min Ji,Kim, Ji Hoon,Hah, J. Hun,Kwon, Tack-Kyun,Kim, Kwang Hyun,Sung, Myung-Whun Elsevier 2018 Auris, nasus, larynx Vol.45 No.4
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>The purpose of this study was to correlate the CT imaging features and histopathological findings of pleomorphic adenomas (PA), and also try to identify its clinical significance.</P> <P><B>Methods</B></P> <P>Totally 262 PAs in the parotid gland including 18 recurrent cases were retrospectively reviewed with preoperative CT and pathologic slides. Each pathologic slide was reviewed by two pathologists to calculate mean value of epithelial/mesenchymal component, and the results were correlated with features of CT scans.</P> <P><B>Results</B></P> <P>PAs showing high contrast enhancement were correlated with high proportion of epithelial components in histopathologic findings. PAs with smooth border tend to have high proportion of epithelial components. The margin on CT imaging did not consisted with pathologic margin of resected specimens. In recurrent PAs, there was a significant difference on CT contrast enhancement, not in proportion of epithelial component.</P> <P><B>Conclusion</B></P> <P>The histopathology and CT imaging features of PAs were variable, but we can find the correlation of epithelial component and CT contrast enhancement. Further large scale study would be expected to identify the clinical significance of CT imaging features and histopathologic findings of PAs.</P>
Antiangiogenic Activity of <i>Acer tegmentosum</i> Maxim Water Extract in Vitro and in Vivo
Kim, Eok-Cheon,Kim, So Hun,Piao, Shan-Ji,Kim, Tack-Joong,Bae, Kiho,Kim, Han Sung,Hong, Soon-Sun,Lee, Byoung Ick,Nam, Moonsuk The Korean Academy of Medical Sciences 2015 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.30 No.7
Kim, Tack-Joong,Yun, Yeo-Pyo Pharmaceutical Society of Japan 2007 Biological & pharmaceutical bulletin Vol.30 No.1
<P>Atherosclerosis, a disease of the large arteries, is the primary cause of heart disease and stroke. The abnormal proliferation of vascular smooth muscle cells (VSMCs) in arterial walls is an important pathogenetic factor of vascular disorders like atherosclerosis and restenosis after angioplasty. In the present study, the possible anti-proliferative effect of a synthetic 1,4-naphthoquinone derivative, 2-chloro-3-(4-hexylphenyl)-amino-1,4-naphthoquinone (NQ304) was investigated on rat aortic VSMCs. NQ304 was shown to potently inhibit 5% fetal bovine serum (FBS)-induced the growth of VSMCs. Pre-treatment of VSMCs with NQ304 (1—10 μ<SMALL>M</SMALL>) for 24 h resulted in significant cell number decreases, <I>i.e.</I>, inhibition percentages were 44.75±10.77, 73.85±6.38 and 89.77±6.52% at NQ304 concentrations of 1, 5 and 10 μ<SMALL>M</SMALL>, respectively. NQ304 was also found to significantly inhibit 5% FBS-induced DNA synthesis in a concentration-dependent manner. Furthermore, NQ304 elevated p21<SUP>cip1</SUP> and p27<SUP>kip1</SUP> mRNA levels and caused G<SUB>0</SUB>/G<SUB>1</SUB> phase arrest in cell cycle progression. However, no evidence of NQ304-induced apoptotic or necrotic cell death was obtained, as determined by flow cytometery analysis and DNA fragmentation assays. To investigate the mechanism underlying the anti-proliferative effect of NQ304, we examined the effects of NQ304 on c-fos mRNA expression, activator protein-1 (AP-1) binding activity and extracellular signal-regulated kinase1/2 (ERK1/2) and Akt activation. Pre-treatment of VSMCs with NQ304 (1—10 μ<SMALL>M</SMALL>) was found to significantly inhibit the 5% FBS-induced phosphorylations of ERK1/2 and Akt, the activation of AP-1 and the expression of c-fos. These data suggest that the anti-proliferative and cell cycle arresting effects of NQ304 on serum-induced VSMCs may be mediated by AP-1 activation downregulation <I>via</I> the suppression of phosphatidylinositol 3-kinase (PI3K)/Akt and ERK1/2 signaling pathways, and it may contribute to the prevention of atherosclerosis through inhibition of VSMC proliferation.</P>
Kim, Tack-Joong,Han, Hyeong-Jun,Jung, Jae-Chul,Oh, Seikwan,Yun, Yeo-Pyo The Pharmaceutical Society of Japan 2011 Journal of Health Science Vol.57 No.1
<P>One of the principal regulators of mitogenesis in vascular smooth muscle cells (VSMCs) is platelet-derived growth factor-BB (PDGF-BB). An increase of PDGF-BB expression has been observed in atherosclerotic lesions. The aim of this study was to elucidate the effects and molecular mechanism of (2E)-3-(4-hydroxy-3-methoxyphenyl) phenylpro-2-en-1-one (KTJ2242), a newly synthesized benzylideneacetophenone derivative, on PDGF-BB-stimulated rat aortic VSMCs. KTJ2242 induced accumulation of cells in the G1 phase of the cell cycle of VSMCs. We observed that KTJ2242 inhibited PDGF-BB-stimulated [<SUP>3</SUP>H]-thymidine incorporation into the DNA of VSMCs, and the cell number was significantly reduced in a concentration-dependent manner. Also, we observed that KTJ2242 decreased PDGF-BB-stimulated extracellular-regulated kinase 1 and 2 (ERK1/2) and Akt phosphorylation. These results suggest the possibility that KTJ2242 may be a potential agent with which to control vascular disorders and its antiproliferative mechanism may be mediated through partial Akt and ERK1/2-dependent signaling pathways.</P>
Kim, Tack-Joong,Han, Hyeong-Jun,Kim, Yong-Jae,Jung, Jae-Chul,Yu, Ji-Yeon,Lee, Jung-Jin,Yun, Yeo-Pyo Pharmaceutical Society of Japan 2010 Biological & pharmaceutical bulletin Vol.33 No.5
<P>Benzylideneacetophenone analogues are known to have several significant biological activities, including antiinflammatory, antitumor, antibacterial, antiviral, and gastric-protective activities. However, the antiproliferative effects of benzylideneacetophenone analogues on vascular smooth muscle cells (VSMCs) are unknown. The aim of this study was to elucidate the antiproliferative effects and molecular mechanism of BST406, a newly synthesized benzylideneacetophenone derivative, on platelet-derived growth factor (PDGF)-BB-stimulated rat aortic VSMCs. BST406 inhibited [<SUP>3</SUP>H]-thymidine incorporation into DNA in VSMCs following treatment with PDGFBB 25 ng/ml. PDGF-BB-stimulated DNA synthesis was significantly reduced. Moreover, pretreatment with BST406 (0—10μ<SMALL>M</SMALL>) suppressed the proliferation of PDGF-BB-stimulated cells in a concentration-dependent manner. We also investigated the mechanism of the antiproliferative effects of BST406 in PDGF-BB-stimulated VSMCs. In Western blot analysis, PDGF-BB-stimulated (25 ng/ml) phospholipase-C (PLC)γ1 and Akt phosphorylation was inhibited by BST406 (0—10μ<SMALL>M</SMALL>). However, BST406 did not inhibit the PDGF-receptor β-chain (PDGF-Rβ) and extracellular-regulated kinase 1 and 2 (ERK1/2) phosphorylation induced by PDGF-BB. To confirm that the inhibitory effects of BST406 are mediated through the inhibition of PLCγ1 or Akt, the effects of inhibitors on cell viability were examined. U73122 completely inhibited PDGF-BB-induced proliferation of VSMCs. However, LY294002 10μ<SMALL>M</SMALL> had no significant effects on PDGF-BB-induced proliferation. These findings suggest that the inhibitory effects of BST406 on the proliferation of PDGF-BB-stimulated VSMCs are mediated by suppression of the PLCγ1 signaling pathways. Our observations may explain, in part, the mechanistic basis for the prevention of cardiovascular disease (such as atherosclerosis and restenosis after coronary angioplasty) by BST406.</P>