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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.
Tack-Joong Kim,Jin-Ho Kim,Yong-Ri Jin,윤여표 대한약학회 2006 Archives of Pharmacal Research Vol.29 No.1
The abnormal proliferation of aortic vascular smooth muscle cells (VSMCs) plays a central role in the pathogenesis of atherosclerosis and restenosis after angioplasty and possibly also in the development of hypertension. The present study was designed to examine the inhibitory effects and the mechanism of luteolin 7-glucoside (L7G) on the platelet-derived growth factor (PDGF)-BB-induced proliferation of VSMCs. L7G significantly inhibited the PDGF-BB-induced proliferation and the DNA synthesis of the VSMCs in a concentration-dependent manner. Preincubation of the VSMCs with L7G significantly inhibited the PDGF-BB-induced extracellular signal-regulated kinase 1/2 (ERK1/2), Akt and the phospholipase C (PLC)-γ1 activation. However, L7G had almost no affect on the phosphorylation of PDGF-β receptor tyrosine kinase, which was induced by PDGF-BB. These results suggest that L7G inhibits the PDGFBB- induced proliferation of VSMCs via the blocking of PLC-γ1, Akt, and ERK1/2 phosphorylation.
Kim, Tack-Joong,Jeon, Jinseon,Jin, Yong-Ri,Son, Dong-Ju,Yoo, Hwan-Soo,Hong, Jin-Tae,Ryu, Chung-Kyu,Shin, Hwa-Sup,Lee, Kwang-Ho,Yun, Yeo-Pyo Raven Press 2007 Journal of cardiovascular pharmacology Vol.49 No.5
<P>Hyperproliferation of platelet-derived growth factor (PDGF)-BB-induced vascular smooth muscle cell (VSMC) is a hallmark of atherosclerosis and related vascular disorders. In the previous study, we reported that KTJ740 [2-chloro-3-(4-(ethylcarboxy)-phenyl)-amino-1,4-naphthoquinone], a newly synthesized vitamin K derivative, has potent antithrombotic effects in mice and antiplatelet activity in vitro and ex vivo. In the present study, we have tested that KTJ740 could inhibit PDGF-BB-stimulated VSMC proliferation. We have examined the potential inhibitory effect of this compound on rat aortic smooth muscle cells (RASMCs). Our results show that this compound significantly inhibits PDGF-BB-stimulated RASMC number and DNA synthesis in a concentration-dependent manner. Furthermore, we have examined its effect on cell cycle progression by flow cytometry. KTJ740 treatment resulted in a significant arrest in cell cycle progression of RASMCs induced by PDGF-BB, and this effect was achieved by suppressing activation of PDGF-beta receptor (PDGF-Rbeta) tyrosine kinase pathway. These results suggest that a possibility of KTJ740 can be a potential agent to control vascular disorders and its antiproliferative mechanism may be mediated through PDGF-Rbeta tyrosine kinase-dependent signaling pathway.</P>
Kim, Tack-Joong,Han, Hyeong-Jun,Hong, Seong-Su,Hwang, Ji-Hye,Hwang, Bang-Yeon,Yoo, Hwan-Soo,Jin, Yong-Ri,Lee, Jung-Jin,Yu, Ji-Yeon,Lee, Kwang-Ho,Kang, Byoung-Won,Yun, Yeo-Pyo Pharmaceutical Society of Japan 2007 Biological & pharmaceutical bulletin Vol.30 No.4
<P>Platelet derived growth factor (PDGF)-BB is one of the most potent vascular smooth muscle cell (VSMC) proliferative factors, and abnormal VSMC proliferation by PDGF-BB plays an important role in the development and progression of cardiovascular problems, including restenosis after coronary angioplasty and atherosclerosis. Previous phytochemical studies on the stems or root barks of <I>Cudrania tricuspidata</I> (Moraceae) resulted in the isolation of various isoprenylated xanthones and flavonoids, some of which have anti-cancer, hepatoprotective, anti-inflammatory and anti-oxidant activities. In the present study, we investigated the antiproliferative effect of cudratricusxanthone A isolated from the root bark of <I>C. tricuspidata</I> and its underlying mechanism in VSMCs. Antiproliferative effects of cudratricusxanthone A on VSMCs were examined by direct cell counting and [<SUP>3</SUP>H]-thymidine incorporation assays. Cudratricusxanthone A inhibited [<SUP>3</SUP>H]-thymidine incorporations into DNA in VSMCs that occurred in response to treatment with 50 ng/ml PDGF-BB. PDGF-BB-stimulated DNA synthesis was significantly reduced to 86.1, 80.2, 64.2 and 25.1% at concentrations of 0.1, 1, 2 and 3 μ<SMALL>M</SMALL>, respectively. Moreover, pre-treatment with cudratricusxanthone A (0.1—3 μ<SMALL>M</SMALL>) suppressed this PDGF-BB-stimulated cell number in a concentration-dependent manner. The inhibition percentages were 11.1, 22.7, 51.3 and 81.5% at the concentrations of 0.1, 1, 2 and 3 μ<SMALL>M</SMALL>, respectively. We also investigated the mechanism of antiproliferative effects by cudratricusxanthone A in PDGF-BB-stimulated VSMCs. In Western blot analysis, 50 ng/ml PDGF-BB-stimulated phospholipase C (PLC)γ1, Ras, and extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylations were inhibited by cudratricusxanthone A (0.1—3 μ<SMALL>M</SMALL>). Consisted with these findings, cudratricusxanthone A inhibited PDGF-receptor β chain (PDGF-Rβ) phosphorylation induced by PDGF-BB in a concentration-dependent manner. These findings suggest that the inhibitory effects of cudratricusxanthone A on DNA synthesis and proliferation by PDGF-BB-stimulated VSMCs are mediated by the suppressions of the PDGF-Rβ and its downstream signaling pathways. Our observation may explain in part mechanistic basis for the prevention of cardiovascular diseases, such as atherosclerosis and restenosis after coronary angioplasty by cudratricusxanthone A.</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,Kim, Jin-Ho,Jin, Yong-Ri,Yun, Yeo-Pyo The Pharmaceutical Society of Korea 2006 Archives of Pharmacal Research Vol.29 No.1
The abnormal proliferation of aortic vascular smooth muscle cells (VSMCs) plays a central role in the pathogenesis of atherosclerosis and restenosis after angioplasty and possibly also in the development of hypertension. The present study was designed to examine the inhibitory effects and the mechanism of luteolin 7-glucoside (L7G) on the platelet-derived growth factor (PDGF)-BB-induced proliferation of VSMCs. L7G significantly inhibited the PDGF-BB-induced proliferation and the DNA synthesis of the VSMCs in a concentration-dependent manner. Pre-incubation of the VSMCs with L7G significantly inhibited the PDGF-BB-induced extracellular signal-regulated kinase 1/2 (ERK1/2), Akt and the phospholipase C $(PLC)-{\gamma}1$ activation. However, L7G had almost no affect on the phosphorylation of $PDGF-{\beta}$ receptor tyrosine kinase, which was induced by PDGF-BB. These results suggest that L7G inhibits the PDGF-BB-induced proliferation of VSMCs via the blocking of $(PLC)-{\gamma}1$, Akt, and ERK1/2 phosphorylation.