• Molecules and Cells
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• v.26 no.5
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• pp.468-473
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• 2008

Low-density lipoprotein (LDL) induces cell proliferation in human aortic smooth muscle cells (hAoSMCs), which may be involved in atherogenesis and intimal hyperplasia. Recent studies have demonstrated that $Cl^-$ channels are related to vessel cell proliferation induced by a variety of stimuli. In this study, we investigated a potential role of $Cl^-$ channels in the signaling pathway of LDL effects on hAoSMC proliferation with a focus on the activation of Erk1/2-PI3K/Akt and the subsequent upregulation of Egr-1. $Cl^-$ channel blockers, DIDS, but neither NPPB nor Furosemide, completely abolished the LDL-induced DNA synthesis and cell proliferation. Moreover, DIDS, but not NPPB, significantly decreased LDL-stimulated $Cl^-$ concentration, as judged by flow cytometry analysis using MQAE as a $Cl^-$-detection dye. DIDS pretreatment completely abolished the activation of Erk1/2 and PI3K/Akt in a dose-dependent manner that is the hallmark of LDL activation, as judged by Western blot and proliferation assays. Moreover, pretreatment with DIDS ($Cl^-$ channel blockers) but not LY294002 (PI3K inhibitors) completely abolished the LDL-induced upregulation of Egr-1 to the same extent as PD98059 (MEK inhibitors to inhibit Erk), as judged by Western blot and luciferase reporter assays. This is the first report, to our knowledge, that DIDS-sensitive $Cl^-$-channels play a key role in the LDL-induced cell proliferation of hAoSMCs via the activation of Erk1/2 and PI3K/Akt and the upregulation of Egr-1.

• Journal of the Korean Institute of Telematics and Electronics S
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• v.35S no.10
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• pp.42-51
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• 1998

This paper suggests a congestion control scheme for CL (ConnectionLess) overlay network using the feedback loops between CL user and CL server, between CL servers, and between end-to-end CL users, and the header translation table of CL server. The CL overlay network for CBDS(Connectionless Broadhand Data Service) defined by ITU-T((International Telecommunication Union-Telecommunication) consists of CL servers which route frames and links which connect between CL user and CL server or between CL servers. In the CL overlay network, two kinds of congestion, CL link congestion and CL server congestion, may occur. We considered the schemes to solve the congestion. link-by-link method[18] has used the ABR feedback loops of ATM layer between CL user and CL server or between CL servers, and the congestion table using header translation table of CL server. As in congestion of output virtual channel this method has an effect on all the traffic transmitting through the link, then it has an effect on the traffic that has not caused the congestion. As a result, the link utilization of output virtual channel that does not bring the congestion and outputs the traffic is decreased. To overcome this drawback of link-by-link, we proposed the hybrid method that are using the ABR feedback loops of link-by-link method, the feedback loop between CL users in end-to-end, the congestion table using and the header translation table. This scheme deals with teh congestion immediately by link-by-link loops and the header translation table, and then regulates the sending rate of CL user that causes the congestion by end-to-end loop.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.133-145
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• 1998

$Ca^{2+}-signals$ in endothelial cells are determined by release from intracellular stores and entry through the plasma membrane. In this review, the nature of $Ca^{2+}$ entry and mechanisms of its control are reviewed. The following ion channels play a pivotal role in regulation of the driving force for $Ca^{2+}$ entry: an inwardly rectifying $K^+$ channel, identified as Kir2.1, a big-conductance, $Ca^{2+}-activated$ $K^+$ channel (hslo) and at least two $Cl^-$ channels (a volume regulated $Cl^-$ channel, VRAC, and a $Ca^{2+}$ activated $Cl^-$ channel, CaCC). At least two different types of $Ca^{2+}$-entry channels exist: 1. A typical CRAC-like, highly selective $Ca^{2+}$ channel is described. Current density for this $Ca^{2+}$ entry is approximately 0.1pA/pF at 0 mV and thus 10 times smaller than in Jurkat or mast cells. 2. Another entry pathway for $Ca^{2+}$ entry is a more non-selective channel, which might be regulated by intracellular $Ca^{2+}$. Although detected in endothelial cells, the functional role of trp1,3,4 as possible channel proteins is unclear. Expression of trp3 in macrovascular endothelial cells from bovine pulmonary artery induced non-selective cation channels which are probably not store operated or failed to induce any current. Several features as well as a characterisation of $Ca^{2+}$-oscillations in endothelial cells is also presented.

• Proceedings of the Ginseng society Conference
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• 2005.11a
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• pp.32-40
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• 2005

The last two decades have shown a marked expansion in publications of diverse effects of Panax ginseng. Ginsenosides, as active ingredients of Panax ginseng, are saponins found in only ginseng. Recently, a line of evidences shows that ginsenosides regulate various types of ion channel activity such as Ca$^{2+}$, K$^+$, Na$^+$, Cl$^-$, or ligand gated ion channels (i.e. 5-HT$_3$, nicotinic acetylcholine, or NMDA receptor) in neuronal, non-neuronal cells, and heterologously expressed cells. Ginsenosides inhibit voltage-dependent Ca$^{2+}$, K$^+$, and Na$^+$ channels, whereas ginsenosides activate Ca$^{2+}$-activated Cl$^-$ and Ca$^{2+}$-activated K$^+$ channels. Ginsenosides also inhibit excitatory ligand-gated ion channels such as 5-HT$_3$. nicotinic acetylcholine, and NMDA receptors. This presentation will introduce recent findings on the ginsenoside-induced differential regulations of ion channel activities as a ligand as other drugs do.

• Biomolecules & Therapeutics
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• v.16 no.4
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• pp.328-335
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• 2008

This study was undertaken to investigate whether honokiol could enhance the pentobarbitalinduced sleeping behaviors through $\gamma$-aminobutyric acid (GABA) receptor $Cl^-$ channel activation. Thirty minutes after the oral administration of honokiol, mice were received sodium pentobarbital (42 mg/kg, i.p.). The time elapsed from pentobarbital injection to the loss of the righting reflex was taken as sleeping latency. The time elapsed between the loss and voluntary recovery of the righting reflex was considered as the total sleeping time. Western blot technique and $Cl^-$ sensitive fluorescence probe were used to detect the expression of $GABA_A$ receptor subunits and $Cl^-$ influx in the primary cultured cerebellar granule cells. Honokiol (0.1 and 0.2 mg/kg) prolonged the sleeping time induced by pentobarbital (42 mg/kg) in a dosage-dependent manner. Honokiol (20 and 50 ${\mu}M$) increased $Cl^-$ influx in primary cultured cerebellar granule cells, and selectively increased the $GABA_A$ receptor $\alpha$-subunit expression, but had no effect on the abundance of $\beta$ or $\gamma$-subunits. Chronic treatment with 20 ${\mu}M$ honokiol in primary cultured cerebellar neurons did not affect the abundance of GAD65/67. The results suggested that honokiol could potentiate pentobarbital-induced sleeping through $GABA_A$ receptor $Cl^-$ channel activation.

• Journal of Ginseng Research
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• v.24 no.4
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• pp.168-175
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• 2000

Relatively little is known about the signaling mechanism of ginseng saponins (ginsenosides), active ingredients of ginseng, in non-neuronal cells. Here, we describe that ginsenosides utilize a common pathway of receptor-mediated signaling pathway in Xenopus oocytes: increase in intracellular $Ca^{2+}$ concentration via phospholipase C (PLC) and $Ca^{2+}$ mobilization. Ginsenosides induced a marked and robust artivation of $Ca^{2+}$-activated Cl- channels in Xenopus oocytes. The effect of ginsenosides was completely reversible, in a dose-dependent manner with EC$_{50}$ of 4.4 $\mu\textrm{g}$/mi, and specifically blocked by niflumic acid, an inhibitor of $Ca^{2+}$-activated Cl- channel. Intracellular injection of BAPIA abolished the effect of ginsenosides. Intracellular injection of GTP${\gamma}$S also abolished the effect of ginsenosides. The effect of gin senosides on $Ca^{2+}$-activated Cl- currents was greatly reduced by the intracellular injection of heparin, an IP$_3$ receptorantagonist or the pretreatment of PLC inhibitor. These results indicate that ginsenosides activate endogenous $Ca^{2+}$-activated Cl- channels via the activation of PLC and the release of $Ca^{2+}$ from the IP$_3$-sensitive intracellular store following the initial interaction with membrane component(s) from extracellular side. This signaling pathway of ginsenosides may be one of the action mechanisms for the pharmacological effects of ginseng.ts of ginseng.

• 한국가시화정보학회:학술대회논문집
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• 2005.12a
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• pp.80-84
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• 2005

Many important properties in colloidal systems are usually determined by surface charge ($\zeta$-potential) of the contacted solid surface. In this study, $\zeta$-potential of glass $\mu$-channel was evaluated from the electro-osmotic velocity distribution. The electro-osmotic velocity inside a glass $\mu$-channel was measured using a micro-PIV velocity field measurement technique. This evaluation method is more simple and easy to approach, compared with the traditional streaming potential technique. The $\zeta$-potential in the glass $\mu$-channel was measured for two different mole NaCl solutions. The effect of an anion surfactant, sodium dodecyl sulphate (SDS), on the electro-osmotic velocity and $\zeta$-potential in the glass surface was also studied. In the range of $0\∼6$mM, the surfactant SDS was added to NaCl solution in four different mole concentrations. As a result, the addition of SDS increases $\zeta$-potential in the surface of the glass $\mu$-channel. The measured $\zeta$-potential was found to vary from-260 to-70mV. When negatively charged particles were used, the flow direction was opposite compared with that of neutral particles. The $\zeta$-potential has a positive sign for the negative particles.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.30 no.10 s.253
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• pp.935-941
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• 2006

Many important properties in colloidal systems are usually determined by surface charge $({\zeta}-potential)$ of the contacted solid surface. In this study, ${\zeta}-potential$ of glass ${\mu}-channel$ was evaluated from the electro-osmotic velocity distribution. The electro-osmotic velocity inside a glass f-channel was measured using a micro-PIV velocity field measurement technique. This evaluation method is more simple and easy to approach, compared with the traditional streaming potential technique. The ${\zeta}-potential$ in the glass ${\mu}-channel$ was measured fur two different mole NaCl solutions. The effect of an anion surfactant, sodium dodecyl sulphate (SDS), on the electro-osmotic velocity and f-potential in the glass surface was also studied. In the range of $0{\sim}6mM$, the surfactant SDS was added to NaCl solution in few different mole concentrations. As a result, the addition of SDS increases ${\zeta}-potential$ in the surface of the glass ${\mu}-channel$. The measured $\zeta-potential$ was found to vary from -260 to -70mV. When negatively charged particles were used, the flow direction was opposite compared with that of neutral particles. The ${\zeta}-potential$ has a positive sign for the negative particles.

• Journal of Ginseng Research
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• v.29 no.1
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• pp.19-26
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• 2005

The last two decades have shown a marked expansion in publications of diverse effects of Panax ginseng. Ginsenosides, as active ingredients of Panax ginseng, are saponins found in only ginseng. Recently, a line of evidences shows that ginsenosides regulate various types of ion channel activity such as $Ca^{2+},\;K^+,\;Na^+,\;Cl^-$, or ligand gated ion channels (i.e. $5-HT_3$, nicotinic acetylcholine, or NMDA receptor) in neuronal, non-neuronal cells, and heterologously expressed cells. Ginsenosides inhibit voltage-dependent $Ca^{2+},\;K^+,\;and\;Na^+$ channels, whereas ginsenosides activate $Ca^{2+}-activated\;Cl^-\;and\;Ca^{2+}-activated\;K^+$ channels. Ginsenosides also inhibit excitatory ligand-gated ion channels such as $5-HT_3$, nicotinic acetylcholine, and NMDA receptors. This review will introduce recent findings on the ginsenoside-induced differential regulations of ion channel activities and will further expand the possibilities how these ginsenoside-induced ion channel regulations are coupled to biological effects of Panax ginseng.

• Journal of the Institute of Electronics Engineers of Korea TC
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• v.45 no.12
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• pp.13-19
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• 2008

In this paper, we propose a new CL-OSTBC (Closed Loop Orthogonal Space-Time Block Code) scheme for four transmit antennas and compare the scheme with existing closed loop schemes on the performance of BER (Bit Error Rate). In the proposed scheme, a transmitter receives channel feedback information and combines modulated symbols by the symbol combiner, and transmits the symbols encoded by the space-time block encoder. As a result, the proposed scheme achieves full-rate and maximal channel gains by more efficient utilization of the channel feedback information. Moreover, the scheme can reduce computation complexity by using a linear detector. Simulation results on the BER performance show that the proposed CL-OSTBC scheme outperforms existing CL-OSTBC schemes.