• The Korean Journal of Physiology and Pharmacology
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• 제9권2호
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• pp.131-135
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• 2005

Potassium channels in human skin fibroblast have been studied as a possible site of Alzheimer disease pathogenesis. Fibroblasts in Alzheimer disease show alterations in signal transduction pathway such as changes in $Ca^{2+}$ homeostasis and/or $Ca^{2+}-activated$ kinases, phosphatidylinositol cascade, protein kinase C activity, cAMP levels and absence of specific $K^+$ channel. However, little is known so far about electrophysiological and pharmacological characteristics of large-conductance $Ca^{2+}$-activated $K^+$ ($BK_{Ca}$) channel in human fibroblast (CRL-1474). In the present study, we found Iberiotoxin- and TEA-sensitive outward rectifying oscillatory current with whole-cell recordings. Single channel analysis showed large conductance $K^{+}$ channels (106 pS of chord conductance at +40 mV in physiological $K^+$ gradient). The 106 pS channels were activated by membrane potential and $[Ca^{2+}]_i$, consistent with the known properties of $BK_{Ca}$ channels. $BK_{Ca}$ channels in CRL-1474 were positively regulated by adenylate cyclase activator ($10{\mu}M$ forskolin), 8-Br-cyclic AMP ($300{\mu}M$) or 8-Br-cyclic GMP ($300{\mu}M$). These results suggest that human skin fibroblasts (CR-1474) have typical $BK_{Ca}$ channel and this channel could be modulated by c-AMP and c-GMP. The electrophysiological characteristics of fibroblasts might be used as the diagnostic clues for Alzheimer disease.

• Progress in Superconductivity
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• 제3권1호
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• pp.41-44
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• 2001

We report the current transport properties of a normal metal/organic conductor/ superconductor tunnel junction as a novel high- $T_{c}$ superconducting three terminal device. The organic copper (II) phthalocyanine (Cu-Pc) layer was used far a polaronic quasiparticle (QP) injector. The injection of polaronic QP from the Cu-Pc interlayer into a superconductor $Bi_2$$Sr_2$$CaCu_2$ $O_{8+}$ $\delta$/(BSCCO) thin film generated a substantially larger nonequilibrium effect as compared to the normal QP injection current. The tunneling spectroscopy of an Au/cu-PC/BSCCO junction exhibited a zero bias conductance peak which may be due to Andreev reflection at a Cu-Pc/d-wave superconductor junction.n..

• 한국재료학회지
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• 제14권12호
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• pp.857-862
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• 2004

Production of titanium powder directly from tantalum oxides ($TiO_2$) pellet through an electronically mediated reaction (EMR) by calciothermic reduction has been investigated. Feed material ($TiO_2\;pellet$) and reductant (Ca-Ni alloy) were charged into electronically isolated locations in a molten calcium chloride ($CaCl_2$) bath at $950^{\circ}C$. The current flow through an external circuit between the feed (cathode) and reductant (anode) locations was monitored during the reduction of $TiO_2$. The current approximately 3.2A was measured during the reaction in the external circuit connecting cathode and anode location. After the reduction experiment, pure titanium powder with low nickel content was obtained even though Ca-Ni alloy was used as a reductant. These results demonstrate that titanium powder can be produced without direct physical contact between the feed and reductant. In certain experimental conditions, pure titanium powder with approximately $99.5\;mass\%$ purity was successfully obtained.

• 한국전기전자재료학회논문지
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• 제21권2호
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• pp.173-177
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• 2008

We have developed the transparent passivation layer for top emission organic light emitting diodes using CsCl thin film by the thermal evaporation method. The CsCl film was deposited on the Ca/Ag semitransparent cathode. The optical transmittance of Ca/ Ag/CsCl triple layer is higher than that of Ca/Ag double layer in the visible range. The device with a structure of glass/Ni/2-TNATA/a-NPD/Alq3:C545T/BCP/Alq3/Ca/Ag/CsCl results in higher efficiency than the device without CsCl passivation layer. The device without CsCl thin film shows a current efficiency of 7 cd/A, whereas the device passivated with CsCl layer shows an efficiency of 10 cd/A. This increase of efficiency isresulted from the increased optical extraction by the CsCl passivation layer.

• 한국전기전자재료학회:학술대회논문집
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• 한국전기전자재료학회 1996년도 춘계학술대회 논문집
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• pp.252-255
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• 1996

Superconducting current lead is one of the promising applications of the oxide high-Tc superconductors, because they have the advantage of decreasing heat conduction to low temperature region, comparing with a conventional cooper alloy lead. High critical current density is a key factor for the applications such as current lead. (Bi,Pb)$_2$Sr$_2$Ca$_2$Cu$_3$O$\_$x/ high Tc superconductor haute been investigated in terms of critical current density. Bi-2223 superconducting current lead made by CIP and solid state sintering process. Bi-2223 current lead that heat treated at 836$^{\circ}C$ for 240 h in 1/13 P$\_$O$_2$/ had over 150 A/$\textrm{cm}^2$ of critical current density at 77K. We knew that the superconducting properties of tube type current leads were better than rods type of them. And we investigated the relation of Bi-2223 formation and heat treatment condition by XRD and SEM analysis.

• The Korean Journal of Physiology and Pharmacology
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• 제5권2호
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• pp.139-146
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• 2001

L-type $Ca^{2+}$ channels play an important role in regulating cytosolic $Ca^{2+}$ and thereby regulating hormone secretions in neuroendocrine cells. Since hormone secretions are also regulated by various kinds of protein kinases, we investigated the role of some kinase activators and inhibitors in the regulation of the L-type $Ca^{2+}$ channel currents in rat pituitary $GH_3$ cells using the patch-clamp technique. Phorbol 12,13-dibutyrate (PDBu), a protein kinase C (PKC) activator, and vanadate, a protein tyrosine phosphatase (PTP) inhibitor, increased the $Ba^{2+}$ current through the L-type $Ca^{2+}$ channels. In contrast, bisindolylmaleimide I (BIM I), a PKC inhibitor, and genistein, a protein tyrosine kinase (PTK) inhibitor, suppressed the $Ba^{2+}$ currents. Forskolin, an adenylate cyclase activator, and isobutyl methylxanthine (IBMX), a non-specific phosphodiesterase inhibitor, reduced $Ba^{2+}$ currents. The above results show that the L-type $Ca^{2+}$ channels are activated by PKC and PTK, and inhibited by elevation of cyclic nucleotides such as cAMP. From these results, it is suggested that the regulation of hormone secretion by various kinase activity in $GH_3$ cells may be attributable, at least in part, to their effect on L-type $Ca^{2+}$ channels.

• The Korean Journal of Physiology and Pharmacology
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• 제2권3호
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• pp.353-359
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• 1998

In gastrointestinal smooth muscle, muscarinic stimulation by carbachol (CCh) activates nonselective cation channel current ($I_{CCh}$) which is facilitated by intracellular [$Ca^{2+}$] increase. Caffeine is widely used in experiments to mobilize $Ca^{2+}$ from intracellular stores. This study shows a strong inhibitory effect of caffeine on $I_{CCh}$ in guinea-pig gastric myocyte. In this study, the underlying mechanism of the inhibitory effect of caffeine was investigated. $I_{CCh}$ was completely suppressed by the addition of caffeine (10 mM) to the superfusing solution. Inhibition of $I_{CCh}$ by caffeine was not related to the intracellular cAMP accumulation which was expected from the phosphodiesterase-inhibiting effect of caffeine. The blockade of $InsP_3-induced$ $Ca^{2+}$ release by heparin had no significant effects on the activation of $I_{CCh}$. When the same cationic current had been induced by intracellular dialysis of $GTP[{\gamma}S]$ in order to bypass the muscarinic receptor, the inhibitory effect of caffeine was significantly attenuated. The results of this study indicate that both intracellular signalling pathways for $I_{CCh}$, proximal and distal to G-protein activation, are suppressed by caffeine. A major inhibition was observed at the proximal level.

• The Korean Journal of Physiology and Pharmacology
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• 제17권3호
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• pp.223-228
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• 2013

The calcium-activated $K^+$ ($BK_{Ca}$) channel is one of the potassium-selective ion channels that are present in the nervous and vascular systems. $Ca^{2+}$ is the main regulator of $BK_{Ca}$ channel activation. The $BK_{Ca}$ channel contains two high affinity $Ca^{2+}$ binding sites, namely, regulators of $K^+$ conductance, RCK1 and the $Ca^{2+}$ bowl. Lysophosphatidic acid (LPA, 1-radyl-2-hydroxy-sn-glycero-3-phosphate) is one of the neurolipids. LPA affects diverse cellular functions on many cell types through G protein-coupled LPA receptor subtypes. The activation of LPA receptors induces transient elevation of intracellular $Ca^{2+}$ levels through diverse G proteins such as $G{\alpha}_{q/11}$, $G{\alpha}_i$, $G{\alpha}_{12/13}$, and $G{\alpha}s$ and the related signal transduction pathway. In the present study, we examined LPA effects on $BK_{Ca}$ channel activity expressed in Xenopus oocytes, which are known to endogenously express the LPA receptor. Treatment with LPA induced a large outward current in a reversible and concentration-dependent manner. However, repeated treatment with LPA induced a rapid desensitization, and the LPA receptor antagonist Ki16425 blocked LPA action. LPA-mediated $BK_{Ca}$ channel activation was also attenuated by the PLC inhibitor U-73122, $IP_3$ inhibitor 2-APB, $Ca^{2+}$ chelator BAPTA, or PKC inhibitor calphostin. In addition, mutations in RCK1 and RCK2 also attenuated LPA-mediated $BK_{Ca}$ channel activation. The present study indicates that LPA-mediated activation of the $BK_{Ca}$ channel is achieved through the PLC, $IP_3$, $Ca^{2+}$, and PKC pathway and that LPA-mediated activation of the $BK_{Ca}$ channel could be one of the biological effects of LPA in the nervous and vascular systems.

• The Korean Journal of Physiology and Pharmacology
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• 제13권6호
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• pp.437-442
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• 2009

A non-steroidal anti-inflammatory drug (NSAID) has many adverse effects including cardiovascular (CV) risk. Diclofenac among the nonselective NSAIDs has the highest CV risk such as congestive heart failure, which resulted commonly from the impaired cardiac pumping due to a disrupted excitationcontraction (E-C) coupling. We investigated the effects of diclofenac on the L-type calcium channels which are essential to the E-C coupling at the level of single ventricular myocytes isolated from neonatal rat heart, using the whole-cell voltage-clamp technique. Only diclofenac of three NSAIDs, including naproxen and ibuprofen, significantly reduced inward whole cell currents. At concentrations higher than $3\;{\mu}M$, diclofenac inhibited reversibly the $Na^+$ current and did irreversibly the L-type $Ca^{2+}$ channels-mediated inward current $(IC_{50}=12.89\pm0.43\;{\mu}M)$ in a dose-dependent manner. However, nifedipine, a well-known L-type channel blocker, effectively inhibited the L-type $Ca^{2+}$ currents but not the $Na^+$ current. Our finding may explain that diclofenac causes the CV risk by the inhibition of L-type $Ca^{2+}$ channel, leading to the impairment of E-C coupling in cardiac myocytes.

• The Korean Journal of Physiology
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• 제25권1호
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• pp.17-26
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• 1991

Single smooth muscle cells of the rabbit pulmonary artery were isolated by treatment with collagenase and elastase. Using the patch clamp technique, potassium channel activity was recorded from the inside-out membrane patch. The channel had a sin히e channel conductance of about 360 pS in symmetrical concentration of K on both sides of the patch, 150 mM, and had a linear current-voltage relationship. During the application of 10 mM tetraethylammonium (TEA) to the intracellular membrane surface, the amplitude of single channel current was reduced and very rapid flickering appeared. The open probability $(P_0)$ of this channel was increased by increasing positivity of the potential across the patch membrane, with e-fold increase by 20 mV depolarization, and by increasing the internal $Ca^{2+}$ concentration. These findings are consistent with those of large conductance Ca-activated K channels reported in other tissues. But the shortening of the mean open time by increasing $[Ca^{2+}]_i$, was an unexpected result and one additional closed state which might be arisen from a block of the open channel by Ca binding was suggested. The $P_0-membrane$ potential relationship was modulated by internal pH. Decreasing pH reduced $P_0$. Increasing pH not only increased $P_0$ but also weakened the voltage dependency of the channel opening. The modulation of Ca-activated K channel by pH was thought to be related to the mechanism of regulation of vascular tone by the pH change.