• Applied Chemistry for Engineering
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• v.23 no.5
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• pp.474-479
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• 2012

Possibility of the selective removal of $Ca^{2+}$ ions from a mixed solution of $Na^{+}$ and $Ca^{2+}$ ions using membrane capacitive deionization (MCDI) was investigated. Adsorption equilibrium experiments were conducted to determine the selectivity of the CMX cation-exchange membrane toward $Ca^{2+}$ ions. In addition, desalination experiments for a mixed solution (5 meq/L NaCl + 2 meq/L $CaCl_{2}$) were performed using an MCDI cell. The adsorption equilibrium of CMX membrane showed that the equivalent fraction of $Ca^{2+}$ ions in the solution and the CMX membrane were 28.6 and 87.2%, respectively, which indicates the CMX membrane's high selectivity toward $Ca^{2+}$ ions. Desalination experiments were performed by applying a constant current to the MCDI cell until the cell potential reached 1.0 V. The amount of ions adsorbed did not significantly change as the applied current was changed. However, the equivalent fractions of $Ca^{2+}$ ions among the adsorbed ions were inversely proportional to the applied currents: 81.4, 78.4, 77.0, and 74.5% at 200, 300, 500, and $700\;A/m^{2}$ of applied current density, respectively. This result is attributed to the increased fraction of $Ca^{2+}$ ions adsorbed by the CMX membrane at lower applied current densities.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.19-19
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• 2003

We have developed a cardiac cell model (Kyoto Model) for the sinoatrial node and ventricle, which is composed of a common set of kinetic equations of membrane ionic currents, Ca$\^$2+/dynamics of sarcoplasmic reticulum and contractile protein. To expand this model by including metabolic pathways, the intracellular ATP metabolism, which is pivotal in cardiac excitation - contraction coupling, was incorporated. ATP consumption by the sarcolemmal Na$\^$+/ pump and the Ca pump in the sarcoplasmic reticulum were calculated with stoichiometry of 3Na:2K:1ATP and 2Ca:1ATP, respectively. ATP consumption by contraction was estimated according to experimental data. Dependence of contraction on ATP and inorganic phosphate was modeled, based on data of skinned cardiac fiber. in production by mitochondrial oxidative phosphorylation was modified from Korzeniewski '||'&'||' Zoladz (2001), and creatine kinase and adenylate kinase reactions were incorporated. ATP dependence of ATP-sensitive K channel and L type Ca channel were also included.

• BMB Reports
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• v.50 no.3
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• pp.109-110
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• 2017

The nature of encoded information in neural circuits is determined by neuronal firing patterns and frequencies. This paper discusses the molecular identity and cellular mechanisms of spike-frequency adaptation in the central nervous system (CNS). Spike-frequency adaptation in thalamocortical (TC) and CA1 hippocampal neurons is mediated by the $Ca^{2+}$-activated $Cl^-$ channel (CACC) anoctamin-2 (ANO2). Knockdown of ANO2 in these neurons results in increased number of spikes, in conjunction with significantly reduced spike-frequency adaptation. No study has so far demonstrated that CACCs mediate afterhyperpolarization currents, which result in the modulation of neuronal spike patterns in the CNS. Our study therefore proposes a novel role for ANO2 in spike-frequency adaptation and transmission of information in the brain.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.3
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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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• v.3 no.1
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• pp.101-117
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• 1999

Amyotrophic lateral sclerosis (ALS) is a degenerative neuromuscular disease of unknown etiology in which the upper and lower motor neurons are progressively destroyed. Recent evidences support the role of autoimmune mechanisms in the pathogenesis of ALS. This study investigated the effects of sera from ALS patients on neuromuscular transmission in phrenic nerve-hemidiaphragm preparations and on calcium currents of single isolated dorsal root ganglion (DRG) cells in mice. Mice were injected with either control sera from healthy adults or ALS sera from 18 patients with ALS of sporadic form, for three days. Miniature end plate potential (MEPP) and nerve-evoked end plate potential (EPP) were measured using intracellular recording technique and the quantal content was determined. Single isolated DRG cells were voltage-clamped with the whole-cell configuration and membrane currents were recorded. Sera from 14 of 18 ALS patients caused a significant increase in MEPP frequency in normal Ringer's solution $(4.62{\pm}0.14\;Hz)$ compared with the control $(2.18{\pm}0.15\;Hz).$ In a high $Mg^{2+}/low\;Ca^{2+}$ solution, sera from 13 of 18 ALS patients caused a significant increase in MEPP frequency, from $2.18{\pm}0.31$ Hz to $6.09{\pm}0.38$ Hz. Sera from 11 of 18 patients produced a significant increase of nerve-evoked EPP amplitude, from $0.92{\pm}0.05$ mV to $1.30{\pm}0.04$ mV, while the other seven ALS sera did not alter EPP amplitude. In the ALS group, EPP quantal content was also elevated by the sera of 14 patients (from $1.49{\pm}0.07$ to $2.35{\pm}0.07).$ MEPP frequency and amplitude in wobbler mouse were $4.03{\pm}0.53$ Hz and $1.37{\pm}0.18$ mV, respectively, which were significantly higher than those of wobbler controls (wobblers without the symptoms of wobbler). Sera from ALS patients significantly reduced HVA calcium currents of DRG cells to 42.7% at -10 mV. Furthermore, the inactivation curve shifted to more negative potentials with its half-inactivation potential changed by 6.98 mV. There were, however, significant changes neither in the reversal potential of $I_{Ca}$ nor in the I-V curve. From these results it was concluded that: 1) The serum factors of sporadic ALS patients increase neuromuscular transmission and can alter motor nerve terminal presynaptic function. This suggests that ALS serum factors may play an important role in the early stage of ALS, and 2) Calcium currents in DRG cells were reduced and rapidly inactivated by ALS sera, suggesting that in these cells, ALS serum factors may exert interaction with the calcium channel.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.1
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• pp.47-52
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• 2003

The prostate gland contains numerous neuroendocrine cells that are believed to influence the function of the prostate gland. Our recent study demonstrated the expression of both ${\alpha}1$- and ${\alpha}2$-ARs, signaling the release of stored $Ca^{2+}$ and the inhibition of N-type $Ca^{2+}$ channels, respectively, in rat prostate neuroendocrine cells (RPNECs). In this study, the effects of NA on the resting membrane potential (RMP) of RPNECs were investigated using a whole-cell patch clamp method. Fresh RPNECs were dissociated from the ventral lobe of rat prostate and identified from its characteristic shape; round or oval shape with dark cytoplasm. Under zero-current clamp conditions with KCl pipette solution, the resting membrane potential (RMP) of RPNECs was between -35 mV and -85 mV. In those RPNECs with relatively hyperpolarized RMP (＜-60 mV), the application of noradrenaline (NA, $1{\mu}M$) depolarized the membrane to around -40 mV. In contrast, the RPNECs with relatively depolarized RMP (＞-45 mV) showed a transient hyperpolarization and subsequent fluctuation at around -40 mV on application of NA. Under voltage clamp conditions (holding voltage, -40 mV) with CsCl pipette solution, NA evoked a slight inward current (＜-20 pA). NA induced a sharp increase of cytosolic $Ca^{2+}$ concentration ($[Ca^{2+}]_c$), measured by the fura-2 fluorescence, and the voltage clamp study showed the presence of charybdotoxin-sensitive $Ca^{2+}$-activated $K^+$ currents. In summary, adrenergic stimulation induced either depolarization or hyperpolarization of RPNECs, depending on the initial level of RMP. The inward current evoked by NA and the $Ca^{2+}$-activated $K^+$ current might partly explain the depolarization and hyperpolarization, respectively.

• International Journal of Oral Biology
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• v.34 no.3
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• pp.151-155
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• 2009

The role of $Cl^-$ channels in regulatory volume decrease (RVD) in human salivary gland acinar cells was examined using a whole-cell patch clamp technique. Human tissues were obtained from healthy volunteers or from patients with oromaxillofacial tumors. During the measurements, $K^+$-free solutions were employed to eliminate contamination of whole-cell conductance by $K^+$ currents. When the cells were exposed to a 70% hypotonic solution, outward-rectifying currents, which were not observed in the resting state, were found to have significantly increased both in human labial and parotid gland acinar cells. The amplitudes of the currents were reduced in a low $Cl^-$ bath solution. Furthermore, the addition of $100{\mu}M$ 5-Nitro-2- (3-phenyl propylamino) benzoic acid (NPPB) or $100{\mu}M$ 4,4'-diisothio cyanatostilbene-2,2'-disulphonic acid (DIDS), known to partially block $Cl^-$ channels, significantly inhibited these currents. Its outward-rectifying current profile, shift in reversal potential in a low $Cl^-$ bath solution and pharmacological properties suggest that this is a $Ca^{2+}$-independent, volume activated $Cl^-$ current. We conclude therefore that volume activated $Cl^-$ channels play a putative role in RVD in human salivary gland acinar cells.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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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.

• Animal cells and systems
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• v.12 no.3
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• pp.137-141
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• 2008

Molecular cloning revealed the three isoforms($Ca_v3.1,\;Ca_v3.2,\;and\;Ca_v3.3$) of the T-type calcium channel subfamily. Expression studies exhibited their distinctive electrophysiological and pharmacological properties, accounting for diverse properties of T-type calcium channel currents previously characterized from isolated cells. However, electrophysiological properties of ion channels have shown to be more diversified by their splice variants. We here searched splice variants of rat $Ca_v3.1$ T-type channel by reverse-transcription-polymerase chain reaction(RT-PCR) to further explore diversity of $Ca_v3.1$. Interestingly, analyses of cloned RT-PCR products displayed that there were at least four splicing variants of rat $Ca_v3.1$ in the loop connecting repeats III and IV. Southern blot analyses indicated that the predominantly detected variant in brain was $Ca_v3.1a$(492 bp), which were rarely detected in most of peripheral tissues. Other two variants($Ca_v3.1c$, 546 bp; $Ca_v3.1d$, 525 bp) were detected in most of the tissues examined. The smallest isoform($Ca_v3.1b$, 471 bp) was rarely detected all the tissues. Electrophysiological characterization of the splicing variants indicated that the splice variants differ in inactivation kinetics and the voltage dependence of activation and inactivation as well.

• Proceedings of the Korean Biophysical Society Conference
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• 1997.07a
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• pp.31-31
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• 1997

Rapidly activating delayed K current (IKr) in cardiac muscles plays an important in repolarization. Expression of HERG cloned by the study on inherited LQT revealed that it encodes a potassium channel with biophysical properties similar to those of IKr in cardiac myocytes： outward currents activating on depolarization with large tail currents on repolarization, implying the inward rectifying property.(omitted)