• Journal of the Korea Academia-Industrial cooperation Society
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• v.13 no.6
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• pp.2484-2490
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• 2012

This study reports on the development and performance verification of cell simulation boards of simulator and the embedded program for board control of the battery management system (BMS) of electric vehicle (EV) cars, which manages the next-generation automotive lithium-ion battery pack. Here, we have improved the speed of the simulator by using operational (OP) amplifier and transistors that were connected in series. In addition, using a digital analog converter (DAC) in each channel, we have improved the performance by channel-to-channel isolation (isolation) as compared to the traditional methods. Furthermore, by constructing a current-limiting protection circuit, one can be protected from disturbance and, by utilizing a precision shunt resistor for the current sensor, we have increased the precision of the current control. In order to verify the performance of the developed simulator, we have performed the experiment 10 times, with values ranging from 0.5 V to 5 V, and a voltage drop step of 0.5 V. Significance analysis of experimental data, and repeatability tests were performed, showing an average standard deviation of 0.001~0.004 V, indicating high repeatability and high statistical significance of the current method and system.

• Progress in Medical Physics
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• v.17 no.2
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• pp.96-104
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• 2006

Experiments from several groups Including ours have demonstrated that $Ca^{2+}$ can enhance the inactivation of N-type calcium channels. However, it is not clear if this effect can be ascribed to a 'classic' $Ca^{2+}$-dependent inactivation (CDI) mechanism. One method that has been used to demonstrate CDI of L-type calcium channels is to alter the intracellular and extracellular concentration of $Ca^{2+}$. In this paper we replaced the external divalent cation to monovalent ion ($MA^+$) to test CDI. In the previous paper, we could separate fast (${\tau}{\sim}150ms$) and slow (${\tau}{\sim}2,500ms$) components of inactivation in both $Ba^{2+}$ and $Ca^{2+}$ using 5-sec voltage step. Lowering the external divalent cation concentration to zero abolished fast inactivation with relatively little effect on slow inactivation. Slow inactivation ${\tau}$ correspond very well with provided the $MA^+$ data is shifted 10 mV hyperpolarized and slow inactivation ${\tau}$ decreases with depolarization voltage in both $MA^+\;and\;Ba^{2+}$, which consistent with a classical voltage dependent inactivation (VDI) mechanism. These results combined with those of our previous paper lead us to hypothesize that external divalent cations are required to produce fast N-channel inactivation and this divalent cation-dependent inactivation is a different mechanism from classic CDI or VDI.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.25-33
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• 2016

Ion channels in carcinoma and their roles in cell proliferation are drawing attention. Intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$)-dependent signaling affects the fate of cancer cells. Here we investigate the role of $Ca^{2+}$-activated $K^+$ channel (SK4) in head and neck squamous cell carcinoma cells (HNSCCs) of dif-ferent cell lines; SNU-1076, OSC-19 and HN5. Treatment with $1{\mu}M$ ionomycin induced cell death in all the three cell lines. Whole-cell patch clamp study suggested common expressions of $Ca^{2+}$-activated $Cl^-$ channels (Ano-1) and $Ca^{2+}$-activated nonselective cation channels (CAN). 1-EBIO, an activator of SK4, induced outward $K^+$ current (ISK4) in SNU-1076 and OSC-19. In HN5, ISK4 was not observed or negligible. The 1-EBIO-induced current was abolished by TRAM-34, a selective SK4 blocker. Interestingly, the ionomycin-induced cell death was effectively prevented by 1-EBIO in SNU-1076 and OSC-19, and the rescue effect was annihilated by combined TRAM-34. Con-sistent with the lower level of ISK4, the rescue by 1-EBIO was least effective in HN5. The results newly demonstrate the role of SK4 in the fate of HNSCCs under the $Ca^{2+}$ overloaded condition. Pharmacological modulation of SK4 might provide an intriguing novel tool for the anti-cancer strategy in HNSCC.

• Journal of the Korean Vacuum Society
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• v.2 no.2
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• pp.188-198
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• 1993

We have developed a technique for growing thin oxides (6~10 nm) by the Last step TCA method. N-channel metal-oxide-semiconductor (n-MOS) capacitor and n-channel metal-oxide-semiconductor field-effect transistor's (MOSFET's) having a gate oxide with chlorine incorporated $SiO_2/Si$ interface have been analyzed by electrical measurements and physical methods, such as secondary ion mass spectrometry (SIMS) and electron spectroscopy for chemical analysis (ESCA). The gate oxide grown with the Last strp TCA method has good characteristics as follows: the electron mobility of the MOSFET's with the Last step TCA method was increased by about 7% and the defect density at the $SiO_2/Si$ interface decreases slightly compared with that with No TCA method. In reliability estimation, the breakdown field was 18 MV/cm, 0.6 MV/cm higher than that of the gate oxide with No TCA method, and the lifetime estimated by TDDB measurement was longer than 20 years. The device lifetime estimated from hot-carrier reliability was proven to be enhanced. As the results, the gate oxide having a $SiO_2/Si$ interface incorporated with chlorine has good characteristics. Our new technique of Last step TCA method may be used to improve the endurance and retention of MOSFET's and to alleviate the degradation of thin oxides in short-channel MOS devices.

• Molecules and Cells
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• v.20 no.1
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• pp.69-73
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• 2005

The flavonoid, quercetin, is a low molecular weight substance found in apple, tomato and other fruit. Besides its antioxidative effect, quercetin, like other flavonoids, has a wide range of neuropharmacological actions including analgesia, and motility, sleep, anticonvulsant, sedative and anxiolytic effects. In the present study, we investigated its effect on mouse 5-hydroxytryptamine type 3 ($5-HT_{3A}$) receptor channel activity, which is involved in pain transmission, analgesia, vomiting, and mood disorders. The $5-HT_{3A}$ receptor was expressed in Xenopus oocytes, and the current was measured with the two-electrode voltage clamp technique. In oocytes injected with $5-HT_{3A}$ receptor cRNA, quercetin inhibited the 5-HT-induced inward peak current ($I_{5-HT}$) with an $IC_{50}$ of $64.7{\pm}2.2{\mu}M$. Inhibition was competitive and voltage-independent. Point mutations of pre-transmembrane domain 1 (pre-TM1) such as R222T and R222A, but not R222D, R222E and R222K, abolished inhibition, indicating that quercetin interacts with the pre-TM1 of the $5-HT_{3A}$ receptor.

• Journal of the Institute of Electronics Engineers of Korea SD
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• v.38 no.8
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• pp.34-42
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• 2001

The 1${\times}$2, 1${\times}$4 and 1${\times}$8 multimode interference(MMI) optical power splitters are fabricated by using $Ag^+-Na^+$ ion exchange on BK7 glass. Before fabricating the MMI optical power splitters, we find the refractive index of the channel waveguide and calculate the multimode section length and width. The multimode section lengths and widths are 887${\mu}m$, 1666${\mu}m$ and 1834${\mu}m$ and 40${\mu}m$, 80${\mu}m$ and 120${\mu}m$ for 1${\times}$2, 1${\times}$4 and 1${\times}$8 MMI optical power splitters respectively. The measured properties of the fabricated MMI optical power splitters show that the unbalance ratios of the 1${\times}$2, 1${\times}$4 and 1${\times}$8 MMI optical power splitters are 1.4[dB], 1.7[dB] and 2.0[dB] and the excess losses of those sre 0.96[dB], 2.26[dB] and 1.67[dB]. respectively.

• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.410-417
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• 2016

Quercetin is a flavonoid usually found in fruits and vegetables. Aside from its antioxidative effects, quercetin, like other flavonoids, has a various neuropharmacological actions. Quercetin-3-O-rhamnoside (Rham1), quercetin-3-O-rutinoside (Rutin), and quercetin-3-(2(G)-rhamnosylrutinoside (Rham2) are mono-, di-, and tri-glycosylated forms of quercetin, respectively. In a previous study, we showed that quercetin can enhance ${\alpha}7$ nicotinic acetylcholine receptor (${\alpha}7$ nAChR)-mediated ion currents. However, the role of the carbohydrates attached to quercetin in the regulation of ${\alpha}7$ nAChR channel activity has not been determined. In the present study, we investigated the effects of quercetin glycosides on the acetylcholine induced peak inward current ($I_{ACh}$) in Xenopus oocytes expressing the ${\alpha}7$ nAChR. $I_{ACh}$ was measured with a two-electrode voltage clamp technique. In oocytes injected with ${\alpha}7$ nAChR copy RNA, quercetin enhanced $I_{ACh}$, whereas quercetin glycosides inhibited $I_{ACh}$. Quercetin glycosides mediated an inhibition of $I_{ACh}$, which increased when they were pre-applied and the inhibitory effects were concentration dependent. The order of $I_{ACh}$ inhibition by quercetin glycosides was Rutin${\geq}$Rham1>Rham2. Quercetin glycosides-mediated $I_{ACh}$ enhancement was not affected by ACh concentration and appeared voltage-independent. Furthermore, quercetin-mediated $I_{ACh}$ inhibition can be attenuated when quercetin is co-applied with Rham1 and Rutin, indicating that quercetin glycosides could interfere with quercetin-mediated ${\alpha}7$ nAChR regulation and that the number of carbohydrates in the quercetin glycoside plays a key role in the interruption of quercetin action. These results show that quercetin and quercetin glycosides regulate the ${\alpha}7$ nAChR in a differential manner.

• JSTS:Journal of Semiconductor Technology and Science
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• v.7 no.3
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• pp.196-208
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• 2007

An analytical model is proposed for an optically controlled Metal Semiconductor Field Effect Transistor (MESFET), known as Optical Field Effect Transistor (OPFET) considering the diffusion fabrication process. The electrical parameters such as threshold voltage, drain-source current, gate capacitances and switching response have been determined for the dark and various illuminated conditions. The Photovoltaic effect due to photogenerated carriers under illumination is shown to modulate the channel cross-section, which in turn significantly changes the threshold voltage, drainsource current, the gate capacitances and the device switching speed. The threshold voltage $V_T$ is reduced under optical illumination condition, which leads the device to change the device property from enhancement mode to depletion mode depending on photon impurity flux density. The resulting I-V characteristics show that the drain-source current IDS for different gate-source voltage $V_{gs}$ is significantly increased with optical illumination for photon flux densities of ${\Phi}=10^{15}\;and\;10^{17}/cm^2s$ compared to the dark condition. Further more, the drain-source current as a function of drain-source voltage $V_{DS}$ is evaluated to find the I-V characteristics for various pinch-off voltages $V_P$ for optimization of impurity flux density $Q_{Diff}$ by diffusion process. The resulting I-V characteristics also show that the diffusion process introduces less process-induced damage compared to ion implantation, which suffers from current reduction due to a large number of defects introduced by the ion implantation process. Further the results show significant increase in gate-source capacitance $C_{gs}$ and gate-drain capacitance $C_{gd}$ for optical illuminations, where the photo-induced voltage has a significant role on gate capacitances. The switching time ${\tau}$ of the OPFET device is computed for dark and illumination conditions. The switching time ${\tau}$ is greatly reduced by optical illumination and is also a function of device active layer thickness and corresponding impurity flux density $Q_{Diff}$. Thus it is shown that the diffusion process shows great potential for improvement of optoelectronic devices in quantum efficiency and other performance areas.

• Korean Journal of Veterinary Research
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• v.38 no.4
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• pp.712-719
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• 1998

Thyroid function is mainly regulated through cAMP and phophatidylinositol, and it is well known that TSH-stimulated thyroxine ($T_4$) release is inhibited by catecholamine from mouse thyroids via the ${\alpha}_1$-adrenoceptor stimulation. Previous study has established that the inhibition of $T_4$ release by ${\alpha}_1$-adrenoceptor stimulation results in activated protein kinase C (PKC). The purpose of this study was to determine if ion transport systems are involved in the inhibition of $T_4$ release elicited by ${\alpha}_1$-adrenergic agonist in mouse thyroids. TSH-, IBMX- and cAMP analogue-stimulated $T_4$ release were significantly inhibited by methoxamine, R59022 (diacylglycerol kinase inhibitor), and MDL (adenylate cyclase inhibitor). TSH-stimulated $T_4$ release could be inhibited by Bay K 8644 and cyclopiazoic acid, but not by verapamil and tetrodotoxin. The addition of nifedipine ($Ca^{2+}$ channel blocker), tetrodotoxin and lidocaine ($Na^+$ channel blockers), but not amiloride (EIPA) and ryanodine, completely blocked the inhibitory effects of methoxamine on $T_4$ release. TSH-stimulated $T_4$ release was also inhibited by benzamil ($Na^+-Ca^{2+}$ exchange inhibitor). TSH-, IBMX- and cAMP-stimulated $T_4$ release were inhibited by methoxamine or R59022, these effects were reversed by nifedipine. but not by verapamil. Furthermore, nifedipine reversed the inhibitory effects of benzamil and R59022 on TSH-stimulated $T_4$ release. These data suggest that the observed ${\alpha}_1$-adrenoceptor-mediated inhibition of $T_4$ release in mouse thyroids is the result of an increase in intracellular $Na^+$ or $Ca^{2+}$ effected via activation of fast $Na^+$ or nifedipine-sensitive $Ca^{2+}$ channels, and that $Na^+-Ca^{2+}$ exchange may play an important role in reducing thyroid hormone by increasing intracellular $Ca^{2+}$.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.259-265
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• 2017

Excessive influx and the subsequent rapid cytosolic elevation of $Ca^{2+}$ in neurons is the major cause to induce hyperexcitability and irreversible cell damage although it is an essential ion for cellular signalings. Therefore, most neurons exhibit several cellular mechanisms to homeostatically regulate cytosolic $Ca^{2+}$ level in normal as well as pathological conditions. Delayed rectifier $K^+$ channels ($I_{DR}$ channels) play a role to suppress membrane excitability by inducing $K^+$ outflow in various conditions, indicating their potential role in preventing pathogenic conditions and cell damage under $Ca^{2+}$-mediated excitotoxic conditions. In the present study, we electrophysiologically evaluated the response of $I_{DR}$ channels to hyperexcitable conditions induced by high $Ca^{2+}$ pretreatment (3.6 mM, for 24 hours) in cultured hippocampal neurons. In results, high $Ca^{2+}$-treatment significantly increased the amplitude of $I_{DR}$ without changes of gating kinetics. Nimodipine but not APV blocked $Ca^{2+}$-induced $I_{DR}$ enhancement, confirming that the change of $I_{DR}$ might be targeted by $Ca^{2+}$ influx through voltage-dependent $Ca^{2+}$ channels (VDCCs) rather than NMDA receptors (NMDARs). The VDCC-mediated $I_{DR}$ enhancement was not affected by either $Ca^{2+}$-induced $Ca^{2+}$ release (CICR) or small conductance $Ca^{2+}$-activated $K^+$ channels (SK channels). Furthermore, PP2 but not H89 completely abolished $I_{DR}$ enhancement under high $Ca^{2+}$ condition, indicating that the activation of Src family tyrosine kinases (SFKs) is required for $Ca^{2+}$-mediated $I_{DR}$ enhancement. Thus, SFKs may be sensitive to excessive $Ca^{2+}$ influx through VDCCs and enhance $I_{DR}$ to activate a neuroprotective mechanism against $Ca^{2+}$-mediated hyperexcitability in neurons.