• 대한전기학회:학술대회논문집
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• 대한전기학회 2015년도 제46회 하계학술대회
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• pp.1106-1107
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• 2015

A flux pump (FP) can inject the DC current into high temperature superconducting (HTS) field coils of a HTS rotating machine without slip ring and current lead. However, it has limits to improve the value of DC current, and has time constants of DC current according to inductances of the HTS field coils. When a large-scale HTS generator with the FP is designed, a proper point about the inductance, field current, and time constant is demanded to decide parameters of the generator. In this paper, a parameter tuning skill of a large-scale superconducting wind power generator for applying a FP has been proposed. The design of the FP has been fixed, and 12 MW HTS generators have been variously designed by adjusting parameters related with the inductance of the HTS field coil. The induced current values have been calculated based on the FP design. The time constants of the induced currents depending on the DC current values and inductances of the generator have been represented. The results of the parameter tuning of the HTS generator have been discussed in detail.

• 한국해안해양공학회지
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• 제13권1호
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• pp.1-8
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• 2001

파랑으로 인해 발생되는 흐름은 연안에서 질량수송의 일련의 과정을 야기시키므로 연안유역의 관리에 파랑과 흐름의 상호작용에 대한 정확한 이해가 요구된다. 본 논문은 적응가능한 사면 구조 격자에 근간을 둔 파랑장과 흐름장을 혼합한 수치모델을 기술하였다. 사용한 모델은 쇄파, 천수, 굴절, 회절, 파랑과 흐름의 상호작용, 평균해면의 저하와 상승, 혼합 과정, 바닥 마찰 효과 그리고 해안선에 접한 운동 등을 해석할 수 있다. 주기와 수심으로 평균한 지배 방정식은 단계적으로 엇갈린 사면구조 격자에 적응 가능한 Adam-Bashforth 2차 유한 차분 기법으로 양해적으로 모델화 되었다. 본 모델로부터의 결과는 평면 해변에서 경사 입사파에 의해 발생된 연안류의 실험치와 타당한 일치를 보였다.

• The Korean Journal of Physiology
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• 제26권2호
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• pp.99-111
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• 1992

Permissive action of thyroid hormone at the level of Ca channel and responsible mechanisms underlying thyroid hormone-induced change in myocardial contractile state and $T_3-induced$ arrhythmias were investigated in rabbit ventricular or atrial myocytes using whole cell patch clamp technique. Single cells were isolated by Langendorff perfusion with collagenase. Cardiac myocytes were incubated in $low-Cl^-,$, $high-K^+$ medium containing $1_{\mu}M\;L-triiodothyronine\;(T_3)$ at $4^{\circ}C$ for 2.10 hours. The calcium currrent $(I_{Ca})$ was increased in $T_3$ loaded cells, however, the shape of current voltage curve and reverse potential did not altered. Cyclic AMP, cyclic GMP, isoprenaline and 3-isobutyl-1-methyl-xanthine increased $I_{Ca}$ in euthyroid and hyperthyroid conditions, and acetylcholine blocked the increase of $I_{Ca}\;in\;T_3$ loaded cells. The amplitude of $I_{Ca}$ was much larger after perfusing cGMP than cGMP in both conditions, whereas the degree of increase of $I_{Ca}$ was greater after perfusing cAMP than cGMP in $T_3$ loaded cells. The degree of increase of $I_{Ca}$ after perfusing isoprenaline or IBMX also was greater in $T_3$ loaded cells than in control cells. Background current induced by isoprenaline also increased in $T_3$ loaded cells. The Ca release dependent inward current was increased in amplitude but its activation and inactivation time course was not changed in $T_3$ loaded cells. Activation of Na pump current was not changed in $T_3$ loaded cells. From the above results it is suggested that thyroid hormone induced increase in the contractile state of cardiac myocytes are accompanied by augmented $I_{Ca}$ and the increase of Ca release from sarcoplasmic reticulum and the permissive action of thyroid hormone to catecholamines could induce arrhythmias through the increase of $I_{Ca}$ and background current.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1999년도 학술발표회 진행표 및 논문초록
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• pp.61-62
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• 1999

;The mechanisms inducing hypertension are actively investigated and are still challenging topics. Basically hypertension must be caused by the disorder of $Ca^{2+}$ metabolism in vascular smooth muscle, such as the increase of $Ca^{2+}$ influx, the decrease of ci+ efflux, or the change of sensitivity of contractile protein etc. The one of cause of the increase of ci+ influx may be the change of ci+ channel activity. Even though the relationships of ci+ channel activity and hypertension were studied using various hypertension models, still it is not clear how much change of $Ca^{2+}$ channel activity in diabetes mellitus (DM) induced hypertension is occurred. We induced DM hypertension in SD rat and compared the $Ca^{2+}$ channel activity with age-matched normotensive SD rat. For inducing DM hypertension, left kidney was removed with 200 gm rat and, after 1 month, 60 mg/kg of streptozotocin was injected into peritoneal space to induce diabetes mellitus. Usually after 4-6 weeks, hypertension was fully induced. For isolating vascular smooth muscle cells (VSMC), we used mesenteric arteriole (3rd - 4th branch of mesenteric artery) of which diameter is below 150 urn. VSMCs were isolated enzymatically. $Ca^{2+}$ current was measured using whole cell patch clamp technique. All experiments were performed at $37^{\circ}C$. The cell membrane area of VSMC of DM hypertensive rat is larger than that of control VSMC($36.6{\pm}3.64{\;}pF{\;}vs{\;}22.4{\pm}1.29{\;}pF, {\;}mean{\pm}S.E.$) When we compared the current amplitude, the $Ca^{2+}$ current amplitude in VSMC of DM hypertensive rat is much larger than that in VSMC of normotensive age-matched rat. After $Ca^{2+}$ current amplitude was normalized by cell membrane area, the current amplitude in DM hypertension is increased to $249.1{\pm}15.9{\;}%{\;}(mean{\pm}S.E.M)$, which means the ;absolute current amplitude is about 4 times larger in DM hypertension. When we compared the steady state activation and inactivation. there were no noticeable differences. From these results. one of cause of the DM hypertension is due to the increase of $Ca^{2+}$ current amplitude. But it need further study why the $Ca^{2+}$ current is so large in VSMC of DM hypertension and how much $Ca^{2+}$ influx through $Ca^{2+}$ channel contribute to the increase of intracellular $Ca^{2+}$ and eventually contribute to development of hypertension.ypertension.

• 한국자기학회:학술대회 개요집
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• 한국자기학회 2004년도 동계학술연구발표회 논문개요집
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• pp.151-151
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• 2004

• 대한전기학회:학술대회논문집
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• 대한전기학회 1988년도 추계학술대회 논문집 학회본부
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• pp.229-232
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• 1988

Induced voltage causing disturbances on the communication lines of electric train is dealt with when the AT power supply system is employed. In the paper we obtain an algorithm to calculate the induced voltages on the communication lines in the AT system and an algorithm for the induced current in case of the accident that the line falls to the ground. These algorithms are developed to a package of computer programs and their validity was checked on a simulated system.

• 대한전기학회:학술대회논문집
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• 대한전기학회 2003년도 하계학술대회 논문집 A
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• pp.500-502
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• 2003

This paper reviews calculating of induced voltage onto a communication line from 22.9kV-Y Distribution Lines. The coexistence of both power line and communication line in parallel generates the induction of significant longitudinal voltage in the weak current line. In order to evaluate a precise induced voltage, this paper indicated some problems about coefficient and numerical formula. It also presents some induced voltage production technology standard application.

• Journal of Korean Neurosurgical Society
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• 제29권11호
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• pp.1429-1436
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• 2000

Objectives : This study was performed in cultured rat hippocampal neurons to investigate the acute electrophysiological features of ionotropic glutamate receptors which act as a major excitatory neurotransmitter in mammalian brain. Method : Glutamate receptor agonists were applied into the bath solution embedding in whole-cell patch-clamp recording of single hippocampal neuron. Results : In voltage-clamped at -60mV and the presence of 1mmol $Mg^{2+}$, extracellulary applied NMDA did not induce any inward current. Both the elimination of $Mg^{2+}$ and addition of glycine in bath, however, elicited a NMDAinduced inward current. $Mg^{2+}$ block current was increased gradually in more negative potentials from -30mV, showing a negative slope in I-V plot with $Mg^{2+}$. Glutamate-induced current represented an outward rectification. A non-NMDA receptor component occupied about 40% of glutamate-induced current in the voltage range of -80mV to +60mV. Conclusion : Present study suggests that glutamate activates acutely the non-NMDA receptors which induces an inward current in the level of resting membrane potential. This makes the membrane potential increase and can activate the NMDA receptors that permit calcium influx against $Mg^{2+}$ block. At the depolarized state of neuron, there may be recovery mechanisms of membrane potential to repolarize irrespective of voltage-dependent potassium channels in the hippocampal neurons.

• The Journal of Korean Physical Therapy
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• 제15권4호
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• pp.442-454
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• 2003

The aim of this study was to demonstrate the effects of silver spike point (SSP) low frequency electrical stimulation on plasma vasoactive intestinal polypeptide (VIP) activities measured by radioimmunoassay from volunteer and the effects of VIP on pain substance-induced contraction investigated by isometric tension methode in animal. The current of 3 Hz continue type, but not 100 Hz continue type, of SSP low frequency electrical stimulation significantly increased in plasma VIP from normal volunteer. The pain substance, such as norepinephrine, serotonin, and prostaglandin $F2{\alpha}$, increased vascular smooth muscle contraction, respectively. These responses were inhibited by VIP applied cumulatively (1 nM - $1\;{\mu}M$), but not serotonin-induced contraction. In addition, serotonin, and prostaglandin $F2{\alpha}$ induced uterine smooth muscle contraction from rat. However, these responses were inhibited by VIP ($1\;{\mu}M$), only serotonin-induced contraction. These results suggest that the VIP regulates pain substance in part and that the SSP low frequency electrical stimulation, specifically current of 3 Hz continue type, significantly increases plasma VIP from volunteer.

• The Korean Journal of Physiology and Pharmacology
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• 제5권1호
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• pp.33-40
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• 2001

The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier $K^+\;(K_{DR})$ channel function in isoproterenol-induced hypertrophy. It has been proposed that $K_{DR}$ channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary $K_{DR}$ channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present study was carried out to compare the properties of coronary $K_{DR}$ channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the study are as follows: (1) the $K_{DR}$ current density was decreased without changes of the channel kinetics in isoproterenol-induced hypertrophy; (2) the sensitivity of coronary $K_{DR}$ channels to 4-AP was increased in isoproterenol-induced hypertrophy. From the above results, we suggest for the first time that the alteration of $K_{DR}$ channels may limit vasodilating responses to several stimuli and may be involved in impaired coronary reserve in isoproterenol-induced hypertrophy.