• 해양환경안전학회지
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• 제24권2호
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• pp.179-187
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• 2018

수치모델실험을 사용하여 한국 서남해 압해도 주변 해역의 조류 및 조석잔차류 분포를 파악하였다. 조류는 대체로 반 일주조가 탁월하며, 조류 주방향은 압해도 주변 다도해역이 좁은 협수로인 관계로 대부분 수로를 따라 형성되었다. 조류타원 형태는 주변수심 및 인근에 산재한 섬 주위 해저지형의 영향으로 대부분 직선에 가까운 왕복성이었으나, 매화도~증도 사이 기점도, 화도, 당사도 주위에 약한 회전성 조류타원 형태였다. 창조류는 화원반도 서쪽 연안을 따라 팔금도~암태도, 암태도~증도 수로에서 북동류한 조류와 함께 압해도 북서쪽 다도해로 빠지고, 낙조류는 반대로 북서 다도해의 협수로를 따라 암태도~증도, 암태도~팔금도를 통과하고 암태도~증도에서의 조류는 팔금도~화원반도 서쪽 연안을 따라 남류했다. 압해도 연안은 창조시 북류한 흐름이 해안에서 동서로 분류되어 압해도 서쪽과 동쪽을 따라 흐르고 낙조시는 조간대 만곡부에서 남류한 흐름과 섬 서쪽과 동쪽에서 남~남동류한 흐름이 팔금도~화원반도 사이로 흘렀다. 조류유속이 강한 곳은 암태도~압해도 사이 합류역이었다. 조석잔차류는 다도해 협수로의 빠른 유속으로 섬 주변 흐름 하류역에 후류와 또는 지형성와류가 형성되었다. 압해도 서쪽에 약한 반시계방향 와류와 압해도 북서 만곡부에 시계방향 환류가 존재했다. 북쪽 협수로를 제외한 압해도 연안은 조간대가 발달되어 조석잔차류 유속이 미약하였다.

• Nuclear Engineering and Technology
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• 제47권5호
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• pp.513-522
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• 2015

The present paper aims at improving the modeling of turbulence for the upward turbulent bubbly flow through the use of experimental databases that contain data on small and large vertical ducts. First, the role of bubble-induced turbulence was analyzed, which indicated the dominant role of the bubble-induced turbulence in the duct center for relatively high void fraction cases. Therefore, the turbulence therein was mainly focused on, which indicated that the stronger turbulence could be induced by bubbles in large ducts with similar void fractions as compared to that in small ducts. Next, the turbulence of upward turbulent bubbly flow near the wall is discussed to understand the interaction between the wall-induced and bubble-induced turbulence. It showed that the existence of a wall could suppress the bubble-induced turbulence given the same void fraction, and the existence of bubbles could also suppress the solely wall-induced turbulence as compared to the single-phase turbulent flow, even though the total turbulence is enhanced. The above characteristics indicated that the current turbulence modeling method needs to be modified, especially when the bubble-induced turbulence plays a dominant role.

• The Korean Journal of Physiology and Pharmacology
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• 제1권5호
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• pp.485-493
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• 1997

We investigated the effect of ${\alpha}-adrenergic$ and cholinergic receptor agonists on $Ca^{2+}$ current in adult rat trigeminal ganglion neurons using whole-cell patch clamp methods. The application of acetylcholine, carbachol, and oxotremorine ($50\;{\mu}M\;each$) produced a rapid and reversible reduction of the $Ca^{2+}$ current by $17{\pm}6%,\;19{\pm}3%,\;and\;18{\pm}4%$, respectively. Atropine, a muscarinic antagonist, blocked carbachol- induced $Ca^{2+}$ current inhibition to $3{\pm}1%$. Norepinephrine ($50\;{\mu}M$) reduced $Ca^{2+}$ current by $18{\pm}2%$, while clonidine ($50\;{\mu}M$), an ${\alpha}2-adrenergic$ receptor agonist, inhibited $Ca^{2+}$ current by only $4{\pm}1%$. Yohimbine, an ${\alpha}2-adrenergic$ receptor antagonist, did not block the inhibitory effect of norepinephrine on $Ca^{2+}$ current, whereas prazosin, an ${\alpha}1-adrenergic$ receptor antagonist, attenuated the inhibitory effect of norepinephrine on $Ca^{2+}$ current to $6{\pm}1%$. This pharmacology contrasts with ${\alpha}2-adrenergic$ receptor modulation of $Ca^{2+}$ channels in rat sympathetic neurons, which is sensitive to clonidine and blocked by yohimbine. Our data suggest that the modulation of voltage dependent $Ca^{2+}$ channel by norepinephrine is mediated via an α1-adrenergic receptor. Pretreatment with pertussis toxin (250 ng/ml) for 16 h greatly reduced norepinephrine- and carbachol-induced $Ca^{2+}$ current inhibition from $17{\pm}3%\;and\;18{\pm}3%\;to\;2{\pm}1%\;and\;2{\pm}1%$, respectively. These results demonstrate that norepinephrine, through an ${\alpha}1-adrenergic$ receptor, and carbachol, through a muscarinic receptor, inhibit $Ca^{2+}$ currents in adult rat trigeminal ganglion neurons via pertussis toxin sensitive GTP-binding proteins.

• The Korean Journal of Physiology and Pharmacology
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• 제5권6호
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• pp.487-494
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• 2001

During depolarization, extrusion of $Ca^{2+}$ from sarcoplasmic reticulum through forward-mode $Na^+-Ca^{2+}$ exchange was studied in the rat ventricular myocytes patch-clamped in whole-cell configuration. In order to confine the $Ca^{2+}$ responses in a micro-domain by limiting the $Ca^{2+}$ diffusion time, rat ventricular myocytes were dialyzed with high (14 mM) EGTA. $K^+$ current was suppressed by substituting KCl with 105 mM CsCl and 20 mM TEA in the pipette filling solution and by omitting KCl in the external Tyrode solution. $Cl^-$ current was suppressed by adding 0.1 mM DIDS in the external Tyrode solution. During stimulation roughly mimicking action potential, the initial outward current was converted into inward current, $47{\pm}1%$ of which was suppressed by 0.1 mM $CdCl_2.$ 10 mM caffeine increased the remaining inward current after $CdCl_2$ in a cAMP-dependent manner. This caffeine-induced inward current was blocked by $1\;{\mu}M$ ryanodine, $10\;{\mu}M$ thapsigargin, 5 mM $NiCl_2,$ or by $Na^+\;and\;Ca^{2+}$ omission, but not by $0.1\;{\mu}M$ isoproterenol. The $I{\sim}V$ relationship of the caffeine-induced current elicited inward current from -45 mV to +3 mV with the peak at -25 mV. Taken together, it is concluded that, during activation of the rat ventricular myocyte, forward-mode $Na^+-Ca^{2+}$ exchange extrudes a fraction of $Ca^{2+}$ released from sarcoplasmic reticulum mainly by voltage-sensitive release mechanism in a micro-domain in the t-tubule, which is functionally separable from global $Ca^{2+}{_i}$ by EGTA.

• 대한물리치료과학회지
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• 제10권2호
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• pp.199-207
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• 2003

The present study examined that in vivo/vitro test is investigated in normotensive sham-operated rats(NSR) and aldosterone-analogue deoxycorticosterone acetate (DOCA)-salt hypertensive rats(ADHR) and that the antiliypertensive effect was induced by silver spike point(SSP) electrical stimulation at meridian points(CV-3, -4, Ki-12, SP-6, LR-3, BL-25, -28, -32, -52), specifically, such as aldosterone in 24 hour urine analysis from normal volunteer. The heart weight, the tickness of vascular wall, collagen fiber and the systolic blood pressure were significantly increased in ADHR than that in NSR. The required time of PSS-induced resting tone and the phosphorylation of stress-activated protein kinase/c-Jun N-terminal protein kinase(SAPK/JNK) were significantly increased in ADHR than that in NSR. However, the Kv currents were significantly decreased in ADHR than that in NSR. The current of 1 Hz continue type of SSP electrical stimulation significantly decreased in excretion of urine aldosterone from normal volunteer. These results suggest that the development of aldosterone analogue-induced hypertension is associated with changed heart weight, content of collagen fiber, tickness of vascular wall, blood pressure, resting tone, voltage-dependent K+ current(Kv) and phosphorylation of SAPK/JNK, which directly affects blood pressure. Therefore the hypertension is a risk factor on cerebrovascular disease. Moreover, These results suggest that the SSP electrical stimulation, especially current of 1 Hz continue type, significantly regulates excretion of urine aldosterone from volunteer.

• The Korean Journal of Physiology and Pharmacology
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• 제12권1호
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• pp.31-35
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• 2008

Lysophosphatidylcholine (LPC), a metabolite of membrane phospholipids by phospholipase $A_2$, has been considered responsible for the development of abnormal vascular reactivity during atherosclerosis. $Ca^{2+}$ influx was shown to be augmented in atherosclerotic artery which might be responsible for abnormal vascular reactivity. However, the mechanism underlying $Ca^{2+}$ influx change in atherosclerotic artery remains undetermined. The purpose of the present study was to examine the effects of LPC on L-type $Ca^{2+}$ current $(I_{Ca(L)})$ activity and to elucidate the mechanism of LPC-induced change of $I_{Ca(L)}$ in rabbit portal vein smooth muscle cells using whole cell patch clamp. Extracellular application of LPC increased $I_{Ca(L)}$ through whole test potentials, and this effect was readily reversed by washout. Steady state voltage dependency of activation or inactivation properties of $I_{Ca(L)}$ was not significantly changed by LPC. Staurosporine (100 nM) or chelerythrine $(3{\mu}M)$, which is a potent inhibitor of PKC, significantly decreased basal $I_{Ca(L)}$, and LPC-induced increase of $I_{Ca(L)}$ was significantly suppressed in the presence of PKC inhibitors. On the other hand, application of PMA, an activator of PKC, increased basal $I_{Ca(L)}$ significantly, and LPC-induced enhancement of $I_{Ca(L)}$ was abolished by pretreatment of the cells with PMA. These findings suggest that LPC increased $I_{Ca(L)}$ in vascular smooth muscle cells by a pathway that involves PKC, and that LPC-induced increase of $I_{Ca(L)}$ might be, at least in part, responsible for increased $Ca^{2+}$ influx in atherosclerotic artery.

• 한국결정성장학회지
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• 제8권3호
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• pp.411-418
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• 1998

LPCVD 방법으로 실리콘 산화막 두께 10nm에서 80nm인 MOS를 제작하였다. 그리고 스트레스 전계 산화막 전류의 두께 의존성을 조사하였다. 산화막 전류는 스트레스 전류와 전이전류로 구성되어 있음을 보여 주었다. 스트레스 전류는 스트레스 유기 누설전류와 직류전류로 이루어졌으며 산화막을 통하는 트립 어시스트 터널링으로 행해진다. 전이전류는 계면에서 트랩의 터널링 충전과 방전에 의해 이루어진다. 스트레스 전류는 산화막 전류의 두계 한계를 평가하는데 이용되고 전이전류는 기억소자에서 데이터 유지에 사용된다.

• 한국전기전자재료학회:학술대회논문집
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• 한국전기전자재료학회 2002년도 하계학술대회 논문집 Vol.3 No.2
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• pp.699-702
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• 2002

A DC current sensor is disclosed in which two pairs of saturable cores are provided so as enclose a conductor carrying a direct current to be measured. On each of the saturable cores, a bias winding, a feedback winding and an output winding are wound. Circuit for detection of an asymmetry in the magnetization current, generated by a reference alternating voltage, in a signal-conditioner. The reference alternating voltage is fed to the respective series circuits such that no resultant induction current is induced in the modulating current. The voltages over the resistor form input signals for two peak value detectors, the strength of the output signal of which represents the degree of asymmetry of magnetization current. This paper describes the development a DC current sensor and its signal-conditioner.

• 대한전기학회논문지:전력기술부문A
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• 제53권2호
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• pp.80-86
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• 2004

During magnetic inrush or over-excitation, saturation of the core in a transformer draws a large exciting current, which can cause mal-operation of a differential relay. This paper proposes a modified current differential relay for transformer protection. The relay calculates core-loss current from the induced voltage and the core-loss resistance; the relay calculates the magnetizing current from the core flux and the magnetization curve. Finally, the relay obtains the modified differential current by subtracting the core-loss and the magnetizing currents from the conventional differential current. Comparison study with the conventional differential relay with harmonic blocking is also shown. The proposed technique not only discriminates magnetic inrush and over-excitation from an internal fault, but also improves the speed of the conventional relay.

• JSTS:Journal of Semiconductor Technology and Science
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• 제9권1호
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• pp.29-36
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• 2009

Power supply noise is fundamentally caused by large current peaks. Since large current peaks are induced by simultaneous switching of many circuit elements, power supply noise can be minimized by deliberate clock scheduling which utilizes nonzero clock skew. In this paper, nonzero skew clock scheduling is used to avoid the large peak current and consequently reduce power supply noise. While previous approaches require extra characterization efforts to acquire current waveform of a circuit, we approximate it only with existing cell library information to be easily adapted to conventional design flow. A simulated annealing based algorithm is performed, and the peak current values are estimated for feasible clock schedules found by the algorithm. The clock schedule with the minimum peak current is selected for a solution. Experimental results on ISCAS89 benchmark circuits show that the proposed method can effectively reduce the peak current.