• The Korean Journal of Physiology and Pharmacology
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• 제10권5호
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• pp.255-261
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• 2006

Melittin-induced nociceptive responses are mediated by selective activation of capsaicin-sensitive primary afferent fibers and are modulated by excitatory amino acid receptor, cyclooxygenase, protein kinase C and serotonin receptor. The present study was undertaken to investigate the peripheral and spinal actions of voltage-gated calcium channel antagonists on melittin-induced nociceptive responses. Changes in mechanical threshold and number of flinchings were measured after intraplantar (i.pl.) injection of melittin $(30\;{\mu}g/paw)$ into mid-plantar area of hindpaw. L-type calcium channel antagonists, verapamil [intrathecal (i.t.), 6 or $12\;{\mu}g$; i.pl.,100 & $200\;{\mu}g$; i.p., 10 or 30 mg], N-type calcium channel blocker, ${\omega}-conotoxin$ GVIA (i.t., 0.1 or $0.5\;{\mu}g$; i.pl., $5\;{\mu}g$) and P-type calcium channel antagonist, ${\omega}-agatoxin$ IVA (i.t., $0.5\;{\mu}g$; i.pl., $5\;{\mu}g$) were administered 20 min before or 60 min after i.pl. injection of melittin. Intraplantar pre-treatment and i.t. pre- or post-treatment of verapamil and ${\omega}-conotoxin$ GVIA dose-dependently attenuated the reduction of mechanical threshold, and melittin-induced flinchings were inhibited by i.pl. or i.t. pre-treatment of both antagonists. P-type calcium channel blocker, ${\omega}-agatoxin$ IVA, had significant inhibitory action on flinching behaviors, but had a limited effect on melittin-induced decrease in mechanical threshold. These experimental findings suggest that verapamil and ${\omega}-conotoxin$ GVIA can inhibit the development and maintenance of melittin-induced nociceptive responses.

• 유체기계공업학회:학술대회논문집
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• 유체기계공업학회 2003년도 유체기계 연구개발 발표회 논문집
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• pp.121-125
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• 2003

Micromixer plays an important role in Bio-MEMS or ${\mu}-TAS$. Mixing is generally generated by turbulence and interdiffusion of two fluids. Because of low Reynolds number(Re << 2000) in ${\mu}-channel$, it is difficult to generate turbulence, so mixing mainly depends on interdiffusion. Thus long channel distance is required to mix two different fluids. To reduce the channel length required for mixing, we propose the a new active ${\mu}-mixer$ that two fluids are effectively mixed in ${\mu}-channel$ by the ultrasonic wave which is generated by PZT. The ultrasonic wave is radiated into a chamber in the cross-section directional direction to interface with the two fluids. The two fluids are positioned one on top of the other. Mixing state is measured by the changing of color due to the reaction of NaOH and phenolphtalein.

• The Korean Journal of Pain
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• 제24권3호
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• pp.131-136
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• 2011

Background: Pregabalin is an anticonvulsant and analgesic agent that interacts selectively with the voltage-sensitive-$Ca^{2+}$-channel alpha-2-delta subunit. The aim of this study was to evaluate whether the analgesic action of intrathecal (IT) pregabalin is associated with KATP channels in the rat formalin test. Methods: IT PE-10 catheters were implanted in male Sprague-Dawley rats (250.300 g) under inhalation anesthesia using enflurane. Nociceptive behavior was defined as the number of hind paw flinches during 60 min after formalin injection. Ten min before formalin injection, IT drug treatments were divided into 3 groups: normal saline (NS) $20\;{\mu}l$ (CON group); pregabalin 0.3, 1, 3 and $10\;{\mu}g$ in NS $10\;{\mu}l$ (PGB group); glibenclamide $100\;{\mu}g$ in DMSO $5\;{\mu}l$ with pregabalin 0.3, 1, 3 and $10\;{\mu}g$ in NS $5\;{\mu}l$ (GBC group). All the drugs were flushed with NS $10\;{\mu}l$. Immunohistochemistry for the $K_{ATP}$ channel was done with a different set of rats divided into naive, NS and PGB groups. Results: IT pregabalin dose-dependently decreased the flinching number only in phase 2 of formalin test. The log dose response curve of the GBC group shifted to the right with respect to that of the PGB group. Immunohistochemistry for the $K_{ATP}$ channel expression on the spinal cord dorsal horn showed no difference among the groups 1 hr after the formalin test. Conclusions: The antinociceptive effect of pregabalin in the rat formalin test was associated with the activation of the $K_{ATP}$ channel. However, pregabalin did not induce $K_{ATP}$ channel expression in the spinal cord dorsal horn.

• 대한전자공학회논문지SD
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• 제49권1호
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• pp.8-14
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• 2012

전체 채널 폭은 같지만 핀 수와 핀 폭이 다른 n-채널 MuGFET의 특성을 측정 비교 분석하였다. 사용된 소자는 Pi-gate 구조의 MuGFET이며 핀 수가 16이며 핀 폭이 55nm인 소자와 핀 수가 14이며 핀 폭이 80nm인 2 종류의 소자이다. 측정 소자성능은 문턱전압, 이동도, 문턱전압 roll-off, DIBL, inverse subthreshold slope, PBTI, hot carrier 소자열화 및 드레인 항복전압 이다. 측정 결과 핀 폭이 작으며 핀 수가 많은 소자의 단채널 현상이 우수한 것을 알 수 있었다. PBTI에 의한 소자열화는 핀 수가 많은 소자가 심하며 hot carrier에 의한 소자열화는 비슷한 것을 알 수 있었다. 그리고 드레인 항복 전압은 핀 폭이 작고 핀 수가 많은 소자가 높은 것을 알 수 있었다. 단채널 현상과 소자열화 및 드레인 항복전압 특성을 고려하면 MuGFET소자 설계 시 핀 폭을 작게 핀 수를 많게 하는 것이 바람직하다.

• Biomolecules & Therapeutics
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• 제9권2호
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• pp.96-103
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• 2001

These studies were investigated about influence of SKP 450, a $K^{+}$ channel opener, on the pressor actions induced by norepinephrine, angiotensin II and carotid artery occlusion in rats. Before these studies, effect of SKP 450 itself on blood pressure was examinated. SKP 450 produced the depressor action in proportionaly to dose of 0.3, 1.0 and 3.0 $\mu$g/kg given intravenously and this depressor action was weakened by pretreatment of glibenclamide, a $K^{+}$ channel blocker. The pressor action induced by norepinephrine, an alpha-adrenergic agonist, was blocked 1 hr after administation of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v. and directly after in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The pressor action induced by angiotensin II was blocked immediatly after treatment of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v.. The pressor action caused by carotid artery occlusion was not affected by SKP 450 of 3.0 $\mu\textrm{g}$/kg, i.v., whereas markedly blocked by SKP 450 of 6.0 $\mu\textrm{g}$/㎦, i.v.. The potentiated-pressor actions of norepinephrine and angiotensin II by pretreatment of chlorisondamine, a autonomic ganglionic blocking agent, were also blocked by administration of SKP 450 in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The weakened-pressor action of carotid artery occlusion by pretreatment of chlorisondamine was more weakened by SKP 450 6.0 $\mu\textrm{g}$/kg, i.v.. The results suggest that hyperpolarization formed through $K^{+}$ channel opening in cell membrane inhibits the pressor action induced norepinephrine ; angiotensin II ; and carotid artery occlusion.usion.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1992년도 제1회 신약개발 연구발표회 초록집
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• pp.45-45
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• 1992

Calcium channel에 작용하는 dihydropyridine(DHP) 계열의 calcium channel 효능제와 길항제의 caicium channel에 대한 작용과 muscarinic receptor에 대한 작용과의 관계를 조사하기 위하여 [$^3$H]QNB와 [$^3$H]nitrendipine 결합실험을 시행하고 이를 지표로 하여 칼슘효능제와 길항제의 이들 receptors에 대한 결합성질을 검토하였다. 본 연구결과 칼슘 channel 효능제인 Bay K 8644는 칼슘길항제인 nicardipine 및 nimodipine과 같이 고농도에서 muscarinic receptor에 대한 [$^3$H]QNB결합을 경쟁적으로 억제하였으며 이들 약물의 muscarinic receptor에 대한 Ki치는 각각 16.7 $\mu$M, 3.5 $\mu$M, 및 15.5 $\mu$M이었다. 한편, 이들 약물은 다같이 칼슘 channel의 high affinity DHP결합부위에 대한 [$^3$H]nitrendipine 결합을 억제하였으나 이 부위에 대한 Bay K 8644, nicardipine, 및 nimodipine의 Ki치는 각각 4 nM, 0.1 nM, 및 0.2 nM로서 muscarinic receptor에 대한 Ki치 보다 4,000-75,000배 작았다. 뿐만 아니라 [$^3$H]QNB결합을 완전히 차단하는 고농도의 atropine(1 $\mu$M)에 의해서도 [$^3$H]nitrendipine결합이 전혀 영향을 받지 않았다. 따라서 DHP계 약물의 muscarinic receptor에 대한 작용은 칼슘channel에 대한 이들 약물의 작용을 연구하거나 임상적 치료 목적으로 사용할때는 나타나지 않을 것으로 생각된다.

• 한국재료학회지
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• 제18권5호
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• pp.272-276
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• 2008

In submicron MOSFET devices, maintaining the ratio between the channel length (L) and the channel depth (D) at 3 : 1 or larger is known to be critical in preventing deleterious short-channel effects. In this study, n-type SOI-MOSFETs with a channel length of $0.1\;{\mu}m$ and a Si film thickness (channel depth) of $0.033\;{\mu}m$ (L : D = 3 : 1) were virtually fabricated using a TSUPREM-4 process simulator. To form functioning transistors on the very thin Si film, a protective layer of $0.08\;{\mu}m$-thick surface oxide was deposited prior to the source/drain ion implantation so as to dampen the speed of the incoming As ions. The p-type boron doping concentration of the Si film, in which the device channel is formed, was used as the key variable in the process simulation. The finished devices were electrically tested with a Medici device simulator. The result showed that, for a given channel doping concentration of $1.9{\sim}2.5\;{\times}\;10^{18}\;cm^{-3}$, the threshold voltage was $0.5{\sim}0.7\;V$, and the subthreshold swing was $70{\sim}80\;mV/dec$. These value ranges are all fairly reasonable and should form a 'magic region' in which SOI-MOSFETs run optimally.

• 한국산학기술학회논문지
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• 제12권6호
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• pp.2660-2667
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• 2011

TREK-1 채널은 two-pore 도메인 포타슘 (K2P) 채널로서 세포내 pH, 세포막의 신전, 불 포화 지방산, 온도, 휘발성 마취제, 신경세포방어물질에 의해 잘 조절된다. TREK-1 채널은 포타슘 이동에 의해 신경세포의 흥분성과 안정막전압을 조절한다. 최근 TREK-1은 전립선 암세포에서도 과발현됨이 확인되었다. 이러한 중요성에도 불구하고, TREK-1 채널에 대한 플라보노이드 효과는 거의 알려지지 않았다. 본 연구의 목적은 전기생리학적 방법 중의 하나인 excised inside-out patch기법을 이용하여 TREK-1 채널을 조절하는 플라보노이드를 탐색하는 것이다. TREK-1 채널이 발현된 CHO 세포에서 단일채널 팻취고정 방법을 이용하여 커큐민 (curcumin), EGCG (epigallocatechin-3-gallate), 퀘르세틴 (quercetin)에 의한 TREK-1 채널의 차단효과를 증명하였다. 퀘르세틴과 커큐민의 차단효과는 가역적으로 회복되었으나 EGCG는 거의 회복되지 않았다. 퀘르세틴, EGCG, 커큐민의 상대적 채널 활성도 (relative channel activity)는 $73{\pm}2.3%$ (n=5), $91{\pm}3.2%$ (n=7), $94{\pm}5.6%$ (n=4)까지 감소하였다. CHO 세포에 발현된 TREK-1 채널에 대한 커큐민, 퀘르세틴, EGCG의 $IC_{50}$는 각각 $1.04{\pm}0.19\;{\mu}M$, $1.13{\pm}0.26\;{\mu}M$, $13.5{\pm}2.20\;{\mu}M$ 이었다. 이러한 결과는 플라보노이드가 TREK-1 채널을 억제하며, 이 조절은 신경계 또는 종양세포에서 플라보노이드의 약리학적 작용 중의 하나임을 제시한다.

• 전자공학회논문지D
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• 제34D권8호
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• pp.35-40
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• 1997

To suppress the short channel effects in nMOSFET with 0.1.mu.m channel length, we have fabricated and characterized the ISRC n MOSFET with several process condition. When the recess oxide thickness is 100nm and the channel dose for threshold voltge adjustment is 6*10$^{12}$ /c $m^{-2}$ , B $F_{2}$$^{+}$, the maximum transconductance at $V_{DS}$ =2.0V is 455mS/mm and the BIDL is kept within 67mV. By comparing the ISRC n MOSFET with the conventioanl SHDD (shallowly heavily dopped drain) nMOSFET, we verify the suppression of short channel effects ISRC structure.e.

• JSTS:Journal of Semiconductor Technology and Science
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• 제8권4호
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• pp.302-310
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• 2008

This paper puts forward an advanced consideration on the design of scaled multiple-gate FET (MuGFET); the aspect ratio ($R_{h/w}$) of the fin height (h) to fin width (w) of MuGFET is considered with the aid of 3-D device simulations. Since any change in the aspect ratio must consider the trade-off between drivability and short-channel effects, it is shown that optimization of the aspect ratio is essential in designing MuGFET's. It is clearly seen that the triple-gate (TG) FET is superior to the conventional FinFET from the viewpoints of drivability and short-channel effects as was to be expected. It can be concluded that the guideline of w < L/3, where L is the channel length, is essential to suppress the short-channel effects of TG-FET.