• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2005.07a
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• pp.105-106
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• 2005

The impact ionization MOS (I-MOS) transistor with 50nm channel length is presented by using 2-D device simulator ISE-TCAD. The subthreshold slope cannot be steeper than kT/q since the subthreshold conduction is due to diffusion current. As MOSFETs are scaled down, this problem becomes significant and the subthreshold slope degrades which leads an increase in the off-current and off-state power dissipation. The I-MOS is based on a gated p-i-n structure and the subthreshold conduction is induced by impact ionization. The simulation results show that the subthreshold slope is 11.7 mV/dec and this indicates the I-MOS improves the switching speed and off-state characteristics.

• Proceedings of the KIEE Conference
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• 1995.07c
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• pp.1205-1208
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• 1995

The optically-gated p-i-n diode switches have been fabricated with gold-compensated silicon. The turn-on and turn-off delay times and the rise and fall times were measured as a function of optical power level, bias, and pulse width. The turn-on characteristics shows a strong dependence an optical pulse power and a delay time(${\delta}{\iota}$) between two pulses, but a weak dependence on the width of optical pulse. Actually there is no turn-off delay in gold-doped p-i-n switches and the fall time is negligible.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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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.

• JSTS:Journal of Semiconductor Technology and Science
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• v.12 no.3
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• pp.370-376
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• 2012

In this work, design considerations for high-performance silicon photodetector are thoroughly investi- gated. Besides the critical dimensions of device, guidelines for process architecture are suggested. Abiding by those criteria for improving both direct-current (DC) and alternating-current (AC) perfor- mances, a high-speed low-operation power silicon photodetector based on p-i-n structure for optical interconnect has been designed by device simulation. An $f_{-3dB}$ of 80 GHz at an operating voltage of 1 V was obtained.

• The Korean Journal of Nuclear Medicine
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• v.31 no.1
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• pp.57-66
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• 1997

We performed 1st day Tc-99m-sestamibi gated SPECT with dipyridamole/rest T1-201 SPECT and 2nd day 24 hour delay T1-201 SPECT/rest Tc-99m-sestamibi gated SPECT in 27 patients with coronary artery disease(24) or having chest pain(3). Stress and rest Tc-99m-sestamibi gated SPECT was acquired at 60min post-injection. A 4-point scoring system(0 to 3 for normal to absent tracer uptake) for 17 segments was used. Wall motion was scored on another 4 point scale(0 to 3 for normal to dyskinesia) in the 1st day post-stress gated and the 2nd day rest gated SPECT. Post-stress gated SPECT showed wall motion abnormality in 94 segments(20%). Fifty-five segments among these 94 showed the same wall motion between post-stress and rest gated SPECT: i.e. 1-1 23 segments, 2-2: 29 segments, 3-3: 3 segments. Remaining 39 segments(41.5%) showed different wall motion between post- stress and rest Tc-99m-sestamibi gated SPECT. Twenty one segments with wall motion abnormality had normal perfusion(rest : 15 segments, 24 hour delay: 6 segments) at either rest or 24 hour delay. Fifteen among these 21 segments showed persistent post-stress and the 2nd day rest wall motion abnormality(persistent stunning). However, in 6 segments with pro-longed (1 hour after stress) stunning, abnormal wall motion did improve in the 2nd day rest Tc-99m-sestamibi gated SPECT(transient prolonged stunning). These 6 segments had normal perfusion at rest(n=4) or at 24 hour delay(n=2). Post stress wall motions showed significantly higher scores in persistent stunning than in prolonged transient stunning(P value<0.05). It was concluded that we could find stunned myocardium with gated Tc-99m-sestamibi SPECT at either post-stress or rest and that some myocardial walls of post-stress 1 hour gated SPECT did not show truly rest wall motion. So, we should be cautious if we use post-stress Tc-99m-sestamibi wall motion to assess rest wall motion.

• Proceedings of the Korean Biophysical Society Conference
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• 1996.07a
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• pp.8-8
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• 1996

The regulatory role of A$\_$2A/ adenosine receptors on the P purinoceptor-mediated calcium signaling was investigated in rat pheochromocytoma (PC 12) cells. When PC 12 cells were treated with 2-p-(2-carboxyethyl) phenethylamino- 5' - N -ethylcarboxamido-adenosine (CGS21680), a specific agonist of the A$\_$2A/ adenosine receptor, extracellular ATP-evoked [Ca$\^$2+/]$\_$I/ rise was inhibited by -20%. (omitted)

• Development and Reproduction
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• v.24 no.4
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• pp.297-306
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• 2020

Repetitive changes in the intracellular calcium concentration ([Ca²⁺]i) triggers egg activation, including cortical granule exocytosis, resumption of second meiosis, block to polyspermy, and initiating embryonic development. [Ca²⁺]i oscillations that continue for several hours, are required for the early events of egg activation and possibly connected to further development to the blastocyst stage. The sources of Ca²⁺ ion elevation during [Ca²⁺]i oscillations are Ca²⁺ release from endoplasmic reticulum through inositol 1,4,5 tri-phosphate receptor and Ca²⁺ ion influx through Ca²⁺ channel on the plasma membrane. Ca²⁺ channels have been characterized into voltage-dependent Ca²⁺ channels (VDCCs), ligand-gated Ca²⁺ channel, and leak-channel. VDCCs expressed on muscle cell or neuron is specified into L, T, N, P, Q, and R type VDCs by their activation threshold or their sensitivity to peptide toxins isolated from cone snails and spiders. The present study was aimed to investigate the localization pattern of N and P/Q type voltage-dependent calcium channels in mouse eggs and the role in fertilization. [Ca²⁺]i oscillation was observed in a Ca²⁺ contained medium with sperm factor or adenophostin A injection but disappeared in Ca²⁺ free medium. Ca²⁺ influx was decreased by Lat A. N-VDCC specific inhibitor, ω-Conotoxin CVIIA induced abnormal [Ca²⁺]i oscillation profiles in SrCl₂ treatment. N or P/Q type VDC were distributed on the plasma membrane in cortical cluster form, not in the cytoplasm. Ca²⁺ influx is essential for [Ca²⁺]i oscillation during mammalian fertilization. This Ca²⁺ influx might be controlled through the N or P/Q type VDCCs. Abnormal VDCCs expression of eggs could be tested in fertilization failure or low fertilization eggs in subfertility women.

• Journal of the Korean Institute of Electrical and Electronic Material Engineers
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• v.13 no.5
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• pp.371-375
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• 2000

In this paper a new conductivity modulated power transistor called the Lateral Insulated Gated Bipolar Transistor which included n+ ring and p-channel gate is presented. A new lateral IGBT structure is proposed to suppress latch-up and to improve turn off time by imploying n+ ring and p-channel gate and verified by MEDICI. The simulated I-V characteristics at $V_{G}$=15V show that the latch up occurs at $V_{A}$=18V and 6.9$\times$10$^{-5}$ A/${\mu}{\textrm}{m}$ for the proposed LIGBT while the conventional LIGBT latches at $V_{A}$=1.3V and 1.96${\mu}{\textrm}{m}$10$^{-5A}$${\mu}{\textrm}{m}$. It is shown that turn off characteristic of new LIGBT is 8 times than that of conventional LIGBT. And noble LIGBT is not n+ buffer layer because that It includes p channel gate and n+ ring. Therefore Mask for the buffer layer isn’t needed. The concentration of n+ ring is and the numbers of n+ ring and p channel gate are three for the optimal design.n.n.n.n.

• Journal of Ginseng Research
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• v.27 no.3
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• pp.120-128
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• 2003

Alternative medicines such as herbal products are increasingly being used for preventive and therapeutic purposes. Ginseng is the best known and most popular herbal medicine used worldwide. In spite of some beneficial effects of ginseng on the nervous system, little scientific evidence shows at the cellular level. In the present study, I have examined the direct modulation of ginseng total saponins and individual ginsenosides on the activation of $Ca^{2+}$ channels and NMDA-gated channels in cultured rat dorsal root ganglion (DRG) and hippocampal neurons, respectively. In DRG neurons, application of ginseng total saponins suppressed high-voltage-activated $Ca^{2+}$ channel currents and ginsenoside Rg$_3$, among the 11 ginsenosides tested, produced the strongest inhibition on $Ca^{2+}$ channel currents. Occlusion experiments using selective $Ca^{2+}$ channel blockers revealed that ginsenoside Rg$_3$ could modulate L-, N-, and P/Q-type currents. In addition, ginsenoside Rg$_3$ also proved to be an active component of ginseng actions on NMDA receptors in cultured hippocampal neurons. Application of ginsenoside Rg$_3$ suppressed NMDA-induced [Ca$^{2+}$]$_{i}$ increase and -gated channels using fura-2-based digital imaging and patch-clamp techniques, respectively. These results suggest that the modulation of $Ca^{2+}$ channels and NMDA receptors by ginsenoside Rg$_3$ could be part of the pharmacological basis of ginseng actions in the peripheral and central nervous systems.ous systems.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.1
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• pp.21-28
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• 2010

Phenolic compounds affect intracellular free $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) signaling. The study examined whether the simple phenolic compound octyl gallate affects ATP-induced $Ca^{2+}$ signaling in PC12 cells using fura-2-based digital $Ca^{2+}$ imaging and whole-cell patch clamping. Treatment with ATP ($100\;{\mu}M$) for 90 s induced increases in $[Ca^{2+}]_i$ in PC12 cells. Pretreatment with octyl gallate (100 nM to $20\;{\mu}M$) for 10 min inhibited the ATP-induced $[Ca^{2+}]_i$ response in a concentration-dependent manner ($IC_{50}=2.84\;{\mu}M$). Treatment with octyl gallate ($3\;{\mu}M$) for 10 min significantly inhibited the ATP-induced response following the removal of extracellular $Ca^{2+}$ with nominally $Ca^{2+}$-free HEPES HBSS or depletion of intracellular $Ca^{2+}$ stores with thapsigargin ($1\;{\mu}M$). Treatment for 10 min with the L-type $Ca^{2+}$ channel antagonist nimodipine ($1\;{\mu}M$) significantly inhibited the ATP-induced $[Ca^{2+}]_i$ increase, and treatment with octyl gallate further inhibited the ATP-induced response. Treatment with octyl gallate significantly inhibited the $[Ca^{2+}]_i$ increase induced by 50 mM KCI. Pretreatment with protein kinase C inhibitors staurosporin (100 nM) and GF109203X (300 nM), or the tyrosine kinase inhibitor genistein ($50\;{\mu}M$) did not significantly affect the inhibitory effects of octyl gallate on the ATP-induced response. Treatment with octyl gallate markedly inhibited the ATP-induced currents. Therefore, we conclude that octyl gallate inhibits ATP-induced $[Ca^{2+}]_i$ increase in PC12 cells by inhibiting both non-selective P2X receptor-mediated influx of $Ca^{2+}$ from extracellular space and P2Y receptor-induced release of $Ca^{2+}$ from intracellular stores in protein kinase-independent manner. In addition, octyl gallate inhibits the ATP-induced $Ca^{2+}$ responses by inhibiting the secondary activation of voltage-gated $Ca^{2+}$ channels.