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RISS 인기검색어
- 검색키워드
- 저자 : Shu-Kuei Huang (검색결과 5 건)
- 무료
- 기관 내 무료
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Design and Analysis of an Interactive Motion Simulator in Space Entertainment System
( Kuei-shu Hsu ),( Wei-ting Cho ),( Chin-feng Lai ),( Xiaofei Wang ),( Yueh-min Huang ) 한국인터넷정보학회 2012 KSII Transactions on Internet and Information Syst Vol.6 No.1
In this paper, the analysis and design of a motion simulator (based on the approach taken by interactive virtual reality (VR) entertainment systems) is conducted. The main components of the system include a bilateral control interface, simulation and a motion simulator control scheme. The space entertainment system uses a virtual environment that enables operators to feel the actual feedback sensing and distorted motion from the virtual environment, just as they would in the real environment. The space entertainment system integrates the dynamics of the motion simulator and the virtual environment and the operator maneuvers a steering wheel to interact with the system. The multiple bilateral control schemes employ a dynamical controller, which is designed by considering the velocity and acceleration that the operator imposes on the joystick, the environmental changes imposed on the motion simulator. In addition, we develop a calculated method to evaluate the Ratio of the simulation results. It is shown that the proposed control scheme can improve the performance of the visual entertainment system. Experiments are conducted on the virtual reality entertainment system to validate the theoretical developments.
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Lu, Cheng-Wei,Huang, Shu-Kuei,Lin, Tzu-Yu,Wang, Su-Jane The Korean Society of Pharmacology 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.3
Echinacoside, an active compound in the herb Herba Cistanche, has been reported to inhibit glutamate release. In this study, we investigated the effects of echinacoside on spontaneous excitatory synaptic transmission changes induced by 4-aminopyridine (4-AP), by using the in vitro rat hippocampal slice technique and whole-cell patch clamp recordings from CA3 pyramidal neurons. Perfusion with echinacoside significantly suppressed the 4-AP-induced epileptiform activity in a concentration-dependent manner. Echinacoside reduced 4-AP-induced increase in frequency of spontaneous excitatory postsynaptic currents (sEPSCs) but it did not affect the amplitude of sEPSCs or glutamate-activated currents, implicating a presynaptic mechanism of action. Echinacoside also potently blocked sustained repetitive firing, which is a basic mechanism of antiepileptic drugs. These results suggest that echinacoside exerts an antiepileptic effect on hippocampal CA3 pyramidal neurons by simultaneously decreasing glutamate release and blocking abnormal firing synchronization. Accordingly, our study provides experimental evidence that echinacoside may represent an effective pharmacological agent for treating epilepsy.
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Cheng Wei Lu,Shu-Kuei Huang,Tzu Yu Lin,Su-Jane Wang 대한약리학회 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.3
Echinacoside, an active compound in the herb Herba Cistanche, has been reported to inhibit glutamate release. In this study, we investigated the effects of echinacoside on spontaneous excitatory synaptic transmission changes induced by 4-aminopyridine (4-AP), by using the in vitro rat hippocampal slice technique and whole-cell patch clamp recordings from CA3 pyramidal neurons. Perfusion with echinacoside significantly suppressed the 4-AP-induced epileptiform activity in a concentration-dependent manner. Echinacoside reduced 4-AP-induced increase in frequency of spontaneous excitatory postsynaptic currents (sEPSCs) but it did not affect the amplitude of sEPSCs or glutamate-activated currents, implicating a presynaptic mechanism of action. Echinacoside also potently blocked sustained repetitive firing, which is a basic mechanism of antiepileptic drugs. These results suggest that echinacoside exerts an antiepileptic effect on hippocampal CA3 pyramidal neurons by simultaneously decreasing glutamate release and blocking abnormal firing synchronization. Accordingly, our study provides experimental evidence that echinacoside may represent an effective pharmacological agent for treating epilepsy.
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Tzu Yu Lin,Cheng Wei Lu,Shu-Kuei Huang,Su-Jane Wang 한국식품영양과학회 2013 Journal of medicinal food Vol.16 No.2
This study investigated the effects and possible mechanism of ferulic acid, a naturally occurring phenolic compound, on endogenous glutamate release in the nerve terminals of the cerebral cortex in rats. Results show that ferulic acid inhibited the release of glutamate evoked by the K+ channel blocker 4-aminopyridine (4-AP). The effect of ferulic acid on the evoked glutamate release was prevented by chelating the extracellular Ca2+ ions, but was insensitive to the glutamate transporter inhibitor DL-threo-beta-benzyl-oxyaspartate. Ferulic acid suppressed the depolarization-induced increase in a cytosolic-free Ca2+ concentration, but did not alter 4-AP–mediated depolarization. Furthermore, the effect of ferulic acid on evoked glutamate release was abolished by blocking the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channels, but not by blocking ryanodine receptors or mitochondrial Na+/Ca2+ exchange. These results show that ferulic acid inhibits glutamate release from cortical synaptosomes in rats through the suppression of presynaptic voltage-dependent Ca2+ entry.
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Myricetin Inhibits the Release of Glutamate in Rat Cerebrocortical Nerve Terminals
Yi Chang,Chia-Ying Chang,Su-Jane Wang,Shu-Kuei Huang 한국식품영양과학회 2015 Journal of medicinal food Vol.18 No.5
The excessive release of glutamate is a critical element in the neuropathology of acute and chronic brain disorders. The purpose of the present study was to investigate the effect and possible mechanism of myricetin, a naturally occurring flavonoid with a neuroprotective profile, on endogenous glutamate release in the nerve terminals (synaptosomes) of the rat cerebral cortex. The release of glutamate was evoked by the K+ channel blocker 4-aminopyridine (4-AP) and measured by one-line enzyme-coupled fluorometric assay. We also used a membrane potential-sensitive dye to assay the synaptosomal plasma membrane potential, and a Ca2 + indicator Fura-2 to monitor cytosolic Ca2 + concentrations ([Ca2 + ]C). Results show that myricetin inhibited 4-AP-evoked glutamate release, and this effect was prevented by chelating extracellular Ca2 + ions and the vesicular transporter inhibitor bafilomycin A1. However, the glutamate transporter inhibitor dl-threo-beta-benzyl-oxyaspartate had no effect on myricetin action. Myricetin did not alter the synaptosomal membrane potential, but decreased 4-APinduced increases in the cytosolic free Ca2 + concentration. Furthermore, the myricetin effect on 4-AP-evoked glutamate release was prevented by blocking the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channels, but not by blocking intracellular Ca2 + release. These results suggest that myricetin inhibits glutamate release from cerebrocortical synaptosomes by attenuating voltage-dependent Ca2 + entry. This implies that the inhibition of glutamate release is an important pharmacological activity of myricetin that may play a critical role in the apparent clinical efficacy of this compound.
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