A multi-gap and multi-channel gas switch with convexo-convex discal planet electrodes was designed and investigated. Eight gaps are formed in series by a trigger electrode, six intermediate electrodes and two high vol...A multi-gap and multi-channel gas switch with convexo-convex discal planet electrodes was designed and investigated. Eight gaps are formed in series by a trigger electrode, six intermediate electrodes and two high voltage electrodes with a uniform gap length of 5 ram. The self breakdown and triggered breakdown performance of the switch are reported. Both the delay time and jitter decrease with the increase in the trigger voltage, switching coefficient and the decrease in the trigger isolating resistor. The delay time of the switch is about 40 ns, and the jitter is less than 2 ns when charged with 4-85 kV and triggered by a voltage pule of -75 kV. The inductance of the switch is about 30 nH.展开更多
目的分解单通道表面肌电信号(surface electromyography,sEMG),获得组成肌电信号的运动单元动作电位(motor unit action potential,MUAP)的波形及发放频率。方法首先对单通道的sEMG信号进行候选MUAP信号段检测,然后使用基于模糊K-均值...目的分解单通道表面肌电信号(surface electromyography,sEMG),获得组成肌电信号的运动单元动作电位(motor unit action potential,MUAP)的波形及发放频率。方法首先对单通道的sEMG信号进行候选MUAP信号段检测,然后使用基于模糊K-均值聚类的Gap Statistic聚类分析处理获取参与肌肉活动的运动单元发放的模板MUAP,最后使用广义互相关求时延的方法完成对低收缩水平的表面肌电信号的分解,并获得所有模板MUAP的发放频率。结果对模拟的单通道表面肌电信号进行分解,MUAP的准确识别率可达80%以上;并对真实采集的低收缩水平的等长收缩表面肌电信号进行分解,得到了MUAP波形和发放信息。结论本文提出的方法能够有效的对单通道表面肌电信号进行分解,具有较好的分解效果。展开更多
Spontaneous, rhythmical contractions, or vasomotion, can be recorded from cerebral vessels under both normal physiological and pathophysiological conditions. We investigated the cellular mechanisms underlying vasomoti...Spontaneous, rhythmical contractions, or vasomotion, can be recorded from cerebral vessels under both normal physiological and pathophysiological conditions. We investigated the cellular mechanisms underlying vasomotion in the cerebral basilar artery （BA） of Wistar rats. Pressure myograph video microscopy was used to study the changes in cerebral artery vessel diameter. The main results of this study were as follows： （1） The diameters of BA and middle cerebral artery （MCA） were 314.5±15.7 μm （n=15） and 233.3±10.1 μm （n=12） at 10 mmHg working pressure （P〈0.05）, respectively. Pressure-induced vasomotion occurred in BA （22/28, 78.6%）, but not in MCA （4/31, 12.9%） from 0 to 70 mmHg working pressure. As is typical for vasomotion, the contractile phase of the response was more rapid than the relaxation phase; （2） The frequency of vasomotion response and the diameter were gradually increased in BA from 0 to 70 mmHg working pressure. The amplitude of the rhythmic con- tractions was relatively constant once stable conditions were achieved. The frequency of contractions was variable and the highest value was 16.7±4.7 （n=13） per 10 min at 60 mmHg working pressure; （3） The pressure-induced vasomotion of the isolated BA was attenuated by nifedipine, NFA, 181]-GA, TEA or in Ca2＋-free medium. Nifedipine, NFA, 18^-GA or Ca2＋-free medium not only dampened vasomotion, but also kept BA in relaxation state. In contrasts, TEA kept BA in contraction state. These results sug- gest that the pressure-induced vasomotion of the isolated BA results from an interaction between Ca2＋-activated C1- channels （CaCCs） currents and Kca currents. We hypothesize that vasomotion of BA depends on the depolarizing of the vascular smooth muscle cells （VSMCs） to activate CaCCs. Depolarization in turn activates voltage-dependent Ca2＋ channels, synchronizing contractions of adjacent cells through influx of extracellular calcium and the flow of calcium through gap junctions. Subsequent calcium-induced calcium release from ryanodine-sensitive stores activates Kca channels and hyperpo- larizes VSMCs, which provides a negative feedback loop for regenerating the contractile cycle.展开更多
基金supported by National Natural Science Foundation of China(Nos.50477019,50637010)the State Key Laboratory of Electrical Insulation and Power Equipment of China(EIPE.09207)
文摘A multi-gap and multi-channel gas switch with convexo-convex discal planet electrodes was designed and investigated. Eight gaps are formed in series by a trigger electrode, six intermediate electrodes and two high voltage electrodes with a uniform gap length of 5 ram. The self breakdown and triggered breakdown performance of the switch are reported. Both the delay time and jitter decrease with the increase in the trigger voltage, switching coefficient and the decrease in the trigger isolating resistor. The delay time of the switch is about 40 ns, and the jitter is less than 2 ns when charged with 4-85 kV and triggered by a voltage pule of -75 kV. The inductance of the switch is about 30 nH.
基金supported by grants from National Basic Research Program of China(No.2012CB52660000)National Natural Science Foundation of China(No.81000411,No.31100829,and No.31260247)
文摘Spontaneous, rhythmical contractions, or vasomotion, can be recorded from cerebral vessels under both normal physiological and pathophysiological conditions. We investigated the cellular mechanisms underlying vasomotion in the cerebral basilar artery （BA） of Wistar rats. Pressure myograph video microscopy was used to study the changes in cerebral artery vessel diameter. The main results of this study were as follows： （1） The diameters of BA and middle cerebral artery （MCA） were 314.5±15.7 μm （n=15） and 233.3±10.1 μm （n=12） at 10 mmHg working pressure （P〈0.05）, respectively. Pressure-induced vasomotion occurred in BA （22/28, 78.6%）, but not in MCA （4/31, 12.9%） from 0 to 70 mmHg working pressure. As is typical for vasomotion, the contractile phase of the response was more rapid than the relaxation phase; （2） The frequency of vasomotion response and the diameter were gradually increased in BA from 0 to 70 mmHg working pressure. The amplitude of the rhythmic con- tractions was relatively constant once stable conditions were achieved. The frequency of contractions was variable and the highest value was 16.7±4.7 （n=13） per 10 min at 60 mmHg working pressure; （3） The pressure-induced vasomotion of the isolated BA was attenuated by nifedipine, NFA, 181]-GA, TEA or in Ca2＋-free medium. Nifedipine, NFA, 18^-GA or Ca2＋-free medium not only dampened vasomotion, but also kept BA in relaxation state. In contrasts, TEA kept BA in contraction state. These results sug- gest that the pressure-induced vasomotion of the isolated BA results from an interaction between Ca2＋-activated C1- channels （CaCCs） currents and Kca currents. We hypothesize that vasomotion of BA depends on the depolarizing of the vascular smooth muscle cells （VSMCs） to activate CaCCs. Depolarization in turn activates voltage-dependent Ca2＋ channels, synchronizing contractions of adjacent cells through influx of extracellular calcium and the flow of calcium through gap junctions. Subsequent calcium-induced calcium release from ryanodine-sensitive stores activates Kca channels and hyperpo- larizes VSMCs, which provides a negative feedback loop for regenerating the contractile cycle.
