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异常电活动
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  abnormal electric activities
     Conclusions:By inhibiting the calcium current through L type calcium channel and decreasing the“run down”of the current,RA could prevent intracellular calcium overload and abnormal electric activities caused by virus infection.
     结论:黄芪通过抑制感染细胞经 L 型钙通道的跨膜钙内流和稳定 L 型钙通道的作用,可防止病毒感染可能导致的细胞内钙超载和异常电活动,从而对感染细胞起到保护作用
短句来源
     CONCLUSIONS:By counteracting the effects of CVB 3 to L-type voltage dependent calcium channel and Na +/Ca 2+ exchange, AM could prevent intracellular calcium overload and abnormal electric activities caused by virus infection.
     结论:黄芪通过拮抗CVB3感染对L型钙通道和钠钙交换电流的影响,可防止病毒感染可能导致的细胞内钙超载和异常电活动,从而对感染细胞起到保护作用。
短句来源
     also, it may be the cause of cell damage and the occurrence of abnormal electric activities induced by CVB3 infection.
     可能是病毒感染后细胞损伤和产生异常电活动的原因。
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  “异常电活动”译为未确定词的双语例句
     Bar 30 μmol/L was found to be able to block delayed after-depolarization and to stop abnormal automatic activity.
     Ber 30μmol/L明显抑制缺氧再给氧所致迟后除极,完全消除异常电活动
短句来源
     Evidence showed that the application of Ga~(2+) and Ca~(2+) channel blockers modulated the abnormal activity of the injured nerve. Ga~(2+) facilitation was dependent on its concentration (in the range of 10~20mol/L), while 40mol/L Ca~(2+) always abolished firing.
     5mmol/L Ca~(2+)不能使受损神经异常放电频率改变,10~20mmol/L Ca~(2+)总能引起兴奋效应,40mmol/L Ca~(2+)则可使异常电活动频率降低。 静脉或局部应用异搏定不但可抑制受损神经自发性异常电活动,还可阻断四乙胺(TEA)诱发的电活动。
短句来源
     The present data suggested that the C and Aδ units with lowered mechanical threshold contribute to the decrease of the behavioral nociceptive threshold of diabetic rats and abnormal discharge of the C and Aδ units may be a peripheral factor in hypersensitivity to painful stimuli and paresthesia of diabetic rats.
     结果表明,糖尿病大鼠C单位和Aδ单位机械阈值的降低有助于其行为伤害性阈值的下降,C单位和Aδ单位的异常电活动是糖尿病大鼠产生对痛刺激敏感性升高和感觉异常的外周因素。
短句来源
     It is suggested that newly formed Ca~(2+) channels on the naked axolemma are largely responsible for the abnormal afferent activities following demyelination of the nerve.
     提示神经损伤区轴突膜上形成了Ca~(2+)通道,而来自损伤区的异常电活动与Ca~(2+)通道密切相关。
短句来源
     In addition, IHC66 did not antagonized abnormal automaticity induced by aconitine (AC).
     但对乌头碱(aconitine,AC)诱发的异常电活动无明显对抗作用。
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  相似匹配句对
     Ca~(2+) Channels and the Abnormal Electrical Activity of Demyelinated Nerve
     钙离子对神经异常活动的影响
短句来源
     EEG showed abnormal electrical activity on temporal lobe.
     脑图检查颞叶呈异常活动
短句来源
     Abnormal colonic electricity activity and motion of visceral hypersensitive rat
     内脏高敏感大鼠结肠活动及运动异常
短句来源
     Activities
     活动
短句来源
     No abnormal movement to either side occurred.
     均无侧方异常活动
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The result of intelligence observation of 40 adult epileptic patients

40例成人癫痢患者智能检查结果,病人组总智商(F/Q)为85.4±20·9,对照组为10·8±9·5(P<0.05),病人组总智商低于平常者19例,对照组仅1例(10%);总智商为边界或缺陷智商者病人组16例,对照组无,两组智力有显著差异(P<0.05)。可能影响癫痫患者智力的因素有:病程长,癫痫频繁发作和有癫痫持续状态史。癫痫患者脑异常电活动本身是脑损伤的基本原因。患者智力减退,可能是癫痫导致脑损伤的一个佐证。

An intracellular microelectrode technique was used to evaluate the changes of electric activities of cultured rat beating heart cells with hypoxia and reoxygenation injury. The results (n = 37) showed that hypoxia caused decreases in the maximal diastolic potential (MDP), Vmax . overshoot (OS) and action potential amplitude (APA), shortening in action potential duration (APD50 and APD100), increase in beating frequency and lots of multiform arrhythmias. After exposure to pure nitrogen 31 cells (83.8%) stopped...

An intracellular microelectrode technique was used to evaluate the changes of electric activities of cultured rat beating heart cells with hypoxia and reoxygenation injury. The results (n = 37) showed that hypoxia caused decreases in the maximal diastolic potential (MDP), Vmax . overshoot (OS) and action potential amplitude (APA), shortening in action potential duration (APD50 and APD100), increase in beating frequency and lots of multiform arrhythmias. After exposure to pure nitrogen 31 cells (83.8%) stopped beating within 30 min while 6 cells (16.2%) stopped beating within 50 min or so. Most cells (86.5%) resumed beating following treatment with oxygen (95%) and carbon dioxide (5%) for 5 min, whereas the values of electric activity parameters of reheating cell during reoxygenation for 30 min were lower than those of normoxic cells (p<0.05). In addition, all reheating cells showed multiform arrhythmias. However, 5 cells (13.5%) could not reheat following reoxygenation and 4 cells (12.5%) stopped beating again within 10 min after reoxygenation.The results indicated that this model exhibited some significance for studying the elec-trophysiological changes in hypoxia and reoxygenation injury of heart cells.

应用细胞内微电极技术记录到37个培养大鼠搏动心肌细胞充氮前后和复氧后的电活动参数。结果提示:充氮10min后,最大舒张电位(MDP),最大除极速度(V_(max)),动作电位振幅(APA)和动作电位时程(APD)等参数明显降低;自发节律增快,并出现多种形式的节律失常。83.8%细胞在充氮后30min内停搏,16.2%在50min左右停搏。复氧后,86.5%细胞在5min内复跳,13.5%未能复跳;12.5%复跳细胞在复跳10min内再次停搏。复跳细胞的各项电活动参数在30min内未能恢复到充氮前水平(p<0.05),且呈现不同程度的各类异常电活动。本结果对进一步研究心肌细胞缺氧和复氧损伤有一定意义。

Peripheral nerve injury by chronic compression caused a decrease in conductive velocity or a delay in the transmission of the action potential, later blocking it completely following demyelination of the damaged nerve region.Abnormal firing activities were recorded from the injured peripheral nerve fibers after the 6-7th postoperative day. There were different patterns of abnormal firing from fibers. Regular tonic ectopic firings with high frequency were always recorded from Aβ fibers. Aδ/C fibers, however,had...

Peripheral nerve injury by chronic compression caused a decrease in conductive velocity or a delay in the transmission of the action potential, later blocking it completely following demyelination of the damaged nerve region.Abnormal firing activities were recorded from the injured peripheral nerve fibers after the 6-7th postoperative day. There were different patterns of abnormal firing from fibers. Regular tonic ectopic firings with high frequency were always recorded from Aβ fibers. Aδ/C fibers, however,had burst or irregular spikes. A single antidromic shock to the damaged region sometimes induced ectopic spikes following the expected one.The demyelinated region of the damaged nerve was very sensitive to both tetraethylammonium, a K+ channel blocker, and noradrenalin. The authors suggest that new ion channels or receptors, absent in normal, form in the damaged region.

外周神经受到损伤的初期,损伤区传递冲动能力减弱和速度减慢,随后发生传导阻滞和神经髓鞘膜脱落的形态学病变。此时可记录到不同类型的传入神经纤维的异常传入放电活动,粗纤维产生规则的高频的异位放电,细纤维有不规则的阵发性放电。对脱髓鞘膜区进行逆行性刺激可引起放电频率增加,单次脉冲的逆行性刺激可使部分C类纤维产生多次的异位放电。脱髓鞘膜区对K~+通道阻断剂以及外源性的去甲肾上腺素异常敏感,提示异常电活动是受伤神经区轴突膜上离子通道和介质受体发生变化的结果。

 
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