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神经元钙
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  neuronal calcium
     Regulatory effects of corticotropin release hormone on hypothalamic neuronal calcium signals and CREB
     促肾上腺皮质激素释放激素对下丘脑神经元钙信号和CREB的调节作用(英文)
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     Lomerizine acts as dual sodium and calcium channel blocker. It has high nmol·L -1 to μmol·L -1 activity at multiple sites, including both vascular and neuronal calcium channels, sodium channel,α 1 adrenoceptors and 5-HT 2 receptors,as well as a free radical scavenger.
     洛美利嗪与氟桂利嗪等钙通道拮抗剂不同 ,具有钙通道和钠通道双重阻断作用 ,洛美利嗪在nmol·L-1至 μmol·L-1水平 ,在多部位具有生物活性 ,包括血管和神经元钙通道、钠通道、α1肾上腺素受体和 5 HT2 受体 ,以及自由基清除作用。
短句来源
     Evidences from heredity investigation indicate that eleven genes are correlated with absence epilepsy, of which four encode the neuronal calcium channel subunits.
     现共发现有11个基因与失神癫痫有关联,其中有4种编码神经元钙通道亚单位。
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  neuron calcium
     Conclusions In the early stage of brain injury, ACh can cause neuron calcium overload, oxide free radical reaction, cerebral vasospasm, and increase blood-brain barry(BBB) permeability. Scopolamine, a muscarinic receptor antagonist, can improve these pathologic changes. As a result, Sco has protective effects on brain tissue injury.
     结论 :脑外伤后早期ACh可致神经元钙超载、氧自由基反应、脑血管痉挛和血脑屏障 (BBB)通透性增强 ,M受体拮抗剂东莨菪硷可改善这些病理变化 ,具有脑保护作用
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  “神经元钙”译为未确定词的双语例句
     Results MgSO_4 and Mg~ 2+ -ATP reduced the calcium influx of anoxic cortical neuron ( P<0.05), lowered the level of LDH, K~+, NSE in the culture fluid (P<0.05) and significantly decreased the mortality of neurons( P<0.05).
     结果MgSO4和Mg2+-ATP能减少缺氧状态下的脑皮质神经元钙内流(P<0.05),降低培养液中LDH、K+、NSE浓度(P<0.05),明显降低神经元死亡率(P<0.05)。
短句来源
     Effect of 2,5 - hexanedione on calcium homeostasis of motor neuron
     2,5-己二酮对运动神经元钙稳态的影响
短句来源
     Conclusion Mg 2+ may protect the neurons by activating the Ca 2+ -activated potassium channels.
     结论 Mg2 +对海马神经元钙激活钾通道的激活作用可能为Mg2 +抗缺血性脑损伤的重要机制之一。
短句来源
     Effect of acute hypoxia on calcium-activated potassium channels in Rat Hippocampal neurons
     急性缺氧对大鼠海马神经元钙激活钾通道的作用
短句来源
     RECTIFICATION OF CALCIUM-ACTIVATED POTASSIUM CHANNELS IN HYPOTHALAMIC NEURONS
     下丘脑神经元钙激活钾通道的整流现象
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     CONCLUSION: PNS is a calcium channel blocker in neurons.
     结论:PNS是神经元通道的阻滞剂.
短句来源
     EFFECTS OF “ISCHEMIA” ON CALCIUM CHANNELS OF RAT CEREBRAL CORTICAL NEURONS
     “缺血”对大鼠大脑皮层神经元通道的影响
短句来源
     A summary of calcium fertilizer
     肥综述
短句来源
     KIDNEY CALCIUM MILK
     肾
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     Pyknosis of neurons was observed occasionally.
     个别神经元固缩。
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  neuronal calcium
Increased production of neurotoxic forms of amyloid β-peptide (Aβ) and abnormalities in neuronal calcium homeostasis play central roles in the pathogenesis of Alzheimer's disease (AD).
      
Evaluation of the long-term memory for thermosensation regulated by neuronal calcium sensor-1 in Caenorhabditis elegans
      
The discriminative stimulus (DS) properties ofd-amphetamine (AMP) are thought to be mediated by enhanced release of catecholamines, which may involve neuronal calcium influx through voltage sensitive channels.
      
Evidence is accumulating that these modifications are triggered by a transient neuronal calcium (Ca) influx.
      
Immunohistochemical investigations with calretinin, a neuronal calcium binding protein, were made in the vestibular end organs of five guinea pigs and one chinchilla.
      
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  neuron calcium
An understanding of their mechanism of modulation provides an added impetus for the molecular characterization of bag cell neuron calcium channels.
      
This is also true of the two bag cell neuron calcium currents.
      
These were the best-fit values for the squid neuron calcium channel.
      


Application of Fura - 2/AM measured the calcium concentration [Ca~(2+)] and the significant inhibitory effects of the extracts of 5 species of Hippocampus on exitatory amino acid L - glutamic acid induced Ca2+ influx in rats'neurons have been reported. The extracts from H. kuda showed the strongest effects and the extract from H. japonicus did weakly. This results are in line with traditional medical material quality evaluation.

用Fura—2/AM测定细胞内钙离子浓度,结果表明,5种海马提取物对L—谷氨酸致大鼠神经元钙内流有明显的抑制作用。其中大海马H.kuda的抑制作用最强,日本海马作用最弱,这与传统药材质量评价相一致。

n order to investigate relationship between chole-cystokinin octapeptide(CCK-8 peptide)and seizuresusceptibility of audiogenic epilepsy-prone rats(P77PMC),CCK-8 peptide content at corticocerebral,subcortical,and hippocampal regions of developmentalbrain in epilepsy-prone.(P77PMC)and epilepsy-resis-tant rats (Wistar)was assayed with RIA.The effectof exogenous CCK-8 on free intracellular Ca ̄(++) concen-tration in corticocerebral cells of normal newbron ratswas measured using Fura-Z/AM method.The resultsshowed...

n order to investigate relationship between chole-cystokinin octapeptide(CCK-8 peptide)and seizuresusceptibility of audiogenic epilepsy-prone rats(P77PMC),CCK-8 peptide content at corticocerebral,subcortical,and hippocampal regions of developmentalbrain in epilepsy-prone.(P77PMC)and epilepsy-resis-tant rats (Wistar)was assayed with RIA.The effectof exogenous CCK-8 on free intracellular Ca ̄(++) concen-tration in corticocerebral cells of normal newbron ratswas measured using Fura-Z/AM method.The resultsshowed that CCK-8 peptide level at different regions ofP77PMC rat brain was significantly lower than that ofWistar rats during postnatal days 0-7(P<0. 05).Af-ter postnatal day 14,the increase of CCK-8 peptide atabove 3 regions of P77PMC rat brain was obviouslyfaster than that of Wistar rat and it was higher thanthat of Wistar rat at 21~28 days after birth,but therewas no significant difference, CCK-8 peptide signifi-cantly inhhted calcium influx in corticocerebral cells ofnewborn rats(P<0.05 ).These results suggest thatlow level of CCK-8 peptide at early postnatal stage maybe related to convulsion susceptibility of P77PMC.Thefact that CCK-8 peptide in the brain of P77PMC ratsrapidly increased in later posetnatal period represents acompensatory mechanism.CCK-8 peptide may act asan inhibitory neuromodulator in central nervous sys- tem.

为探讨胆囊收缩素8肽(CCK-8肽)与惊厥易感性的关系,采用放射免疫法,以惊厥不易感(Wistar)大鼠为对照,测定听源性惊厥易感(P77PMC)大鼠发育中脑内皮层、皮层下及海马各区的CCK-8肽含量变化。同时应用Fura-2技术检测CCK-8肽对正常新生大鼠皮层神经细胞内游离钙的影响。结果表明,P77PMC大鼠生后0~7天各区CCK-8肪含量显著低于对照(P均<0.05);出生14天后各区CCK-8肽含量增加明显快于对照,21~28天后分别超过对照;CCK-8肽对皮层神经元钙内流具有明显的抑制作用。提示CCK-8肽为一种神经兴奋性的抑制性调质;P77PMC大鼠生后初期低水平CCK-8肽与惊厥易感有关,但随日龄的增长可代偿性增加。

Aim: To study the alteration of neuronal calcium currents after brain injury and the effect of antagonist of Ca 2+ channels on the currents. Methods: The brain impact injury in Wistar rats was made by a free drop impacting device. Neurons around the traumatic area and in the same area of the opposite semisphere were isolated by enzymatic and mechanical method and the voltage dependent calcium currents (I Ca ) in these neurons were recorded with the whole cell patch clamp technique. Results: I Ca...

Aim: To study the alteration of neuronal calcium currents after brain injury and the effect of antagonist of Ca 2+ channels on the currents. Methods: The brain impact injury in Wistar rats was made by a free drop impacting device. Neurons around the traumatic area and in the same area of the opposite semisphere were isolated by enzymatic and mechanical method and the voltage dependent calcium currents (I Ca ) in these neurons were recorded with the whole cell patch clamp technique. Results: I Ca of traumatic neurons was -240±46pA( n =6) and I Ca of normal neurons was -143 ±38pA ( n =8). The increasing rate of I Ca in traumatic neurons was 68.5%. After irrigating nimodipine 10 μmol/L I Ca was -108±37pA( n =6) in the traumatic neurons, and -112±35pA( n =6) in the normal neurons. The decreasing rates of I Ca were 55.0% in the traumatic neurons and 21.6% in the normal neurons. Conclusion: The influx of Ca 2+ increased much more in the injured neurons than in the normal neurons. The effect of nimodipine on the reduction of I Ca is more effective in the traumatic neurons than in the normal neurons. Nimodipine could inhibit the inflow of Ca 2+ into the neurons. Therefore, neuronal damage may be reduced by nimodipine after brain injury.

目的:研究颅脑撞击伤后皮层神经元钙离子通道电流变化及钙离子通道拮抗剂对该电流的影响.方法:采用自由落体撞击装置对大鼠大脑左顶部进行硬膜外撞击致伤.伤后分离出损伤灶边缘区及健侧相应部位神经元,用膜片钳技术的全细胞方式记录神经元钙离子通道电流.结果:伤侧Ca2+电流(ICa)为-240±46pA,较健侧-143±38pA平均增加68.5%.分别用10μmol/L尼莫地平灌流后,伤侧下降至-108±37pA,下降率为55.0%,健侧下降至-112±35pA,下降率为21.6%.结论:脑创伤后Ca2+内流增加,可能为细胞内Ca2+超载的主要原因之一.尼莫地平对创伤后神经元Ca2+电流的抑制作用较正常神经元更明显,对阻止Ca2+内流,减轻神经细胞损害有一定作用.

 
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