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chronic constriction injury cci
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     Analgesia effect of lactoferrin in rat chronic constriction injury (CCI) model
     乳铁蛋白在大鼠坐骨神经慢性束缚损伤模型产生镇痛作用
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     Objective To study the analgesic effect of lappaconitine in rats with chronic constriction injury (CCI).
     目的研究氢溴酸高乌甲素对大鼠慢性缩窄性损伤(CCI)模型神经病理性疼痛的镇痛作用。
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     Effect of lappaconitine on chronic constriction injury rats
     氢溴酸高乌甲素对神经病理性疼痛大鼠的影响
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     Objective: To investigate the central mechanism of trigeminal neuralgia following chronic constriction injury (CCI).
     目的 :探讨慢性压缩性损害引起三叉神经痛的中枢机制。
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     Conclusion:Intraperitoneal injection LF has analgesic effect in chronic constriction injury(CCI) model of rats.
     结论:腹腔注射乳铁蛋白在大鼠坐骨神经慢性束缚损伤模型产生剂量依赖性镇痛作用。
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  chronic constriction injury cci
The aim of the present study was to test the sensitivity of PDE5 inhibitor sildenafil in chronic constriction injury (CCI) model a rat model of neuropathic pain.
      
Chronic constriction injury (CCI) and partial ligation (PSNL) of the sciatic nerve induce a similar neuropathic pain syndrome in rats.
      
Chronic constriction injury (CCI) of the rat sciatic nerve increases the dorsal horn excitability.
      
We aimed to investigate whether such osteopathic changes occurred in rats with chronic constriction injury (CCI) of the sciatic nerve.
      
In order to evaluate effect of MCS in experimental animals we applied MCS to rats with neuropathic pain, which was evoked by chronic constriction injury (CCI) to the left sciatic nerve.
      
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Objective To investigate the changes in small-diameter sensory neuron (SNS)/ peripheral nerve type 3(PN3) Na+ channel transcript and in tetrodotoxin-resistant (TTX-R) Na+ current in dorsal root ganglion (DRG) neurons in a chronic constriction injury (CCI) model of neuropathic pain. Methods Eighteen rats were divided into 6 groups of 3 animals each. Chronic constriction injury model was established after Dib-Hajj et al. Pain threshold was significantly lowered after CCI...

Objective To investigate the changes in small-diameter sensory neuron (SNS)/ peripheral nerve type 3(PN3) Na+ channel transcript and in tetrodotoxin-resistant (TTX-R) Na+ current in dorsal root ganglion (DRG) neurons in a chronic constriction injury (CCI) model of neuropathic pain. Methods Eighteen rats were divided into 6 groups of 3 animals each. Chronic constriction injury model was established after Dib-Hajj et al. Pain threshold was significantly lowered after CCI as compared with that in control group. The animals were deeply anesthetized and rapidly decapitated 14 days after surgery. The L4-5 DRG of the operated side was removed and crushed and total RNA was extracted with trizol reagent. The DRG of the contralateral side was used as control. The change in SNS/PN3 Na + channel expression was determined by semi-reverse transcriptase-PCR. The DRG neurons were isolated enzymatically and the change in voltage-gated TTX-R Na+ current was recorded using whole-cell patch clamp technique. Results Sensory neuron specific TTX-R Na+ channel transcript SNS/PN3 was down-regulated by 60% 14 days after CCI as compared with that in control group. TTX-R Na+ current density was significantly reduced but its activation and steady state inactivation were unchanged. Conclusions Na+ channel SNS/PN3 is involved in the hyperextability of the primary sensory neurons after CCI.

目的 通过观察背根神经节(DRG)电压门控钠通道SNS/PN3在大鼠坐骨神经压迫性损伤(CCI)的变化,以探讨慢性神经痛的发生机制。方法 对大鼠建立慢性神经痛模型,14d后,将神经痛模型大鼠18只,均分为6组,每组3只,组内同侧(CCI)与对侧自体对照(Control),在深麻醉下快速断头,分别取L4和 L5 DRG,用Trizol试剂提取DRG总RNA。以逆转录多聚酶链反应(RT-PCR)半定量分析CCI后大鼠背根神经节钠通道SNS/PN3转录物的变化,以及全细胞膜片钳技术记录CCI对急性分离大鼠背根神经节TTX-R钠电流的影响。结果CCI术后14d,感觉神经元特异性的TTX-R钠通道转录物 SNS/PN3下调,与对照组相比,下降了大约60%,TTX-R钠电流密度明显减弱,但不影响其激活与稳态失活。结论 钠通道 SNS/PN3与慢性神经痛后初级感觉神经元过度兴奋有关。

Objective To investigate the changes in TNFα content of sciatic nerve induced by chronic constriction injury (CCI) of sciatic nerve to determine the role of TNFa in the development of neuropathic pain. Methods Eight-four female health SD rats weighing 250-300g were anesthetized with sodium barbiturate. Unilateral sciatic nerve was exposed and ligated at the middle of thigh. Three ligatures (chromic catgut 4.0) were placed around the sciatic nerve and tied. The distance between the two...

Objective To investigate the changes in TNFα content of sciatic nerve induced by chronic constriction injury (CCI) of sciatic nerve to determine the role of TNFa in the development of neuropathic pain. Methods Eight-four female health SD rats weighing 250-300g were anesthetized with sodium barbiturate. Unilateral sciatic nerve was exposed and ligated at the middle of thigh. Three ligatures (chromic catgut 4.0) were placed around the sciatic nerve and tied. The distance between the two ligatures was about 1 mm. Sham operation was performed on the contralateral thigh. The sciatic nerve was exposed and mobilized but not ligated. The thermal nociceptive threshold was determined by measuring the withdrawal latency of hindpaw placed on a 58℃ hot plate on days 0.5, 1, 3, 5, 7, 9, 11, 13 and 14 after surgery. Animals were sacrificed on days 0.5, 1, 3, 7, 10 and 14 after surgery. Sciatic nerves were removed from both thighs and frozen at - 80℃ for determination of TNFα content. Sciatic nerve from healthy animals was used as control. The percentage of maximal possible response (% MPR) , was determined for each group (CCI, sham operation, control) % MPR= (new withdrawal latency- average baseline latency)/( 15-average baseline latency) . The distribution of TNFα between supernatant and sediment was also determined. Results The average baseline nociceptive threshold (withdrawal latency) was (7.9±0.2)s. There was significant different in %MPR between the two hindpaws on days 1, 3, 5, 7, 9 and 11 after surgery. The TNFα content of sciatic nerve from healthy rats was (40.62± 0.24) pg/mg protein. The TNFα content of the ligated sciatic nerve was elevated abruptly in 12h after ligation, then abruptly declined to a plateau but was still significantly higher than that of sham-operated side on days 1 and 3. There was no significant difference in TNFα content of sciatic nerve between control group and sham-operation group. The relative content of TNFα content in the sediment of ligated sciatic nerve gradually increased and reached the peak on day 7 and then gradually decreased. Conclusion The TNFα content of peripheral nerves plays an important role in the development of neuropathic pain. Membrane-combined TNFα is involved in the process of nerve repairing.

目的 通过大鼠坐骨神经慢性压榨伤(CCI)神经病理痛模型热痛敏阈值及坐骨神经中TNFα含量的变化,探讨外周源性TNFα在神经病理痛形成中的作用及可能机制。方法 雌性健康SD大鼠84只,在巴比妥钠麻醉下于大腿中部暴露并结扎坐骨神经。对侧大腿暴露坐骨神经作为模拟对照(Sham)。术后0.5、1、3、5、7、9、11、13、14d测定手术大鼠(n=12)两侧后爪的热痛敏阈值。于术后0.5、1、3、7、10、14d(每时点n=12)处死大鼠,切取两侧坐骨神经片断匀浆。对照组(n=12)标本取自健康大鼠。用酶联免疫法测定TNFα含量及上清液与沉淀物中的相对分布。结果 大鼠热痛敏基础值为(7.9± 0.2)s,大鼠双侧后爪(CCI及Sham)的%MPR在术后 1、3、5、7、9、11d有显著性差异;健康大鼠坐骨神经TNFα含量为(40.62±0.24)pg/mg,CCI侧坐骨神经TNFα含量于术后12h内急剧升高,显著高于Sham侧(P<0.01),后急剧下降至平台期,但 1、3 d仍高于Sham侧(P<0.05)。Sham侧TNFα含量不同时间点比较及与对照组比较均无显著性差异(P>0.05)。结扎侧坐骨神经TNFα在...

目的 通过大鼠坐骨神经慢性压榨伤(CCI)神经病理痛模型热痛敏阈值及坐骨神经中TNFα含量的变化,探讨外周源性TNFα在神经病理痛形成中的作用及可能机制。方法 雌性健康SD大鼠84只,在巴比妥钠麻醉下于大腿中部暴露并结扎坐骨神经。对侧大腿暴露坐骨神经作为模拟对照(Sham)。术后0.5、1、3、5、7、9、11、13、14d测定手术大鼠(n=12)两侧后爪的热痛敏阈值。于术后0.5、1、3、7、10、14d(每时点n=12)处死大鼠,切取两侧坐骨神经片断匀浆。对照组(n=12)标本取自健康大鼠。用酶联免疫法测定TNFα含量及上清液与沉淀物中的相对分布。结果 大鼠热痛敏基础值为(7.9± 0.2)s,大鼠双侧后爪(CCI及Sham)的%MPR在术后 1、3、5、7、9、11d有显著性差异;健康大鼠坐骨神经TNFα含量为(40.62±0.24)pg/mg,CCI侧坐骨神经TNFα含量于术后12h内急剧升高,显著高于Sham侧(P<0.01),后急剧下降至平台期,但 1、3 d仍高于Sham侧(P<0.05)。Sham侧TNFα含量不同时间点比较及与对照组比较均无显著性差异(P>0.05)。结扎侧坐骨神经TNFα在沉淀物中的相对含量逐渐增加,7d达高峰,后逐渐降低。结论 外周神经源性TNFα是热痛敏产生及维持的主要诱发因素。膜结合型TNFα可能在神经修复中有重要作用。

The present study was to investigate the changes of TTX R sodium currents and NaN/SNS2 sodium channel transcripts in DRG neurons in chronic constriction injury (CCI) of sciatic nerve 14 days after surgery. The transcript of NaN, a sensory neuron specific TTX R sodium channel, was significantly down regulated as well as the TTX R sodium current. The TTX R current density was significantly decreased in CCI group. At the same time, the properties of the TTX R currents revealed...

The present study was to investigate the changes of TTX R sodium currents and NaN/SNS2 sodium channel transcripts in DRG neurons in chronic constriction injury (CCI) of sciatic nerve 14 days after surgery. The transcript of NaN, a sensory neuron specific TTX R sodium channel, was significantly down regulated as well as the TTX R sodium current. The TTX R current density was significantly decreased in CCI group. At the same time, the properties of the TTX R currents revealed in the activation curve and steady state inactivation curve were unchanged. These results may provide at least a partial basis for the hyperexcitability of DRG neurons that contributes to hyperalgesia in this model.

目的 :观察电压门控钠通道NaN /SNS2在大鼠坐骨神经慢性压迫性损伤 (chronicconstric tioninjury ,CCI) 14天后的变化 ,探讨慢性神经痛的发生机制。方法 :以逆转录多聚酶链反应(RT PCR)半定量分析CCI后大鼠背根神经节 (Dorsalrootgamglion ,DRG)钠通道NaN/SNS2转录物的变化 ,以及全细胞膜片钳技术记录CCI对急性分离大鼠背根神经节TTX R钠电流的影响。结果 :CCI术后 14天 ,感觉神经元特异性的TTX R钠通道转录物NaN/SNS2下调 ,与对照组相比 ,下降了大约 30 % ,TTX R钠电流密度明显减弱 ,但不影响其激活与稳态失活。其激活曲线的V1/2 分别为 - 2 6 .6 378mV、- 2 6 .6 30 6mV ,k为 6 .786 4mV、6 .732 3mV ;失活曲线的V1/2 分别为 -35 .5 84 4mV、- 37.2 188mV ,k为 8.2 792mV、8.4 6 47mV。结论 :钠通道NaN/SNS2与慢性神经痛后初级感觉神经元过度兴奋有关。

 
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