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The effects could be attributed to the selective action of BmK Ⅰ on the TTX-S Na〓 channel: slowing the inactivation process of Na〓 channel, increasing the amplitude of peak Na〓 currents; 2 BmK abT, a new-type neurotoxin with higher sequence homology to β-type scorpion neurotoxin, was found to slow the inactivation process of Na〓 channel and prolong the duration of action potential in DRG neurons.

这些结果提示BmK IT2和BmK AS-1的外周抗伤害性效应可能是通过它们对小直径DRG神经元外周游离末梢即C纤维末梢上的TTX-S和TTX-R钠通道的门控调节所致,且BmK IT2对角叉菜胶致炎大鼠较强的抗伤害性作用可能是由于它对TTX-R钠通道较高的敏感性所致。二。特异性钠通道调制剂-东亚钳蝎神经毒素的电生理特征。

The purposes of this study are to investigate the harmful situations which are cognized by self-injurious adolescents in daily lives, the responsive contents of self-injurious behaviors which are induced, and the coping strategies which can effectively reduce or even terminate self-injurious behaviors.

本研究旨在探讨自我伤害青少年所认知生活中具伤害性境遇及所引发的自我伤害行为反应内涵,以及能有效降低甚至终止自我伤害行为之相关因应策略。

Neuroscience 2001;104:523-538.[12]Ma WL, Zhang WB, Zhang YF. Projection of the calbindin D-28k neurons receiving visceral nociceptive information from interstitial nucleus of the spinal trigeminal tract to nucleus of the solitary tract in the rat. Acta Anat Sin 2003;34:(in Chinese with English abstract).

表明CB同样存在于经INV至PB的伤害性信息传导径路内,且传递内脏伤害性信息的CB神经元多于传递躯体伤害性信息的神经元,提示含CB的神经元可能也参与了经INV中继的外周伤害性信息向PB的传递。

In the central, 5-HT can induce the release of inhibitory neurotransmitter γ-aminobutyric acid etc. through 5-HT2A receptor resulting in analgesia. In the peripheral, 5-HT can active the nociceptor and advance the traumatic information transmission.

在中枢可以通过2A受体引起抑制性神经递质γ-丁氨酸等的释放,从而发挥镇痛作用;在外周参与伤害性感受器的活化,促进伤害性信息的传递。

Mizumura K,Kumazawa T. Modification of nociceptor responses by inflammatory mediators and second messengers implicated in their actiona study in canine testicular polymodal receptors.

痛过敏的产生有赖于许多炎症介质的参与,如PGs,缓激肽,5-羟色胺和白介素B4等,这些炎症介质有的可敏化伤害性感受器,使它们的阈值降低,有的可激活伤害性感受器,有的具有敏化和激活双重作用[4~6]。

Rectal distension as a reliably noxious visceral stimulus produces visceromotor responses, which can reflect visceral sensitivity, c-Fos expression can be seen as the marker of activated neurons, NO is a kind of important transmitter and modulator in the pathway of pain, which can affect visceral sensation.

直肠扩张作为一种可靠的内脏伤害性刺激,可以反映内脏的敏感性。c-Fos表达可以作为伤害性神经元兴奋的标志和神经通路的示踪物。

After dialyzing for 10~20 min, SNP at a concentration of 1 μmol/L increased the induced responses to innocuous mechanical stimulation and decreased those to noxoius mechanical stimulation. The induced responses to both innocuous and noxious mechanical stimulations were all decreased after dialyzing the same dose of SNP for 20~30 min. The decrease was shown within 7~15 min dialysis when SNP was used at a concentration of 20 μmol/L.

脊髓深层神经元透析1 μmol/L SNP, 10~20 min后,非伤害性机械刺激诱发的反应增强,伤害性机械刺激诱发的反应减弱;透析20~30 min后,伤害性和非伤害性机械刺激诱发的反应均减弱;透析20 μmol/L SNP 7~15 min内伤害性和非伤害性机械刺激诱发的反应均降低。

VR1 selectively expressed on small-to medium-diameter DRG neurons and it was recently considered as a molecular integrating multiple pain-producing stimuli.

VR1特异地表达在初级伤害性感受器上,被认为是汇集伤害性刺激的一个信号转导分子。

The latedischarges decreased from 9.29 ± 0.97 to 6.71 ± 0.68 with the A-fiberconditioning stimulus increasing from 1 to 5 (n〓8, P〓0. 05).(7) The intervalbetween the conditioning stimulus and test stimulus (C-T interval) wasincreasing, the inhibition tended to plateau off. At shorter time intervalsthe inhibition became more effective. When C-T interval was limited in 50ms,the inhibitory effects was the strongest, here, the late discharges reducedfrom 12.57±1.21to 2.29±0.42 (n=11, P<0. 01).(8) Behavior research showedthat the rat model of snake venom exhibited neuropathic pain with heathyperalgesia, cold and mechanical allodynia, which corresponding to the acuteelectrophysiological findings.

此时轻刷WDR神经元的感受野不能引起其活动改变,但伤害性齿镊夹捏仍可引起WDR神经元放电增多;〓5〓晚成分放电的潜伏期缩短,即宁静期的时程变短,由给蛇毒前的118.83〓3.67ms降至50.72〓1.36ms〓n〓32,P〓0.01〓;〓6〓在正常动物,如果预先给予只激活A纤维的弱条件电刺激〓mA,100μs〓可抑制随后的伤害性检验刺激所诱发的WDR神经元的晚成分放电,当条件刺激个数从1增加至5时,每次伤害性检验刺激所诱发的晚成分放电数从9.29〓0.97个降至6.71〓0.68个〓n〓8,P〓0.05〓;〓7〓固定条件刺激数为1个,当条件刺激与检验刺激之间的间隔增大时,A纤维条件刺激对WDR神经元晚成分放电的抑制作用逐渐减弱,当条件刺激与检验刺激之间的间隔在50 ms以内时,抑制效应最为显著,此时,晚成分放电数由正常时的12.57〓1.21个降至2.29〓0.42个〓n〓11,P〓0.01〓;〓8〓与急性研究中的WDR神经元电活动的变化结果相匹配,利用蛇毒制备的大鼠模型在行为学上表现为热痛觉过敏、冷觉的痛性感觉异常及机械痛觉过敏等慢性痛症状。

At the same time, most WDR neurons failedto respond to the light brush applied to the receptive fields, but they couldbe intensively excited by the noxious pinch.(5) The latency of the latedischarges was shortened from 118.83 ± 3.67ms to 50.72 ± 1.36ms (n〓32, P〓0. 01).(6) Preceding graded number of A〓fiber conditioning inputs (〓mA, 100 μs) delayed the C-activity evoked by the following nociceptive teststimulus activating both A- and C-fiber applied to the sciatic nerve. The latedischarges decreased from 9.29 ± 0.97 to 6.71 ± 0.68 with the A-fiberconditioning stimulus increasing from 1 to 5 (n〓8, P〓0. 05).(7) The intervalbetween the conditioning stimulus and test stimulus (C-T interval) wasincreasing, the inhibition tended to plateau off. At shorter time intervalsthe inhibition became more effective. When C-T interval was limited in 50ms,the inhibitory effects was the strongest, here, the late discharges reducedfrom 12.57±1.21to 2.29±0.42 (n=11, P<0. 01).(8) Behavior research showedthat the rat model of snake venom exhibited neuropathic pain with heathyperalgesia, cold and mechanical allodynia, which corresponding to the acuteelectrophysiological findings.

此时轻刷WDR神经元的感受野不能引起其活动改变,但伤害性齿镊夹捏仍可引起WDR神经元放电增多;〓5〓晚成分放电的潜伏期缩短,即宁静期的时程变短,由给蛇毒前的118.83〓3.67ms降至50.72〓1.36ms〓n〓32,P〓0.01〓;〓6〓在正常动物,如果预先给予只激活A纤维的弱条件电刺激〓mA,100μs〓可抑制随后的伤害性检验刺激所诱发的WDR神经元的晚成分放电,当条件刺激个数从1增加至5时,每次伤害性检验刺激所诱发的晚成分放电数从9.29〓0.97个降至6.71〓0.68个〓n〓8,P〓0.05〓;〓7〓固定条件刺激数为1个,当条件刺激与检验刺激之间的间隔增大时,A纤维条件刺激对WDR神经元晚成分放电的抑制作用逐渐减弱,当条件刺激与检验刺激之间的间隔在50 ms以内时,抑制效应最为显著,此时,晚成分放电数由正常时的12.57〓1.21个降至2.29〓0.42个〓n〓11,P〓0.01〓;〓8〓与急性研究中的WDR神经元电活动的变化结果相匹配,利用蛇毒制备的大鼠模型在行为学上表现为热痛觉过敏、冷觉的痛性感觉异常及机械痛觉过敏等慢性痛症状。

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