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neuron相关的网络例句

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与 neuron 相关的网络例句 [注:此内容来源于网络,仅供参考]

Unlike previous models in which overexpression of the amyloid precursor protein results in amyloid plaque formation, have produced mice that overexpress only Aβ40 or Aβ42 and prove that Aβ42 is critical for the formation of amyloid deposits in vivo.

不同于早先调控淀粉样蛋白前体蛋白的动物模型,McGowan 等(Neuron, Vol 47, 191-199, 21 July 2005)培养了专一表达Aβ40或者 Aβ42的老鼠,结果直接证明了Aβ42 确实是引起淀粉样蛋白沉淀的主要因素,而不是Aβ40。

Especially for severe extremities disabled such as Injury to spinal cord, Motor neuron disease and so on, who are paralyses in a bed for a long-term. The people who have communication and action disabled, they couldn't do them well, so their lives are full of inconvenience. If they want to associate with the normal people, the most easy method is to make some word cards of reading. With these word cards to guess what he need from his health or psychology, such as the weathers turns cold,"cold","hot","wearing clothes" and so on, But it couldn't express all the thought from patients. Therefore, it often caused that we can't know what the patients want or their condition. It's too inconvenient for their lives.

尤其是重度肢体障碍患者,如脊髓损伤、运动神经元疾病患者等长期瘫痪在床的病人,对於沟通和行动障碍两者并存的患者而言,其日常生活起居处处充满著不便,一般与此类患者沟通最简单的方式就是制作一些简易读字卡,依著基本的身体或心理层面去推敲他的需要,如天气转凉了,「冷」「热」「穿衣服」等…,但这并不能完全表达患者的需求,因此常造成无法满足患者需求的情况,造成生活上非常的不方便。

In addition, ER-associated apoptosis was activated in penumbral area which may be responsible for neuron death caused by acute cerebral ischemia.

结果显示edaravone可以改善大鼠的神经功能缺损症状,减轻脑水肿,显著降低大鼠脑组织缺血急性期的GRP78表达水平,使caspase-12激活减少。

LTA-induced delayed PC can prevent brain damage caused by peroxidate reaction and reduce the destruction of ultrastructure of the neuron. The neuroprotective mechanisms of LTA pretreatment may be associated with anti-free radical effect and decreased the cytotoxic effect of NO.

结论LTA诱导的延迟预适应能显著减少大鼠脑组织再灌注损伤,减少脑组织坏死,其作用机制与减少脑I/R后自由基和NO毒性作用有关。

Two kinds changes of neuron plasticity are confirmed being related to GAP-43:(1)synaptic structural change makes GAP-43 increase ;(2) changes of synaptic transduction efficacy that long term potential and long term depression can alter GAP-43 phosphatize state and mRNA expression.

突触素(synaptophysin,P38)系一相对分子质量为38000的膜结构蛋白,存在于突触前囊泡膜,与突触的结构和功能密切相关。P38作为突触前终末特异性标记物,常用来反映突触的密度和分布。

They are already being evaluated in clinical trials as potential therapeutic agents for major human neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and motor neuron disease. However, delivery of polypeptide growth factors to compromised neurons in the CNS is problematic because their plasmatic half-life are very short and their abilities to cross the blood-brain barrier are theoretically null.

然而由于中枢神经系统中存在血脑屏障,神经营养因子类物质难以通过血脑屏障而到达靶部位;同时又因为神经营养因子在体内生物半衰期较短,使得全身性用药效果不够理想,另外还往往产生意想不到的副作用,如何解决这些问题对于深入研究神经营养因子在神经损伤及神经系统退行性疾病中的作用及开展临床应用前景研究有着十分重要的意义。

Results The neurological defects score was singificiant lower in D group (41.50±8.18) than that in group A(82.20±8.08), B(63.60±6.22) and C (61.00±6.58)(all P.01). Compared with groups A, C, group D showed that the cellular nucleus was shrinkaged slightly, the gap of cells was nomal roughly and the degree of rarefaction in neurofibra net was not serious under the light microscope. Under the electron microscope, the neuron was degenerated, the cellular membrane was integrated and the plastosome was swelled lightly in the group D. The physiological demage were slighter in D group.

结果 D组神经功能缺损评分(41.50±8.18)明显低于A组(82.20±8.08)、B组(63.60±6.22)和C组(61.00±6.58)(均P.01);光镜下D组神经细胞核轻度皱缩,细胞周围间隙大致正常,神经纤维网疏程度不严重;电镜下D组神经元轻度变性,细胞核无皱缩,核膜完整,线粒体轻度肿胀;脑组织病理损害程度较B组和C组明显减轻。

MMN should be differentiated from motor neuron disease and chronic inflammatory demyelinating polyneuropathy.

MMN应与运动神经元病和慢性炎性脱髓鞘性多发性神经根神经病鉴别。

RESULTS: Lidocaine inhibited both EPSP and the response foracetylcholine of the postsynaptic neuron.

结果:利多卡因同时抑制了兴奋性突触后电位和突触后神经元对乙酰胆碱的反应。

The immediate effects of this pharmacologic action are to increase the availability of norepinephrine and serotonin in the synapse and to increase stimulation of the postsynaptic neuron.

药理学活性的瞬即效应是为了提高突触对去甲肾上腺素和 5-羟色胺的利用率,也为了增值突触后神经元的兴奋。

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