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An infectious viral disease occurring in dogs, characterized by loss of appetite, a catarrhal discharge from the eyes and nose, vomiting, fever, lethargy, partial paralysis caused by destruction of myelinated nerve tissue, and sometimes death.

犬热病发生在狗身上的一种传染性病毒引起的疾病,主要特征是:无食物欲,眼鼻处有黏液,呕吐,发烧,昏睡,由于有髓鞘的神经组织受到损害而部分麻痹,有时会导致死亡

Inthe present study, we sought to determine whether RTX-inducedreversible sciatic nerve block results in the degenerative changesof unmyelinated fibers.

在本研究中,我们拟确定 RTX 诱发的可逆性坐骨神经阻滞是否可以导致无髓鞘神经纤维退行性变。

In contrast to white fat, brown fat is richly vascularized and has numer unmyelinated nerves which provide sympathetic stimulation to the adipocytes.

和白色脂肪组织比较起来,棕色组织有充分的血管浸润,而且有许多无髓鞘的神经提供交感神经对脂肪细胞的刺激。

One rarely observed finding was the irregularlycompacted membranous deposits in the unmyelinated axons.

一个很罕见的发现是无髓鞘神经轴突上有不规则的紧密膜状沉积物。

Studies using perineural vanilloids inhigh concentrations suggest that they can cause a degenerationof unmyelinated fibers.

在神经周围给予高浓度 vanilloids 的研究发现,它们可导致无髓鞘神经纤维退行性变。

Beyond or distal to a ganglion (referring especially to the unmyelinated fibers that originate from cells in autonomic ganglia).

超出神经节后部或末端的(尤指发源于自主神经中枢细胞的无髓鞘神经纤维)。

In this paper, we first analyze the mechanism of action potential propagated alongan unmyelinated fiber, and present a hypothesis that the velocity of transmembranecurrent is the equivalent of the propagation velocity of action potential. Then usingthe H-H model and the cable equation we obtain the formula of the velocity. Insuccession, we apply a similar method to analyze the mechanism of action potentialpropagated along a myelinated fiber. Using the McNeal model and the CRRSS model,we obtain the formula of the velocity.

接下来,应用与无髓鞘神经纤维相类似的方法,分析了动作电位在有髓鞘神经纤维上的传递机制,同样得出了可用跨膜电流的移动速度来等效动作电位传递速度的结论,利用 McNeal 模型和 CRRSS 模型,建立了有髓神经纤维在兴奋传递期间等效电路模型,并推导出了速度的计算模型。

Recently, many foreign researchers found that the tetrodotoxin-resistant voltage-gated sodium channel, Nav1.8, which is expressed only by unmyelinated small-diameter sensory neurons associated with nociception in dorsal root ganglion and trigeminal ganglion, is involved in pain pathways and play a key role. Thus it provides a new idea in pain research.

近年来,国外众多学者发现河豚毒素(tetrodotoxin,TTX)不敏感型(TTX-resistant,TTX-R)电压门控钠通道Na_v1.8与疼痛的关系极为密切,其仅分布在背根神经节(dorsal root ganglion,DRG)和三叉神经节(trigeminal ganglion,TG)中的与伤害性感受密切相关的无髓鞘的小直径感觉神经元胞体上,它为疼痛的研究提供了新的思路。

We introduced improved primary mixed glial culture and different-attachment method to isolate and purify the OPCs, the cells were proliferated in serum-free medium, flow cytometry and immunohischemistry methods were employed to estimate the purity of cultured OPCs. Their abilities of differentiation and expression of trophic factors were identified by RT-PCR and immunostaining. Several methods including TUNEL and MTT were adopted to estimate the protective effects of conditioned culture medium from oligodendrocyte lineage cells on the primary cultured cerebellar granule neurons. Intravitreal transplant of OPCs, combined with retrograde fluorescent labeling the superior colliculus and intraorbital optic nerve transection, were used to investigate the protective effects of OPCs on the axotomized RGCs in vivo. Intravitreal transplantof OPCs or NSCs on the newborn rats, and retinal transplant of OPCs on the young rats were performed, to observe the myelin formation in the retina at different stages after cellular transplantation. Optic nerve transection was carried out on some rats with myelinated retinae, to study the influence of myelination on the injuried RGCs.

为此,本研究采用改良的胶质细胞混合培养与差速贴壁方法获得大鼠OPCs,使用无血清培养基进行扩增、培养,用免疫组织化学和流式细胞技术对培养细胞的纯度进行鉴定,对少突胶质系细胞表达部分营养因子的情况进行检测;采用TUNEL、MTT等方法对少突胶质系细胞条件培养基对原代培养小脑颗粒神经元的保护作用进行检测;将OPCs移植入成年SD大鼠玻璃体内,利用上丘逆行荧光标记技术,观察眼内移植的OPCs对眶内视神经切断时的视网膜神经节细胞的保护作用及其持续时间;将OPCs或NSCs移植入新生和幼年SD大鼠玻璃体或视网膜内,观察不同时期视网膜内髓鞘形成与分布特点,分析髓鞘的超微结构,并观察眼内髓鞘形成对损伤神经节细胞的保护作用。

Results Under our experimental conditions, three kinds of NO donors when in lower concentrations could not cause obvious changes of axons while when the concentration of DETA NONOate was doubled, it could induce the non-selective demyelination and Wallerian degeneration of both sensory and motor nerve fibers.

结果:在本实验条件下,应用三种NO供体的低浓度,都不能引起大鼠坐骨神经轴突的改变;将DETA NONOate浓度加倍则可导致轴突脱髓鞘和沃勒变性,但对有髓鞘纤维和无髓鞘纤维并无选择性作用。

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