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Methods: Oxygen–glucose deprivation injury was induced in pure neuronal or neuronal–glial cocultures 24 h after preconditioning with xenon and/or sevoflurane.

缺氧缺糖损伤是预处理氙气和/或七氟醚24 h后纯粹的神经元或神经胶质联合培养所致的。

Using an in itro bioassay, we demonstrated that cytokine-actiated microglia release cytotoxins that kill retinal neurons.

应用体外生物测定技术,我们证明细胞因子活化的小神经胶质细胞释放杀死视网膜神经元的细胞毒素。

Phagocytic microglia release cytokines and cytotoxins that regulate the survival of astrocytes and neurons in culture.

酒精进入神经系统后可对各种细胞产生直接毒性作用,包括减少大脑某些部位神经元细胞的数目和破坏神经元与神经胶质细胞之间的正常关系。

Minocycline represses diabetes-induced inflammatory cytokine production, reduces the release of cytotoxins from actiated microglia, and significantly reduces measurable caspase-3 actiity within the retina.

二甲胺四环素抑制糖尿病诱导的炎性细胞因子的产生,降低来自于活化的小神经胶质细胞的细胞因子的释放,同时显著降低视网膜内可检测的caspase-3的活性。

More than forty percent of growths in the brain are gliomas.

脑部超过40%的瘤都是神经胶质瘤。

More than forty percent of growths in the brain are gliomas.

40%多在脑部生长都是神经胶质瘤。

Clew cerebrospinal fluid or haemal NSE content can mirror nerve colloid cell damages degree, as unusual as electroencephalogram closely related.

提示脑脊液或血液NSE含量可反映神经胶质细胞损害程度,和脑电图异常密切相关。

Furthermore, we provide evidence that the CD36 scavenger receptor and downstream kinases are involved in SYN-mediated microglial activation.

此外,CD36受体和下游的激酶参与SYN介导的小神经胶质的活化。

In conclusion, Hg(superscript 2+) appears to damage retina and glial cells may play an anti-toxic role in retina recovering in loaches.

推测Hg(上标 2+)污染可能对视网膜有伤害性影响,而神经胶质细胞在视网膜修复过程中起了重要作用。

After treatment with the conditional medium of tumor cells, the number of tubules increased in a dose-dependent manner.

结果:血管生成素-2在神经胶质瘤细胞中的表达强度与瘤组织的分级呈正相关(p.05);肿瘤细胞诱导肿瘤血管形成呈浓度依赖效应(p.05)。

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