• 结论星形胶质细胞可能参与青光眼神经纤维进一步损害抑制神经纤维再生

    CONCLUSION: Astrocytes may take part in the further lesion of nerve fiber in glaucoma, and inhibit the regeneration of nerve fiber axis-cylinder.

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  • 结果婴幼儿促纤维增生性星形细胞CT检查表现为巨大囊性病变;

    Results In this case, CT scan presented a massive cystic within tumor of the left temporal lobe.

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  • 胶质纤维酸性蛋白(GFAP)星形胶质细胞特异性标记物活性星形胶质细胞中GFAP的表达相对更高最后GFAP成为胶质疤痕主要成份

    The GFAP is a specific marker of astrocyte, its expression is more higher in the activity astrocyte, and finally the GFAP become the main composition of scar formations.

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  • 目的探讨大鼠脑缺血再灌注损伤麻黄碱治疗星形胶质细胞胶质原纤维酸性蛋白(GFAP)表达水平影响

    Objective To investigate the effects of ephedrine on glial fibrillary acidic protein (GFAP) expression after cerebral ischemia-reperfusion injury in rats.

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  • 方法流式细胞仪检测缺血缺氧不同时间星形胶质细胞细胞周期变化,并用荧光免疫细胞化学技术测定胶质细胞纤维酸性蛋白(GFAP增殖细胞核抗原(PCNA表达水平

    Methods We measured the astrocyte cell cycles in different time after ischemia and anoxia by flow cytometry and detected the levels of GFAP and PCNA with fluorescence immunocytochemistry.

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  • 血清血清浓度下,所分化的胶质细胞原浆星形胶质细胞在高血清浓度下则分化为纤维星形胶质细胞

    The differentiated gliocytes in free and low serum media were protoplasmic astrocytes, and fibrous astrocytes in high fetus serum media.

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  • 目的研究血小板活化因子(PAF)神经元活力星形胶质细胞胶质纤维酸性蛋白(GFAP)表达影响

    AIM: to observe the effect of platelet-activating factor (PAF) on cultured neuronal viability and glial fibrillary acidic protein (GFAP) expression in cultured astrocytes.

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  • 肿瘤细胞纤维细胞免疫细胞星形胶质细胞其它细胞报道可以释放摄取外泌体[7 - 9]。

    Cancer cells, fibroblast cells, immune cells, astrocytes and other cells have all been reported to release or uptake exosomes [7-9].

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  • NECL1恢复表达U251细胞星形胶质细胞分化的趋势,星形胶质细胞标志蛋白神经胶质纤维酸性蛋白的表达上调

    The U251 cells was differentiated potentially to astrocytes, and glial fibrillary acidic protein was up-regulated after the restoration of the NECL1 expression.

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  • NECL1恢复表达U251细胞星形胶质细胞分化的趋势,星形胶质细胞标志蛋白神经胶质纤维酸性蛋白的表达上调

    The U251 cells was differentiated potentially to astrocytes, and glial fibrillary acidic protein was up-regulated after the restoration of the NECL1 expression.

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