结论组织培养方法能够成功体外培养人眼小梁网细胞。
Conclusion Human trabecular meshwork cells can be successfully cultured in vitro.
这种效应被认为是通过小梁网的糖皮质激素受体介导的。
The effect was thought to be mediated via trabecular meshwork glucocorticoid receptors.
小梁网的色素沉积程度同样也不是有统计学意义的预后因子。
The amount of trabecular meshwork pigmentation was not a significant predictor as well.
目的探讨体外培养人眼小梁网细胞的方法并观测其生物学特性。
Objective To culture of human trabecular meshwork cells in vitro and for investigate their biological character. Methods the trabecular tissues from human eyes were cultured.
糖皮质激素对小梁网的作用可作为一个良好模型用于研究青光眼的发病机制。
Glucocorticoid effects on the human trabecular meshwork can be used as a model system in which to study glaucomatous damage to the trabecular meshwork.
电镜下观察可见角巩膜及葡萄膜处的小梁网扩张变形，轴心胶原和弹力样纤维增生；
Under the electron microscope, the trabecular was expanded and deformed, with hyperplasia of collagen and elastic fibers.
本文对7例正常人眼前房角小梁网进行了组织化学——酸性粘多糖及超微结构的研究。
Histochemical and ultrastructural studies of the trabecular meshwork(TM)of 7 normal human eyes were carried out.
青光眼基因治疗的靶目标包括眼前节的小梁网和睫状体、眼后节的视网膜神经节细胞等。
Trabecular meshwork, ciliary body, retina and optic nerve will be the targets for glaucoma gene therapy.
结果所有患者治疗后周边前房深度均明显加深，静态前房角镜检查小梁网可见范围增宽。
ResultsThe results showed that in all these cases, the peripheral anterior chamber depth was increased, the anterior chamber angle was widened.
由于小梁细胞负责去除小梁网沉积的残渣，这些细胞功能的下降可能引起房水流畅系数的下降。
Because these cells function to remove debris deposited in the meshwork, reduced functional activity may lead to reduced outflow facility.
糖皮质激素对小梁网的作用是多方面的，它包括细胞外基质、细胞膜、细胞骨架及细胞核的多重变化。
Glucocorticoids cause multiple effects on the human trabecular meshwork including changes in extracellular matrix metabolism, organization of the cytoskeleton, and changes in gene...
诱导后晚期的模型眼前房角胶原增生，结构破坏。结论复方卡波姆诱导的兔眼慢性高眼压模型房水流出受阻的主要部位在小梁内皮网部。
Conclusions the obstruction of aqueous humor outflow induced by compound Carbomer in rabbit high IOP model is caused mainly by the changes in trabecular endothelial cells.
诱导后晚期的模型眼前房角胶原增生，结构破坏。结论复方卡波姆诱导的兔眼慢性高眼压模型房水流出受阻的主要部位在小梁内皮网部。
Conclusions the obstruction of aqueous humor outflow induced by compound Carbomer in rabbit high IOP model is caused mainly by the changes in trabecular endothelial cells.
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