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演示文稿演讲PPT学习教学课件医学文件教学培训课件
成髓鞘细胞研究和应用进展;安逸生活 pk 艰苦卓绝创业
高原如此艰苦的环境:勇于担当,发挥引领作用
以苦为乐,人生需要有一股精神;特朗普:我拒绝政治正确, 我只做正确的事情
精英政治;2016.10.11. 中英脱髓鞘伦敦会议;要点;Year 1977~ 2016 40年
demyelination remyelination Pubmed文献量趋势图;中枢神经系统(CNS)有髓神经纤维
与周围(PNS)相似结构
有髓鞘和郎飞结
髓鞘外无基膜(神经膜)
相邻神经纤维有时融合(箭头);儿童发育;The final stage of oligodendrocyte development is myelination.
Unlike the peripheral nervous system where there is a strict size-dependent bias for myelination (only axons 1 um diameter enjoy the privilege), in the CNS axons as small as 300 nm are sometimes myelinated.
Nevertheless, CNS myelination is also influenced by axonal size. Surprisingly, cultured oligodendrocytes will begin myelinating even synthetic axon-like tubes lacking the usual neuron-glia signaling cues.
In this type of ‘blind’ myelination, only tubes with a diameter of ≥ 400 nm were myelinated, suggesting this mode of myelination may be particularly important for larger axons.
Moreover, once differentiating, it appears that oligodendrocytes only have a very narrow window of opportunity to select which adjacent axons to myelinate (~5 h in the developing zebrafish and ~12 h in myelinating cultures of rodent derived cells), irrespective of the total number of sheaths being made.
This implies that the signaling pathways mediating this process are likely to be relatively robust. Although in vitro studies have implicated several key pathways, to date no one single molecule has been shown to be indispensable for myelination of CNS axons in vivo, highlighting the great degree of redundancy in the control of this vital process.
Despite this, recent in vivo studies have revealed a great deal about how these various signaling pathways converge to control the extent or timing of myelination, if not overall myelination per se.;髓鞘脱失(脱髓鞘)一种very常见的临床神经病理变化;;多指数T2/磁化转移MRI;provides an important step for understanding ‘typical’ myelin development as well as providing the ability to identify when and where white matter abnormalities occur in neurodevelopmental disor
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