本文選題：神經(jīng)膠質(zhì)細(xì)胞 + 小頭�。� 參考：《中國感染與化療雜志》2017年06期

【摘要】：正對許多原發(fā)性小頭癥進行病理學(xué)檢查顯示,無炎性改變,無壞死。這與胎兒大腦感染寨卡病毒引起小頭癥的研究結(jié)果不同。在胎兒大腦感染中,小頭畸形伴隨著小神經(jīng)膠質(zhì)細(xì)胞的激活,彌漫性神經(jīng)膠質(zhì)增生、壞死,腦室周圍和皮質(zhì)鈣化,以及大腦收縮產(chǎn)生的腦積水。原發(fā)性小頭癥可能是由于缺乏放射狀神經(jīng)膠質(zhì)(radial glia)的神經(jīng)干細(xì)胞所致。Retallack及其同事發(fā)現(xiàn)編碼黃病毒進入細(xì)胞的多個基因在放射狀神經(jīng)膠質(zhì)細(xì)胞、星形細(xì)胞、內(nèi)皮細(xì)胞和小神經(jīng)
[Abstract]:Pathological examination of many primary microcephaly showed no inflammatory changes and no necrosis. This is different from the study of microcephaly caused by Zika virus infection in the fetal brain. In fetal brain infection, microcephaly is associated with activation of microglia, diffuse glial hyperplasia, necrosis, periventricular and cortical calcification, and hydrocephalus caused by brain contraction. Primary microcephaly may be caused by a lack of radial glial neural stem cells. Retallack and his colleagues found that multiple genes encoding the yellow virus enter the cells in the radial glia, astrocytes, endothelial cells and small nerves
【分類號】：R714.5

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