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首页> 外文期刊>Neural development >Ependymal alterations in sudden intrauterine unexplained death and sudden infant death syndrome: possible primary consequence of prenatal exposure to cigarette smoking
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Ependymal alterations in sudden intrauterine unexplained death and sudden infant death syndrome: possible primary consequence of prenatal exposure to cigarette smoking

机译：子宫内原因不明的猝死和婴儿猝死综合征的室管膜改变：产前暴露于吸烟的主要后果

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Background The ependyma, the lining providing a protective barrier and filtration system separating brain parenchyma from cerebrospinal fluid, is still inadequately understood in humans. In this study we aimed to define, by morphological and immunohistochemical methods, the sequence of developmental steps of the human ependyma in the brainstem (ventricular ependyma) and thoracic spinal cord (central canal ependyma) of a large sample of fetal and infant death victims, aged from 17 gestational weeks to 8 postnatal months. Additionally, we investigated a possible link between alterations of this structure, sudden unexplained fetal and infant death and maternal smoking. Results Our results demonstrate that in early fetal life the human ependyma shows a pseudostratified cytoarchitecture including many tanycytes and ciliated cells together with numerous apoptotic and reactive astrocytes in the subependymal layer. The ependyma is fully differentiated, with a monolayer of uniform cells, after 32 to 34 gestational weeks. We observed a wide spectrum of ependymal pathological changes in sudden death victims, such as desquamation, clusters of ependymal cells in the subventricular zone, radial glial cells, and the unusual presence of neurons within and over the ependymal lining. These alterations were significantly related to maternal smoking in pregnancy. Conclusions We conclude that in smoking mothers, nicotine and its derivatives easily reach the cerebrospinal fluid in the fetus, immediately causing ependymal damage. Consequently, we suggest that the ependyma should be examined in-depth first in victims of sudden fetal or infant death with mothers who smoke.
机译：背景技术室管膜，衬里提供了保护性屏障和过滤系统，将脑实质与脑脊液分开，在人类中仍然缺乏了解。在这项研究中，我们旨在通过形态学和免疫组化方法，确定大量胎儿和婴儿死亡受害者的脑干（室管膜室）和胸脊髓（中枢管室管膜）的人类室间隔的发育步骤顺序，年龄从妊娠17周到出生后8个月。此外，我们研究了这种结构改变，无法解释的胎儿和婴儿突然死亡以及孕妇吸烟之间的可能联系。结果我们的结果表明，在人类胎儿早期，室管膜呈伪分层的细胞结构，其中包括许多单核细胞和纤毛细胞，以及在室管膜下层的许多凋亡和反应性星形胶质细胞。妊娠32至34周后，室管膜完全分化，单层均匀细胞。我们观察到猝死受害者的室间隔病变广泛，例如脱屑，脑室下区的室间隔细胞簇，放射状神经胶质细胞以及室间隔内和内膜神经元的异常存在。这些改变与孕期孕妇吸烟显着相关。结论我们得出的结论是，在吸烟的母亲中，尼古丁及其衍生物容易到达胎儿的脑脊液，立即引起室间隔损害。因此，我们建议应首先对吸烟引起的胎儿或婴儿猝死的受害者中的吸烟者首先进行深度检查。

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