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丙烯酰胺对狒狒外周神经系统的影响。

The effect of acrylamide on the peripheral nervous system of the baboon.

作者信息

Hopkins A

出版信息

J Neurol Neurosurg Psychiatry. 1970 Dec;33(6):805-16. doi: 10.1136/jnnp.33.6.805.

DOI:10.1136/jnnp.33.6.805
PMID:5497880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC493596/
Abstract

In the baboon, acrylamide produces a clinical illness characterized by weakness and ataxia of the limbs, weakness of bulbar muscles, and finally tetraplegia. Histological examination shows extensive involvement of peripheral nerves, the main histological change being a Wallerian type of degeneration affecting the distal ends of the largest diameter nerve fibres. The phenomenon of `dying back' has been demonstrated in single teased fibres. Changes also occur in the paranodal myelin; these are not necessarily associated with degeneration of the axon, since intercalated segments and extension of myelin from neighbouring internodes are present in recovering animals. Demyelination of whole internodes is rare. Paranodal changes may be found a few millimetres proximal to complete degeneration, but may also occur on fibres which are otherwise normal in the length examined. The mechanism of the paranodal changes is uncertain, but they may indicate a secondary response of the Schwann cell to a primary change in the axon.

摘要

在狒狒中,丙烯酰胺会引发一种临床疾病,其特征为四肢无力和共济失调、延髓肌肉无力,最终发展为四肢瘫痪。组织学检查显示外周神经广泛受累,主要组织学变化是沃勒氏型变性,影响最大直径神经纤维的远端。在单根分离纤维中已证实存在“逆行性死亡”现象。结旁髓鞘也会发生变化;这些变化不一定与轴突变性相关,因为在恢复的动物中存在插入节段以及相邻结间髓鞘的延伸。整个结间的脱髓鞘现象很少见。在完全变性近端几毫米处可能发现结旁变化,但在检查长度内其他方面正常的纤维上也可能出现。结旁变化的机制尚不确定,但它们可能表明施万细胞对轴突原发性变化的继发性反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/4154bad7c716/jnnpsyc00222-0092-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/5ec8c0d96377/jnnpsyc00222-0086-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/a1b88071a58a/jnnpsyc00222-0086-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/e1135cee10f4/jnnpsyc00222-0087-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/007e706b613a/jnnpsyc00222-0088-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/782e3ae1fda3/jnnpsyc00222-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/92e5c79b3d47/jnnpsyc00222-0089-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/4154bad7c716/jnnpsyc00222-0092-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/5ec8c0d96377/jnnpsyc00222-0086-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/a1b88071a58a/jnnpsyc00222-0086-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/e1135cee10f4/jnnpsyc00222-0087-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/007e706b613a/jnnpsyc00222-0088-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/782e3ae1fda3/jnnpsyc00222-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/92e5c79b3d47/jnnpsyc00222-0089-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f168/493596/4154bad7c716/jnnpsyc00222-0092-a.jpg

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