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维生素B12缺乏的恒河猴脊髓亚急性联合变性的超微结构研究

An ultrastructural study of subacute combined degeneration of the spinal cord in vitamin B12-deficient rhesus monkeys.

作者信息

Agamanolis D P, Victor M, Harris J W, Hines J D, Chester E M, Kark J A

出版信息

J Neuropathol Exp Neurol. 1978 May;37(3):273-99. doi: 10.1097/00005072-197805000-00006.

Abstract

Prolonged deprivation of vitamin B12 in rhesus monkeys produced changes in the central nervous system that were indistinguishable topographically and histologically from those of human subacute combined degeneration. Ultrastructural studies of early lesions of the spinal cord disclosed a degeneration of myelin characterized by separation of myelin lamellae and formation of intramyelinic vacuoles, leading eventually to complete destruction of myelin sheaths. At a later stage, there was degeneration and loss of axons, and marked gliosis. The theories of pathogenesis of subacute combined degeneration are reviewed in the light of these observations.

摘要

恒河猴长期缺乏维生素B12会导致中枢神经系统发生变化,这些变化在拓扑学和组织学上与人类亚急性联合变性无法区分。对脊髓早期病变的超微结构研究发现,髓鞘变性的特征是髓鞘板层分离和髓鞘内空泡形成,最终导致髓鞘完全破坏。在后期,出现轴突变性和丢失,以及明显的胶质细胞增生。根据这些观察结果对亚急性联合变性的发病机制理论进行了综述。

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