Selective vulnerability in acute energy deprivation syndromes
Selective vulnerability in acute energy deprivation syndromes
复制标题
急性能量剥夺综合征的选择性脆弱性
DOI：
--
复制
发表时间：
1993
影响因子：
5
通讯作者：
J. Cavanagh
中科院分区：
文献类型：
--
作者：
J. Cavanagh
由氯糖、6-氨基烟酰胺、二硝基苯和三溴咪唑在动物中引起的实验损伤中的地形和细胞事件被认为与人类急性硫胺素缺乏（韦尼克氏）脑病的这些特征有关，并与利氏病进行比较。仔细检查时，地形和细胞的变化是不同的，并且对于每种情况都是特定的，尽管有一个对所有人来说都是共同的基本细胞过程。每种病症的发病机制必须被视为多因素，并且寻找导致神经轴不同区域的神经元和细胞选择性脆弱性的因素将使我们了解每种情况下疾病过程的发病机制。实验模型为了解人类状况提供了很多帮助，特别是在寻找令人满意的治疗策略方面。
The topography and cellular events in the experimental lesions caused by chlorosugars, 6‐aminonicotinamide, dinitrobenzene and tribromoimidazole in animals are considered in relation to those features in human acute thiamine deficiency (Wernicke's) encephalopathy and for comparison in Leigh's disease. The topography and cellular changes when closely examined are different and particular to each condition, although there is a basic cellular process common to all. The pathogenesis of each condition must be considered as multifactorial and a search for the factors responsible for the neuronal and cellular selective vulnerability of different regions of the neuraxis will lead us to understanding the pathogenesis of the disease process in each instance. The experimental models offer much for the understanding of the human conditions, particularly in the search for satisfactory therapeutic strategies.