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[维罗毒素诱导的溶血尿毒综合征:神经系统受累的病理生理学]

[Verotoxin induced hemolytic uremic syndrome: pathophysiology of neurological involvement].

作者信息

Takagi C, Naruse T

机构信息

Third Department of Internal Medicine, Gunma University School of Medicine.

出版信息

Nihon Rinsho. 1997 Mar;55(3):731-5.

PMID:9086789
Abstract

Hemolytic uremic syndrome (HUS) is caused by endothelial cell damages. Ninety percent of children with HUS have verotoxin-producing E.coli infection. Verotoxin binds to glycolipid receptors globotriaosyl ceramide (Gb3), and the difference of Gb3 expression level in each organ would lead to specific organ involvement. The receptors are expressed in human renal cortex and medulla. The expression level of Gb3 in normal human brain has not been characterized completely. However involvement of central nervous system is a severe complication of HUS. Spreading of microvascular thrombosis caused by combined effects of lipopolysaccharide, cytokine, enhanced shear stress, and verotoxin would play a major role in the development of central nervous dysfunction.

摘要

溶血尿毒综合征(HUS)由内皮细胞损伤引起。90%的HUS患儿有产志贺毒素大肠杆菌感染。志贺毒素与糖脂受体球三糖神经酰胺(Gb3)结合,各器官Gb3表达水平的差异会导致特定器官受累。这些受体在人肾皮质和髓质中表达。正常人类大脑中Gb3的表达水平尚未完全明确。然而,中枢神经系统受累是HUS的严重并发症。脂多糖、细胞因子、增强的剪切应力和志贺毒素共同作用导致的微血管血栓形成扩散在中枢神经功能障碍的发展中起主要作用。

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