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首页> 外文期刊>Advances in Experimental Medicine and Biology >Chronic Mild Hypoxia Ameliorates Chronic Inflammatory Activity in Myelin Oligodendrocyte Glycoprotein (MOG) Peptide Induced Experimental Autoimmune Encephalomyelitis (EAE)
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Chronic Mild Hypoxia Ameliorates Chronic Inflammatory Activity in Myelin Oligodendrocyte Glycoprotein (MOG) Peptide Induced Experimental Autoimmune Encephalomyelitis (EAE)

机译:慢性轻度缺氧改善骨髓蛋白寡核细胞糖蛋白(MOG)肽诱导实验性自身免疫脑脊髓炎(EAE)的慢性炎症活性

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摘要

Abstract While the pathologic events associated with multiple sclerosis (MS), diffuse axonal injury, cognitive damage, and white matter plaques, have been known for some time, the etiology of MS is still unknown and therapeutic efforts are somewhat disappointing. This may be due to a lack of fundamental knowledge on how to buffer the brain from secondary injury following immune attack. Maintenance of central nervous system (CNS) homeostasis is a complex set of regulatory adjustments by the neurovascular unit that includes induction of adaptive angiogenesis. Although aspects of adaptive angiogenesis are induced in MS and experimental autoimmune encephalomyelitis (EAE), vascular remodeling is ineffective and the balance between metabolic need and oxygen (O2) and glucose availability is disrupted.
机译:摘要在一段时间内已知与多发性硬化症(MS)相关的病理事件,弥漫性轴突损伤,认知损伤和白质斑块,MS的病因仍然是未知的,治疗努力有点令人失望。 这可能是由于在免疫发作后如何从继发伤害中缓冲大脑的基本知识。 中枢神经系统的维持(CNS)稳态是由神经血管单元的复杂调节调整,包括诱导适应性血管生成。 尽管在MS和实验性自身免疫脑脊髓炎(EAE)中诱导适应性血管生成的方面,但血管重塑是无效的,并且代谢需求与氧气(O2)之间的平衡被破坏。

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