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[神经肌肉传递障碍的免疫学方面。2. 实验性自身免疫性重症肌无力和兰伯特-伊顿肌无力综合征]

[Immunologic aspects of disorders of neuromuscular transmission. 2. Experimental autoimmune myasthenia gravis and the Lambert-Eaton myasthenic syndrome].

作者信息

Andreis I, Lovnićki T J, Beara N, Taradi M

机构信息

Zavod za fiziologiju Medicinskog fakulteta Sveucilista u Zagrebu.

出版信息

Lijec Vjesn. 1994 May-Jun;116(5-6):158-61.

PMID:7968205
Abstract

This paper describes two condition caused by disfunction of neuromuscular transport: experimental autoimmune myasthenia gravis (EAMG) and Lambert-Eaton myasthenic syndrome (LEMS). EAMG can be caused by immunization with acetylcholine receptors (AChR). As in myasthenia gravis, anti-AChR antibodies reduce the number of these receptors, which impedes normal neuromuscular transmission. LEMS patients have normal AChR function: however there is a disfunction of acetylcholine release from the presynaptic terminals. This is due to the formation of antibodies against the voltage gated calcium channels on the presynaptic nerve terminals.

摘要

本文描述了由神经肌肉传递功能障碍引起的两种病症

实验性自身免疫性重症肌无力(EAMG)和兰伯特-伊顿肌无力综合征(LEMS)。EAMG可由用乙酰胆碱受体(AChR)进行免疫接种引起。与重症肌无力一样,抗AChR抗体减少了这些受体的数量,这阻碍了正常的神经肌肉传递。LEMS患者的AChR功能正常:然而,突触前终末乙酰胆碱释放存在功能障碍。这是由于针对突触前神经终末上电压门控钙通道的抗体形成所致。

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