Nelson I, Bonne G, Degoul F, Marsac C, Ponsot G, Lestienne P
U 298 INSERM, CHR, Angers.
Neuropediatrics. 1992 Aug;23(4):199-205. doi: 10.1055/s-2008-1071341.
The progressive syndrome of Kearns-Sayre has been studied at the clinical, biochemical and genetic levels in a patient. Clinical arguments suggest an evolution from Pearson's disease to Kearns-Sayre syndrome. The respiratory chain activities were low, and Southern blot analysis, together with gene sequencing, showed a heteroplasmic deletion of 7767 base pairs in a significant proportion of the mitochondrial DNA in different tissues. Protein synthesis studies on lymphoblasts did not reveal any translation of the new reading frame created by the deletion, although the corresponding deleted mitochondrial DNA sequence is transcribed.
我们对一名患有进行性Kearns-Sayre综合征的患者进行了临床、生化及遗传学层面的研究。临床证据表明该疾病由Pearson病发展而来。患者呼吸链活性较低,Southern印迹分析及基因测序显示,不同组织中相当比例的线粒体DNA存在7767个碱基对的异质性缺失。尽管缺失的线粒体DNA序列能够转录,但对淋巴母细胞进行的蛋白质合成研究未发现由该缺失产生的新阅读框发生任何翻译。