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Elena Schlapakow Viktoriya Peeva Gábor Zsurka Monika Jeub Bettina Wabbels Cornelia Kornblum Wolfram S. Kunz 《Neuromuscular disorders : NMD》2019,29(5):358-367
Chronic progressive external ophthalmoplegia (CPEO) is a frequent clinical manifestation of disorders caused by pathogenic mitochondrial DNA mutations. However, for diagnostic purposes skeletal muscle tissue is used, since extraocular muscle tissue is usually not available for work-up. In the present study we aimed to identify causative factors that are responsible for extraocular muscle to be primarily affected in CPEO. We performed comparative histochemical and molecular genetic analyses of extraocular muscle and skeletal muscle single fibers in a case of isolated CPEO caused by the heteroplasmic m.5667G>A mutation in the mitochondrial tRNAAsn gene (MT-TN). Histochemical analyses revealed higher proportion of cytochrome c oxidase deficient fibers in extraocular muscle (41%) compared to skeletal muscle (10%). However, genetic analyses of single fibers revealed no significant difference either in the mutation loads between extraocular muscle and skeletal muscle cytochrome c oxidase deficient single fibers (extraocular muscle 86% ± 4.6%; skeletal muscle 87.8 %± 5.7%, p = 0.246) nor in the mutation threshold (extraocular muscle 74% ± 3%; skeletal muscle 74% ± 4%). We hypothesize that higher proportion of cytochrome c oxidase deficient fibers in extraocular muscle compared to skeletal muscle might be due to facilitated segregation of the m.5667G>A mutation into extraocular muscle, which may explain the preferential ocular manifestation and clinically isolated CPEO. 相似文献
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best practice onkologie - 相似文献
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Matthias Christgen MD PhD Oleg Gluz MD Nadia Harbeck MD Ronald E. Kates PhD Mieke Raap MD Henriette Christgen Michael Clemens MD Wolfram Malter MD Benno Nuding MD Bahriye Aktas MD Sherko Kuemmel MD Toralf Reimer MD Andrea Stefek MD Petra Krabisch MD Marianne Just MD Doris Augustin MD Monika Graeser MD Frederick Baehner MD Rachel Wuerstlein MD Ulrike Nitz MD Hans Kreipe MD the West German Study Group PlanB Investigators 《Cancer》2020,126(22):4847-4858
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Herbert Schulz Ann‐Kathrin Ruppert Federico Zara Francesca Madia Michele Iacomino Maria S. Vari Ganna Balagura Carlo Minetti Pasquale Striano Amedeo Bianchi Carla Marini Renzo Guerrini Yvonne G. Weber Felicitas Becker Holger Lerche Claudia Kapser Christoph J. Schankin Wolfram S. Kunz Rikke S. Mller Karen L. Oliver Susannah T. Bellows Saul A. Mullen Samuel F. Berkovic Ingrid E. Scheffer Hande Caglayan Ugur Ozbek Per Hoffmann Sara Schramm Despina Tsortouktzidis Albert J. Becker Thomas Sander 《Epilepsia》2019,60(5):e31-e36
Juvenile myoclonic epilepsy (JME) is a common syndrome of genetic generalized epilepsies (GGEs). Linkage and association studies suggest that the gene encoding the bromodomain‐containing protein 2 (BRD2) may increase risk of JME. The present methylation and association study followed up a recent report highlighting that the BRD2 promoter CpG island (CpG76) is differentially hypermethylated in lymphoblastoid cells from Caucasian patients with JME compared to patients with other GGE subtypes and unaffected relatives. In contrast, we found a uniform low average percentage of methylation (<4.5%) for 13 CpG76‐CpGs in whole blood cells from 782 unrelated European Caucasians, including 116 JME patients, 196 patients with genetic absence epilepsies, and 470 control subjects. We also failed to confirm an allelic association of the BRD2 promoter single nucleotide polymorphism (SNP) rs3918149 with JME (Armitage trend test, P = 0.98), and we did not detect a substantial impact of SNP rs3918149 on CpG76 methylation in either 116 JME patients (methylation quantitative trait loci [meQTL], P = 0.29) or 470 German control subjects (meQTL, P = 0.55). Our results do not support the previous observation that a high DNA methylation level of the BRD2 promoter CpG76 island is a prevalent epigenetic motif associated with JME in Caucasians. 相似文献
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