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Kay E. Davies

Researcher at University of Oxford

Publications -  580
Citations -  40236

Kay E. Davies is an academic researcher from University of Oxford. The author has contributed to research in topics: Duchenne muscular dystrophy & Dystrophin. The author has an hindex of 100, co-authored 573 publications receiving 38462 citations. Previous affiliations of Kay E. Davies include Case Western Reserve University & Technische Universität München.

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Linkage analysis of two cloned DNA sequences, DXS197 and DXS207, in hypophosphatemic rickets families.

TL;DR: Multilocus linkage analysis mapped the DXS197 and DXS207 loci distal to HYP and demonstrated the locus order Xpter-DXS85-(DXS207, DXS43,DXS197)-HYP- DXS41-Xcen, which will be useful as alternative markers in the genetic counseling of some families.
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The emerging family of dystrophin-related proteins

TL;DR: Duchenne and Becker muscular dystrophy are caused by mutations in the gene encoding dystrophin, a component of the subsarcolemmal cytoskeleton, a part of the neuromuscular junction.
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A Phase 1b Trial to Assess the Pharmacokinetics of Ezutromid in Pediatric Duchenne Muscular Dystrophy Patients on a Balanced Diet

TL;DR: This study provides assurance that, with the formulation tested (F3) and instructions regarding food, 2500 mg BID of ezutromid achieves plasma concentrations that, based on preclinical studies, should be able to modulate utrophin expression in future clinical trials.
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The ARRIVE guidelines, a welcome improvement to standards for reporting animal research.

TL;DR: The ARRIVE (Animal Research: Reporting In Vivo Experiments) guidelines are introduced, produced by the National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC3Rs), which are published in this issue of the journal with the authors' endorsement.
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Microarray analysis of mdx mice expressing high levels of utrophin: Therapeutic implications for dystrophin deficiency

TL;DR: This study confirms that a strategy to up-regulate utrophin is likely to be beneficial in dystrophin deficiency and produces a global gene expression profile more similar to that seen for the wild-type mouse.