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Boris Schmitz
Researcher at University of Münster
Publications - 58
Citations - 918
Boris Schmitz is an academic researcher from University of Münster. The author has contributed to research in topics: High-intensity interval training & Interval training. The author has an hindex of 17, co-authored 58 publications receiving 712 citations. Previous affiliations of Boris Schmitz include University of Copenhagen & Leibniz Association.
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Journal ArticleDOI
Serum-Mediated Inhibition of Enzyme Replacement Therapy in Fabry Disease
TL;DR: Agalsidase inhibition was associated with higher lyso-globotriaosylceramide levels and worse disease severity scores in patients, and affected patients presented more often with FD-typical symptoms, such as diarrhea, fatigue, and neuropathic pain, among others.
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The Yo-Yo Intermittent Tests: A Systematic Review and Structured Compendium of Test Results.
Boris Schmitz,Carina Pfeifer,Kiana Kreitz,Matthias Borowski,Andreas Faldum,Stefan-Martin Brand +5 more
TL;DR: There is evidence that Yo-Yo intermittent tests reference values differ with respect to the type and level of sport performed, as well as statistical aggregation of published data.
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Alpha-Galactosidase A p.A143T, a non-Fabry disease-causing variant
Malte Lenders,Frank Weidemann,Christine Kurschat,Sima Canaan-Kühl,Thomas Duning,Jörg Stypmann,Boris Schmitz,Stefanie Reiermann,Johannes Krämer,Johannes Krämer,Daniela Blaschke,Christoph Wanner,Stefan-Martin Brand,Eva Brand +13 more
TL;DR: It is suggested that p.A143T patients with stroke/transient ischemic attacks of unknown etiology should be further evaluated, since the diagnosis of FD is not probable and subsequent ERT or chaperone treatment should not be an unreflected option.
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Salt controls endothelial and vascular phenotype
TL;DR: The potential clinical implication of direct (amiloride) and indirect (spironolactone) EnNaC inhibition on vascular function and the link between salt-induced changes of the endothelial and vascular phenotype and its clinical implications are outlined.
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Multifocal White Matter Lesions Associated with the D313Y Mutation of the α-Galactosidase A Gene
Malte Lenders,Thomas Duning,Michael Schelleckes,Boris Schmitz,Sonja Ständer,Arndt Rolfs,Stefan-Martin Brand,Eva Brand +7 more
TL;DR: Evidence is provided that GLA D313Y is potentially involved in neural damage with significant WML, demonstrating the necessity of evaluating patients carrying D 313Y more thoroughly.