Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy. - Wikidata - wikimedia - TriplyDB

Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy.

Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy.

http://www.wikidata.org/entity/Q34332718

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Modifier genes and their effect on Duchenne muscular dystrophy A Reduction in Selenoprotein S Amplifies the Inflammatory Profile of Fast-Twitch Skeletal Muscle in the mdx Dystrophic Mouse.Muscular dystrophy in the mdx mouse is a severe myopathy compounded by hypotrophy, hypertrophy and hyperplasia.Prednisone/prednisolone and deflazacort regimens in the CINRG Duchenne Natural History Study.Elusive sources of variability of dystrophin rescue by exon skipping TNF-α-Induced microRNAs Control Dystrophin Expression in Becker Muscular Dystrophy Deep RNA profiling identified CLOCK and molecular clock genes as pathophysiological signatures in collagen VI myopathy Molecular Signatures of Membrane Protein Complexes Underlying Muscular Dystrophy.Association Study of Exon Variants in the NF-κB and TGFβ Pathways Identifies CD40 as a Modifier of Duchenne Muscular Dystrophy.Immune-mediated pathology in Duchenne muscular dystrophy.Inflammation during skeletal muscle regeneration and tissue remodeling: application to exercise-induced muscle damage management.Outside in: The matrix as a modifier of muscular dystrophy.Redox Control of Skeletal Muscle Regeneration.Renin-angiotensin-aldosterone system inhibitors improve membrane stability and change gene-expression profiles in dystrophic skeletal muscles.Major hnRNP proteins act as general TDP-43 functional modifiers both in Drosophila and human neuronal cells.NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation.Genetic modifiers of muscular dystrophy act on sarcolemmal resealing and recovery from injury.Glucocorticoids Improve Myogenic Differentiation In Vitro by Suppressing the Synthesis of Versican, a Transitional Matrix Protein Overexpressed in Dystrophic Skeletal Muscles.SPP1 genotype and glucocorticoid treatment modify osteopontin expression in Duchenne muscular dystrophy cells.Divergent impact of Toll-like receptor 2 deficiency on repair mechanisms in healthy muscle versus Duchenne muscular dystrophy.Impact of Inflammation and Anti-inflammatory Modalities on Skeletal Muscle Healing: From Fundamental Research to the Clinic.Non-Glycanated Biglycan and LTBP4: Leveraging the extracellular matrix for Duchenne Muscular Dystrophy therapeutics.Expression profiling of disease progression in canine model of Duchenne muscular dystrophy.Phase 1 trial of vamorolone, a first-in-class steroid, shows improvements in side effects via biomarkers bridged to clinical outcomes.Multiscale analysis of a regenerative therapy for treatment of volumetric muscle loss injury.Optical prediction of single muscle fiber force production using a combined biomechatronics and second harmonic generation imaging approach Expression of the OAS Gene Family Is Highly Modulated in Subjects Affected by Juvenile Dermatomyositis, Resembling an Immune Response to a dsRNA Virus Infection

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P2860

Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy.

http://www.wikidata.org/entity/Q34332718

description

2014 nî lūn-bûn

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2014 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2014 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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Asynchronous remodeling is a d ...... n Duchenne muscular dystrophy.

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Eric P Hoffman

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Helen Johnston

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Jianhua Xuan

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Mamta Giri

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Robert J Freishtat

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Sherry Dadgar

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Terence A Partridge

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Yi-Wen Chen

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Yue Wang

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P2860

SPP1 genotype is a determinant of disease severity in Duchenne muscular dystrophy

Sources of variability and effect of experimental approach on expression profiling data interpretation

Gene expression profiling in DQA1*0501+ children with untreated dermatomyositis: a novel model of pathogenesis

Distinct roles for the alpha and beta subunits in the functions of integrin alphaMbeta2

Glucocorticoid-treated mice are an inappropriate positive control for long-term preclinical studies in the mdx mouse

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

In vivo filtering of in vitro expression data reveals MyoD targets.

VISDA: an open-source caBIG analytical tool for data clustering and beyond.

Probabilistic principal component subspaces: a hierarchical finite mixture model for data visualization.

Probe set algorithms: is there a rational best bet?

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