نتایج جستجو برای: dmd

تعداد نتایج: 4377  

2017
Zaïda Koeks Catherine L. Bladen David Salgado Erik van Zwet Oksana Pogoryelova Grace McMacken Soledad Monges Maria E. Foncuberta Kyriaki Kekou Konstantina Kosma Hugh Dawkins Leanne Lamont Matthew I. Bellgard Anna J. Roy Teodora Chamova Velina Guergueltcheva Sophelia Chan Lawrence Korngut Craig Campbell Yi Dai Jen Wang Nina Barišić Petr Brabec Jaana Lähdetie Maggie C. Walter Olivia Schreiber-Katz Veronika Karcagi Marta Garami Agnes Herczegfalvi Venkatarman Viswanathan Farhad Bayat Filippo Buccella Alessandra Ferlini En Kimura Janneke C. van den Bergen Miriam Rodrigues Richard Roxburgh Anna Lusakowska Anna Kostera-Pruszczyk Rosário Santos Elena Neagu Svetlana Artemieva Vedrana Milic Rasic Dina Vojinovic Manuel Posada Clemens Bloetzer Andrea Klein Jordi Díaz-Manera Eduard Gallardo A. Ayşe Karaduman Tunca Oznur Haluk Topaloğlu Rasha El Sherif Angela Stringer Andriy V. Shatillo Ann S. Martin Holly L. Peay Jan Kirschner Kevin M. Flanigan Volker Straub Kate Bushby Christophe Béroud Jan J. Verschuuren Hanns Lochmüller

BACKGROUND Recent short-term clinical trials in patients with Duchenne Muscular Dystrophy (DMD) have indicated greater disease variability in terms of progression than expected. In addition, as average life-expectancy increases, reliable data is required on clinical progression in the older DMD population. OBJECTIVE To determine the effects of corticosteroids on major clinical outcomes of DMD...

2016
Jean-Paul Iyombe-Engembe Dominique L Ouellet Xavier Barbeau Joël Rousseau Pierre Chapdelaine Patrick Lagüe Jacques P Tremblay

The CRISPR/Cas9 system is a great revolution in biology. This technology allows the modification of genes in vitro and in vivo in a wide variety of living organisms. In most Duchenne muscular dystrophy (DMD) patients, expression of dystrophin (DYS) protein is disrupted because exon deletions result in a frame shift. We present here the CRISPR-induced deletion (CinDel), a new promising genome-ed...

Journal: :Nucleic acids research 2016
Ignazio Maggio Luca Stefanucci Josephine M Janssen Jin Liu Xiaoyu Chen Vincent Mouly Manuel A F V Gonçalves

Duchenne muscular dystrophy (DMD) is a fatal X-linked muscle-wasting disorder caused by mutations in the 2.4 Mb dystrophin-encoding DMD gene. The integration of gene delivery and gene editing technologies based on viral vectors and sequence-specific designer nucleases, respectively, constitutes a potential therapeutic modality for permanently repairing defective DMD alleles in patient-derived m...

Journal: :Molecular and cellular biology 2006
Joanne L Thorvaldsen Andrew M Fedoriw Son Nguyen Marisa S Bartolomei

The differentially methylated domain (DMD) of the mouse H19 gene is a methylation-sensitive insulator that blocks access of the Igf2 gene to shared enhancers on the maternal allele and inactivates H19 expression on the methylated paternal allele. By analyzing H19 DMD deletion alleles H19DeltaDMD and H19Delta3.8kb-5'H19 in pre- and postimplantation embryos, we show that the DMD exhibits positive...

Journal: :PLoS ONE 2009
Isabelle Desguerre Christo Christov Michele Mayer Reinhard Zeller Henri-Marc Becane Sylvie Bastuji-Garin France Leturcq Catherine Chiron Jamel Chelly Romain K. Gherardi

BACKGROUND To explore clinical heterogeneity of Duchenne muscular dystrophy (DMD), viewed as a major obstacle to the interpretation of therapeutic trials METHODOLOGY/PRINCIPAL FINDINGS A retrospective single institution long-term follow-up study was carried out in DMD patients with both complete lack of muscle dystrophin and genotyping. An exploratory series (series 1) was used to assess phen...

2015
Jonathan H. Soslow Stephen M. Damon Kimberly Crum Mark A. Lawson James C. Slaughter Meng Xu Andrew E. Arai Douglas B. Sawyer David A. Parra Bruce M. Damon Larry W. Markham

BACKGROUND Duchenne muscular dystrophy (DMD) cardiomyopathy is a progressive disease for which there is no cure. Disease-specific therapies are needed that can be initiated before irreversible myocardial damage ensues. In order to evaluate therapeutic efficacy, surrogate endpoints other than ejection fraction must be found. The hypothesis of this study is that T1 and extracellular volume fracti...

Journal: :Nucleic acids research 1985
K E Davies A Speer F Herrmann A W Spiegler S McGlade M H Hofker P Briand R Hanke M Schwartz V Steinbicker

Two DNA markers, a random DNA fragment 754 and the cDNA sequence encoding the gene for ornithine transcarbamylase (OTC) have been studied in kindreds segregating for Duchenne muscular dystrophy. 754 and OTC are located close physically to the mutation in the region Xp21 below the breakpoints in two Duchenne females. The genetic distance was found to be approximately 10cM between 754 and DMD (tw...

2015
J. Patrick Gonzalez Jayalakshmi Ramachandran Lai-Hua Xie Jorge E. Contreras Diego Fraidenraich

Duchenne muscular dystrophy (DMD) is caused by an X-linked mutation that leads to the absence of dystrophin, resulting in life-threatening arrhythmogenesis and associated heart failure. We targeted the gap junction protein connexin43 (Cx43) responsible for maintaining cardiac conduction. In mild mdx and severe mdx:utr mouse models of DMD, and human DMD tissues, Cx43 was found to be pathological...

Journal: :Journal of pediatric psychology 2009
Jos G M Hendriksen James T Poysky Debby G M Schrans Eric G W Schouten Albert P Aldenkamp Johan S H Vles

OBJECTIVE The primary aim of this study was to establish the psychometric properties and clinical utility of the Personal Adjustment and Role Skills Scale (PARS-III) for assessing psychosocial adjustment in males with Duchenne muscular dystrophy (DMD). METHODS The parents of 287 male patients with DMD aged 5-18 years completed the PARS-III and Revised Rutter Scale. RESULTS The alpha coeffic...

Journal: :Cornea 2016
Ricardo M Nosé Maria Daniela Rivera-Monge Adriana S Forseto Walton Nosé

PURPOSE To report a case series of 4 patients with Descemet membrane detachment (DMD) after undergoing femtosecond laser-assisted cataract surgery incisions. METHODS Case report. RESULTS DMD was noted at the secondary incision (n = 2) or at the main incision (n = 2). All the secondary incision and 1 main incision DMD were resolved with intraoperative maneuvers. Delay in recognizing DMD intr...

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