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Non-invasive electromechanical cell-based biosensors for improved investigation of 3D cardiac models.
Biosens Bioelectron
January 2019
Department of Informatics, Bioengineering Robotics and Systems Engineering, University of Genova, Via All'Opera Pia, 13, 16145 Genova, Italy. Electronic address:
Cardiomyocytes (CM) placed on microelectrode array (MEA) were simultaneously probed with cantilever from atomic force microscope (AFM) system. This electric / nanomechanical combination in real time recorded beating force of the CMs cluster and the triggering electric events. Such "organ-on-a-chip" represents a tool for drug development and disease modeling.
View Article and Find Full Text PDFCatheter ablation of multiple accessory pathways in duchenne muscular dystrophy.
Korean Circ J
February 2013
Krankenanstalt Rudolfstiftung, Vienna, Austria.
A 23-year-old male with Duchenne muscular dystrophy (DMD) experienced self-limiting palpitations at age 19 years for the first time. Palpitations recurred not earlier than at age 23 years, and were attributed to narrow complex tachycardia, which could be terminated with adenosine. Since electrocardiography showed a delta-wave, Wolff-Parkinson-White (WPW) syndrome was diagnosed, ajmaline prescribed and radio-frequency catheter ablation of three accessory pathways carried out one week later.
View Article and Find Full Text PDFDiltiazem and verapamil protect dystrophin-deficient muscle fibers of MDX mice from degeneration: a potential role in calcium buffering and sarcolemmal stability.
Muscle Nerve
February 2009
Departamento de Anatomia, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), Campinas, São Paulo, 13083-970, Brazil.
The lack of dystrophin in mdx mice and in Duchenne muscular dystrophy causes sarcolemmal breakdown and increased calcium influx followed by myonecrosis. We examined whether the calcium channel blockers diltiazem and verapamil protect dystrophic muscles from degeneration. Mdx mice received daily intraperitoneal injections of diltiazem or verapamil for 18 days, followed by removal of the sternomastoid, diaphragm, tibialis anterior, and cardiac muscles.
View Article and Find Full Text PDFCalcium antagonists for Duchenne muscular dystrophy.
Cochrane Database Syst Rev
October 2008
Division of Rehabilitation Medicine, University of Nottingham, Arkwright House, Derby City Hospital, Derby, UK, DE22 3NE.
Background: Duchenne muscular dystrophy (DMD) is a progressive muscle condition starting in childhood, leading to severe disability and a shortened life span. It is due to severe deficiency of the protein dystrophin which performs both structural and signalling roles within skeletal and cardiac myocytes. Calcium accumulates in dystrophic muscle cells and plays a role in cell damage.
View Article and Find Full Text PDFMuscle regeneration in dystrophic mdx mice is enhanced by isosorbide dinitrate.
Neurosci Lett
July 2005
Departamento de Anatomia, Instituto de Biologia, Universidade Estadual de Campinas, CP 6109, Campinas 13084-971, São Paulo, Brazil.
Activation of muscle satellite cells, a fundamental step in the success of muscle regeneration is mediated by nitric oxide (NO). In this study, we investigated whether isosorbide dinitrate (ISD), an NO donor, could improve muscle regeneration in dystrophic mdx mice. The right tibialis anterior muscle of mdx and C57Bl/10 mice was injected with bupivacaine (0.
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