Results 81 to 90 of about 21,845 (197)
The Journal of Physiology, EarlyView.Abstract figure legend The results from this study show that maximal cardiac output, stroke volume and leg blood flow are similar between highly trained females and males after normalisation to lean body mass (LBM). However, the 10% higher haemoglobin concentration ([Hb]) and arterial O2 content in males result in higher systemic and leg O2 delivery ...
Øyvind Skattebo +11 more
wiley +1 more source
Caenorhabditis elegans as an in vivo model system for human inherited primary arrhythmia syndromes
The Journal of Physiology, EarlyView.Abstract figure legend Most genes involved in inherited primary arrhythmia syndromes (IPAS) are conserved in Caenorhabditis elegans, where genetic manipulation enables functional characterization of variants, identification of regulatory proteins, and in vivo drug testing.
Antoine Delinière +6 more
wiley +1 more source
The interaction of actin with dystrophin
FEBS Letters, 1990 Proton NMR spectroscopy of synthetic peptides corresponding to defined regions of human dystrophin has been employed to study the interaction with F‐actin. No evidence of interaction with a C‐terminal region corresponding to amino acid residues 3429–3440 was obtained.
Levine, B.A. +3 more
openaire +2 more sources
The Journal of Physiology, EarlyView.Abstract figure legend In healthy young males, we found that skeletal muscle hypertrophy following a period of resistance exercise training (RET) was consistent within and between subjects, as assessed using a variety of established methods. The skeletal muscle hypertrophic response was independent of external load.
Matthew J. Lees +11 more
wiley +1 more source
Duchenne muscular dystrophy treatment with lentiviral vector containing mini‐dystrophin gene in vivo
MedCommDuchenne muscular dystrophy (DMD) is an incurable X‐linked recessive genetic disease caused by mutations in the dystrophin gene. Many researchers aim to restore truncated dystrophin via viral vectors.
Xiaoyu Wang +11 more
doaj +1 more source
Journal of Translational Medicine, 2009 The dystrophin gene, located at Xp21, codifies dystrophin, which is part of a protein complex responsible for the membrane stability of muscle cells. Its absence on muscle causes Duchenne Muscular Dystrophy (DMD), a severe disorder, while a defect of ...
Gollop Thomaz R +6 more
doaj +1 more source
Dystrophin and the brain [PDF]
Developmental Medicine & Child Neurology, 2010 Ricotti, Valeria +2 more
openaire +3 more sources
Vascular smooth muscle cell mechanotransduction: Pathways, phenotypes and emerging technologies
The Journal of Physiology, EarlyView.Abstract figure legend Vascular smooth muscle cells are exposed to mechanical stimuli from the blood flow and the extracellular matrix. The cells sense the signals from cyclic stretch, shear stress, hydrostatic pressure and matrix stiffness through specialized mechanosensors, such as mechanosensitive ion channels or cell surface receptors including ...
Nivethitha Kota Lakshminaraasimulu +3 more
wiley +1 more source
Molecular Therapy: Nucleic Acids, 2018 Duchenne muscular dystrophy is a fatal muscle disease, caused by mutations in DMD, leading to loss of dystrophin expression. Phosphorodiamidate morpholino splice-switching oligonucleotides (PMO-SSOs) have been used to elicit the restoration of a ...
Ugur Akpulat +6 more
doaj +1 more source
The Journal of Physiology, EarlyView.Abstract figure legend Cardiac cellular electrophysiology is modulated by multiple factors, including temperature, extracellular K+, heart rate/pacing frequency, and drugs. These modulators can have distinct effects on ion‐channel gating and transcription/trafficking over time.
Stefan Meier +3 more
wiley +1 more source