Results 151 to 160 of about 17,660 (277)

PatternJ: an ImageJ toolset for the automated and quantitative analysis of regular spatial patterns found in sarcomeres, axons, somites, and more

Biology Open
Mélina Baheux Blin, Vincent Loreau, Frank Schnorrer, Pierre Mangeol   +3 more
doaj   +1 more source

Intramuscular pathways of maladaptation in overtraining syndrome

The Journal of Physiology, EarlyView.
Abstract figure legend The transition from adaptive overreaching to maladaptive overtraining and mechanisms through which excessive training load can lead to performance decline. Four interconnected pathophysiological domains are highlighted: neural fatigue, involving both central and peripheral components such as altered sensory feedback and reflex ...
Emily Shorter, Oscar Horwath, Sabrina Tzivia Barsky, Ferdinand von Walden, Johanna T. Lanner   +4 more
wiley   +1 more source

Human Variant in the Cardiac Troponin I Switch Domain Causes Diastolic Dysfunction in a Novel Mouse Model

Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Elizabeth Silver, Jason M. Duran, Betul Beyza Gunes, Axel J. Fenwick, Sofie Maisel, Tsui‐Min Wang, Ana Maria Manso, Marina Sampaio Cruz, Yusu Gu, Joshua Fong, Aysen Shathaya, Chao Chen, Angel Soto‐Hermida, Wei Feng, Yoshitake Cho, Julius Bogomolovas, Jill M. Gelow, Ahmad Masri, Kelly A. Frazer, Robert S. Ross, Ju Chen, Catherine A. Makarewich, Anthony Cammarato, Andrew D. McCulloch, Paul Bushway, Eric D. Adler   +25 more
doaj   +1 more source

Hypoxia and hypercapnia elicit overlapping but distinct skeletal muscle toxicities

The Journal of Physiology, EarlyView.
Abstract figure legend Hypoxia and hypercapnia cause overlapping skeletal muscle phenotypes, including atrophy, change in myofibre metabolic profile and myogenic response to injury. Both signals operate via distinct cellular pathways. Abstract Skeletal muscle dysfunction is strongly associated with elevated mortality in acute and chronic pulmonary ...
Joseph Balnis, Ariel Jaitovich
wiley   +1 more source

Asynchronous movement of sarcomeres in myocardium under living conditions: role of titin

In summary, recent nano-imaging studies have revealed that the length of each sarcomere does not change in a synchronous fashion throughout excitation-contraction coupling in myocytes in the beating heart in vivo (Kobirumaki-Shimozawa et al., 2016 ...
Tomohiro Nakanishi, Fuyu Kobirumaki-Shimozawa, Oyama Kotaro, Shin’ichi Ishiwata, Norio Fukuda   +4 more
core   +1 more source

Computational model of haemodynamics during atrial fibrillation

The Journal of Physiology, EarlyView.
Abstract figure legend We developed a simplified computational model that replicates patient‐specific haemodynamics during both normal sinus rhythm and atrial fibrillation (AF). Our computational model comprises: (1) an electrical subsystem that generates unco‐ordinated atrial and irregular ventricular activation times characteristic of AF and (2) a ...
Felix Plappert, Pim J.A. Oomen, Clara E. Jones, Emmanouil Charitakis, Lars O. Karlsson, Pyotr G. Platonov, Mikael Wallman, Frida Sandberg   +7 more
wiley   +1 more source

Residual force depression in single sarcomeres is abolished by MgADP-induced activation

, 2015
The mechanisms of force depression commonly observed during active shortening in skeletal muscles remain elusive. One major limitation to force depression research has been the inability of experimental preparations to directly isolate the two most ...
Trecarten, Neal
core  

Energetic microdomains and the vascular control of neuronal and muscle excitability: Toward a unified model

The Journal of Physiology, EarlyView.
Abstract figure legend The capillary–mitochondria–ion channel (CMIC) axis scales structural resources to match functional workload. (Left) In settings of restricted energetic capacity (e.g. cortical neurons), sparse capillary networks and modest mitochondrial pools set a lower energetic ceiling, sufficient to support phasic, low‐workload excitability. (
L. Fernando Santana, Scott Earley
wiley   +1 more source

Human‐derived cardiac‐neural microtissues reveal catecholaminergic polymorphic ventricular tachycardia is also a disease of the sympathetic neuron

The Journal of Physiology, EarlyView.
Abstract figure legend Schematic diagram illustrating the proposed pathway in which regulatory defects might occur in sympathetic neurons derived from hiPSC in catecholaminergic polymorphic ventricular tachycardia (CPVT). Specifically, enhanced calcium transients appeared to derive from three sources: enhanced membrane excitability (due to loss of ...
Ni Li, Chenchen Zhang, Mengying Xu, YoonYoung Choi, Davi Sidarta‐Oliveira, Ruirui Dong, Xinyu Hu, Enrique M. Toledo, Cesar A. Prada‐Medina, Finbar Argus, Kun Liu, Mingyu Li, Linna Zhou, Hagan Bayley, Corey Smith, Chris Denning, Ana I. Domingos, Guoliang Hao, Dan Li, David J. Paterson   +19 more
wiley   +1 more source

Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction. [PDF]

J Mol Cell Cardiol Plus
McCauley MD, Solaro RJ.
europepmc   +1 more source