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Parasympathetic stimulation of the heart has been shown to protect against ventricular arrhythmias.
The computational modeling of the heart has been shown to be a very useful tool.
Importantly, purified mitochondrial aconitase (m-aconitase) isolated from bovine heart has been shown to be a source of hydroxyl radical formation (.OH), presumably via Fenton chemistry initiated by the co-released Fe2+ and hydrogen peroxide (H2O2) [10] (Equation 2).
Selective stimulation of the cardiac sympathetic nerves by transvascular stimulation of the heart has been shown [ 63, 64].
More recently, local administration of DKK-2 in the infarcted heart has been shown to enhance neovascularization [ 74].
Its use in combination with dynamic [O]H2O scans of the heart has been shown [ 18, 19], although it was found that frequent operator intervention was required.
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In particular, radiation techniques that have incorporated large volumes of the heart have been shown to negatively impact on overall survival [52].
In mice the transcriptional effects of TTA in the heart have been shown to be mediated almost exclusively via PPAR α[ 38].
Different progenitor cell populations, resident in the adult heart, have been shown to differentiate into cardiomyocytes or vascular structures both in vitro and in vivo [ 5, 6, 29].
In an animal model of diabetes collagen synthesis and ventricular stiffening in the heart have been shown to be dependent on mannose-binding lectin and activation of the lectin pathway [ 22].
Indeed, transgenic mice expressing a kinase dead form of AMPK in the heart have been shown to exhibit greater myocardial necrosis and apoptosis after ischaemia/reperfusion [134] and cannot be preconditioned [135].
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Justyna Jupowicz-Kozak
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