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Our results demonstrate that CRF/CRF1R activation may contribute to the adaptive changes induced by naloxone-precipitated withdrawal in the heart and in the brain areas which modulate the cardiac sympathetic function and suggest that CRF/CRF1R pathways could be contributing to cardiovascular disease associated to opioid addiction.
The compounds aim to modulate the cardiac ventricular L-type Ca2+ current (ICaL).
Besides proteomic analysis, cardiac hypertrophy induced by Ang II in the dTGR model was also shown by gas-chromatography TOF to modulate the cardiac metabolome in more than 100 metabolites [ 70].
The pro-redox components of multipollutant mixtures could modulate the cardiac myocytes' Ca2+ handling by reducing the intracellular Ca2+, or cause a change in the sensitivity of the contractile proteins to Ca2+, resulting in decreased cardiac contractility.
Interestingly, a recent work from the Paolocci group [ 95] reported that a tyrosine kinase-receptor such as TrkB, with its endogenous ligand BDNF, is able to modulate the cardiac excitation-contraction coupling process directly, independently and in parallel to G protein-coupled receptor signaling.
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These data suggested that RASSF1A is involved in modulating the cardiac contractile response following TNF-α stimulation.
Accordingly, we sought to further explore the in vivo role of ASIC3 in modulating the cardiac autonomic nervous system in conscious mice, since cardiac autonomic function has been suggested to reveal the healthy condition of humans.
These effects were not observed when the rise in fatty acid levels was pharmacologically prevented, thus underscoring the causal role of an extramyocardial supply of fatty acids in modulating the cardiac lipid pool (10).
It protects cells from oxidative stress [ 75], preserves anoxic heart function [ 76], protects the gut [ 77], lung [ 78], liver [ 79] and kidney [ 80] from ischaemia/reperfusion injury, modulates the cardiac preconditioning response [ 81] and acts as a preconditioning agent in its own right [ 82].
Regardless of the underlying pathophysiologic mechanisms, various compensatory feedback systems, including the sympathetic nervous system and renin angiotensin aldosterone system, are activated in patients with heart failure which aim to modulate the deprived cardiac pump function within a normal homeostatic range [ 4– 7].
Current evidence suggests that immune processes modulate the risk for cardiac involvement in HIV-infected persons.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com