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David Montaigne

Researcher at university of lille

Publications -  120
Citations -  3158

David Montaigne is an academic researcher from university of lille. The author has contributed to research in topics: Internal medicine & Medicine. The author has an hindex of 25, co-authored 95 publications receiving 2250 citations. Previous affiliations of David Montaigne include Centre Hospitalier Regional et Universitaire de Lille & Lille University of Science and Technology.

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Comment on Patel et al. ACE2 Deficiency Worsens Epicardial Adipose Tissue Inflammation and Cardiac Dysfunction in Response to Diet-Induced Obesity. Diabetes 2016;65:85-95.

TL;DR: The authors read with interest, but concern, the recently published article, which focused on potential links between angiotensin-converting enzyme 2 (ACE2) deficiency, epicardial adipose tissue (EAT) inflammation, and cardiac dysfunction in a high-fat diet mouse model.
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Right ventricular pacing with mechanical dyssynchrony causes apoptosis interruptus and calcium mishandling.

TL;DR: In this article, a pacemaker was inserted into the right jugular vein and positioned either in the right atrium or at the right ventricular (RV) apex for 3 weeks to test whether ventricular dyssynchrony would elicit myocardial alterations in LV calcium handling regulation.
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The synthetic pentasaccharide fondaparinux prevents coronary microvascular injury and myocardial dysfunction in the ischemic heart.

TL;DR: It is demonstrated that fondaparinux can attenuate inflammatory responses and oxidative stress in connection with IR heart injury and could represent a potential therapeutic strategy for the prevention of myocardial dysfunction.

Basic Research Right Ventricular Pacing With Mechanical Dyssynchrony Causes Apoptosis Interruptus and Calcium Mishandling

TL;DR: Slow rate RV pacing causes mechanical dyssynchrony and profound LV alterations in both apoptotic pathways and calcium handling in the early stages of pacing-induced cardiomyopathy.
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Differential effects of inhibitory G protein isoforms on G protein-gated inwardly rectifying K+ currents in adult murine atria.

TL;DR: It is found that mice with deletion of Gαi2 had increased basal and agonist-activated currents, particularly in the right atria while in contrast those with G αi1/Gαi3 deletion had reduced currents.