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Jos G. Maessen

Researcher at Maastricht University

Publications -  453
Citations -  12346

Jos G. Maessen is an academic researcher from Maastricht University. The author has contributed to research in topics: Atrial fibrillation & Medicine. The author has an hindex of 51, co-authored 416 publications receiving 10525 citations. Previous affiliations of Jos G. Maessen include Maastricht University Medical Centre & Central Texas College.

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Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction.

TL;DR: Galectin-3, a macrophage-derived mediator, induces cardiac fibroblast proliferation, collagen deposition, and ventricular dysfunction, which implies that HF therapy aimed at inflammatory responses may need to be targeted at the early stages of HF and probably needs to antagonize multiple inflammatory mediators, including galectIn-3.
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miR-133 and miR-30 Regulate Connective Tissue Growth Factor Implications for a Role of MicroRNAs in Myocardial Matrix Remodeling

TL;DR: The results show that both miR-133 and mi-30 directly downregulate CTGF, a key profibrotic protein, and thereby establish an important role for these miRNAs in the control of structural changes in the extracellular matrix of the myocardium.
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A protocol is not enough to implement an enhanced recovery programme for colorectal resection.

TL;DR: This international observational study evaluated the implementation of an enhanced recovery programme in five European centres and examined the determinants affecting recovery and length of hospital stay.
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Post-operative atrial fibrillation: a maze of mechanisms

TL;DR: The mechanistic interaction between predisposing factors and the electrophysiological mechanisms resulting in POAF and their therapeutic implications are discussed and show that POAF is ‘multi-factorial’.
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Impact of Blood Transfusions on Inflammatory Mediator Release in Patients Undergoing Cardiac Surgery

TL;DR: Intraoperative PC transfusions do contribute to the inflammatory response after cardiac surgery both by enhancing part of the response and by directly changing plasma concentrations of inflammatory mediators.