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Bart van de Sluis

Researcher at University Medical Center Groningen

Publications -  90
Citations -  10769

Bart van de Sluis is an academic researcher from University Medical Center Groningen. The author has contributed to research in topics: Inflammation & LDL receptor. The author has an hindex of 39, co-authored 90 publications receiving 7992 citations. Previous affiliations of Bart van de Sluis include University of Adelaide & University Medical Center Utrecht.

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Clearance of p16 Ink4a -positive senescent cells delays ageing-associated disorders

TL;DR: Data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.
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Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

TL;DR: Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.
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Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel

TL;DR: In this paper, the authors proposed a method to solve the problem of the problem: this paper ] of "uniformity" of the distribution of data points in the data set.
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Chronic inflammation induces telomere dysfunction and accelerates ageing in mice

TL;DR: It is shown that chronic, progressive low-grade inflammation induced by knockout of the nfkb1 subunit of the transcription factor NF-κB induces premature ageing in mice, and frequency of senescent cells in liver and intestinal crypts quantitatively predict mean and maximum lifespan in both short- and long-lived mice cohorts.
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Identification of a new copper metabolism gene by positional cloning in a purebred dog population.

TL;DR: The discovery of a mutated MURR1 gene in Bedlington terriers with copper toxicosis provides a new lead to disentangling the complexities of copper metabolism in mammals.