Jesper Lundström

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Despite the well-documented effects of plasma lipid lowering regimes halting atherosclerosis lesion development and reducing morbidity and mortality of coronary artery disease and stroke, the transcriptional response in the atherosclerotic lesion mediating these beneficial effects has not yet been carefully investigated. We performed transcriptional(More)
Environmental exposures filtered through the genetic make-up of each individual alter the transcriptional repertoire in organs central to metabolic homeostasis, thereby affecting arterial lipid accumulation, inflammation, and the development of coronary artery disease (CAD). The primary aim of the Stockholm Atherosclerosis Gene Expression (STAGE) study was(More)
BACKGROUND The stability of atherosclerotic plaques determines the risk for rupture, which may lead to thrombus formation and potentially severe clinical complications such as myocardial infarction and stroke. Although the rate of plaque formation may be important for plaque stability, this process is not well understood. We took advantage of the(More)
The quest to determine cause from effect is often referred to as reverse engineering in the context of cellular networks. Here we propose and evaluate an algorithm for reverse engineering a gene regulatory network from time-series and steady-state data. Our algorithmic pipeline, which is rather standard in its parts but not in its integrative composition,(More)
Uncovering interactions between genes, gene networks, is important to increase our understanding of intrinsic cellular processes and responses to external stimuli such as drugs. Gene networks can be computationally inferred from repeated measurements of gene expression, using algorithms, which assume that each gene is controlled by only a small number of(More)
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