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Wesley Abplanalp

Researcher at Goethe University Frankfurt

Publications -  43
Citations -  1515

Wesley Abplanalp is an academic researcher from Goethe University Frankfurt. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 14, co-authored 26 publications receiving 774 citations. Previous affiliations of Wesley Abplanalp include University of Louisville.

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Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation.

TL;DR: Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes, which could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.
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Cell type-specific expression of the putative SARS-CoV-2 receptor ACE2 in human hearts.

TL;DR: This poster presents a poster presented at the 2016 European Conference on Cardiovascular Regeneration and Cardiopulmonary Institute (ECAS) at the University of Heidelberg, Germany, on the topic of regenerative medicine and cardiothoracic surgery.
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Clonal Hematopoiesis–Driver DNMT3A Mutations Alter Immune Cells in Heart Failure

TL;DR: This study demonstrates that circulating monocytes and T cells of patients with HF harboring clonal hematopoiesis–driver mutations in DNMT3A exhibit a highly inflamed transcriptome, which may contribute to the aggravation of chronic HF.
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Association of Clonal Hematopoiesis of Indeterminate Potential With Inflammatory Gene Expression in Patients With Severe Degenerative Aortic Valve Stenosis or Chronic Postischemic Heart Failure.

TL;DR: Gene ontology term analyses of regulated genes revealed that the most significantly upregulated genes encode for leukocyte-activation and interleukin-signaling pathways in monocytes of individuals with DNMT3A (myeloid leukocytes activation), as well as the NLRP3 inflammasome complex, a cellular receptor capable of mediating infection, macrophage activation syndrome, and other genes involved in cytokine response syndrome.