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Paul Hasler

Researcher at University of Basel

Publications -  51
Citations -  2757

Paul Hasler is an academic researcher from University of Basel. The author has contributed to research in topics: Neutrophil extracellular traps & Rheumatoid arthritis. The author has an hindex of 20, co-authored 48 publications receiving 2241 citations. Previous affiliations of Paul Hasler include University Hospital of Basel.

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Activated endothelial cells induce neutrophil extracellular traps and are susceptible to NETosis-mediated cell death

TL;DR: Findings offer new insight into mechanisms whereby NETs trigger damage to the endothelium in sepsis, small vessel vasculitis and possibly the villous trophoblast in preeclampsia.
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Induction of Neutrophil Extracellular DNA Lattices by Placental Microparticles and IL-8 and Their Presence in Preeclampsia

TL;DR: Large numbers of NETs were present directly in the intervillous space of preeclamptic placentae, and their increased presence in preeclampsia suggests that NETs may play a role in the underlying pathology.
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Preliminary criteria for the very early diagnosis of systemic sclerosis: results of a Delphi Consensus Study from EULAR Scleroderma Trials and Research Group

Jérôme Avouac, +127 more
TL;DR: A core set of preliminary items considered as important for the very early diagnosis of systemic sclerosis were identified in a Delphi exercise among 110 experts in the field of SSc.
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Enhanced neutrophil extracellular trap generation in rheumatoid arthritis: analysis of underlying signal transduction pathways and potential diagnostic utility

TL;DR: Signaling elements associated with the extrusion of NETs are significantly enhanced to promote NETosis in RA compared with healthy controls, and the quantitation of NETosis-derived products may be a useful complementary tool to discriminate between healthy controls and RA cases.
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Efficient Neutrophil Extracellular Trap Induction Requires Mobilization of Both Intracellular and Extracellular Calcium Pools and Is Modulated by Cyclosporine A

TL;DR: The data regarding the calcineurin antagonists, ascomycin and cyclosporine A, open the possibility to therapeutically supress or modulate NETosis and provide new insight into the mechanism whereby such immune suppressive drugs render transplant patients susceptible to opportunistic fungal infections.