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Jacqueline A. Madison

Researcher at University of Michigan

Publications -  20
Citations -  2437

Jacqueline A. Madison is an academic researcher from University of Michigan. The author has contributed to research in topics: Neutrophil extracellular traps & Antiphospholipid syndrome. The author has an hindex of 11, co-authored 16 publications receiving 1222 citations.

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Neutrophil extracellular traps in COVID-19.

TL;DR: Sera from patients with COVID-19 have elevated levels of cell-free DNA, myeloperoxidase(MPO)-DNA, and citrullinated histone H3 (Cit-H3); the latter two are highly specific markers of NETs, which may contribute to cytokine release and respiratory failure.
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Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19.

TL;DR: Higher titers of aPL antibodies were associated with neutrophil hyperactivity, including the release of neutrophils extracellular traps (NETs), higher platelet counts, more severe respiratory disease, and lower clinical estimated glomerular filtration rate.
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Neutrophil extracellular traps and thrombosis in COVID-19.

TL;DR: Remains of NETs and neutrophil-derived S100A8/A9 (calprotectin) in patient sera were associated with higher risk of morbid thrombotic events in spite of prophylactic anticoagulation, and underscore the need for urgent investigation into the potential relationship betweenNETs and unrelentingThrombosis in COVID-19.
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Plasma tissue plasminogen activator and plasminogen activator inhibitor-1 in hospitalized COVID-19 patients.

TL;DR: In this article, the authors measured plasma antigen levels of tissue-type plasminogen activator (tPA) and PLSA inhibitor-1 (PAI-1) and performed spontaneous clot-lysis assays.
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Neutrophil calprotectin identifies severe pulmonary disease in COVID-19.

TL;DR: Serious cases of coronavirus disease 2019 (COVID‐19) are regularly complicated by respiratory failure, and levels of neutrophil activation marker S100A8/A9 (calprotectin) track closely with current and future CO VID‐19 severity, implicating neutrophils as potential perpetuators of inflammation and respiratory compromise.