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Ruth D E Fritsch-Stork

Researcher at Utrecht University

Publications -  45
Citations -  1378

Ruth D E Fritsch-Stork is an academic researcher from Utrecht University. The author has contributed to research in topics: Antiphospholipid syndrome & Population. The author has an hindex of 18, co-authored 43 publications receiving 1005 citations. Previous affiliations of Ruth D E Fritsch-Stork include University Medical Center Utrecht & Sigmund Freud University Vienna.

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A framework for remission in SLE: consensus findings from a large international task force on definitions of remission in SLE (DORIS)

Ronald F van Vollenhoven, +58 more
TL;DR: An international task force of 60 specialists and patient representatives agreed on eight key statements regarding remission in SLE and three principles to guide the further development of remission definitions, which provides a framework for testing different definitions of remission against long-term outcomes.
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Alterations in peripheral blood memory B cells in patients with active rheumatoid arthritis are dependent on the action of tumour necrosis factor

TL;DR: The data suggest that decreases in peripheral blood IgD+CD27+ pre-switch memory B cells in RA reflect their accumulation in the synovial tissue, and indicates that trafficking ofMemory B cells into inflamed tissue in RA patients is regulated by TNF and can be corrected by neutralising TNF.
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Performance of the 2012 Systemic Lupus International Collaborating Clinics classification criteria versus the 1997 American College of Rheumatology classification criteria in adult and juvenile systemic lupus erythematosus. A systematic review and meta-analysis

TL;DR: Evaluating the performance in classifying systemic lupus erythematosus by the 2012 Systemic Lupus International Collaborating Clinics criteria versus the revised American College of Rheumatology criteria from 1997 found ACR'97 is best for juvenile SLE even if associated with lower sensitivity.
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Ligation of signal inhibitory receptor on leukocytes-1 suppresses the release of neutrophil extracellular traps in systemic lupus erythematosus.

TL;DR: SIRL-1 engagement can dampen spontaneous and anti-neutrophil antibody-induced NET formation in SLE, likely by suppressing NAPDH oxidase and MEK-ERK activity.