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Rafal Pawlinski

Researcher at University of North Carolina at Chapel Hill

Publications -  119
Citations -  7414

Rafal Pawlinski is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Tissue factor & Inflammation. The author has an hindex of 37, co-authored 112 publications receiving 6482 citations. Previous affiliations of Rafal Pawlinski include Scripps Research Institute & Jagiellonian University.

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Excess of heme induces tissue factor-dependent activation of coagulation in mice

TL;DR: The results indicate that heme promotes tissue factor-dependent coagulation activation and induces tissue factor expression on leukocytes in vivo and that free heme may contribute to thrombin generation in a mouse model of sickle cell disease.
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Protease-Activated Receptor 2 Deficiency Reduces Cardiac Ischemia/Reperfusion Injury

TL;DR: PAR-2 deficiency reduces myocardial infarction and heart remodeling after I/R injury and PAR-2−/− mice were protected from postinfarction remodeling and showed less impairment in heart function compared with wild-type littermates up to 4 weeks after I-R injury.
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Enterococcus faecalis Gelatinase Mediates Intestinal Permeability via Protease-Activated Receptor 2

TL;DR: It is demonstrated that GelE from E. faecalis can regulate enteric epithelial permeability via PAR2, and this protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a dysbiotic enteric microbiota can lead to disease.
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Using heparin molecules to manage COVID-2019

TL;DR: Encouraging clinical data suggest that heparin‐like molecules may represent a useful approach to treat or prevent severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, and a novel strategy is proposed using “designer” heparIn molecules that are fabricated using a synthetic biology approach.
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Protease-activated receptors and myocardial infarction.

TL;DR: Results between genetic and pharmacological approaches indicate that further studies are needed to determine the role of different PARs in the injured heart, and it is possible that the major cellular target of the PAR‐4 inhibitor is platelets, which has been shown to contribute to inflammation in thejured heart, whereasPAR‐4 signaling in cardiomyocytes may be protective.