id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-346413-2njl0fd3	Nakazawa, Daigo	Immunothrombosis in severe COVID-19	2020-08-15		.txt	text/plain	836	52	39	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spread all over the world immediately after the first patient infected with this virus was discovered in Wuhan, China, in December 2019. It has been demonstrated that SARS-CoV-2 infection induces vascular endothelial injury, resulting from coagulation [3] . Because these are degradation products of fibrin or neutrophil extracellular traps (NETs), an enhanced turnover of coagulation and NET formation appears to characterize severe COVID-19. Based on the loss of CD31 + cells in the endothelium that were close to the aggregated NETs, Leppkes and coworkers suggested that the injury of vascular endothelial cells infected with SARS-CoV-2 could trigger neutrophil attraction and NET formation (Fig. 1) . Leppkes and coworkers suggested that the prevention of excessive NET formation and aggregation could provide an approach to inhibit vascular occlusion and the development of severe COVID-19. When SARS-CoV-2 injures vascular endothelial cells, coagulation is invoked, and simultaneously, DAMPs are secreted from the damaged cells.	./cache/cord-346413-2njl0fd3.txt	./txt/cord-346413-2njl0fd3.txt