id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-282547-ehr9aaix	Chang, Jae C.	Acute Respiratory Distress Syndrome as an Organ Phenotype of Vascular Microthrombotic Disease: Based on Hemostatic Theory and Endothelial Molecular Pathogenesis	2019-11-28		.txt	text/plain	11511	637	33	7 Recently, two proposed hemostatic mechanisms have opened the door in the understanding of ARDS from molecular pathogenesis associated with endotheliopathy that promotes inflammation and coagulation disorder in sepsis and other critical illnesses [8] [9] [10] [11] ; one is "two-activation theory of the endothelium" in which endothelial pathogenesis activates inflammatory pathway and microthrombotic pathway and the other is a novel "two-path unifying theory" of hemostasis in which hemostasis initiates thrombogenesis and promotes microthrombogenesis, leading to vascular microthrombotic disease (VMTD). ARDS indicates acute respiratory distress syndrome; DIT, disseminated intravascular thrombosis; EA-VMTD, endotheliopathy-associated vascular microthrombotic disease; ECs, endothelial cells; HC, hepatic coagulopathy; MAHA/aMAHA, microangiopathic hemolytic anemia/atypical microangiopathic hemolytic anemia; MODS: multi-organ dysfunction syndrome; MOF, multi-organ failure; TMA, thrombotic microangiopathy; SIRS, systemic inflammatory response syndrome; TTP, thrombotic thrombocytopenic purpura; ULVWF, unusually large von Willebrand factor multimers activates ULVWF path, but TF path is not activated if subendothelial tissue (SET)/extravascular tissue (EVT) illustrated in Figure 2 is not compromised.	./cache/cord-282547-ehr9aaix.txt	./txt/cord-282547-ehr9aaix.txt