id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-006700-df8ard9o	Müller-Redetzky, Holger C.	Dynamics of pulmonary endothelial barrier function in acute inflammation: mechanisms and therapeutic perspectives	2014-03-06		.txt	text/plain	10609	582	32	However, upon infectious or sterile inflammatory stimulation via either the alveolar (e.g., in pneumonia and mechanical ventilation) or the vascular lumen (e.g., in bacteremia and sepsis), pulmonary endothelial barrier homeostasis may be disturbed, resulting in increased permeability, protein-rich fluid extravasation, lung oedema and finally acute respiratory distress syndrome (ARDS) with mortality rates ranging from 27 to 45 % depending on severity (Ranieri, et al. Although the underlying mechanisms of leukocyte mediated barrier failure are of highest scientific interest, therapeutic interference to ameliorate acute lung injury by depletion or blocking of cell recruitment should raise concerns as neutrophils and monocytes are key players of pulmonary and systemic innate immune responses and therapeutic intervention at this level might leave the patient functionally immunosuppressed. In mice, Ang-1-induced Tie-2 receptor phosphorylation stimulated the p190RhoGTPaseactivating protein (p190RhoGAP) via PI3-kinase and Rac1 to inactivate RhoA, resulting in reduced F-actin stress fibre formation and diminished endothelial permeability (Mammoto et al.	./cache/cord-006700-df8ard9o.txt	./txt/cord-006700-df8ard9o.txt