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Id: 109: parkin mediates endothelial pro-inflammatory responses in acute lung injury
Conclusion These results suggest that endothelial parkin mediates EC activation and neutrophil adhesion/migration after LPS, and therefore it may represent a new potential therapeutic target in ALI/ARDS.
Source: Journal of Investigative Medicine - March 21, 2016 Category: Research Authors: Letsiou, E., Wang, H., Belvitch, P., Dudek, S., Sammani, S. Tags: Pulmonary/Critical Care Source Type: research

Id: 124: abl family kinases mediate lung vascular permeability and inflammation in acute lung injury
Conclusions The Abl family kinases c-Abl and Arg play complementary but distinct roles in mediating vascular permeability and inflammation following LPS challenge. The promoter of Abl1 (c-Abl) contains antioxidant response elements and LPS causes an increase in c-Abl expression. Additionally, LPS increases the mRNA expression of c-Abl, but not Arg. C-Abl contributes to LPS-induced NFB signaling; whereas Arg contributes to inter-endothelial gap formation and adherens junction stability. Inhibition of both of these kinases may be of benefit in patients with ARDS.
Source: Journal of Investigative Medicine - March 21, 2016 Category: Research Authors: Rizzo, A., Letsiou, E., Dudek, S., Sun, X., Garcia, J. Tags: Pulmonary/Critical Care Source Type: research