Excess circulating angiopoietin-2 may contribute to pulmonary vascular leak in sepsis in humans.

Background: Acute respiratory distress syndrome (ARDS) is a devastating complication of numerous underlying conditions, most notably sepsis. Although pathologic vascular leak has been implicated in the pathogenesis of ARDS and sepsis-associated lung injury, the mechanisms promoting leak are incompletely understood. Angiopoietin-2 (Ang-2), a known antagonist of the endothelial Tie-2 receptor, was originally described as a naturally occurring disruptor of normal embryonic vascular development otherwise mediated by the Tie-2 agonist angiopoietin-1 (Ang-1).

Automating terminological networks to link heterogeneous biomedical databases.

As cross-disciplinary research escalates, researchers are facing the challenge of linking disparate biomedical databases that have been developed without common indexes. Manually indexing these large-scale databases is laborious and often impractical. Solutions involving mediating terminologies have been proposed, but coordination of terms from the databases of interest to these mediating terminologies is also laborious, and regular synchronization between indexes is an additional problem.