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Vascular damage, initiated by host inflammatory cells, is a component of the pathophysiology of many acute and chronic inflammatory disorders. Neutrophil-mediated tissue damage is mediated primarily hyproteinases, particularly elastase and cathepsin G. In this study we have identified endothelial binding of two key serine proteinase inhibitors (serpins), α1-antitrypsin, the inhibitor of elastase, and α1-antichymotrypsin, the inhibitor of cathepsin G. These serpins are shed from the endothelium into the supernatant when neutrophils adherent to the endothelium are activated. Endothelium activated by lipopolysaccharide (LPS) augments this process, Serpin-proteinase complexes activate neutrophils and induce further cytokine release, thereby amplifying inflammatory processes. Strategies aimed at preventing endothelial serpin depletion may help minimize vascular damage during inflammation. [ABSTRACT FROM AUTHOR]

The article presents a study of carbonyl iron as a tool for non-toxic iron loading of the mussel Mytilus edulis. It says that carbonyl iron can be used for the iron loading method, with the ability to maintain a relatively high iron concentration. It states that the method rejects the use of filter system to avoid the build up of iron hydroxide.