English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Neutral proteinases such as elastase and cathepsin G are liberated from secretory granules of PMN leukocytes in the course of diseases like septicemia, acute myelocytic leukemia or emphysema. Despite the presence of a high antiproteinase potential (α1-antitrypsin, α2-macroglobulin, anti-thrombin III, α2-antiplasmin, α1-antichymotrypsin) in plasma these proteinases are able to degrade clotting and other plasma factors unspecifically thus contributing to severe coagulation disorders. Evidence is presented that the plasma inhibitors (antithrombin III, α2-anti- plasmin and α1-antichymotrypsin) which are not able to inhibit granulocytic elastase, are rapidly inactivated by this proteinase and may thereby intensify consumption of clotting and other plasma proteins during inflammation.

Coagulation Defects Due To Inactivation Of Plasma Inhibitors By Granulocytic Elastase