The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Serine proteases as mediators of radiographic contrast media toxicity.

Iodipamide, iodoxamine, iothalamate, diatrizoate, and ioxitalamate exhibit a dose-dependent prolongation of coagulation time of global and monospecific functional coagulation tests. This is due to an inhibition of fibrin polymerization induced by these contrast media. Furthermore, a dose-dependent generation of fibrinolytic split products by RCM was found. At low doses, biliary RCM cause hypercoagulation by binding to spontaneously existing fibrinolytic products. Biliary RCM cause a dose-dependent decrease of hemolytic complement activity and decrease of complement factors of C3, B, and, to a lesser extent, C4. Nephrotopic RCM do not show these effects. By crossed immunoelectrophoresis B and C3 split products were not detected after in vitro incubation of iodipamide in serum or EDTA-blood. In contrast, zymosan, inulin, and dextran sulfate incubation of sera readily resulted in Bb and C3b generation. The failure to demonstrate complement split products was not due to artifacts. As a working hypothesis unspecific binding of RCM to blood proteins followed by interference with antithrombin and antiplasmin inhibitor functions is proposed. Possibly other antiproteases might be involved too. This results in a lowering of the clinical manifestation threshold of coagulation and fibrinolysis. The mechanism of complement activation remains unclear, since it is not influenced by EDTA, aprotinin, steroids, or by specific sera depleted of prekallikrein, Hageman factor, C2, and gamma-globulins.[1]


WikiGenes - Universities