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Saturday, 10/07/2006 1:39:16 AM

Saturday, October 07, 2006 1:39:16 AM

Post# of 346182
My earlier posts about exposed PS on activate platelets appear to have addressed correctly only one of two reasons for the increase in pro-time and APTT.

"A prolonged aPTT means that clotting is taking longer to occur than expected and may be caused by a variety of factors (see the list below). Often, this suggests that there may be a coagulation factor deficiency or a specific or nonspecific inhibitor affecting the body’s clotting ability. (snip) Inhibitors may be antibodies that specifically target certain coagulation factors, such as Factor VIII antibodies, or they may be non specific inhibitors, such as lupus antibodies and anticardiolipin antibodies that bind to chemicals called phospholipids found on the surface of platelets. Since phospholipids assist in the clotting process, and since the aPTT test reagents (chemicals used to run the tests) contain phospholipids, such antibodies may prolong the aPTT even though they are usually associated with thrombosis instead of bleeding.

http://www.labtestsonline.org/understanding/analytes/aptt/test.html

So, not only do we have to assume that Bavi will bind with the PS displayed on the activated platelets (just as ACL and lupus antibodies can), delaying the cascade and reducing its magnitude of its expression, but it appears that Bavi will also bind to phoshpolipids in the test reagents themselves, just as ACL and lupus antibodies do.



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