Flash Forward is a show about possible (and not so possible) future scenarios. What would the warranty on a sex robot look like? How would diplomacy work if we couldn’t lie? Could there ever be a fecal transplant black market? (Complicated, it wouldn’t, and yes, respectively, in case you’re curious.) Hosted and produced by award winning science journalist Rose Eveleth, each episode combines audio drama and journalism to go deep on potential tomorrows, and uncovers what those futures might re ...
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Thrombosis and novel hemophilia therapies: the fine line between clotting and bleeding
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Manage episode 303647537 series 1443907
Content provided by Blood Advances Talks. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Blood Advances Talks or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://player.fm/legal.
The availability of novel nonfactor therapeutics is revolutionizing the management of hemophilia in individuals with inhibitory antibodies, as well as making prophylaxis more convenient even in the absence of inhibitors. Unfortunately, the use of these products has been associated with thrombotic events that are not typically seen with factor replacement. These are primarily seen when a patient on a nonfactor therapy experiences breakthrough bleeding and concomitantly receives another hemostatic agent. This video addresses thrombotic complication in 3 nonfactor products: (1) emicizumab, a bispecific antibody that mimics the cofactor activity of factor VIII; (2) fitusiran, an small interfering RNA that knocks down synthesis of antithrombin; and (3) concizumab, an antibody that blocks inhibition of factor Xa by tissue factor pathway inhibitor. The latter 2 agents were developed on the premise that hemostasis in hemophilia could be “rebalanced” by reducing the levels of anticoagulant activity to compensate for the defect in procoagulant activity. Each of these approaches increases peak levels of thrombin achieved in assays on plasma from treated subjects and reduces bleeding rates in individuals with or without inhibitors. However, we do not yet have a good mechanistic model for precisely how these approaches affect hemostasis in vivo. It is not only the total amount of active thrombin produced that determines the effectiveness of hemostasis but also how thrombin generation is regulated. Therefore, it is currently difficult to predict how these new agents will interact with other perturbations or therapeutic manipulations of the coagulation system.
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28 episodes
MP3•Episode home
Manage episode 303647537 series 1443907
Content provided by Blood Advances Talks. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Blood Advances Talks or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://player.fm/legal.
The availability of novel nonfactor therapeutics is revolutionizing the management of hemophilia in individuals with inhibitory antibodies, as well as making prophylaxis more convenient even in the absence of inhibitors. Unfortunately, the use of these products has been associated with thrombotic events that are not typically seen with factor replacement. These are primarily seen when a patient on a nonfactor therapy experiences breakthrough bleeding and concomitantly receives another hemostatic agent. This video addresses thrombotic complication in 3 nonfactor products: (1) emicizumab, a bispecific antibody that mimics the cofactor activity of factor VIII; (2) fitusiran, an small interfering RNA that knocks down synthesis of antithrombin; and (3) concizumab, an antibody that blocks inhibition of factor Xa by tissue factor pathway inhibitor. The latter 2 agents were developed on the premise that hemostasis in hemophilia could be “rebalanced” by reducing the levels of anticoagulant activity to compensate for the defect in procoagulant activity. Each of these approaches increases peak levels of thrombin achieved in assays on plasma from treated subjects and reduces bleeding rates in individuals with or without inhibitors. However, we do not yet have a good mechanistic model for precisely how these approaches affect hemostasis in vivo. It is not only the total amount of active thrombin produced that determines the effectiveness of hemostasis but also how thrombin generation is regulated. Therefore, it is currently difficult to predict how these new agents will interact with other perturbations or therapeutic manipulations of the coagulation system.
…
continue reading
28 episodes
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