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Comparative Factor Ⅻ Contact Activation at Hydrophilic and Hydrophobic Surfaces and Interactions with Prekallikrein and Factor Ⅺ

机译:比较因子Hydro亲水和疏水表面的接触活化以及与前激肽释放酶和因子Inter的相互作用

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Blood coagulation resulting from contact activation due to blood - material interactions remains a challenge in the use of blood-contacting devices. The initiating step of the intrinsic pathway of plasma coagulation cascade is widely accepted to be surface contact activation of the blood zymogen FⅫ (Hageman Factor) into an active-enzyme form (FⅫa). This activation facilitates the assembly of a contact activation complex that is essential for enzyme amplification via reciprocal-activation prekallkrein (PK) and then FⅫ, as well as cascade propagation by FⅫa-mediated factor Ⅺ hydrolysis. This study seeks to clarify the differences between active FⅫ arising from interactions with hydrophilic vs. hydrophobic surfaces, and subsequent interactions of activated FⅫ with PK and coagulation factor FⅪ.
机译:在使用血液接触装置时,由于血液与物质的相互作用而引起的接触活化引起的血液凝结仍然是一个挑战。血浆凝血级联反应的内在途径的起始步骤被广泛接受为将血液酶原FⅫ(Hageman因子)转化为活性酶形式(FⅫa)的表面接触活化。这种活化作用促进了接触活化复合物的组装,这对于通过相互活化前kallkrein(PK)然后通过F 3进行酶扩增以及通过F 3a介导的β3水解进行级联繁殖是必不可少的。这项研究试图弄清由于与亲水性表面与疏水性表面相互作用而产生的活性F 3与活化的F 3与PK和凝血因子F 3的后续相互作用之间的差异。

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