China 
Africa 
Explore chapters and articles related to this topic
Introduction to Host-Biomaterial Interactions
Published in Nina M. K. Lamba, Kimberly A. Woodhouse, Stuart L. Cooper, Polyurethanes in Biomedical Applications, 2017
Nina M. K. Lamba, Kimberly A. Woodhouse, Stuart L. Cooper
The intrinsic pathway also is referred to as contact phase activation. It is initiated by the actions of factor XII (FXII, Hageman factor), prekallikrein (PK) and high molecular weight kininogen (HMWK), when FXII contacts surfaces such as glass or collagen. FXII is activated to FXIIa, which acts as an enzyme, catalyzing the activation of factor XI (FXI) to FXIa. FXIa then acts in the presence of Ca2+ to activate factor IX (FIX). FIXa then activates FX, and at this stage the reaction proceeds along the common pathway. The common pathway commences with the activation of FX, which converts prothrombin (FII) to thrombin. Thrombin cleaves fibrinopeptides A and B from fibrinogen molecules, and the resulting fibrin monomers are then able to polymerize into a gel, forming the fibrin network required for the stabilization of the platelet plug. Thrombin and factor XIII (FXIII) stabilize the fibrin network by forming covalent bonds between fibrin molecules, essentially providing a crosslinked structure. An overview of coagulation is given in Figure 3.
Biocompatibility of Powdered Materials: The Influence of Surface Characteristics
Published in Michel Nardin, Eugène Papirer, Powders and Fibers, 2006
Patrick Frayssinet, Patrice Laquerriere
Surface charge is known to activate the coagulation cascade. Initiation of the intrinsic pathway occurs when prekallikrein, high-molecular-weight kininogen, factor XI, and XII are exposed to a negatively charged surface.
A human whole-blood model to study the activation of innate immunity system triggered by nanoparticles as a demonstrator for toxicity
Published in Science and Technology of Advanced Materials, 2019
Kristina N Ekdahl, Karin Fromell, Camilla Mohlin, Yuji Teramura, Bo Nilsson
The plasma contact system is linked to both the coagulation system and the kallikrein/bradykinin system: its primary function is to maintain hemostasis, but it also has an important role in inflammation. Factor XII (FXII) is the primary recognition molecule within the contact system and in particular (but not exclusively) it binds to various negatively charged substances such as heparin, lipopolysaccharide (LPS), and biomaterials (including NPs) which leads to its autoactivation to FXIIa. FXIIa, an active protease which can activate prekallikrein to kallikrein which then releases the highly potent inflammatory mediator BK from high molecular weight kininogen (HMWK). Alternatively, FXIIa can start the intrinsic pathway of coagulation by cleaving FXI to FXIa which then initiates the generation of FXa, thrombin and subsequent fibrin formation and clotting.
Immobilizing argatroban and mPEG-NH2 on a polyethersulfone membrane surface to prepare an effective nonthrombogenic biointerface
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Yanling Dai, Siyuan Dai, Xiaohui Xie, Jianping Ning
The intrinsic pathway and complement system are activated by the contact activation of high molecular weight kininogen (HMWK), prekallikrein and factor XII, and those molecules require contact with negatively charged surfaces for zymogen activation in vitro [54, 55]. The charge density is another important factor that can influence the hemocompatibility of the membrane. The surface charge properties of the unmodified and modified membranes were measured, and streaming potential measurements were carried out at pH 3–10 (1 mM KCl solution at 25 °C). As shown in Figure 6, the zeta potential of the pure PES was −18.27 ± 1.87 mV at pH 7.4 (simulating the in vivo pH). The PES-PDA membrane value decreased to −31.69 ± 1.87 mV due to the introduction of the abundant negative charges of the phenol hydroxyl groups. For the AG-immobilized PES-PDA membrane, the zeta potential further declines to −52.84 ± 1.76 mV, which might be related to the –COOH group of at AG. Electrically neutral mPEG-NH2 had a shadowing effect on the negative charges, contributing to an increase of in zeta potential (−15.34 ± 1.74 mV). Some researchers proposed that the presence of negative charges on the membrane surface cause electrostatic repulsion with negatively charged components of the blood, such as proteins, erythrocytes and platelets. Others [51, 56, 57] reported that the contact phase activation after the blood contacts with the negatively charged surface was improved via neutralizing the electronegative charges.