The role of platelets in blood coagulation during thrombus formation in flow

Hemostatic plug covering the injury site (or a thrombus in the pathological case) is formed due to the complex interaction of aggregating platelets with biochemical reactions in plasma that participate in blood coagulation. The mechanisms that control clot growth and which lead to growth arrest are not yet completely understood. We model them with numerical simulations based on a hybrid DPD-PDE model. Dissipative particle dynamics (DPD) is used to model plasma flow with platelets while fibrin concentration is described by a simplified reaction-diffusion-convection equation. The model takes into account consecutive stages of clot growth. First, a platelet is weakly connected to the clot and after some time this connection becomes stronger due to other surface receptors involved in platelet adhesion. At the same time, the fibrin network is formed inside the clot. This becomes possible because flow does not penetrate the clot and cannot wash out the reactants participating in blood coagulation. Platelets covered by the fibrin network cannot attach new platelets. Modelling shows that the growth of a hemostatic plug can stop as a result of its exterior part being removed by the flow thus exposing its non-adhesive core to the flow

Hybrid model of clot formation in flow

The process of blood coagulation and clot formation in vivo is not yet completely understood. One of the main questions related to haemostasis is why the clot stops growing in normal conditions before it completely obstructs the flow in the vessel, whereas, in pathologic cases, it can continue to grow, often with fatal consequences. Hence, revealing the mechanisms by which the clot grows and stops growing in the flow remains of great importance. In order to study this topic we have developed a hybrid DPD-PDE method where Dissipative Particle Dynamics (DPD) is used to model plasma flow and platelets, while the protein regulatory network is described by a system of partial differential equations. The model describes the interaction between blood flow, platelet aggregation and plasma coagulation. As a result of modelling we propose a new mechanism of clot growth and growth arrest in flow. The developed model and its parts can be used as a base to modelling of different physiological phenomena related to cell-cell interactions and blood flows

Hybrid model of clot formation in flow

The process of blood coagulation and clot formation in vivo is not yet completely understood. One of the main questions related to haemostasis is why the clot stops growing in normal conditions before it completely obstructs the flow in the vessel, whereas, in pathologic cases, it can continue to grow, often with fatal consequences. Hence, revealing the mechanisms by which the clot grows and stops growing in the flow remains of great importance. In order to study this topic we have developed a hybrid DPD-PDE method where Dissipative Particle Dynamics (DPD) is used to model plasma flow and platelets, while the protein regulatory network is described by a system of partial differential equations. The model describes the interaction between blood flow, platelet aggregation and plasma coagulation. As a result of modelling we propose a new mechanism of clot growth and growth arrest in flow. The developed model and its parts can be used as a base to modelling of different physiological phenomena related to cell-cell interactions and blood flows

Existence of Reaction-Diffusion Waves with Nonlinear Boundary Conditions

The paper is devoted to a reaction-diffusion equation in an infinite two-dimensional strip with nonlinear boundary conditions. The existence of travelling waves is proved in the bistable case by the Leray-Schauder method. It is based on a topological degree for elliptic problems in unbounded domains and on a priori estimates of solutions

Modeling of the effects of IL-17 and TNF-α on endothelial cells and thrombus growth [Modélisation des effets des cytokines IL-17 and TNF-α sur les cellules endothéliales et la croissance du thrombus]

Rheumatoid and psoriatic arthritis are chronic inflammatory diseases, with massive increase of cardiovascular events (CVE), and contribution of the cytokines TNF-α and IL-17. Chronic inflammation inside the joint membrane or synovium results from the activation of fibroblasts/synoviocytes, and leads to the release of cytokines from monocytes (Tumor Necrosis Factor or TNF) and from T lymphocytes (Interleukin-17 or IL-17). At the systemic level, the very same cytokines affect endothelial cells and vessel wall. We have previously shown [1,2 that IL-17 and TNF-α specifically when combined, increase procoagulation, decrease anticoagulation and increase platelet aggregation, leading to thrombosis. These results are the basis for the models of interactions between IL-17 and TNF, and genes expressed by activated endothelial cells. This work is devoted to mathematical modeling and numerical simulations of blood coagulation and clot growth under the influence of IL-17 and TNF-α. We show that they can provoke thrombosis, leading to the complete or partial occlusion of blood vessels. The regimes of blood coagulation and conditions of occlusion are investigated in numerical simulations and in approximate analytical models. The results of mathematical modeling allow us to predict thrombosis development for an individual patient. © 2017 Académie des science

Modeling of the effects of IL-17 and TNF-α on endothelial cells and thrombus growth [Modélisation des effets des cytokines IL-17 and TNF-α sur les cellules endothéliales et la croissance du thrombus]

Rheumatoid and psoriatic arthritis are chronic inflammatory diseases, with massive increase of cardiovascular events (CVE), and contribution of the cytokines TNF-α and IL-17. Chronic inflammation inside the joint membrane or synovium results from the activation of fibroblasts/synoviocytes, and leads to the release of cytokines from monocytes (Tumor Necrosis Factor or TNF) and from T lymphocytes (Interleukin-17 or IL-17). At the systemic level, the very same cytokines affect endothelial cells and vessel wall. We have previously shown [1,2 that IL-17 and TNF-α specifically when combined, increase procoagulation, decrease anticoagulation and increase platelet aggregation, leading to thrombosis. These results are the basis for the models of interactions between IL-17 and TNF, and genes expressed by activated endothelial cells. This work is devoted to mathematical modeling and numerical simulations of blood coagulation and clot growth under the influence of IL-17 and TNF-α. We show that they can provoke thrombosis, leading to the complete or partial occlusion of blood vessels. The regimes of blood coagulation and conditions of occlusion are investigated in numerical simulations and in approximate analytical models. The results of mathematical modeling allow us to predict thrombosis development for an individual patient. © 2017 Académie des science

Hybrid model of blood coagulation

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Hybrid model of clot formation in flow and its applications

info:eu-repo/semantics/nonPublishe

Modelling of thrombus growth in flow with a DPD-PDE method

info:eu-repo/semantics/nonPublishe