ﻻ يوجد ملخص باللغة العربية
We present the first mathematical model of flow-mediated primary hemostasis in an extravascular injury, which can track the process from initial deposition to occlusion. The model consists of a system of ordinary differential equations (ODE) that describe platelet aggregation (adhesion and cohesion), soluble-agonist-dependent platelet activation, and the flow of blood through the injury. The formation of platelet aggregates increases resistance to flow through the injury, which is modeled using the Stokes-Brinkman equations. Data from analogous experimental (microfluidic flow) and partial differential equation models informed parameter values used in the ODE model description of platelet adhesion, cohesion, and activation. This model predicts injury occlusion under a range of flow and platelet activation conditions. Simulations testing the effects of shear and activation rates resulted in delayed occlusion and aggregate heterogeneity. These results validate our hypothesis that flow-mediated dilution of activating chemical ADP hinders aggregate development. This novel modeling framework can be extended to include more mechanisms of platelet activation as well as the addition of the biochemical reactions of coagulation, resulting in a computationally efficient high throughput screening tool.
In the last decades, the interest to understand the connection between brain and body has grown notably. For example, in psychoneuroimmunology many studies associate stress, arising from many different sources and situations, to changes in the immune
The formation of new bone involves both the deposition of bone matrix, and the formation of a network of cells embedded within the bone matrix, called osteocytes. Osteocytes derive from bone-synthesising cells (osteoblasts) that become buried in bone
We present a novel mathematical model of heterogeneous cell proliferation where the total population consists of a subpopulation of slow-proliferating cells and a subpopulation of fast-proliferating cells. The model incorporates two cellular processe
We propose a strange-attractor model of tumor growth and metastasis. It is a 4-dimensional spatio-temporal cancer model with strong nonlinear couplings. Even the same type of tumor is different in every patient both in size and appearance, as well as
In this paper I have given a mathematical model of Cell reprogramming from a different contexts. Here I considered there is a delay in differential regulator rate equations due to intermediate regulators regulations. At first I gave some basic mathem