Modification of the RLA model for presenting a cluster system of a composite material with a fractal filler structure

The paper proposes a modification of the diffusion-limited aggregation model to study the properties of a cluster system. A computational experiment to determine the mutual influence of the sticking probability and the volume concentration of particles on the formation of fractal clusters in a cluster system was carried out in accordance with the second-order orthogonal central compositional plan (OCCP). As a result of a computational experiment in accordance with the OCCP, an equation was obtained for the dependence of the mass fractal dimension of clusters on the volume of particle concentration and the probability of adhesion of diffusing particles and cluster particles in the adhesion zone. This dependence was obtained in a range of volume concentration of particles from 2 to 5 % and the probability of adhesion of diffusing particles and particles of clusters in the adhesion zone from 0.2 to 1.

The participation of signal transduction and gene regulation mechanisms in the cascade of MAPK p38 (mitogen-activated protein kinases) in the repair of damage to the serous membrane of the abdominal cavity

Objective: to assess the activity of р38 МАРК in serosal injury.Material and methods. We modelled adhesive process in abdomen in 40 Wistar rats. Adhesion zone was immunohistochemically stained for p38 MAPK and p38 MAPK Phospho. Expression of р38 МАР-coding genes was studied the in the injured zone using RT PCR. The control group consisted of 5 intact Wistar rats.Results. As a result of immunohistochemical staining of adhesion zone we determined that peak of p38 expression is registered on the 14th day after surgery, but phosphorylated p38 MAPK activity peak — on the 3rd day. Assessment of p38 MAPK genes expression showed that Mapk12 genes was expression peaks on the 3rd и 14th day, Mapk13 — in 12 hours and on the 7th day, Mapk11 and Mapk14 — on the 14th day. Statistical significance in comparison with data obtained in intact animals (р < 0,05) for MAPK12 was registered on the 3rd day, for MAPK13 — in 12 hours, on the 3rd and 7th day.Conclusion. Our research allowed us to determine р38 МАРК cascade expression in non-changed reparative process. It was found that p38 MAPK cascade activation starts from the 6thhour after the surgery and lasts up to 30th day with its maximum on the 14th day.

Adhesion and Cohesion

The phenomena of adhesion and cohesion are reviewed and discussed with particular reference to dentistry. This review considers the forces involved in cohesion and adhesion together with the mechanisms of adhesion and the underlying molecular processes involved in bonding of dissimilar materials. The forces involved in surface tension, surface wetting, chemical adhesion, dispersive adhesion, diffusive adhesion, and mechanical adhesion are reviewed in detail and examples relevant to adhesive dentistry and bonding are given. Substrate surface chemistry and its influence on adhesion, together with the properties of adhesive materials, are evaluated. The underlying mechanisms involved in adhesion failure are covered. The relevance of the adhesion zone and its importance with regard to adhesive dentistry and bonding to enamel and dentin is discussed.

Kinetics of Membrane Spreading on Compliant Bio-Adhesive Substrates

The contact formation between cell membrane and a bio-adhesive substrate is driven by binding between transmembrane mobile receptors (e.g., integrin) and complementary ligand molecules on the substrate (fibronectin, collagen, etc.) This short range specific adhesion is alleviated by a phalanx of interfacial non-specific forces. In addition to cell-substrate interfacial interactions, cell adhesion can be mediated by a wide range of substrate physiochemical properties. In particular, mechanical stiffness of the substrate has been recognized as one of the major regulators for bio-adhesion. Cells in general, exhibit an apparent adhesion preference for stiffer substrates and switch from a round to spread morphology as the substrate stiffness increases. Understanding the mechano-chemical pathways mediating the interplay between the substrate properties and cell behavior could be critical for effective performance of synthetic biomaterials in tissue engineering applications. In this study, we consider the effect of substrate elasticity on the dynamics of membrane spreading and growth of focal adhesion zone. The formation and growth of the focal adhesion points during the early stage of adhesion process is a result of spontaneous spreading of membrane on the substrate. This can be considered as a non-equilibrium kinetic process which is controlled by the diffusibility of receptor molecules. In order to study the effect of substrate elasticity on the kinetics of membrane-substrate association, receptors are assumed as ideal solute particles laterally diffusing within the plane of the membrane until they are stabilized through association with their complementary ligands which are immobilized on the surface of a compliant substrate. Considering different mechanical stiffness for the substrates, the displacement and speed of spreading at the edge of adhesion zone are predicted as a function of time. Results show that decreasing the stiffness of bio-adhesive substrates reduces the rate of membrane spreading, due to a weaker thermodynamic force which drives the membrane-substrate association. This mechanism restrains the growth of focal adhesion zones on compliant substrates and can be considered as a reason for smaller spread area of the cells after stabilization of adhesion.

Finite Element Modelling of Cell Adhesion Mediated by Receptor-Ligand Binding

The process of cell adhesion and spreading on the extracellular matrix (ECM) protein layer is mediated by the interaction of cell receptors and ECM ligands [1]. Receptors diffuse along the cell membrane surface and interact with ligands in ECM to form bonds. Cells spread and the adhesion zone grows as bond formation at the adhesion front increases to a critical level. This process involves coupling of reaction-diffusion and mechanical contact between cells and ECM. In this study, a novel numerical algorithm is developed to implement this coupling into the finite element method for modeling the process of cell adhesion and spreading. By taking the mass diffusion and the user-defined gap conductance features provided in a commercial FEM code, Abaqus [2], the process has been solved in an integrated and fully coupled manner. Preliminary results have been obtained from the simulation of cell spreading on a rigid substrate. The influence of glycocalyx layer (present at cell surface) on the adhesion development has also been incorporated into the modeling.