An a priori assumption in micromechanical analysis of polymeric networks is that the constitutive polymer strands are of equal length. Monodisperse distribution of strands, however, is merely a simplifying assumption. This paper relaxes this assumption and considers a vulcanized network with a broad distribution of strand length. In the light of this model, this study predicts the damage initiation and stress–stretch dependency in filled polymer networks with random internal structures. The degradation of network mechanical behavior is assumed to be controlled by the adhesive failure of the strands adsorbed to the filler surface. This study shows that the short adsorbed strands are the culprits for damage initiation and their finite extensibility is a key determinant of the mechanical strength.

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Adhesion of carrier particles to the luminal surface of endothelium under hemodynamic flow conditions is critical for successful vascular drug delivery. Endothelial cells line the inner surface of blood vessels. The effect of mechanical behavior of this compliant surface on the adhesion of blood-borne particles is unknown. In this contribution, we use a phase-plane method, first developed by Hammer and Lauffenburger [Biophysical Journal, 52, 475 (1987)], to analyze the stability of specific adhesion of a spherical particle to a compliant interface layer. We construct a phase diagram that predicts the state of particle adhesion, subjected to an incident simple shear flow, in terms of interfacial elasticity, shear rate, binding affinity of cell adhesive molecules, and their surface density. The main conclusion is that the local deformation of the flexible interface inhibits the stable adhesion of the particle. In comparison with adhesion to a rigid substrate, a greater ligand density is required to establish a stable adhesion between a particle and a compliant interface. The results can be used for the rational design of particles in vascular drug delivery.

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