We investigate the interaction of intracellular calcium spatio-temporal variations with the self-sustained contractions in cardiac myocytes. A consistent mathematical model is presented considering a hyperelastic description of the passive mechanical properties of the cell, combined with an active-strain framework to explain the active shortening of myocytes and its coupling with cytosolic and sarcoplasmic calcium dynamics. A finite element method based on a Taylor-Hood discretization is employed to approximate the nonlinear elasticity equations, whereas the calcium concentration and mechanical activation variables are discretized by piecewise linear finite elements. Several numerical tests illustrate the ability of the model in predicting key experimentally established characteristics including: (i) calcium propagation patterns and contractility, (ii) the influence of boundary conditions and cell shape on the onset of structural and active anisotropy and (iii) the high localized stress distributions at the focal adhesions. Besides, they also highlight the potential of the method in elucidating some important subcellular mechanisms affecting, e.g. cardiac repolarization.

Vesicles under flow constitute a model system for the study of red blood cells (RBCs) dynamics and blood rheology. In the blood circulatory system the Reynolds number (at the scale of the RBC) is not always small enough for the Stokes limit to be valid. We develop a numerical method in two dimensions based on the level set approach and solve the fluid/membrane coupling by using an adaptive finite element technique. We find that a Reynolds number of order one can destroy completely the vesicle tumbling motion obtained in the Stokes regime. We analyze in details this phenomenon and discuss some of the far reaching consequences. We suggest experimental tests on vesicles.