Blood clot contraction plays an important role in prevention of bleeding and in thrombotic disorders. We will unveil and quantify the structural mechanisms of clot contraction at the level of single platelets. In contrast to other cell–matrix systems in which cells migrate along fibers, we will demonstrate that the “hand-over-hand” longitudinal pulling causes shortening and bending of platelet-attached fibers, resulting in formation of fiber kinks [1]. The revealed platelet-driven mechanisms of blood clot contraction demonstrate an important new biological application of cell motility principles. Recently developed multi-scale discrete worm-like chain model will be used to demonstrate mechanisms of governing non-linear mechanical properties of stretched and contracted fibrin network. Also, a novel multi-phase model will be described that simulates active interactions between platelets and fibrin network and which is used to study the impact of various physiologically relevant blood shear flow conditions on deformation and embolization of a partially obstructive clot [2].

In the second half of the talk, mechanism of mitotic rounding within packed embryonic tissue will be analyzed using a newly developed multi-scale subcellular element computational model that is calibrated using experimental data from developing Drosophila imaginal wing discs. Regression analysis of predictive model simulation results revealed the relative contributions of osmotic pressure, cell-cell adhesion and cortical stiffness to mitotic rounding. Mitotic area expansion is shown to be largely driven by regulation of cytoplasmic pressure. Surprisingly, mitotic shape roundness within physiological ranges is most sensitive to variation in cell-cell adhesivity and stiffness [3]. An understanding of how perturbed mechanical properties impact mitotic rounding has important potential implications on, amongst others, how tumors progressively become more genetically unstable due to increased chromosomal aneuploidy and more aggressive.