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We derive sharp-interface models for one-dimensional brittle fracture via the inverse-deformation approach. Methods of Γ -convergence are employed to obtain the singular limits of previously proposed models. The latter feature a local, non-convex stored energy of inverse strain, augmented by small interfacial energy, formulated in terms of the inverse-strain gradient. They predict spontaneous fracture with exact crack-opening discontinuities, without the use of damage (phase) fields or pre-existing cracks; crack faces are endowed with a thin layer of surface energy. The models obtained herewith inherit the same properties, except that surface energy is now concentrated at the crack faces in the Γ -limit. Accordingly, we construct energy-minimizing configurations. For a composite bar with a breakable layer, our results predict a pattern of equally spaced cracks whose number is given as an increasing function of applied load. 

Through mechanical forces, biological cells remodel the surrounding collagen network, generating striking deformation patterns. Tethers—tracts of high densification and fibre alignment—form between cells, thinner bands emanate from cell clusters. While tethers facilitate cell migration and communication, how they form is unclear. Combining modelling, simulation and experiment, we show that tether formation is a densification phase transition of the extracellular matrix, caused by buckling instability of network fibres under cell-induced compression, featuring unexpected similarities with martensitic microstructures. Multiscale averaging yields a two-phase, bistable continuum energy landscape for fibrous collagen, with a densified/aligned second phase. Simulations predict strain discontinuities between the undensified and densified phase, which localizes within tethers as experimentally observed. In our experiments, active particles induce similar localized patterns as cells. This shows how cells exploit an instability to mechanically remodel the extracellular matrix simply by contracting, thereby facilitating mechanosensing, invasion and metastasis. 

A mathematical model is proposed for shape evolution and locomotion of fish epidermal keratocytes on elastic substrates. The model is based on mechanosensing concepts: cells apply contractile forces onto the elastic substrate, while cell shape evolution depends locally on the substrate stress generated by themselves or external mechanical stimuli acting on the substrate. We use the level set method to study the behaviour of the model numerically, and predict a number of distinct phenomena observed in experiments, such as (i) symmetry breaking from the stationary centrosymmetric to the well-known steadily propagating crescent shape, (ii) asymmetric bipedal oscillations and travelling waves in the lamellipodium leading edge, (iii) response to remote mechanical stress externally applied to the substrate (tensotaxis) and (iv) changing direction of motion towards an interface with a rigid substrate (durotaxis).