Davide Riccobelli

We argue that nucleation of brittle cracks in initially flawless soft elastic solids is preceded by a continuum instability which cannot be captured without accounting for geometrically and physical nonlinearities of the constitutive response. To corroborate this somewhat counterintuitive claim, we present a theoretical and numerical study of the simplest model where a homogeneous elastic body subjected to tension is weakened by a free surface which then serves as a site of crack nucleation. We show that in this prototypical setting, brittle fracture starts as a symmetry breaking elastic instability activated by softening and involving large elastic rotations. The implied bifurcation of the homogeneous elastic equilibrium is highly unconventional due to its extraordinary sensitivity to geometry, reminiscent of the transition to turbulence. We trace the development of the instability beyond the limits of continuum elasticity by using quasi-continuum theory allowing one to capture the ultimate strain localization indicative of the formation of actual cracks.

Modeling the behavior of biological tissues and organs often necessitates the knowledge of their shape in the absence of external loads. However, when their geometry is acquired in-vivo through imaging techniques, bodies are typically subject to mechanical deformation due to the presence of external forces, and the load-free configuration needs to be reconstructed. This paper addresses this crucial and frequently overlooked topic, known as the inverse elasticity problem (IEP), by delving into both theoretical and numerical aspects, with a particular focus on cardiac mechanics. In this work, we extend Shield’s seminal work to determine the structure of the IEP with arbitrary material inhomogeneities and in the presence of both body and active forces. These aspects are fundamental in computational cardiology, and we show that they may break the variational structure of the inverse problem. In addition, we show that the inverse problem might have no solution even in the presence of constant Neumann boundary conditions and a polyconvex strain energy functional. We then present the results of extensive numerical tests to validate our theoretical framework, and to characterize the computational challenges associated with a direct numerical approximation of the IEP. Specifically, we show that this framework outperforms existing approaches both in terms of robustness and optimality, such as Sellier’s iterative procedure, even when the latter is improved with acceleration techniques. A notable discovery is that multigrid preconditioners are, in contrast to standard elasticity, not efficient, where a one-level additive Schwarz and generalized Dryja–Smith–Widlund provide a much more reliable alternative. Finally, we successfully address the IEP for a full-heart geometry, demonstrating that the IEP formulation can compute the stress-free configuration in real-life scenarios where Sellier’s algorithm proves inadequate.

We report surprising morphological changes of suspension droplets (containing class II hydrophobin protein HFBI from Trichoderma reesei in water) as they evaporate with a contact line pinned on a rigid solid substrate. Both pendant and sessile droplets display the formation of an encapsulating elastic film as the bulk concentration of solute reaches a critical value during evaporation, but the morphology of the droplet varies significantly: for sessile droplets, the elastic film ultimately crumples in a nearly flattened area close to the apex while in pendant droplets, circumferential wrinkling occurs close to the contact line. These different morphologies are understood through a gravito-elastocapillary model that predicts the droplet morphology and the onset of shape changes, as well as showing that the influence of the direction of gravity remains crucial even for very small droplets (where the effect of gravity can normally be neglected). The results pave the way to control droplet shape in several engineering and biomedical applications.

Understanding the mechanics of brain embryogenesis can provide insights on pathologies related to brain development, such as lissencephaly, a genetic disease which cause a reduction of the number of cerebral sulci. Recent experiments on brain organoids have confirmed that gyrification, i.e. the formation of the folded structures of the brain, is triggered by the inhomo-geneous growth of the peripheral region. However, the rheology of these cellular aggregates and the mechanics of lissencephaly are still matter of debate. In this work, we develop a mathematical model of brain organoids based on the theory of morpho-elasticity. We describe them as non-linear elastic bodies, composed of a disk surrounded by a growing layer called cortex. The external boundary is subjected to a tissue surface tension due the intercellular adhesion forces. We show that the resulting surface energy is relevant at the small length scales of brain organoids and significantly affects the mechanics of cellular aggregates. We perform a linear stability analysis of the radially symmetric configuration and we study the post-buckling behaviour through finite element simulations. We find that the process of gyrification is triggered by the cortex growth and modulated by the competition between two length scales: the radius of the organoid and the capillary length due to surface tension. We show that a solid model can reproduce the results of the in-vitro experiments. Furthermore, we prove that the lack of brain sulci in lissencephaly is caused by a reduction of the cell stiffness: the softening of the organoid strengthens the role of surface tension, delaying or even inhibiting the onset of a mechanical instability at the free boundary.