Davide Riccobelli

Growing experimental evidence highlights the relevant role of mechanics in the physiology of solid tumours, even in their early stages. While most of the mathematical models describe tumour growth as a volumetric increase of mass in the bulk, in vitro experiments on tumour spheroids have demonstrated that cell proliferation occurs in a thin layer at the boundary of the cellular aggregate. In this work, we investigate how elasticity and surface tension interact during the development of tumour spheroids. We model the tumour as a hyperelastic material undergoing boundary accretion, where the newly created cells are deformed by the action of surface tension. This growth leads to a frustrated reference configuration, resulting in the appearance of residual stress. Our theoretical framework is validated through experimental results of tumour spheroid cutting. Similar to fully developed tumours, spheroids tend to open when subject to radial cuts. Remarkably, even newly formed spheroids, which lack residual stress, exhibit this behaviour. Through both analytical solutions and numerical simulations, we show that this phenomenon is driven by elastocapillary interactions, where the residual stress developed in grown spheroids amplifies the tumour opening. Our model’s outcomes align with experimental observations and allow us to estimate the surface tension acting on tumour spheroids.

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.