Cavitation is a common damage mechanism in soft solids. Here, we study this using a phaseseparation technique in stretched, elastic solids to controllably nucleate and grow small cavities by several orders of magnitude. The ability to make stable cavities of different sizes, as well as the huge range of accessible strains, allows us to systematically study the early stages of cavity expansion. Cavities grow in a scale-free manner, accompanied by irreversible bond breakage that is distributed around the growing cavity, rather than being localized to a crack tip. Furthermore, cavities appear to grow at constant driving pressure. This has strong analogies with the plasticity that occurs surrounding a growing void in ductile metals. In particular we find that, although elastomers are normally considered as brittle materials, small-scale cavity expansion is more like a ductile process. Our results have broad implications for understanding and controlling failure in soft solids. arXiv:1811.00841v2 [cond-mat.soft]

Dynamic steady-state spherical cavitation fields are examined with emphasis on material porosity at large strain. Cavity expansion is driven by constant internal pressure in presence of remote tension or compression. The plastic branch of constitutive relations is described by the Gurson model, with arbitrary strain hardening. The mathematical model is reduced to a system of four ordinary nonlinear coupled differential equations. Numerical examples show that a plastic shock wave builds up as expansion velocity approaches a critical value and jump conditions across the shock are accounted for. At critical levels of remote tension, quasi-static cavitation of all internal voids is induced before dynamic cavity expansion occurs.

Cavity expansion can be used to measure the local nonlinear elastic properties in soft materials, regardless of the specific damage or instability mechanism that it may ultimately induce.

Biofilms are aggregates of bacterial cells surrounded by an extracellular matrix. Much progress has been made in studying biofilm growth on solid substrates; however, little is known about the biophysical mechanisms underlying biofilm development in three-dimensional confined environments in which the biofilm-dwelling cells must push against and even damage the surrounding environment to proliferate. Here, combining single-cell imaging, mutagenesis, and rheological measurement, we reveal the key morphogenesis steps of Vibrio cholerae biofilms embedded in hydrogels as they grow by four orders of magnitude from their initial size. We show that the morphodynamics and cell ordering in embedded biofilms are fundamentally different from those of biofilms on flat surfaces. Treating embedded biofilms as inclusions growing in an elastic medium, we quantitatively show that the stiffness contrast between the biofilm and its environment determines biofilm morphology and internal architecture, selecting between spherical biofilms with no cell ordering and oblate ellipsoidal biofilms with high cell ordering. When embedded in stiff gels, cells self-organize into a bipolar structure that resembles the molecular ordering in nematic liquid crystal droplets. In vitro biomechanical analysis shows that cell ordering arises from stress transmission across the biofilm–environment interface, mediated by specific matrix components. Our imaging technique and theoretical approach are generalizable to other biofilm-forming species and potentially to biofilms embedded in mucus or host tissues as during infection. Our results open an avenue to understand how confined cell communities grow by means of a compromise between their inherent developmental program and the mechanical constraints imposed by the environment.

No abstract