Session K53: Fracture and Adhesion of Soft Materials

The Topology and Mechanics of the Formation of Fracture Surface Patterns

How and why are patterns formed on broken surfaces? Faceted fracture surfaces are commonly formed by slow tensile cracks in amorphous materials; hence their formation cannot reflect microscopic order. While fracture mechanics predict that slow crack fronts should be straight and form mirror-like surfaces, facet-forming fronts propagate simultaneously within different planes separated by steps. Why are steps stable, what determines their path and how do they couple to crack front dynamics? By integrating real-time imaging of propagating crack fronts with surface measurements, we demonstrate that steps are topological defects; crack front separation into disconnected overlapping segments provides the condition for step stability. Crack dynamics are enslaved to steps; steps drift at a constant angle to the local front propagation direction while their increased dissipation couples to long-ranged elasticity to determine front shapes. We see how 3D topology couples to 2D fracture dynamics to provide a fundamental picture of how patterned surfaces are generated. We also show that crack front curvature may feed back to deflect step paths via nonlinear focusing of crack fronts, causing steps to converge to form a micro-branch. Thus, our results supply the basis for a unified picture of pattern formation on fracture surfaces.   

Topological adhesion

TBD   

Fracture mechanics of self-healing hydrogels

TBD   

Active superelasticity in three-dimensional epithelia of controlled shape

Fundamental biological processes are carried out by curved epithelial sheets enclosing a pressurized lumen. How these sheets develop and withstand three-dimensional deformations has remained unclear. By combining measurements of epithelial tension and shape with theoretical modeling, here we show that epithelial sheets are active superelastic materials. We produce arrays of epithelial domes with controlled geometry. Quantification of luminal pressure and epithelial tension reveals a tensional plateau over several-fold areal strains. These extreme tissue strains are accommodated by highly heterogeneous cellular strains, in seeming contradiction with the measured tensional uniformity. This phenomenology is reminiscent of superelasticity, a behavior generally attributed to microscopic material instabilities in metal alloys. We show that this instability is triggered in epithelial cells by a stretch-induced dilution of the actin cortex and rescued by the intermediate filament network. Our study unveils a new type of mechanical behavior -active superelasticity- that enables epithelial sheets to sustain extreme stretching under constant tension.   

Towards a Unified Model of Soft Adhesives

Pressure Sensitive Adhesives (PSA) have been widely used in adhesive tapes, stickers, tags in industry and day-to-day use, for decades. PSAs are rate-dependent materials, extremely soft, hence highly deformable. Their bonding strength depends critically on small scale features such the surface properties of the substrates. Understanding quantitatively their behavior has been a enormous challenge. Quite surprisingly, a same adhesive can be described by different models with little connection within each other depending on the adhesion tests used. In this talk, I will present a new modeling strategy to these soft materials [Creton and Ciccotti, Soft Matter, (2016)] based on the identification of the mesoscale mechanisms (cavitation, fibrillation, ...) along with the evaluation of the contribution of the large strain rheology of the PSA into the total work of debonding. I will discuss some original experimental investigations providing insights into the pertinent links between the peel, tack and shear of model PSAs.