Unified scenario for the morphology of crack paths in two-dimensional disordered solids.

A combined experimental and numerical investigation of the roughness of intergranular cracks in two-dimensional disordered solids is presented. We focus on brittle materials for which the characteristic length scale of damage is much smaller than the grain size. Surprisingly, brittle cracks do not follow a persistent path with a roughness exponent ζ≈0.6-0.7 as reported for a large range of materials. Instead, we show that they exhibit monoaffine scaling properties characterized by a roughness exponent ζ=0.50±0.05, which we explain theoretically from linear elastic fracture mechanics. Our findings support the description of the roughening process in two-dimensional brittle disordered solids by a random walk. Furthermore, they shed light on the failure mechanism at the origin of the persistent behavior with ζ≈0.6-0.7 observed for fractures in other materials, suggesting a unified scenario for the geometry of crack paths in two-dimensional disordered solids.

Clearing-induced tisssue shrinkage: A novel observation of a thickness size effect.

The use of clearing agents has provided new insights in various fields of medical research (developmental biology, neurology) by enabling examination of tissue architecture in 3D. One of the challenges is that clearing agents induce tissue shrinkage and the shrinkage rates reported in the literature are incoherent. Here, we report that for a classical clearing agent, benzyl-alcohol benzyl-benzoate (BABB), the shrinkage decreases significantly with increasing sample size, and present an analytical formula describing this.

Discrete dislocation plasticity analysis of loading rate-dependent static friction.

From a microscopic point of view, the frictional force associated with the relative sliding of rough surfaces originates from deformation of the material in contact, by adhesion in the contact interface or both. We know that plastic deformation at the size scale of micrometres is not only dependent on the size of the contact, but also on the rate of deformation. Moreover, depending on its physical origin, adhesion can also be size and rate dependent, albeit different from plasticity. We present a two-dimensional model that incorporates both discrete dislocation plasticity inside a face-centred cubic crystal and adhesion in the interface to understand the rate dependence of friction caused by micrometre-size asperities. The friction strength is the outcome of the competition between adhesion and discrete dislocation plasticity. As a function of contact size, the friction strength contains two plateaus: at small contact length [Formula: see text], the onset of sliding is fully controlled by adhesion while for large contact length [Formula: see text], the friction strength approaches the size-independent plastic shear yield strength. The transition regime at intermediate contact size is a result of partial de-cohesion and size-dependent dislocation plasticity, and is determined by dislocation properties, interfacial properties as well as by the loading rate.

Three-dimensional cross-linked F-actin networks: relation between network architecture and mechanical behavior.

Numerical simulations are reported for the response of three-dimensional cross-linked F-actin networks when subjected to large deformations. In addition to the physiological parameters such as actin and cross-linker concentration, the model explicitly accounts for filament properties and network architecture. Complementary to two-dimensional studies, we find that the strain-stiffening characteristics depend on network architecture through the local topology around cross-links.

Alternative explanation of stiffening in cross-linked semiflexible networks.

Strain stiffening of filamentous protein networks is explored by means of a finite strain analysis of a two-dimensional network model of cross-linked semiflexible filaments. The results show that stiffening is caused by nonaffine network rearrangements that govern a transition from a bending-dominated response at small strains to a stretching-dominated response at large strains. Filament undulations, which are key in the existing explanation of stiffening, merely postpone the transition.