Nanoporous metals are a class of novel nanomaterials with potential applications in many fields such as sensing, catalysis, and fuel cells. The present paper is aimed to investigate atomic mechanisms associated with the uniaxial tensile deformation behavior of nanoporous gold. A phase field method is adopted to generate the bicontinuous open-cell porous microstructure of the material. Molecular dynamics simulations then reveal that the uniaxial tensile deformation in such porous materials is accompanied by an accumulation of stacking faults in ligaments along the loading direction and their junctions with neighboring ligaments, as well as the formation of Lomer–Cottrell locks at such junctions. The tensile strain leads to progressive necking and rupture of some ligaments, ultimately resulting in failure of the material. The simulation results also suggest scaling laws for the effective Young's modulus, yield stress, and ultimate strength as functions of the relative mass density and average ligament size in the material.

Collective cell migration occurs in a diversity of physiological processes such as wound healing, cancer metastasis, and embryonic morphogenesis. In the collective context, cohesive cells may move as a translational solid, swirl as a fluid, or even rotate like a disk, with scales ranging from several to dozens of cells. In this work, an active vertex model is presented to explore the regulatory roles of social interactions of neighboring cells and environmental confinements in collective cell migration in a confluent monolayer. It is found that the competition between two kinds of intercellular social interactions-local alignment and contact inhibition of locomotion-drives the cells to self-organize into various dynamic coherent structures with a spatial correlation scale. The interplay between this intrinsic length scale and the external confinement dictates the migration modes of collective cells confined in a finite space. We also show that the local alignment-contact inhibition of locomotion coordination can induce giant density fluctuations in a confluent cell monolayer without gaps, which triggers the spontaneous breaking of orientational symmetry and leads to phase separation.

The atomic force microscopy (AFM) has been widely used to measure the mechanical properties of biological cells through indentations. In most of existing studies, the cell is supposed to be linear elastic within the small strain regime when analyzing the AFM indentation data. However, in experimental situations, the roles of large deformation and surface tension of cells should be taken into consideration. Here, we use the neo-Hookean model to describe the hyperelastic behavior of cells and investigate the influence of surface tension through finite element simulations. At large deformation, a correction factor, depending on the geometric ratio of indenter radius to cell radius, is introduced to modify the force-indent depth relation of classical Hertzian model. Moreover, when the indent depth is comparable with an intrinsic length defined as the ratio of surface tension to elastic modulus, the surface tension evidently affects the indentation response, indicating an overestimation of elastic modulus by the Hertzian model. The dimensionless-analysis-based theoretical predictions, which include both large deformation and surface tension, are in good agreement with our finite element simulation data. This study provides a novel method to more accurately measure the mechanical properties of biological cells and soft materials in AFM indentation experiments.

Adhesion processes of biological membranes that enclose cells and cellular organelles are essential for immune responses, tissue formation, and signaling. These processes depend sensitively on the binding constant K2D of the membrane-anchored receptor and ligand proteins that mediate adhesion, which is difficult to measure in the "two-dimensional" (2D) membrane environment of the proteins. An important problem therefore is to relate K2D to the binding constant K3D of soluble variants of the receptors and ligands that lack the membrane anchors and are free to diffuse in three dimensions (3D). In this article, we present a general theory for the binding constants K2D and K3D of rather stiff proteins whose main degrees of freedom are translation and rotation, along membranes and around anchor points "in 2D," or unconstrained "in 3D." The theory generalizes previous results by describing how K2D depends both on the average separation and thermal nanoscale roughness of the apposing membranes, and on the length and anchoring flexibility of the receptors and ligands. Our theoretical results for the ratio K2D/K3D of the binding constants agree with detailed results from Monte Carlo simulations without any data fitting, which indicates that the theory captures the essential features of the "dimensionality reduction" due to membrane anchoring. In our Monte Carlo simulations, we consider a novel coarse-grained model of biomembrane adhesion in which the membranes are represented as discretized elastic surfaces, and the receptors and ligands as anchored molecules that diffuse continuously along the membranes and rotate at their anchor points.