Life and death of colloidal bonds control the rate-dependent rheology of gels

Colloidal gels exhibit rich rheological responses under flowing conditions. A clear understanding of the coupling between the kinetics of the formation/rupture of colloidal bonds and the rheological response of attractive gels is lacking. In particular, for gels under different flow regimes, the correlation between the complex rheological response, the bond kinetics, microscopic forces, and an overall micromechanistic view is missing in previous works. Here, we report the bond dynamics in short-range attractive particles, microscopically measured stresses on individual particles and the spatiotemporal evolution of the colloidal structures in different flow regimes. The interplay between interparticle attraction and hydrodynamic stresses is found to be the key to unraveling the physical underpinnings of colloidal gel rheology. Attractive stresses, mostly originating from older bonds dominate the response at low Mason number (the ratio of shearing to attractive forces) while hydrodynamic stresses tend to control the rheology at higher Mason numbers, mostly arising from short-lived bonds. Finally, we present visual mapping of particle bond numbers, their life times and their borne stresses under different flow regimes.

Can oppositely charged polyelectrolyte stars form a gel? A simulational study

A Langevin MD study of an equimolar mixture of monodispersed oppositely charged di- block four-armed polyelectrolyte stars is presented. We determine the minimal charged block length which results in gels and we study the ionic bond kinetics.

Exploring the hydrogen bond kinetics of methanol–water solutions using Raman scattering

Stimulated Raman scattering was used to clearly show the hydrogen bond kinetics of water–methanol mixed solutions.

Evaluating Plastic Deformation and Damage as Potential Mechanisms for Tendon Inelasticity Using a Reactive Modeling Framework

Inelastic behaviors, such as softening, a progressive decrease in modulus before failure, occur in tendon and are important aspects in degeneration and tendinopathy. These inelastic behaviors are generally attributed to two potential mechanisms: plastic deformation and damage. However, it is not clear which is primarily responsible. In this study, we evaluated these potential mechanisms of tendon inelasticity by using a recently developed reactive inelasticity model (RIE), which is a structurally inspired continuum mechanics framework that models tissue inelasticity based on the molecular bond kinetics. Using RIE, we formulated two material models, one specific to plastic deformation and the other to damage. The models were independently fit to published macroscale experimental tensile tests of rat tail tendons. We quantified the inelastic effects and compared the performance of the two models in fitting the mechanical response during loading, relaxation, unloading, and reloading phases. Additionally, we validated the models by using the resulting fit parameters to predict an independent set of experimental stress–strain curves from ramp-to-failure tests. Overall, the models were both successful in fitting the experiments and predicting the validation data. However, the results did not strongly favor one mechanism over the other. As a result, to distinguish between plastic deformation and damage, different experimental protocols will be needed. Nevertheless, these findings suggest the potential of RIE as a comprehensive framework for studying tendon inelastic behaviors.

Multiscale model of integrin adhesion assembly

The ability of adherent cells to form adhesions is critical to several phases of their physiology. The assembly of adhesions is mediated by several types of integrins. These integrins differ in physical properties, including rate of diffusion on the plasma membrane, rapidity of changing conformation from bent to extended, affinity for extracellular matrix ligands, and lifetimes of their ligand-bound states. However, the way in which nanoscale physical properties of integrins ensure proper adhesion assembly remains elusive. We observe experimentally that both beta-1 and beta-3 integrins localize in nascent adhesions at the cell leading edge. In order to understand how different nanoscale parameters of beta-1 and beta-3 integrins mediate proper adhesion assembly, we therefore develop a coarse-grained computational model. Results from the model demonstrate that morphology and distribution of nascent adhesions depend on ligand binding affinity and strength of pairwise interactions. Organization of nascent adhesions depends on the relative amounts of integrins with different bond kinetics. Moreover, the model shows that the architecture of an actin filament network does not perturb the total amount of integrin clustering and ligand binding; however, only bundled actin architectures favor adhesion stability and ultimately maturation. Together, our results support the view that cells can finely tune the expression of different integrin types to determine both structural and dynamic properties of adhesions.

Evaluating Plastic Deformation and Damage as Potential Mechanisms for Tendon Inelasticity using a Reactive Modeling Framework

ABSTRACTInelastic behaviors, such as softening, a progressive decrease in modulus before failure, occur in tendon andare important aspect in degeneration and tendinopathy. These in elastic behaviors are generally attributed to two potential mechanisms: plastic deformation and damage. However, it is not clear which is primarily responsible.In this study, we evaluated these potential mechanisms of tendon in elasticity by using a recently developed reactive in elasticity model (RIE), which is a structurally-inspired continuum mechanics frame work that models tissue in elasticity based on the molecular bond kinetics. Using RIE, we formulated two material models, one specific toplastic deformation and the other to damage. The models were independently fit to published experimental tensiletests of rat tail tendons. We quantified the inelastic effects and compared the performance of the two models infitting the mechanical response during loading, relaxation, unloading, and reloading phases. Additionally, we validated the models by using the resulting fit parameters to predict an independent set of experimental stress-straincurves from ramp-to-failure tests. Overall, the models were both successful in fitting the experiments and predicting the validation data. However, the results did not strongly favor one mechanism over the other. As a result, to distinguish between plastic deformation and damage, different experimental protocols will be needed. Nevertheless, these findings suggest the potential of RIE as a comprehensive framework for studying tendon inelastic behaviors.