21 research outputs found

    Stress-stabilized sub-isostatic fiber networks in a rope-like limit

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    The mechanics of disordered fibrous networks such as those that make up the extracellular matrix are strongly dependent on the local connectivity or coordination number. For biopolymer networks this coordination number is typically between three and four. Such networks are sub-isostatic and linearly unstable to deformation with only central force interactions, but exhibit a mechanical phase transition between floppy and rigid states under strain. Introducing weak bending interactions stabilizes these networks and suppresses the critical signatures of this transition. We show that applying external stress can also stabilize sub-isostatic networks with only tensile central force interactions, i.e., a rope-like potential. Moreover, we find that the linear shear modulus shows a power law scaling with the external normal stress, with a non-mean-field exponent. For networks with finite bending rigidity, we find that the critical stain shifts to lower values under prestress

    Structural features and nonlinear rheology of self-assembled networks of crosslinked semiflexible polymers

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    Random networks of semiflexible filaments are common support structures in biology. Familiar examples include the fibrous matrices in blood clots, bacterial biofilms, and essential components of the cells and tissues of plants, animals, and fungi. Despite the ubiquity of these networks in biomaterials, we have only a limited understanding of the relationship between their structural features and highly strain-sensitive mechanical properties. In this work, we perform simulations of three-dimensional networks produced by the irreversible formation of crosslinks between linker-decorated semiflexible filaments. We characterize the structure of networks formed by a simple diffusion-dependent assembly process and measure their associated steady-state rheological features at finite temperature over a range of applied prestrains encompassing the strain-stiffening transition. We quantify the dependence of network connectivity on crosslinker availability and detail the associated connectivity dependence of both linear elasticity and nonlinear strain stiffening behavior, drawing comparisons with prior experimental measurements of the crosslinker concentration-dependent elasticity of actin gels

    Signatures of irreversibility in microscopic models of flocking

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    Flocking in d=2d=2 is a genuine non-equilibrium phenomenon for which irreversibility is an essential ingredient. We study a class of minimal flocking models whose only source of irreversibility is self-propulsion and use the entropy production rate (EPR) to quantify the departure from equilibrium across their phase diagrams. The EPR is maximal in the vicinity of the order-disorder transition, where reshuffling of the interaction network is fast. We show that signatures of irreversibility come in the form of asymmetries in the steady state distribution of the flock's microstates. They occur as consequences of the time reversal symmetry breaking in the considered self-propelled systems, independently of the interaction details. In the case of metric pairwise forces, they reduce to local asymmetries in the distribution of pairs of particles. This study suggests a possible use of pair asymmetries both to quantify the departure from equilibrium and to learn relevant information about aligning interaction potentials from data.Comment: 8 pages + Appendix; 6 figure

    Cell-induced confinement effects in soft tissue mechanics

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    The mechanical properties of tissues play a critical role in their normal and pathophysiological functions such as tissue development, aging, injury, and disease. Understanding tissue mechanics is important not only for designing realistic biomimetic materials for tissue engineering and drug testing but also for developing novel diagnostic techniques and medical interventions. Tissues are heterogeneous materials consisting of cells confined within extracellular matrices (ECMs), both of which derive their structural integrity, at least in part, from networks of biopolymers. However, the rheology of purified reconstituted biopolymer networks fails to explain many key aspects of tissue mechanics. Notably, purified networks typically soften under applied compression, whereas many soft tissues like liver, fat, and brain instead stiffen when compressed. While continuum models can readily capture this compression-stiffening behavior, the underlying mechanism is not fully understood. In this perspective paper, we discuss several recently proposed microscopic mechanisms that may explain compression stiffening of soft tissues. These mechanisms include (I) interactions between the ECM and volume-preserving inclusions that promote extension-dominated stiffening of fibrous ECMs when subject to uniform compression, (II) ECM interactions with rigid inclusions under non-uniform compression, (III) other internal physical constraints that cause compression stiffening of cells and ECMs, and (IV) propagation of compressive forces through jammed, compression-stiffening cells. We further identify a few of the many open problems in understanding the structure–function relationship of soft-tissue mechanics

    Motor crosslinking augments elasticity in active nematics

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    In active materials, uncoordinated internal stresses lead to emergent long-range flows. An understanding of how the behavior of active materials depends on mesoscopic (hydrodynamic) parameters is developing, but there remains a gap in knowledge concerning how hydrodynamic parameters depend on the properties of microscopic elements. In this work, we combine experiments and multiscale modeling to relate the structure and dynamics of active nematics composed of biopolymer filaments and molecular motors to their microscopic properties, in particular motor processivity, speed, and valency. We show that crosslinking of filaments by both motors and passive crosslinkers not only augments the contributions to nematic elasticity from excluded volume effects but dominates them. By altering motor kinetics we show that a competition between motor speed and crosslinking results in a nonmonotonic dependence of nematic flow on motor speed. By modulating passive filament crosslinking we show that energy transfer into nematic flow is in large part dictated by crosslinking. Thus motor proteins both generate activity and contribute to nematic elasticity. Our results provide new insights for rationally engineering active materials

    Unique Role of Vimentin Networks in Compression Stiffening of Cells and Protection of Nuclei from Compressive Stress

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    In this work, we investigate whether stiffening in compression is a feature of single cells and whether the intracellular polymer networks that comprise the cytoskeleton (all of which stiffen with increasing shear strain) stiffen or soften when subjected to compressive strains. We find that individual cells, such as fibroblasts, stiffen at physiologically relevant compressive strains, but genetic ablation of vimentin diminishes this effect. Further, we show that unlike networks of purified F-actin or microtubules, which soften in compression, vimentin intermediate filament networks stiffen in both compression and extension, and we present a theoretical model to explain this response based on the flexibility of vimentin filaments and their surface charge, which resists volume changes of the network under compression. These results provide a new framework by which to understand the mechanical responses of cells and point to a central role of intermediate filaments in response to compression

    Nonaffinity controls critical slowing down and rheology near the onset of rigidity

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    Fluid-immersed networks and dense suspensions typically reside near a boundary between soft (or fluid-like) and rigid (or solid-like) mechanical regimes. This boundary can be crossed either by varying the concentration or by deformation. Near the onset or loss of rigidity, dissipation limiting nonaffine rearrangements dominate the macroscopic viscoelastic response, giving rise to diverging relaxation times and power-law rheology. Here, we derive a simple relationship between nonaffinity and excess viscosity in fluid-immersed amorphous materials. We then demonstrate this relationship and its rheological consequences in simulations of stress relaxation in strained filament networks and dense suspensions
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