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Register a new userSlow dynamics in a model of the cellulose network
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We present numerical simulations of a model of cellulose consisting of long stiff rods, representing cellulose microfibrils, connected by stretchable crosslinks, representing xyloglucan molecules, hydrogen bonded to the microfibrils. Within a broad range of temperature the competing interactions in the resulting network give rise to a slow glassy dynamics. In particular, the structural relaxation described by orientational correlation functions shows a logarithmic time dependence. The glassy dynamics is found to be due to the frustration introduced by the network of xyloglucan molecules. Weakening of interactions between rod and xyloglucan molecules results in a more marked reorientation of cellulose microfibrils, suggesting a possible mechanism to modify the dynamics of the plant cell wall.
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We study the phase ordering dynamics of a two dimensional model colloidal solid using molecular dynamics simulations. The colloid particles interact with each other with a Hamaker potential modified by the presence of equatorial patches of attractive and negative regions. The total interaction potential between two such colloids is, therefore, strongly directional and has three-fold symmetry. Working in the canonical ensemble, we determine the tentative phase diagram in the density-temperature plane which features three distinct crystalline ground states viz, a low density honeycomb solid followed by a rectangular solid at higher density, which eventually transforms to a close packed triangular structure as the density is increased further. We show that when cooled rapidly from the liquid phase along isochores, the system undergoes a transition to a strong glass while slow cooling gives rise to crystalline phases. We claim that geometrical frustration arising from the presence of many crystalline ground states causes glassy ordering and dynamics in this solid. Our results may be easily confirmed by suitable experiments on patchy colloids.
Spin glasses and many-body localization (MBL) are prime examples of ergodicity breaking, yet their physical origin is quite different: the former phase arises due to rugged classical energy landscape, while the latter is a quantum-interference effect. Here we study quantum dynamics of an isolated 1d spin-glass under application of a transverse field. At high energy densities, the system is ergodic, relaxing via resonance avalanche mechanism, that is also responsible for the destruction of MBL in non-glassy systems with power-law interactions. At low energy densities, the interaction-induced fields obtain a power-law soft gap, making the resonance avalanche mechanism inefficient. This leads to the persistence of the spin-glass order, as demonstrated by resonance analysis and by numerical studies. A small fraction of resonant spins forms a thermalizing system with long-range entanglement, making this regime distinct from the conventional MBL. The model considered can be realized in systems of trapped ions, opening the door to investigating slow quantum dynamics induced by glassiness.
We present a rigorous result on ultra-slow diffusion by solving a Fokker-Planck equation, which describes anomalous transport in a three dimensional (3D) comb. This 3D cylindrical comb consists of a cylinder of discs threaten on a backbone. It is shown that the ultra-slow contaminant spreading along the backbone is described by the mean squared displacement (MSD) of the order of $ln (t)$. This phenomenon takes place only for normal two dimensional diffusion inside the infinite secondary branches (discs). When the secondary branches have finite boundaries, the ultra-slow motion is a transient process and the asymptotic behavior is normal diffusion. In another example, when anomalous diffusion takes place in the secondary branches, a destruction of ultra-slow (logarithmic) diffusion takes place as well. As the result, one observes enhanced subdiffusion with the MSD $sim t^{1-alpha}ln t$, where $0<alpha<1$.
We introduce a 2-layer network model for the study of the immunization dynamics in epidemics. Spreading of an epidemic is modeled as an excitatory process in a small-world network (body layer) while immunization by prevention for the disease as a dynamic process in a scale-free network (head layer). It is shown that prevention indeed turns periodic rages of an epidemic into small fluctuation. The study also reveals that, in a certain situation, prevention actually plays an adverse role and helps the disease survive. We argue that the presence of two different characteristic time scales contributes to the immunization dynamics observed.
We present an exhaustive mathematical analysis of the recently proposed Non-Poissonian Ac- tivity Driven (NoPAD) model [Moinet et al. Phys. Rev. Lett., 114 (2015)], a temporal network model incorporating the empirically observed bursty nature of social interactions. We focus on the aging effects emerging from the Non-Poissonian dynamics of link activation, and on their effects on the topological properties of time-integrated networks, such as the degree distribution. Analytic expressions for the degree distribution of integrated networks as a function of time are derived, ex- ploring both limits of vanishing and strong aging. We also address the percolation process occurring on these temporal networks, by computing the threshold for the emergence of a giant connected component, highlighting the aging dependence. Our analytic predictions are checked by means of extensive numerical simulations of the NoPAD model.
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