26 research outputs found

    Domain coarsening and interface kinetics in the Ising model

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    In this thesis, I investigate in detail two basic problems in nonequilibrium statistical mechanics. First, if a spin system such as a kinetic Ising model or a kinetic Potts model is quenched from supercritical temperature to subcritical temperature, how does the system coarsen, and what complexities arise as the system descends in energy toward one of its equilibrium states? Second, if a kinetic Ising model is evolved from a deterministic initial condition at zero temperature, how do the domain interfaces evolve in time? I first study the nonconserved coarsening of the kinetic spin systems mentioned above. The coarsening of a 2d ferromagnet can be described exactly by an intriguing connection with continuum critical percolation. Furthermore, careful simulations of phase ordering in the 3d Ising model at zero temperature reveal strange nonstatic final states and anomalously slow relaxation modes, which we explain in detail. I find similarly rich phenomena in the zero-temperature evolution of a kinetic Potts model in 2d, where glassy behavior is again manifest. We also find large-scale avalanches in which clusters merge and dramatically expand beyond their original convex hulls at late times in the dynamics. Next, I study the geometrically simpler problem of the evolution of a single corner interface in the Ising model. We extend prior work by investigating the Ising Hamiltonian with longer interaction range. We solve exactly the limiting shapes of the corner interface in 2d for several interaction ranges. In 3d, where analytical treatments are notoriously difficult, we develop novel methods for studying corner interface growth. I conjecture a growth equation for the interface that agrees quite well with simulation data, and I discuss the interface's surprising geometrical features. In the summary, I discuss the broader implications of our findings and offer some thoughts on possible directions for future work

    Life cycle synchronization is a viral drug resistance mechanism

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    Viral infections are one of the major causes of death worldwide, with HIV infection alone resulting in over 1.2 million casualties per year. Antiviral drugs are now being administered for a variety of viral infections, including HIV, hepatitis B and C, and influenza. These therapies target a specific phase of the virus’s life cycle, yet their ultimate success depends on a variety of factors, such as adherence to a prescribed regimen and the emergence of viral drug resistance. The epidemiology and evolution of drug resistance have been extensively characterized, and it is generally assumed that drug resistance arises from mutations that alter the virus’s susceptibility to the direct action of the drug. In this paper, we consider the possibility that a virus population can evolve towards synchronizing its life cycle with the pattern of drug therapy. The periodicity of the drug treatment could then allow for a virus strain whose life cycle length is a multiple of the dosing interval to replicate only when the concentration of the drug is lowest. This process, referred to as “drug tolerance by synchronization”, could allow the virus population to maximize its overall fitness without having to alter drug binding or complete its life cycle in the drug’s presence. We use mathematical models and stochastic simulations to show that life cycle synchronization can indeed be a mechanism of viral drug tolerance. We show that this effect is more likely to occur when the variability in both viral life cycle and drug dose timing are low. More generally, we find that in the presence of periodic drug levels, time-averaged calculations of viral fitness do not accurately predict drug levels needed to eradicate infection, even if there is no synchronization. We derive an analytical expression for viral fitness that is sufficient to explain the drug-pattern-dependent survival of strains with any life cycle length. We discuss the implications of these findings for clinically relevant antiviral strategies

    Growth Inside a Corner: The Limiting Interface Shape

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    We investigate the growth of a crystal that is built by depositing cubes onto the inside of a corner. The interface of this crystal evolves into a limiting shape in the long-time limit. Building on known results for the corresponding two-dimensional system and accounting for the symmetries of the three-dimensional problem, we conjecture a governing equation for the evolution of the interface profile. We solve this equation analytically and find excellent agreement with simulations of the growth process. We also present a generalization to arbitrary spatial dimension.Comment: 4 pages, 2-column revtex4 format. Revised version in response to referee comment

    Indirect Reciprocity with Optional Interactions and Private Information

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    We consider indirect reciprocity with optional interactions and private information. A game is offered between two players and accepted unless it is known that the other person is a defector. Whenever a defector manages to exploit a cooperator, his or her reputation is revealed to others in the population with some probability. Therefore, people have different private information about the reputation of others, which is a setting that is difficult to analyze in the theory of indirect reciprocity. Since a defector loses a fraction of his social ties each time he exploits a cooperator, he is less efficient at exploiting cooperators in subsequent rounds. We analytically calculate the critical benefit-to-cost ratio above which cooperation is successful in various settings. We demonstrate quantitative agreement with simulation results of a corresponding Wright–Fisher process with optional interactions and private information. We also deduce a simple necessary condition for the critical benefit-to-cost ratio
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