Clonal dynamics of surface-driven growing tissues.

The self-organization of cells into complex tissues relies on a tight coordination of cell behavior. Identifying the cellular processes driving tissue growth is key to understanding the emergence of tissue forms and devising targeted therapies for aberrant growth, such as in cancer. Inferring the mode of tissue growth, whether it is driven by cells on the surface or by cells in the bulk, is possible in cell culture experiments but difficult in most tissues in living organisms (in vivo). Genetic tracing experiments, where a subset of cells is labeled with inheritable markers, have become important experimental tools to study cell fate in vivo. Here we show that the mode of tissue growth is reflected in the size distribution of the progeny of marked cells. To this end, we derive the clone size distributions using analytical calculations in the limit of negligible cell migration and cell death, and we test our predictions with an agent-based stochastic sampling technique. We show that for surface-driven growth the clone size distribution takes a characteristic power-law form with an exponent determined by fluctuations of the tissue surface. Our results propose a possible way of determining the mode of tissue growth from genetic tracing experiments.

Effects of lattice dilution on the nonequilibrium phase transition in the stochastic susceptible-infectious-recovered model.

We investigate how site dilution, as would be introduced by immunization, affects the properties of the active-to-absorbing nonequilibrium phase transition in the paradigmatic susceptible-infectious-recovered (SIR) model on regular cubic lattices. According to the Harris criterion, the critical behavior of the SIR model, which is governed by the universal scaling exponents of the dynamic isotropic percolation (DyIP) universality class, should remain unaltered after introducing impurities. However, when the SIR reactions are simulated for immobile agents on two- and three-dimensional lattices subject to quenched disorder, we observe a wide crossover region characterized by varying effective exponents. Only after a sufficient increase of the lattice sizes does it become clear that the SIR system must transition from that crossover regime before the effective critical exponents asymptotically assume the expected DyIP values. We attribute the appearance of this exceedingly long crossover to a time lag in a complete recovery of small disconnected clusters of susceptible sites, which are apt to be generated when the system is prepared with Poisson-distributed quenched disorder. Finally, we demonstrate that this transient region becomes drastically diminished when we significantly increase the value of the recovery rate or enable diffusive agent mobility through short-range hopping.

Social distancing and epidemic resurgence in agent-based susceptible-infectious-recovered models.

Once an epidemic outbreak has been effectively contained through non-pharmaceutical interventions, a safe protocol is required for the subsequent release of social distancing restrictions to prevent a disastrous resurgence of the infection. We report individual-based numerical simulations of stochastic susceptible-infectious-recovered model variants on four distinct spatially organized lattice and network architectures wherein contact and mobility constraints are implemented. We robustly find that the intensity and spatial spread of the epidemic recurrence wave can be limited to a manageable extent provided release of these restrictions is delayed sufficiently (for a duration of at least thrice the time until the peak of the unmitigated outbreak) and long-distance connections are maintained on a low level (limited to less than five percent of the overall connectivity).

Transverse temperature interfaces in the Katz-Lebowitz-Spohn driven lattice gas.

We explore the intriguing spatial patterns that emerge in a two-dimensional spatially inhomogeneous Katz-Lebowitz-Spohn (KLS) driven lattice gas with attractive nearest-neighbor interactions. The domain is split into two regions with hopping rates governed by different temperatures T>T_{c} and T_{c}, respectively, where T_{c} indicates the critical temperature for phase ordering, and with the temperature boundaries oriented perpendicular to the drive. In the hotter region, the system behaves like the (totally) asymmetric exclusion processes (TASEP), and experiences particle blockage in front of the interface to the critical region. To explain this particle density accumulation near the interface, we have measured the steady-state current in the KLS model at T>T_{c} and found it to decay as 1/T. In analogy with TASEP systems containing "slow" bonds, we argue that transport in the high-temperature subsystem is impeded by the lower current in the cooler region, which tends to set the global stationary particle current value. This blockage is induced by the extended particle clusters, growing logarithmically with system size, in the critical region. We observe the density profiles in both high- and low-temperature subsystems to be similar to the well-characterized coexistence and maximal-current phases in (T)ASEP models with open boundary conditions, which are respectively governed by hyperbolic and trigonometric tangent functions. Yet if the lower temperature is set to T_{c}, we detect marked fluctuation corrections to the mean-field density profiles, e.g., the corresponding critical KLS power-law density decay near the interfaces into the cooler region.