No Arabic abstract
Minimizing social contact is an important tool to reduce the spread of diseases, but harms peoples well-being. This and other, more compelling reasons, urge people to walk outside periodically. The present simulation explores how organizing the traffic of pedestrians affects the number of walking or running people passing by each other. By applying certain rules this number can be significantly reduced, thus reducing the contribution of person-to-person contagious to the basic reproductive number, R0. One example is the traffic of pedestrians on sidewalks. Another is the use of walking or running tracks in parks. It is demonstrated here that the number of people crossing each other can be drastically reduced if one-way traffic is enforced and runners are separated from walkers.
Traffic breakdown, as one of the most puzzling traffic flow phenomena, is characterized by sharply decreasing speed, abruptly increasing density and in particular suddenly plummeting capacity. In order to clarify its root mechanisms and model its observed properties, this paper proposes a car-following model based on the following assumptions: (i) There exists a preferred time-varied and speed-dependent space gap that cars hope to maintain; (ii) there exists a region R restricted by two critical space gaps and two critical speeds in the car following region on the speed-space gap diagram, in which cars movements are determined by the weighted mean of the space- gap-determined acceleration and the speed-difference-determined acceleration; and (iii) out of region R, cars either accelerate to the free flow speed or decelerate to keep safety. Simulation results show that this model is able to simultaneously reproduce traffic breakdown and the transition from the synchronized traffic flow to wide moving jams. To our knowledge, this is the first car-following model that is able to fully depict traffic breakdown, spontaneous formation of jams, and the concave growth of the oscillations.
In the present work, we study how the number of simulated clients (occupancy) affects the social distance in an ideal supermarket. For this, we account for realistic typical dimensions and process time (picking products and checkout). From the simulated trajectories, we measure events of social distance less than 2 m and its duration. Between other observables, we define a social distance coefficient that informs how many events (of a given duration) suffer each agent in the system. These kinds of outputs could be useful for building procedures and protocols in the context of a pandemic allowing to keep low health risks while setting a maximum operating capacity.
Pathogens can spread epidemically through populations. Beneficial contagions, such as viruses that enhance host survival or technological innovations that improve quality of life, also have the potential to spread epidemically. How do the dynamics of beneficial biological and social epidemics differ from those of detrimental epidemics? We investigate this question using three theoretical approaches. First, in the context of population genetics, we show that a horizontally-transmissible element that increases fitness, such as viral DNA, spreads superexponentially through a population, more quickly than a beneficial mutation. Second, in the context of behavioral epidemiology, we show that infections that cause increased connectivity lead to superexponential fixation in the population. Third, in the context of dynamic social networks, we find that preferences for increased global infection accelerate spread and produce superexponential fixation, but preferences for local assortativity halt epidemics by disconnecting the infected from the susceptible. We conclude that the dynamics of beneficial biological and social epidemics are characterized by the rapid spread of beneficial elements, which is facilitated in biological systems by horizontal transmission and in social systems by active spreading behavior of infected individuals.
The size that an epidemic can reach, measured in terms of the number of fatalities, is an extremely relevant quantity. It has been recently claimed [Cirillo & Taleb, Nature Physics 2020] that the size distribution of major epidemics in human history is extremely fat-tailed, i.e., asymptotically a power law, which has important consequences for risk management. Reanalyzing this data, we find that, although the fatality distribution may be compatible with a power-law tail, these results are not conclusive, and other distributions, not fat-tailed, could explain the data equally well. As an example, simulation of a log-normally distributed random variable provides synthetic data whose statistics are undistinguishable from the statistics of the empirical data. Theoretical reasons justifying a power-law tail as well as limitations in the current data are also discussed.
Epidemic propagation on complex networks has been widely investigated, mostly with invariant parameters. However, the process of epidemic propagation is not always constant. Epidemics can be affected by various perturbations, and may bounce back to its original state, which is considered resilient. Here, we study the resilience of epidemics on networks, by introducing a different infection rate ${lambda_{2}}$ during SIS (susceptible-infected-susceptible) epidemic propagation to model perturbations (control state), whereas the infection rate is ${lambda_{1}}$ in the rest of time. Through simulations and theoretical analysis, we find that even for ${lambda_{2}<lambda_{c}}$, epidemics eventually could bounce back if control duration is below a threshold. This critical control time for epidemic resilience, i.e., ${cd_{max}}$ can be predicted by the diameter (${d}$) of the underlying network, with the quantitative relation ${cd_{max}sim d^{alpha}}$. Our findings can help to design a better mitigation strategy for epidemics.