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1.
Phys Rev E ; 95(2-1): 022314, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-28297881

RESUMO

Most studies of disease spreading consider the underlying social network as obtained without the contagion, though epidemic influences people's willingness to contact others: A "friendly" contact may be turned to "unfriendly" to avoid infection. We study the susceptible-infected disease-spreading model on signed networks, in which each edge is associated with a positive or negative sign representing the friendly or unfriendly relation between its end nodes. In a signed network, according to Heider's theory, edge signs evolve such that finally a state of structural balance is achieved, corresponding to no frustration in physics terms. However, the danger of infection affects the evolution of its edge signs. To describe the coupled problem of the sign evolution and disease spreading, we generalize the notion of structural balance by taking into account the state of the nodes. We introduce an energy function and carry out Monte Carlo simulations on complete networks to test the energy landscape, where we find local minima corresponding to the so-called jammed states. We study the effect of the ratio of initial friendly to unfriendly connections on the propagation of disease. The steady state can be balanced or a jammed state such that a coexistence occurs between susceptible and infected nodes in the system.

2.
Phys Rev E ; 95(2-1): 022409, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-28297983

RESUMO

Memory has a great impact on the evolution of every process related to human societies. Among them, the evolution of an epidemic is directly related to the individuals' experiences. Indeed, any real epidemic process is clearly sustained by a non-Markovian dynamics: memory effects play an essential role in the spreading of diseases. Including memory effects in the susceptible-infected-recovered (SIR) epidemic model seems very appropriate for such an investigation. Thus, the memory prone SIR model dynamics is investigated using fractional derivatives. The decay of long-range memory, taken as a power-law function, is directly controlled by the order of the fractional derivatives in the corresponding nonlinear fractional differential evolution equations. Here we assume "fully mixed" approximation and show that the epidemic threshold is shifted to higher values than those for the memoryless system, depending on this memory "length" decay exponent. We also consider the SIR model on structured networks and study the effect of topology on threshold points in a non-Markovian dynamics. Furthermore, the lack of access to the precise information about the initial conditions or the past events plays a very relevant role in the correct estimation or prediction of the epidemic evolution. Such a "constraint" is analyzed and discussed.


Assuntos
Evolução Biológica , Epidemias , Memória , Modelos Biológicos , Humanos , Dinâmica não Linear , Fatores de Tempo
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