Large deviations for a mean field model of systemic risk

We consider a system of diffusion processes that interact through their empirical mean and have a stabilizing force acting on each of them, corresponding to a bistable potential. There are three parameters that characterize the system: the strength of the intrinsic stabilization, the strength of the external random perturbations, and the degree of cooperation or interaction between them. The latter is the rate of mean reversion of each component to the empirical mean of the system. We interpret this model in the context of systemic risk and analyze in detail the effect of cooperation between the components, that is, the rate of mean reversion. We show that in a certain regime of parameters increasing cooperation tends to increase the stability of the individual agents but it also increases the overall or systemic risk. We use the theory of large deviations of diffusions interacting through their mean field

Consensus Convergence with Stochastic Effects

We consider a stochastic, continuous state and time opinion model where each agent's opinion locally interacts with other agents' opinions in the system, and there is also exogenous randomness. The interaction tends to create clusters of common opinion. By using linear stability analysis of the associated nonlinear Fokker-Planck equation that governs the empirical density of opinions in the limit of infinitely many agents, we can estimate the number of clusters, the time to cluster formation and the critical strength of randomness so as to have cluster formation. We also discuss the cluster dynamics after their formation, the width and the effective diffusivity of the clusters. Finally, the long term behavior of clusters is explored numerically. Extensive numerical simulations confirm our analytical findings.Comment: Dedication to Willi J\"{a}ger's 75th Birthda

Upregulation of a novel eukaryotic translation initiation factor 5A (eIF5A) in dengue 2 virus-infected mosquito cells

<p>Abstract</p> <p>Background</p> <p>Dengue virus, a mosquito-borne flavivirus, is the etiological agent of dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. It generally induces apoptosis in mammalian cells, but frequently results in persistent infection in mosquito cells. That mechanism remains to be explored. In turn, a genomic survey through subtractive hybridization (PCR-select cDNA subtraction) was conducted in order to find gene(s) that may play a role in interactions between the virus and its host cells.</p> <p>Results</p> <p>Through this technique, we identified a novel eukaryotic translation initiation factor 5A (eIF5A) which is upregulated in <it>Aedes albopictus</it>-derived C6/36 cells infected by the type 2 dengue (Den-2) virus. The full-length of the identified eIF5A gene consisted of 1498 bp of nucleotides with a 41.39% G+C content, and it possessed a higher similarity and shorter evolutionary distance with insects than with other organisms. Upregulation of eIF5A in response to Den-2 virus infection was validated at both the RNA and protein levels. This phenomenon was also observed by confocal microscopy. In addition, cell death obviously occurred when eIF5A activity was inhibited in C6/36 cells even when they were infected by the virus. However, viral multiplication was not obviously affected in infected C6/36 cells when eIF5A activity was reduced.</p> <p>Conclusions</p> <p>Taken together, we postulated that eIF5A plays a role in preventing mosquito cells from death in response to Den-2 viral infection, thus facilitating continued viral growth and potential persistent infection in mosquito cells. It would be worthwhile to further investigate how its downstream factors or cofactors contribute to this phenomenon of dengue infection.</p