Predicting the extinction of Ebola spreading in Liberia due to mitigation strategies

The Ebola virus is spreading throughout West Africa and is causing thousands of deaths. In order to quantify the effectiveness of different strategies for controlling the spread, we develop a mathematical model in which the propagation of the Ebola virus through Liberia is caused by travel between counties. For the initial months in which the Ebola virus spreads, we find that the arrival times of the disease into the counties predicted by our model are compatible with World Health Organization data, but we also find that reducing mobility is insufficient to contain the epidemic because it delays the arrival of Ebola virus in each county by only a few weeks. We study the effect of a strategy in which safe burials are increased and effective hospitalisation instituted under two scenarios: (i) one implemented in mid-July 2014 and (ii) one in mid-August—which was the actual time that strong interventions began in Liberia. We find that if scenario (i) had been pursued the lifetime of the epidemic would have been three months shorter and the total number of infected individuals 80% less than in scenario (ii). Our projection under scenario (ii) is that the spreading will stop by mid-spring 2015.H.E.S. thanks the NSF (grants CMMI 1125290 and CHE-1213217) and the Keck Foundation for financial support. L.D.V. and L.A.B. wish to thank to UNMdP and FONCyT (Pict 0429/2013) for financial support. (CMMI 1125290 - NSF; CHE-1213217 - NSF; Keck Foundation; UNMdP; Pict 0429/2013 - FONCyT)Published versio

Role of bridge nodes in epidemic spreading: Different regimes and crossovers

Power-law behaviors are common in many disciplines, especially in network science. Real-world networks, like disease spreading among people, are more likely to be interconnected communities, and show richer power-law behaviors than isolated networks. In this paper, we look at the system of two communities which are connected by bridge links between a fraction $r$ of bridge nodes, and study the effect of bridge nodes to the final state of the Susceptible-Infected-Recovered model, by mapping it to link percolation. By keeping a fixed average connectivity, but allowing different transmissibilities along internal and bridge links, we theoretically derive different power-law asymptotic behaviors of the total fraction of the recovered $R$ in the final state as $r$ goes to zero, for different combinations of internal and bridge link transmissibilities. We also find crossover points where $R$ follows different power-law behaviors with $r$ on both sides when the internal transmissibility is below but close to its critical value, for different bridge link transmissibilities. All of these power-law behaviors can be explained through different mechanisms of how finite clusters in each community are connected into the giant component of the whole system, and enable us to pick effective epidemic strategies and to better predict their impacts

Structural crossover of polymers in disordered media

We present a unified scaling theory for the structural behavior of polymers embedded in a disordered energy substrate. An optimal polymer configuration is defined as the polymer configuration that minimizes the sum of interacting energies between the monomers and the substrate. The fractal dimension of the optimal polymer in the limit of strong disorder (SD) was found earlier to be larger than the fractal dimension in weak disorder (WD). We introduce a scaling theory for the crossover between the WD and SD limits. For polymers of various sizes in the same disordered substrate we show that polymers with a small number of monomers, N << N*, will behave as in SD, while large polymers with length N >> N* will behave as in WD. This implies that small polymers will be relatively more compact compared to large polymers even in the same substrate. The crossover length N* is a function of \nu and a, where \nu is the percolation correlation length exponent and a is the parameter which controls the broadness of the disorder. Furthermore, our results show that the crossover between the strong and weak disorder limits can be seen even within the same polymer configuration. If one focuses on a segment of size n << N* within a long polymer (N >> N*) that segment will have a higher fractal dimension compared to a segment of size n >> N*

Pengujian Koalisi Likuiditas, Solvabilitas dan Profitabilitas terhadap Harga Saham (Perusahaan Sektor Pertanian Terdaftar di ISSI)

This research was aimed to find out the coalition liquidity, solvency, and profitability testing of stock prices. The population in this research was agricultural companies listed in the ISSI registered in the period 2013-2016 as many as 14 companies. The sample used in this research were only six companies by using sampling technique based on purposive sampling. The results showed that the variables CR, and DAR partially had no significant effect on stock prices. For ROE variable partially had a significant positive effect on stock price. While the simultaneous variables CR, DAR, and ROE had significant influences on stock prices. And based on test results, determination coefficient showed that Adjusted R2 value in regression model of 47% while the remaining 53% was influenced by other factors not included in the regression model

Effect of Disorder Strength on Optimal Paths in Complex Networks

We study the transition between the strong and weak disorder regimes in the scaling properties of the average optimal path $\ell_{\rm opt}$ in a disordered Erd\H{o}s-R\'enyi (ER) random network and scale-free (SF) network. Each link $i$ is associated with a weight $\tau_i\equiv\exp(a r_i)$, where $r_i$ is a random number taken from a uniform distribution between 0 and 1 and the parameter $a$ controls the strength of the disorder. We find that for any finite $a$, there is a crossover network size $N^*(a)$ at which the transition occurs. For $N \ll N^*(a)$ the scaling behavior of $\ell_{\rm opt}$ is in the strong disorder regime, with $\ell_{\rm opt} \sim N^{1/3}$ for ER networks and for SF networks with $\lambda \ge 4$, and $\ell_{\rm opt} \sim N^{(\lambda-3)/(\lambda-1)}$ for SF networks with $3 < \lambda < 4$. For $N \gg N^*(a)$ the scaling behavior is in the weak disorder regime, with $\ell_{\rm opt}\sim\ln N$ for ER networks and SF networks with $\lambda > 3$. In order to study the transition we propose a measure which indicates how close or far the disordered network is from the limit of strong disorder. We propose a scaling ansatz for this measure and demonstrate its validity. We proceed to derive the scaling relation between $N^*(a)$ and $a$. We find that $N^*(a)\sim a^3$ for ER networks and for SF networks with $\lambda\ge 4$, and $N^*(a)\sim a^{(\lambda-1)/(\lambda-3)}$ for SF networks with $3 < \lambda < 4$.Comment: 6 pages, 6 figures. submitted to Phys. Rev.

Radiative Corrections to Neutrino Deep Inelastic Scattering Revisited

Radiative corrections to neutrino deep inelastic scattering are revisited. One-loop electroweak corrections are re-calculated within the automatic SANC system. Terms with mass singularities are treated including higher order leading logarithmic corrections. Scheme dependence of corrections due to weak interactions is investigated. The results are implemented into the data analysis of the NOMAD experiment. The present theoretical accuracy in description of the process is discussed.Comment: 19 pages, two figures are added, discussion of theoretical uncertainties is extende

The polyphenols resveratrol and epigallocatechin-3-gallate restore the severe impairment of mitochondria in hippocampal progenitor cells from a Down syndrome mouse model.

Mitochondrial dysfunctions critically impair nervous system development and are potentially involved in the pathogenesis of various neurodevelopmental disorders, including Down syndrome (DS), the most common genetic cause of intellectual disability. Previous studies from our group demonstrated impaired mitochondrial activity in peripheral cells from DS subjects and the efficacy of epigallocatechin-3-gallate (EGCG) - a natural polyphenol major component of green tea - to counteract the mitochondrial energy deficit. In this study, to gain insight into the possible role of mitochondria in DS intellectual disability, mitochondrial functions were analyzed in neural progenitor cells (NPCs) isolated from the hippocampus of Ts65Dn mice, a widely used model of DS which recapitulates many major brain structural and functional phenotypes of the syndrome, including impaired hippocampal neurogenesis. We found that, during NPC proliferation, mitochondrial bioenergetics and mitochondrial biogenic program were strongly compromised in Ts65Dn cells, but not associated with free radical accumulation. These data point to a central role of mitochondrial dysfunction as an inherent feature of DS and not as a consequence of cell oxidative stress. Further, we disclose that, besides EGCG, also the natural polyphenol resveratrol, which displays a neuroprotective action in various human diseases but never tested in DS, restores oxidative phosphorylation efficiency and mitochondrial biogenesis, and improves proliferation of NPCs. These effects were associated with the activation of PGC-1α/Sirt1/AMPK axis by both polyphenols. This research paves the way for using nutraceuticals as a potential therapeutic tool in preventing or managing some energy deficit-associated DS clinical manifestations