We prove that the exact closure of SIR pairwise epidemic equations on a configuration model network is possible if and only if the degree distribution is Poisson, Binomial, or Negative Binomial. The proof relies on establishing, for these specific degree distributions, the equivalence of the closed pairwise model and the so-called dynamical survival analysis (DSA) edge-based model which was previously shown to be exact. Indeed, as we show here, the DSA model is equivalent to the well-known edge-based Volz model. We use this result to provide reductions of the closed pairwise and Volz models to the same single equation involving only susceptibles, which has a useful statistical interpretation in terms of the times to infection. We illustrate our findings with some numerical examples.
In the chemotactic motion of Escherichia coli, the switching of transmembrane chemoreceptors between active and inactive states is one of the most important steps of the signaling pathway. We study the effect of this switching time-scale on the chemotactic performance of the cell. We quantify performance by the chemotactic drift velocity of the cell. Our extensive numerical simulations on a detailed theoretical model show that as the activity switching rate increases, the drift velocity increases and then saturates. Our data also show the mean duration of a downhill run decreases strongly with the switching rate, while that of an uphill run decreases relatively slowly. We explain this effect from temporal variation of activity along uphill and downhill trajectories. We show that for large and small switching rates the nature of activity variation show qualitatively different behaviors along a downhill run but similar behavior along an uphill run. This results in a stronger dependence of downhill run duration on the switching rate and relatively milder dependence for uphill run duration.
A unique feature of neuromorphic computing is that memory is an implicit part of processing through traces of past information in the system's collective dynamics. The extent of memory about past inputs is commonly quantified by the autocorrelation time of collective dynamics. Based on past experimental evidence, a potential explanation for the underlying autocorrelations are close-to-critical fluctuations. Here, we show for self-organized networks of excitatory and inhibitory leaky integrate-and-fire neurons that autocorrelations can originate from emergent bistability upon reducing external input strength. We identify the bistability as a fluctuation-induced stochastic switching between metastable active and quiescent states in the vicinity of a non-equilibrium phase transition. This bistability occurs for networks with fixed heterogeneous weights as a consequence of homeostatic self-organization during development. Specifically, in our experiments on neuromorphic hardware and in computer simulations, the emergent bistability gives rise to autocorrelation times exceeding 500 ms despite single-neuron timescales of only 20 ms. Our results provide the first verification of biologically compatible autocorrelation times in networks of leaky integrate-and-fire neurons, which here are not generated by close-to-critical fluctuations but by emergent bistability in homeostatically regulated networks. Our results thereby constitute a new, complementary mechanism for emergent autocorrelations in networks of spiking neurons, with implications for biological and artificial networks, and introduces the general paradigm of fluctuation-induced bistability for driven systems with absorbing states.
Genome-wide Association Studies (GWASes) identify genomic variations that are statistically associated with a trait, such as a disease, in a group of individuals. Unfortunately, careless sharing of GWAS statistics might give rise to privacy attacks. Several works attempted to reconcile secure processing with privacy-preserving releases of GWASes. However, we highlight that these approaches remain vulnerable if GWASes utilize overlapping sets of individuals and genomic variations. In such conditions, we show that even when relying on state-of-the-art techniques for protecting releases, an adversary could reconstruct the genomic variations of up to 28.6% of participants, and that the released statistics of up to 92.3% of the genomic variations would enable membership inference attacks. We introduce I-GWAS, a novel framework that securely computes and releases the results of multiple possibly interdependent GWASes. I-GWAScontinuously releases privacy-preserving and noise-free GWAS results as new genomes become available.
The pharmaceutical success of atorvastatin (ATV), a widely employed drug against the "bad" cholesterol (LDL) and cardiovascular diseases, traces back to its ability to scavenge free radicals. Unfortunately, information on its antioxidant properties is missing or unreliable. Here, we report detailed quantum chemical results for ATV and its ortho- and para-hydroxy metabolites (o-ATV, p-ATV) in the methanolic phase. They comprise global reactivity indices, bond order indices, and spin densities as well as all relevant enthalpies of reaction (bond dissociation BDE, ionization IP and electron attachment EA, proton detachment PDE and proton affinity PA, and electron transfer ETE). With these properties in hand, we can provide the first theoretical explanation of the experimental finding that, due to their free radical scavenging activity, ATV hydroxy metabolites rather than the parent ATV, have substantial inhibitory effect on LDL and the like. Surprisingly (because it is contrary to the most cases currently known), we unambiguously found that HAT (direct hydrogen atom transfer) rather than SPLET (sequential proton loss electron transfer) or SET-PT (stepwise electron transfer proton transfer) is the thermodynamically preferred pathway by which o-ATV and p-ATV in methanolic phase can scavenge DPPH$^\bullet$ (1,1-diphenyl-2-picrylhydrazyl) radicals. From a quantum chemical perspective, the ATV's species investigated are surprising because of the nontrivial correlations between bond dissociation energies, bond lengths, bond order indices and pertaining stretching frequencies, which do not fit the framework of naive chemical intuition.
This paper presents a method for time-lapse 3D cell analysis. Specifically, we consider the problem of accurately localizing and quantitatively analyzing sub-cellular features, and for tracking individual cells from time-lapse 3D confocal cell image stacks. The heterogeneity of cells and the volume of multi-dimensional images presents a major challenge for fully automated analysis of morphogenesis and development of cells. This paper is motivated by the pavement cell growth process, and building a quantitative morphogenesis model. We propose a deep feature based segmentation method to accurately detect and label each cell region. An adjacency graph based method is used to extract sub-cellular features of the segmented cells. Finally, the robust graph based tracking algorithm using multiple cell features is proposed for associating cells at different time instances. Extensive experiment results are provided and demonstrate the robustness of the proposed method. The code is available on Github and the method is available as a service through the BisQue portal.