Transport Properties of Random Walks on Scale-Free/Regular-Lattice Hybrid Networks

We study numerically the mean access times for random walks on hybrid disordered structures formed by embedding scale-free networks into regular lattices, considering different transition rates for steps across lattice bonds ($F$) and across network shortcuts ($f$). For fast shortcuts ($f/F\gg 1$) and low shortcut densities, traversal time data collapse onto an universal curve, while a crossover behavior that can be related to the percolation threshold of the scale-free network component is identified at higher shortcut densities, in analogy to similar observations reported recently in Newman-Watts small-world networks. Furthermore, we observe that random walk traversal times are larger for networks with a higher degree of inhomogeneity in their shortcut distribution, and we discuss access time distributions as functions of the initial and final node degrees. These findings are relevant, in particular, when considering the optimization of existing information networks by the addition of a small number of fast shortcut connections.Comment: 8 pages, 6 figures; expanded discussions, added figures and references. To appear in J Stat Phy

Correlation effects in a simple model of small-world network

We analyze the effect of correlations in a simple model of small world network by obtaining exact analytical expressions for the distribution of shortest paths in the network. We enter correlations into a simple model with a distinguished site, by taking the random connections to this site from an Ising distribution. Our method shows how the transfer matrix technique can be used in the new context of small world networks.Comment: 10 pages, 3 figure

Scaling Properties of Random Walks on Small-World Networks

Using both numerical simulations and scaling arguments, we study the behavior of a random walker on a one-dimensional small-world network. For the properties we study, we find that the random walk obeys a characteristic scaling form. These properties include the average number of distinct sites visited by the random walker, the mean-square displacement of the walker, and the distribution of first-return times. The scaling form has three characteristic time regimes. At short times, the walker does not see the small-world shortcuts and effectively probes an ordinary Euclidean network in $d$-dimensions. At intermediate times, the properties of the walker shows scaling behavior characteristic of an infinite small-world network. Finally, at long times, the finite size of the network becomes important, and many of the properties of the walker saturate. We propose general analytical forms for the scaling properties in all three regimes, and show that these analytical forms are consistent with our numerical simulations.Comment: 7 pages, 8 figures, two-column format. Submitted to PR

Equilibration times in numerical simulation of structural glasses: Comparing parallel tempering and conventional molecular dynamics

Generation of equilibrium configurations is the major obstacle for numerical investigation of the slow dynamics in supercooled liquid states. The parallel tempering (PT) technique, originally proposed for the numerical equilibration of discrete spin-glass model configurations, has recently been applied in the study of supercooled structural glasses. We present an investigation of the ability of parallel tempering to properly sample the liquid configuration space at different temperatures, by mapping the PT dynamics into the dynamics of the closest local potential energy minima (inherent structures). Comparing the PT equilibration process with the standard molecular dynamics equilibration process we find that the PT does not increase the speed of equilibration of the (slow) configurational degrees of freedom.Comment: 5 pages, 3 figure

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease