Complex Network Phenomena in Telecommunication Systems

Many networks such as the Internet have been found to possess scale-free and small-world network properties reflected by power-law distributions. Scale-free properties evolve in large complex networks through self-organizing processes and, more specifically, preferential attachment. New nodes in a network tend to attach to other vertices that are already well-connected. Because traffic is routed mainly through a few highly connected and concentrated vertices, the diameter of the network is small in comparison to other network structures, and movement through the network is therefore efficient. At the same time, this efficiency feature puts scale-free networks at risk for becoming disconnected or significantly disrupted when super-connected nodes are removed, either unintentionally or through a targeted attack or external force. The present paper will examine and compare properties of telecommunication networks for both the United States and Europe. Both types of networks will be examined in terms of their network topology and specifically, whether or not they are scale-free networks to be further explored by identifying and plotting power-law © Springer Science + Business Media, Inc. 2005

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