Topology and Evolution of Technology Innovation Networks

The web of relations linking technological innovation can be fairly described in terms of patent citations. The resulting patent citation network provides a picture of the large-scale organization of innovations and its time evolution. Here we study the patterns of change of patents registered by the US Patent and Trademark Office (USPTO). We show that the scaling behavior exhibited by this network is consistent with a preferential attachment mechanism together with a Weibull-shaped aging term. Such attachment kernel is shared by scientific citation networks, thus indicating an universal type of mechanism linking ideas and designs and their evolution. The implications for evolutionary theory of innovation are discussed.Comment: 6 pages, 5 figures, submitted to Physical Review

Robustness of the European power grids under intentional attack

The power grid defines one of the most important technological networks of our times and sustains our complex society. It has evolved for more than a century into an extremely huge and seemingly robust and well understood system. But it becomes extremely fragile as well, when unexpected, usually minimal, failures turn into unknown dynamical behaviours leading, for example, to sudden and massive blackouts. Here we explore the fragility of the European power grid under the effect of selective node removal. A mean field analysis of fragility against attacks is presented together with the observed patterns. Deviations from the theoretical conditions for network percolation (and fragmentation) under attacks are analysed and correlated with non topological reliability measures.Comment: 7 pages, 4 figure

Clinical value of next generation sequencing of plasma cell-free DNA in gastrointestinal stromal tumors

Gastrointestinal stromal tumor (GIST) initiation and evolution is commonly framed by KIT/PDGFRA oncogenic activation, and in later stages by the polyclonal expansion of resistant subpopulations harboring KIT secondary mutations after the onset of imatinib resistance. Thus, circulating tumor (ct)DNA determination is expected to be an informative non-invasive dynamic biomarker in GIST patients. We performed amplicon-based next-generation sequencing (NGS) across 60 clinically relevant genes in 37 plasma samples from 18 GIST patients collected prospectively. ctDNA alterations were compared with NGS of matched tumor tissue samples (obtained either simultaneously or at the time of diagnosis) and cross-validated with droplet digital PCR (ddPCR). We were able to identify cfDNA mutations in five out of 18 patients had detectable in at least one timepoint. Overall, NGS sensitivity for detection of cell-free (cf)DNA mutations in plasma was 28.6%, showing high concordance with ddPCR confirmation. We found that GIST had relatively low ctDNA shedding, and mutations were at low allele frequencies. ctDNA was detected only in GIST patients with advanced disease after imatinib failure, predicting tumor dynamics in serial monitoring. KIT secondary mutations were the only mechanism of resistance found across 10 imatinib-resistant GIST patients progressing to sunitinib or regorafenib. ctDNA evaluation with amplicon-based NGS detects KIT primary and secondary mutations in metastatic GIST patients, particularly after imatinib progression. GIST exhibits low ctDNA shedding, but ctDNA monitoring, when positive, reflects tumor dynamics

Statistical structure of host–phage interactions

Interactions between bacteria and the viruses that infect them (i.e., phages) have profound effects on biological processes, but despite their importance, little is known on the general structure of infection and resistance between most phages and bacteria. For example, are bacteria–phage communities characterized by complex patterns of overlapping exploitation networks, do they conform to a more ordered general pattern across all communities, or are they idiosyncratic and hard to predict from one ecosystem to the next? To answer these questions, we collect and present a detailed metaanalysis of 38 laboratory-verified studies of host–phage interactions representing almost 12,000 distinct experimental infection assays across a broad spectrum of taxa, habitat, and mode of selection. In so doing, we present evidence that currently available host–phage infection networks are statistically different from random networks and that they possess a characteristic nested structure.This nested structure is typified by the finding that hard to infect bacteria are infected by generalist phages (and not specialist phages) and that easy to infect bacteria are infected by generalist and specialist phages. Moreover, we find that currently available host–phage infection networks do not typically possess a modular structure. We explore possible underlying mechanisms and significance of the observed nested host–phage interaction structure. In addition, given that most of the available host–phage infection networks examined here are composed of taxa separated by short phylogenetic distances, we propose that the lack of modularity is a scale-dependent effect, and then, we describe experimental studies to test whether modular patterns exist at macroevolutionary scales.Peer reviewe

Phage-bacteria infection networks

Phage and their bacterial hosts are the most abundant and genetically diverse group of organisms on the planet. Given their dominance, it is no wonder that many recent studies have found that phage-bacteria interactions strongly influence global biogeochemical cycles, incidence of human diseases, productivity of industrial microbial commodities, and patterns of microbial genome diversity. Unfortunately, given the extreme diversity and complexity of microbial communities, traditional analyses fail to characterize interaction patterns and underlying processes. Here, we review emerging systems approaches that combine empirical data with rigorous theoretical analysis to study phage-bacterial interactions as networks rather than as coupled interactions in isolation. © 2012 Elsevier Ltd.This research was supported by grants from the James S. McDonnell Foundation and the Burroughs Wellcome Fund (to J.S.W.), the MELS and FQRNT (to T.P.), the Gordon and Betty Moore Foundation (to M.B.S.), and the Agence National de Recherche (‘EvolStress’) and the James S. McDonnell Foundation (to M.E.H.).Peer Reviewe