Exact solution of bond percolation on small arbitrary graphs

We introduce a set of iterative equations that exactly solves the size distribution of components on small arbitrary graphs after the random removal of edges. We also demonstrate how these equations can be used to predict the distribution of the node partitions (i.e., the constrained distribution of the size of each component) in undirected graphs. Besides opening the way to the theoretical prediction of percolation on arbitrary graphs of large but finite size, we show how our results find application in graph theory, epidemiology, percolation and fragmentation theory.Comment: 5 pages and 3 figure

Adaptive networks: coevolution of disease and topology

Adaptive networks have been recently introduced in the context of disease propagation on complex networks. They account for the mutual interaction between the network topology and the states of the nodes. Until now, existing models have been analyzed using low-complexity analytic formalisms, revealing nevertheless some novel dynamical features. However, current methods have failed to reproduce with accuracy the simultaneous time evolution of the disease and the underlying network topology. In the framework of the adaptive SIS model of Gross et al. [Phys. Rev. Lett. 96, 208701 (2006)], we introduce an improved compartmental formalism able to handle this coevolutionary task successfully. With this approach, we analyze the interplay and outcomes of both dynamical elements, process and structure, on adaptive networks featuring different degree distributions at the initial stage.Comment: 11 pages, 8 figures, 1 appendix. To be published in Physical Review

Les quotidiens du Québec et la Bataille de Seattle : entre l'approche néolibérale et l'analyse radicale

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal

Modeling the dynamical interaction between epidemics on overlay networks

Epidemics seldom occur as isolated phenomena. Typically, two or more viral agents spread within the same host population and may interact dynamically with each other. We present a general model where two viral agents interact via an immunity mechanism as they propagate simultaneously on two networks connecting the same set of nodes. Exploiting a correspondence between the propagation dynamics and a dynamical process performing progressive network generation, we develop an analytic approach that accurately captures the dynamical interaction between epidemics on overlay networks. The formalism allows for overlay networks with arbitrary joint degree distribution and overlap. To illustrate the versatility of our approach, we consider a hypothetical delayed intervention scenario in which an immunizing agent is disseminated in a host population to hinder the propagation of an undesirable agent (e.g. the spread of preventive information in the context of an emerging infectious disease).Comment: Accepted for publication in Phys. Rev. E. 15 pages, 7 figure

Propagation dynamics on networks featuring complex topologies

Analytical description of propagation phenomena on random networks has flourished in recent years, yet more complex systems have mainly been studied through numerical means. In this paper, a mean-field description is used to coherently couple the dynamics of the network elements (nodes, vertices, individuals...) on the one hand and their recurrent topological patterns (subgraphs, groups...) on the other hand. In a SIS model of epidemic spread on social networks with community structure, this approach yields a set of ODEs for the time evolution of the system, as well as analytical solutions for the epidemic threshold and equilibria. The results obtained are in good agreement with numerical simulations and reproduce random networks behavior in the appropriate limits which highlights the influence of topology on the processes. Finally, it is demonstrated that our model predicts higher epidemic thresholds for clustered structures than for equivalent random topologies in the case of networks with zero degree correlation.Comment: 10 pages, 5 figures, 1 Appendix. Published in Phys. Rev. E (mistakes in the PRE version are corrected here

Propagation on networks: an exact alternative perspective

By generating the specifics of a network structure only when needed (on-the-fly), we derive a simple stochastic process that exactly models the time evolution of susceptible-infectious dynamics on finite-size networks. The small number of dynamical variables of this birth-death Markov process greatly simplifies analytical calculations. We show how a dual analytical description, treating large scale epidemics with a Gaussian approximations and small outbreaks with a branching process, provides an accurate approximation of the distribution even for rather small networks. The approach also offers important computational advantages and generalizes to a vast class of systems.Comment: 8 pages, 4 figure

Characterization of dedifferentiating human mature adipocytes from the 6 visceral and subcutaneous fat compartments : fibroblast-activation protein 7 alpha and Dipeptidyl peptidase 4 as major components of matrix remodeling

Mature adipocytes can reverse their phenotype to become fibroblast-like cells. This is achieved by ceiling culture and the resulting cells, called dedifferentiated fat (DFAT) cells, are multipotent. Beyond the potential value of these cells for regenerative medicine, the dedifferentiation process itself raises many questions about cellular plasticity and the pathways implicated in cell behavior. This work has been performed with the objective of obtaining new information on adipocyte dedifferentiation, especially pertaining to new targets that may be involved in cellular fate changes. To do so, omental and subcutaneous mature adipocytes sampled from severely obese subjects have been dedifferentiated by ceiling culture. An experimental design with various time points along the dedifferentiation process has been utilized to better understand this process. Cell size, gene and protein expression as well as cytokine secretion were investigated. Il-6, IL-8, SerpinE1 and VEGF secretion were increased during dedifferentiation, whereas MIF-1 secretion was transiently increased. A marked decrease in expression of mature adipocyte transcripts (PPARγ2, C/EBPα, LPL and Adiponectin) was detected early in the process. In addition, some matrix remodeling transcripts (FAP, DPP4, MMP1 and TGFβ1) were rapidly and strongly up-regulated. FAP and DPP4 proteins were simultaneously induced in dedifferentiating mature adipocytes supporting a potential role for these enzymes in adipose tissue remodeling and cell plasticity

Role of the TGF-β pathway in dedifferentiation of human mature adipocytes

Dedifferentiation of adipocytes contributes to the generation of a proliferative cell population that could be useful in cellular therapy or tissue engineering. Adipocytes can dedifferentiate into precursor cells to acquire a fibroblast-like phenotype using ceiling culture, in which the buoyancy of fat cells is exploited to allow them to adhere to the inner surface of a container. Ceiling culture is usually performed in flasks, which limits the ability to test various culture conditions. Using a new 6-well plate ceiling culture approach, we examined the relevance of TGF-β signaling during dedifferentiation. Adipose tissue samples from patients undergoing bariatric surgery were digested with collagenase and cell suspensions were used for ceiling cultures. Using the 6-well plate approach, cells were treated with SB431542 (an inhibitor of TGF-β receptor ALK5) or human TGF-β1 during dedifferentiation. Gene expression was measured in these cultures and in whole adipose tissue, the stromal-vascular fraction (SVF), mature adipocytes and dedifferentiated fat (DFAT) cells. TGF-β1 and collagen type I alpha 1 (COL1A1) gene expression was significantly higher in DFAT cells compared to whole adipose tissue samples and SVF cells. TGF-β1, COL1A1 and COL6A3 gene expression was significantly higher at day 12 of dedifferentiation compared to day 0. In the 6-well plate model, treatment with recombinant TGFβ1 or SB431542 respectively stimulated and inhibited the TGF-β pathway as shown by increased TGF-β1, TGF-β2, COL1A1 and COL6A3 gene expression and decreased expression of TGF-β1, COL1A1, COL1A2 and COL6A3, respectively. Treatment of DFAT cells with recombinant TGF-β1 increased the phosphorylation level of SMAD 2 and SMAD 3. Thus, a new 6-well plate model for ceiling culture allowed us to demonstrate a role for TGF-β in modulating collagen gene expression during dedifferentiation of mature adipocytes

Bariatric surgery induces hypomethylation of genes related to type 2 diabetes and insulin resistance

Biliopancreatic diversion with duodenal switch (BPD-DS) is a surgical intervention known to induce substantial weight loss and significant long-lasting metabolic improvements including a decrease in insulin resistance (IR) and resolution of type 2diabetes(T2D). The specific mechanisms by which metabolic improvements occur after BPD-DS are still not fully elucidated and the impact of BPD-DS on gene methylation profiles has not been studied. To gain understanding of epigenetic factors that may predispose to metabolic improvements after weight loss surgery, we characterized the methylation signature of genes associated to T2D and IR after BPD-DS. Most of the genes involved in T2D and IR pathways exhibited significant differences in methylation levels after BPD-DS compared to a pre-surgery control group. The majority of these loci were significantly hypomethylated, suggesting an effect of bariatric surgery on the epigenetic signature of genes encoding proteins involved in glucose homeostasis

Gene expression variability in subcutaneous and omental adipose tissue of obese men

We investigated interindividual variability in gene expression in abdominal subcutaneous (SC) and omental (OM) adipose tissue of 10 massively obese men. Affymetrix human U133A microarrays were used to measure gene expression levels. A total of 6811 probesets generated significant signal in both depots in all samples. Interindividual variability in gene expression was rather low, with more than 90% of transcripts showing a coefficient of variation (CV) lower than 23.6% and 21.7% in OM and SC adipose tissues, respectively. The distributions of CV were similar between the two fat depots. A set of highly variable genes was identified for both tissues on the basis of a high CV and elevated gene expression level. Among the set of highly regulated genes, 18 transcripts were involved in lipid metabolism and 28 transcripts were involved in cell death for SC and OM samples, respectively. In conclusion, gene expression interindividual variability was rather low and globally similar between fat compartments, and the adipose tissue transcriptome appeared as relatively stable, although specific pathways were found to be highly variable in SC and OM depots