Phase Transition of a Non-Linear Opinion Dynamics with Noisy Interactions

International audienceIn several real \emph{Multi-Agent Systems} (MAS), it has been observed that only weaker forms of\emph{metastable consensus} are achieved, in which a large majority of agents agree on some opinion while other opinions continue to be supported by a (small) minority of agents. In this work, we take a step towards the investigation of metastable consensus for complex (non-linear) \emph{opinion dynamics} by considering the famous \undecided dynamics in the binary setting, which is known to reach consensus exponentially faster than the \voter dynamics. We propose a simple form of uniform noise in which each message can change to another one with probability $p$ and we prove that the persistence of a \emph{metastable consensus} undergoes a \emph{phase transition} for $p=\frac 16$. In detail, below this threshold, we prove the system reaches with high probability a metastable regime where a large majority of agents keeps supporting the same opinion for polynomial time. Moreover, this opinion turns out to be the initial majority opinion, whenever the initial bias is slightly larger than its standard deviation.On the contrary, above the threshold, we show that the information about the initial majority opinion is ``lost'' within logarithmic time even when the initial bias is maximum.Interestingly, using a simple coupling argument, we show the equivalence between our noisy model above and the model where a subset of agents behave in a \emph{stubborn} way

Biological effects of particles from the paris subway system

Particulate matter (PM) from atmospheric pollution can easily deposit in the lungs and induce recruitment of inflammatory cells, a source of inflammatory cytokines, oxidants, and matrix metalloproteases (MMPs), which are important players in lung structural homeostasis. In many large cities, the subway system is a potent source of PM emission, but little is known about the biological effects of PM from this source. We performed a comprehensive study to evaluate the biological effects of PM sampled at two sites (RER and Metro) in the Paris subway system. Murine macrophages (RAW 264.7) and C57Bl/6 mice, respectively, were exposed to 0.01-10 microg/cm2 and 5-100 microg/mouse subway PM or reference materials [carbon black (CB), titanium dioxide (TiO2), or diesel exhaust particles (DEPs)]. We analyzed cell viability, production of cellular and lung proinflammatory cytokines [tumor necrosis factor alpha (TNFalpha), macrophage inflammatory protein (MIP-2), KC (the murin analog of interleukin-8), and granulocyte macrophage-colony stimulating factor (GM-CSF)], and mRNA or protein expression of MMP-2, -9, and -12 and heme oxygenase-1 (HO-1). Deferoxamine and polymixin B were used to evaluate the roles of iron and endotoxin, respectively. Noncytotoxic concentrations of subway PM (but not CB, TiO2, or DEPs) induced a time- and dose-dependent increase in TNFalpha and MIP-2 production by RAW 264.7 cells, in a manner involving, at least in part, PM iron content (34% inhibition of TNF production 8 h after stimulation of RAW 264.7 cells with 10 microg/cm2 RER particles pretreated with deferoxamine). Similar increased cytokine production was transiently observed in vivo in mice and was accompanied by an increased neutrophil cellularity of bronchoalveolar lavage (84.83+/-0.98% of polymorphonuclear neutrophils for RER-treated mice after 24 h vs 7.33+/-0.99% for vehicle-treated animals). Subway PM induced an increased expression of MMP-12 and HO-1 both in vitro and in vivo. PM from the Paris subway system has transient biological effects. Further studies are needed to better understand the pathophysiological implications of these findings

Role of nitric oxide synthases in elastase-induced emphysema

Nitric oxide (NO) in combination with superoxide produces peroxynitrites and induces protein nitration, which participates in a number of chronic degenerative diseases. NO is produced at high levels in the human emphysematous lung, but its role in this disease is unknown. The aim of this study was to determine whether the NO synthases contribute to the development of elastase-induced emphysema in mice. nNOS, iNOS, and eNOS were quantified and immunolocalized in the lung after a tracheal instillation of elastase in mice. To determine whether eNOS or iNOS had a role in the development of emphysema, mice bearing a germline deletion of the eNOS and iNOS genes and mice treated with a pharmacological iNOS inhibitor were exposed to elastase. Protein nitration was determined by immunofluorescence, protein oxidation was determined by ELISA. Inflammation and MMP activity were quantified by cell counts, RT-PCR and zymography in bronchoalveolar lavage fluid. Cell proliferation was determined by Ki67 immunostaining. Emphysema was quantified morphometrically. iNOS and eNOS were diffusely upregulated in the lung of elastase-treated mice and a 12-fold increase in the number of 3-nitrotyrosine-expressing cells was observed. Over 80% of these cells were alveolar type 2 cells. In elastase-instilled mice, iNOS inactivation reduced protein nitration and increased protein oxidation but had no effect on inflammation, MMP activity, cell proliferation or the subsequent development of emphysema. eNOS inactivation had no effect. In conclusion, in the elastase-injured lung, iNOS mediates protein nitration in alveolar type 2 cells and alleviates oxidative injury. Neither eNOS nor iNOS are required for the development of elastase-induced emphysema

The Ethical Implications of an Elite Press

Newspaper publishers are well into the process of bifurcating what once was a single mass-market product. Particularly for larger papers, website versions are taking over the mass-market role, while remaining print products are moving toward targeting a much smaller and more elite readership. This article explores theoretical and ethical issues raised by such a two-tiered newspaper structure and suggests directions for empirical study. Broadly, concerns center on the widening knowledge gap between print and online newspaper readers and its implications for civic discourse and democratic vitality. More narrowly, issues encompass a potential bifurcation of normative standards, including diverging markers of credibility, accuracy, and privacy

Do tabloids poison the well of social media? Explaining democratically dysfunctional news sharing

This paper was accepted for publication in the journal New Media and Society and the definitive published version is available at https://doi.org/10.1177/1461444818769689The use of social media for sharing political information and the status of news as an essential raw material for good citizenship are both generating increasing public concern. We add to the debates about misinformation, disinformation, and “fake news” using a new theoretical framework and a unique research design integrating survey data and analysis of observed news sharing behaviors on social media. Using a media-as-resources perspective, we theorize that there are elective affinities between tabloid news and misinformation and disinformation behaviors on social media. Integrating four data sets we constructed during the 2017 UK election campaign—individual-level data on news sharing (N = 1,525,748 tweets), website data (N = 17,989 web domains), news article data (N = 641 articles), and data from a custom survey of Twitter users (N = 1313 respondents)—we find that sharing tabloid news on social media is a significant predictor of democratically dysfunctional misinformation and disinformation behaviors. We explain the consequences of this finding for the civic culture of social media and the direction of future scholarship on fake news

Dendritic cells loaded with killed breast cancer cells induce differentiation of tumor-specific cytotoxic T lymphocytes

BACKGROUND: Early clinical trials, mostly in the setting of melanoma, have shown that dendritic cells (DCs) expressing tumor antigens induce some immune responses and some clinical responses. A major difficulty is the extension to other tumors, such as breast carcinoma, for which few defined tumor-associated antigens are available. We have demonstrated, using both prostate carcinoma and melanoma as model systems, that DCs loaded with killed allogeneic tumor cell lines can induce CD8(+ )T cells to differentiate into cytotoxic T lymphocytes (CTLs) specific for shared tumor antigens. METHODS: The present study was designed to determine whether DCs would capture killed breast cancer cells and present their antigens to autologous CD4(+ )and CD8(+ )T cells. RESULTS: We show that killed breast cancer cells are captured by immature DCs that, after induced maturation, can efficiently present MHC class I and class II peptides to CD8(+ )and CD4(+ )T lymphocytes. The elicited CTLs are able to kill the target cells without a need for pretreatment with interferon gamma. CTLs can be obtained by culturing the DCs loaded with killed breast cancer cells with unseparated peripheral blood lymphocytes, indicating that the DCs can overcome any potential inhibitory effects of breast cancer cells. CONCLUSION: Loading DCs with killed breast cancer cells may be considered a novel approach to breast cancer immunotherapy and to identification of shared breast cancer antigens

Cross-priming of cyclin B1, MUC-1 and survivin-specific CD8(+ )T cells by dendritic cells loaded with killed allogeneic breast cancer cells

INTRODUCTION: The ability of dendritic cells (DCs) to take up whole tumor cells and process their antigens for presentation to T cells ('cross-priming') is an important mechanism for induction of tumor specific immunity. METHODS: In vitro generated DCs were loaded with killed allogeneic breast cancer cells and offered to autologous naïve CD8(+ )T cells in 2-week and/or 3-week cultures. CD8(+ )T cell differentiation was measured by their capacity to secrete effector cytokines (interferon-γ) and kill breast cancer cells. Specificity was measured using peptides derived from defined breast cancer antigens. RESULTS: We found that DCs loaded with killed breast cancer cells can prime naïve CD8(+ )T cells to differentiate into effector cytotoxic T lymphocytes (CTLs). Importantly, these CTLs primed by DCs loaded with killed HLA-A*0201(- )breast cancer cells can kill HLA-A*0201(+ )breast cancer cells. Among the tumor specific CTLs, we found that CTLs specific for HLA-A2 restricted peptides derived from three well known shared breast tumor antigens, namely cyclin B1, MUC-1 and survivin. CONCLUSION: This ability of DCs loaded with killed allogeneic breast cancer cells to elicit multiantigen specific immunity supports their use as vaccines in patients with breast cancer