14 research outputs found

    Online Distributed Learning over Random Networks

    Full text link
    The recent deployment of multi-agent systems in a wide range of scenarios has enabled the solution of learning problems in a distributed fashion. In this context, agents are tasked with collecting local data and then cooperatively train a model, without directly sharing the data. While distributed learning offers the advantage of preserving agents' privacy, it also poses several challenges in terms of designing and analyzing suitable algorithms. This work focuses specifically on the following challenges motivated by practical implementation: (i) online learning, where the local data change over time; (ii) asynchronous agent computations; (iii) unreliable and limited communications; and (iv) inexact local computations. To tackle these challenges, we introduce the Distributed Operator Theoretical (DOT) version of the Alternating Direction Method of Multipliers (ADMM), which we call the DOT-ADMM Algorithm. We prove that it converges with a linear rate for a large class of convex learning problems (e.g., linear and logistic regression problems) toward a bounded neighborhood of the optimal time-varying solution, and characterize how the neighborhood depends on~(i)–(iv)\text{(i)--(iv)}. We corroborate the theoretical analysis with numerical simulations comparing the DOT-ADMM Algorithm with other state-of-the-art algorithms, showing that only the proposed algorithm exhibits robustness to (i)--(iv)

    Education and the changing structure of opportunities for young people in England

    Get PDF
    In this article we explore the implications for young people’s life opportunities of rising levels of qualifications in England, drawing on a range of sources, including the OECD’s 2014 Survey and Adult Skills (SAS) and the UK Labour Force Survey. We find that increasing rates of participation in post 16 education and training in England has led to a substantial rise in qualification levels for the current generation of youth compared their parents’ generation. More inclusive participation has also narrowed inequalities in qualification outcomes and slightly reduced the social gaps in attainment of qualifications, at least at the upper secondary level. However, the gains in educational opportunities for young people are to some extent illusory. Improvements in the skills we can measure, like literacy and numeracy, have not kept pace with increasing qualifications rates, and inequalities in skills have reduced much less than those in qualifications, if at all. This suggests that much of rise in qualifications is indeed a question of credential inflation and yields few benefits to young people today in terms of future life prospects. Indeed our analysis of the occupational destinations of people qualified at different levels suggests a steady erosion of the value of qualifications of all levels on the labour market. At the same time career opportunities for young women have generally improved and, arguably, for most young people there is a sense that they are freer to aspire then was the case for their parents

    bag3 gene expression is regulated by heat shock factor 1.

    No full text
    BAG3 protein, a member of the BAG co-chaperones family, sustains cell survival, through its interaction with the heat shock protein (HSP) 70, in a variety of normal and neoplastic cell types. bag3 gene expression is induced by stressful stimuli. Here we report for the first time that two of the three putative heat shock-responsive elements (HSEs) in bag3 promoter interact with the heat shock factor (HSF) 1 in vitro and in vivo. Furthermore, downmodulation of HSF1 protein levels by specific small interfering (si) RNAs results in reducing BAG3 protein levels, indicating that the transcription factor plays a major role in bag3 gene expression. Because of the anti-apoptotic role of BAG3 protein, these results disclose a previously unrecognized pathway, through which HSF1 maintains cell survival

    Identification of a microRNA (miR-663a) induced by ER stress and its target gene PLOD3 by a combined microRNome and proteome approach

    No full text
    Introduction MicroRNAs (miRs) regulate gene expression to support important physiological functions. Significant evidences suggest that miRs play a crucial role in many pathological events and in the cell response to various stresses. Methods With the aim to identify new miRs induced by perturbation of intracellular calcium homeostasis, we analysed miR expression profiles of thapsigargin (TG)-treated cells by microarray. In order to identify miR-663a-regulated genes, we evaluated proteomic changes in miR-663a-overexpressing cells by two-dimensional differential in-gel electrophoresis coupled to mass spectrometric identification of the differentially represented proteins. Microarray and proteomic analyses were supported by biochemical validation. Results Results of microarray revealed 24 differentially expressed miRs; among them, miR-663a turned out to be by ER stress and under the control of the PERK pathway of the unfolded protein response. Proteomic analysis revealed that PLOD3, which is the gene encoding for collagen-modifying lysyl hydroxylase 3 (LH3), is regulated by miR-663a. Luciferase reporter assays demonstrated that miR-663a indeed reduces LH3 expression by targeting to 3′-UTR of PLOD3 mRNA. Interestingly, miR-663a inhibition of LH3 expression generates reduced extracellular accumulation of type IV collagen, thus suggesting the involvement of miR-663a in modulating collagen 4 secretion in physiological conditions and in response to ER stress. Conclusion The finding of the ER stress-induced PERK-miR-663a pathway may have important implications in the understanding of the molecular mechanisms underlying the function of this miR in normal and/or pathological conditions

    Exposure to 50 Hz electromagnetic field raises the level of the anti-apoptotic protein BAG3 in melanoma cells

    No full text
    The expression of the anti-apoptotic protein BAG3 is induced in several cell types by exposure to high temperature, oxidants, and other stressful agents. We investigated whether exposure to 50 Hz electromagnetic fields raised BAG3 levels in the human melanoma cell line M14, in vitro and in orthotopic xenografts. Exposure of cultured cells or xenografts for 6 h or 4 weeks, respectively, produced a significant (P < 0.01) increase in BAG3 protein amounts. Interestingly, at the same times, we could not detect any significant variation in the levels of HSP70/72 protein or cell apoptosis. These results confirm the stressful effect of exposure to ELF in human cells, by identifying BAG3 protein as a marker of ELF-induced stress. Furthermore, they suggest that BAG3 induction by ELF may contribute to melanoma cell survival and/or resistance to therapy
    corecore