Université libre de Bruxelles

About: Université libre de Bruxelles is a education organization based out in Brussels, Belgium. It is known for research contribution in the topics: Population & Breast cancer. The organization has 24974 authors who have published 56969 publications receiving 2084303 citations. The organization is also known as: ULB.

Fom Local Actions to Global Tasks: Stigmergy and Collective Robotics

Abstract: This paper presents a series of experiments where a group of mobile robots gather 81 randomly distributed objects and cluster them into one pile. Coordination of the agents’ movements is achieved through stigmergy. This principle, originally developed for the description of termite building behaviour, allows indirect communication between agents through sensing and modification of the local environment which determines the agents’ behaviour. The efficiency of the work was measured for groups of one to five robots working together. Group size is a critical factor. The mean time to accomplish the task decreases for one, two, and three robots respectively, then increases again for groups of four and five agents, due to an exponential increase in the number of interactions between robots which are time consuming and may eventually result in the destruction of existing clusters. We compare our results with those reported by Deneubourg et al. (1990) where similar clusters are observed in ant colonies, generated by the probabilistic behaviour of workers.

Free Fatty Acids and Cytokines Induce Pancreatic β-Cell Apoptosis by Different Mechanisms: Role of Nuclear Factor-κB and Endoplasmic Reticulum Stress

Abstract: Apoptosis is probably the main form of beta-cell death in both type 1 diabetes mellitus (T1DM) and T2DM. In T1DM, cytokines contribute to beta-cell destruction through nuclear factor-kappaB (NF-kappaB) activation. Previous studies suggested that in T2DM high glucose and free fatty acids (FFAs) are beta-cell toxic also via NF-kappaB activation. The aims of this study were to clarify whether common mechanisms are involved in FFA- and cytokine-induced beta-cell apoptosis and determine whether TNFalpha, an adipocyte-derived cytokine, potentiates FFA toxicity through enhanced NF-kappaB activation. Apoptosis was induced in insulinoma (INS)-1E cells, rat islets, and fluorescence-activated cell sorting-purified beta-cells by oleate, palmitate, and/or cytokines (IL-1beta, interferon-gamma, TNFalpha). Palmitate and IL-1beta induced a similar percentage of apoptosis in INS-1E cells, whereas oleate was less toxic. TNFalpha did not potentiate FFA toxicity in primary beta-cells. The NF-kappaB-dependent genes inducible nitric oxide synthase and monocyte chemoattractant protein-1 were induced by IL-1beta but not by FFAs. Cytokines activated NF-kappaB in INS-1E and beta-cells, but FFAs did not. Moreover, FFAs did not enhance NF-kappaB activation by TNFalpha. Palmitate and oleate induced C/EBP homologous protein, activating transcription factor-4, and immunoglobulin heavy chain binding protein mRNAs, X-box binding protein-1 alternative splicing, and activation of the activating transcription factor-6 promoter in INS-1E cells, suggesting that FFAs trigger an endoplasmic reticulum (ER) stress response. We conclude that apoptosis is the main mode of FFA- and cytokine-induced beta-cell death but the mechanisms involved are different. Whereas cytokines induce NF-kappaB activation and ER stress (secondary to nitric oxide formation), FFAs activate an ER stress response via an NF-kappaB- and nitric oxide-independent mechanism. Our results argue against a unifying hypothesis for the mechanisms of beta-cell death in T1DM and T2DM.

A Large Hadron Electron Collider at CERN

Abstract: This document provides a brief overview of the recently published report on the design of the Large Hadron Electron Collider (LHeC), which comprises its physics programme, accelerator physics, technology and main detector concepts. The LHeC exploits and develops challenging, though principally existing, accelerator and detector technologies. This summary is complemented by brief illustrations of some of the highlights of the physics programme, which relies on a vastly extended kinematic range, luminosity and unprecedented precision in deep inelastic scattering. Illustrations are provided regarding high precision QCD, new physics (Higgs, SUSY) and electron-ion physics. The LHeC is designed to run synchronously with the LHC in the twenties and to achieve an integrated luminosity of O(100)\,fb$^{-1}$. It will become the cleanest high resolution microscope of mankind and will substantially extend as well as complement the investigation of the physics of the TeV energy scale, which has been enabled by the LHC.

SOX2 controls tumour initiation and cancer stem-cell functions in squamous-cell carcinoma

Abstract: Cancer stem cells (CSCs) have been reported in various cancers, including in skin squamous-cell carcinoma (SCC). The molecular mechanisms regulating tumour initiation and stemness are still poorly characterized. Here we find that Sox2, a transcription factor expressed in various types of embryonic and adult stem cells, was the most upregulated transcription factor in the CSCs of squamous skin tumours in mice. SOX2 is absent in normal epidermis but begins to be expressed in the vast majority of mouse and human pre-neoplastic skin tumours, and continues to be expressed in a heterogeneous manner in invasive mouse and human SCCs. In contrast to other SCCs, in which SOX2 is frequently genetically amplified, the expression of SOX2 in mouse and human skin SCCs is transcriptionally regulated. Conditional deletion of Sox2 in the mouse epidermis markedly decreases skin tumour formation after chemical-induced carcinogenesis. Using green fluorescent protein (GFP) as a reporter of Sox2 transcriptional expression (SOX2-GFP knock-in mice), we showed that SOX2-expressing cells in invasive SCC are greatly enriched in tumour-propagating cells, which further increase upon serial transplantations. Lineage ablation of SOX2-expressing cells within primary benign and malignant SCCs leads to tumour regression, consistent with the critical role of SOX2-expressing cells in tumour maintenance. Conditional Sox2 deletion in pre-existing skin papilloma and SCC leads to tumour regression and decreases the ability of cancer cells to be propagated upon transplantation into immunodeficient mice, supporting the essential role of SOX2 in regulating CSC functions. Transcriptional profiling of SOX2-GFP-expressing CSCs and of tumour epithelial cells upon Sox2 deletion uncovered a gene network regulated by SOX2 in primary tumour cells in vivo. Chromatin immunoprecipitation identified several direct SOX2 target genes controlling tumour stemness, survival, proliferation, adhesion, invasion and paraneoplastic syndrome. We demonstrate that SOX2, by marking and regulating the functions of skin tumour-initiating cells and CSCs, establishes a continuum between tumour initiation and progression in primary skin tumours.

Another Report on Harmonic Maps

Abstract: (1.1) Some of the main results described in [Report] are the following (in rough terms; notations and precise references will be given below): (1) A map (f>:{M,g)-+(N,h) between Riemannian manifolds which is continuous and of class L\\ is harmonic if and only if it is a critical point of the energy functional. (2) Let (M, g) and (N, h) be compact, and <̂ 0: (M, g) -> (N, h) a map. Then ^0 can be deformed to a harmonic map with minimum energy in its homotopy class in the following cases: (a) Riem ' f t ^0; (b) dim M = 2 and n2(N) = 0. (3) Any map 0O: S m -> S can be deformed to a harmonic map provided m ^ 7. More generally, suitably restricted harmonic polynomial maps can be joined to provide harmonic maps between spheres. (4) The homotopy class of maps of degree 1 from the 2-torus T to the 2-sphere S has no harmonic representative, whatever Riemannian metrics are put on T and S. (5) If in (2) M has a smooth boundary, then various Dirichlet problems have solutions in case (a) and (b); and also when the boundary data is sufficiently small.