9 resultados para R-MEDIATED PHAGOCYTOSIS
em Universidade do Minho
Resumo:
A search is presented for photonic signatures motivated by generalised models of gauge-mediated supersymmetry breaking. This search makes use of 20.3 fb−1 of proton-proton collision data at s√=8 TeV recorded by the ATLAS detector at the LHC, and explores models dominated by both strong and electroweak production of supersymmetric partner states. Four experimental signatures incorporating an isolated photon and significant missing transverse momentum are explored. These signatures include events with an additional photon, lepton, b-quark jet, or jet activity not associated with any specific underlying quark flavor. No significant excess of events is observed above the Standard Model prediction and model-dependent 95% confidence-level exclusion limits are set.
Resumo:
Recent advances in computation allow for the integration of design and simulation of highly interrelated systems, such as hybrids of structural membranes and bending active elements. The engaged complexities of forces and logistics can be mediated through the development of materials with project specific properties and detailing. CNC knitting with high tenacity yarn enables this practice and offers an alternative to current woven membranes. The design and fabrication of an 8m high fabric tower through an interdisciplinary team of architects, structural and textile engineers, allowed to investigate means to design, specify, make and test CNC knit as material for hybrid structures in architectural scale. This paper shares the developed process, identifies challenges, potentials and future work.
Resumo:
Results of a search for new phenomena in final states with an energetic jet and large missing transverse momentum are reported. The search uses 20.3 fb−1 of s√=8 TeV data collected in 2012 with the ATLAS detector at the LHC. Events are required to have at least one jet with pT>120 GeV and no leptons. Nine signal regions are considered with increasing missing transverse momentum requirements between EmissT>150 GeV and EmissT>700 GeV. Good agreement is observed between the number of events in data and Standard Model expectations. The results are translated into exclusion limits on models with large extra spatial dimensions, pair production of weakly interacting dark matter candidates, and production of very light gravitinos in a gauge-mediated supersymmetric model. In addition, limits on the production of an invisibly decaying Higgs-like boson leading to similar topologies in the final state are presented.
Resumo:
Searches for heavy long-lived charged particles are performed using a data sample of 19.8 fb−1 from proton--proton collisions at a centre-of-mass energy of s√ = 8 TeV collected by the ATLAS detector at the Large Hadron Collider. No excess is observed above the estimated background and limits are placed on the mass of long-lived particles in various supersymmetric models. Long-lived tau sleptons in models with gauge-mediated symmetry breaking are excluded up to masses between 440 and 385 GeV for tan(beta) between 10 and 50, with a 290 GeV limit in the case where only direct tau slepton production is considered. In the context of simplified LeptoSUSY models, where sleptons are stable and have a mass of 300 GeV, squark and gluino masses are excluded up to a mass of 1500 and 1360 GeV, respectively. Directly produced charginos, in simplified models where they are nearly degenerate to the lightest neutralino, are excluded up to a mass of 620 GeV. R-hadrons, composites containing a gluino, bottom squark or top squark, are excluded up to a mass of 1270, 845 and 900 GeV, respectively, using the full detector; and up to a mass of 1260, 835 and 870 GeV using an approach disregarding information from the muon spectrometer.
Resumo:
A summary is presented of ATLAS searches for gluinos and first- and second-generation squarks in final states containing jets and missing transverse momentum, with or without leptons or b-jets, in the s√=8 TeV data set collected at the Large Hadron Collider in 2012. This paper reports the results of new interpretations and statistical combinations of previously published analyses, as well as a new analysis. Since no significant excess of events over the Standard Model expectation is observed, the data are used to set limits in a variety of models. In all the considered simplified models that assume R-parity conservation, the limit on the gluino mass exceeds 1150 GeV at 95% confidence level, for an LSP mass smaller than 100 GeV. Furthermore, exclusion limits are set for left-handed squarks in a phenomenological MSSM model, a minimal Supergravity/Constrained MSSM model, R-parity-violation scenarios, a minimal gauge-mediated supersymmetry breaking model, a natural gauge mediation model, a non-universal Higgs mass model with gaugino mediation and a minimal model of universal extra dimensions.
Resumo:
Activation of the dorsomedial nucleus of the hypothalamus (DMH) by galanin (GAL) induces behavioural hyperalgesia. Since DMH neurones do not project directly to the spinal cord, we hypothesized that the medullary dorsal reticular nucleus (DRt), a pronociceptive region projecting to the spinal dorsal horn (SDH) and/or the serotoninergic raphe-spinal pathway acting on the spinal 5-HT3 receptor (5HT3R) could relay descending nociceptive facilitation induced by GAL in the DMH. Heat-evoked paw-withdrawal latency (PWL) and activity of SDH neurones were assessed in monoarthritic (ARTH) and control (SHAM) animals after pharmacological manipulations of the DMH, DRt and spinal cord. The results showed that GAL in the DMH and glutamate in the DRt lead to behavioural hyperalgesia in both SHAM and ARTH animals, which is accompanied particularly by an increase in heat-evoked responses of wide-dynamic range neurons, a group of nociceptive SDH neurones. Facilitation of pain behaviour induced by GAL in the DMH was reversed by lidocaine in the DRt and by ondansetron, a 5HT3R antagonist, in the spinal cord. However, the hyperalgesia induced by glutamate in the DRt was not blocked by spinal ondansetron. In addition, in ARTH but not SHAM animals PWL was increased after lidocaine in the DRt and ondansetron in the spinal cord. Our data demonstrate that GAL in the DMH activates two independent descending facilitatory pathways: (i) one relays in the DRt and (ii) the other one involves 5-HT neurones acting on spinal 5HT3Rs. In experimental ARTH, the tonic pain-facilitatory action is increased in both of these descending pathways.
Resumo:
Spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an untreatable autosomal dominant neurodegenerative disease, and the most common such inherited ataxia worldwide. The mutation in SCA3 is the expansion of a polymorphic CAG tri-nucleotide repeat sequence in the C-terminal coding region of the ATXN3 gene at chromosomal locus 14q32.1. The mutant ATXN3 protein encoding expanded glutamine (polyQ) sequences interacts with multiple proteins in vivo, and is deposited as aggregates in the SCA3 brain. A large body of literature suggests that the loss of function of the native ATNX3-interacting proteins that are deposited in the polyQ aggregates contributes to cellular toxicity, systemic neurodegeneration and the pathogenic mechanism in SCA3. Nonetheless, a significant understanding of the disease etiology of SCA3, the molecular mechanism by which the polyQ expansions in the mutant ATXN3 induce neurodegeneration in SCA3 has remained elusive. In the present study, we show that the essential DNA strand break repair enzyme PNKP (polynucleotide kinase 3'-phosphatase) interacts with, and is inactivated by, the mutant ATXN3, resulting in inefficient DNA repair, persistent accumulation of DNA damage/strand breaks, and subsequent chronic activation of the DNA damage-response ataxia telangiectasia-mutated (ATM) signaling pathway in SCA3. We report that persistent accumulation of DNA damage/strand breaks and chronic activation of the serine/threonine kinase ATM and the downstream p53 and protein kinase C-d pro-apoptotic pathways trigger neuronal dysfunction and eventually neuronal death in SCA3. Either PNKP overexpression or pharmacological inhibition of ATM dramatically blocked mutant ATXN3-mediated cell death. Discovery of the mechanism by which mutant ATXN3 induces DNA damage and amplifies the pro-death signaling pathways provides a molecular basis for neurodegeneration due to PNKP inactivation in SCA3, and for the first time offers a possible approach to treatment.
Resumo:
Recently, there has been a growing interest in the field of metabolomics, materialized by a remarkable growth in experimental techniques, available data and related biological applications. Indeed, techniques as Nuclear Magnetic Resonance, Gas or Liquid Chromatography, Mass Spectrometry, Infrared and UV-visible spectroscopies have provided extensive datasets that can help in tasks as biological and biomedical discovery, biotechnology and drug development. However, as it happens with other omics data, the analysis of metabolomics datasets provides multiple challenges, both in terms of methodologies and in the development of appropriate computational tools. Indeed, from the available software tools, none addresses the multiplicity of existing techniques and data analysis tasks. In this work, we make available a novel R package, named specmine, which provides a set of methods for metabolomics data analysis, including data loading in different formats, pre-processing, metabolite identification, univariate and multivariate data analysis, machine learning, and feature selection. Importantly, the implemented methods provide adequate support for the analysis of data from diverse experimental techniques, integrating a large set of functions from several R packages in a powerful, yet simple to use environment. The package, already available in CRAN, is accompanied by a web site where users can deposit datasets, scripts and analysis reports to be shared with the community, promoting the efficient sharing of metabolomics data analysis pipelines.
Resumo:
Doctoral thesis in Marketing and Strategy.