1,969 research outputs found

    Joint phase-recovery and demodulation-decoding of AIS signals received by satellite

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    International audienceThis paper presents a demodulation algorithm for automatic identification system (AIS) signals received by a satellite. The main contribution of this work is to consider the phase recovery problem for an unknown modulation index, coupled with a time-varying phase shift. The proposed method is based on a demodulator introduced in a previous paper based on a Viterbi-type algorithm applied to an extended trellis. The states of this extended trellis are composed of a trellis-code state and of a cyclic redundancy check state. The bit stuffing mechanism is taken into account by defining special conditional transitions in the extended trellis. This algorithm estimates and tracks the phase shift by modifying the Euclidean distance used in the trellis. Simulation results obtained with and without phase tracking are presented and compared in the context of the AIS system

    Poursuite de phase durant la démodulation et le décodage des signaux AIS reçus par satellite

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    National audienceThis paper presents a demodulation algorithm for automatic identification system (AIS) signals received by a satellite. The main contribution of this work is to consider the phase recovery problem for an unknown modulation index, coupled with a time-varying phase shift. The proposed method is based on a demodulator introduced in a previous paper based on a Viterbi-type algorithm applied to an extended trellis. The states of this extended trellis are composed of a trellis-code state and of a cyclic redundancy check state. The bit stuffing mechanism is taken into account by defining specific conditional transitions in the extended trellis. This algorithm estimates and tracks the phase shift by modifying the Euclidean distance used in the trellis. Simulation results obtained with and without phase tracking are presented and compared in the context of the AIS system.Cet article présente un algorithme de démodulation des signaux du système d’identification automatique (AIS) reçus par satellite. La principale contribution de ce travail est de considérer le problème d’estimation de la phase pour un indice de modulation inconnu couplé avec un décalage de phase variant dans le temps. La méthode proposée consiste à étendre la méthode de démodulation présentée dans un précédent article utilisant un algorithme de Viterbi appliqué sur un treillis étendu. Les états de ce treillis étendu sont composés d’un état du codeur en treillis et d’un état du contrôle de redondance cyclique (CRC). Les bits de bourrage sont pris en compte en définissant des transitions spécifiques dans le treillis étendu. Cet algorithme estime et poursuit le décalage de phase en modifiant la distance euclidienne utilisée dans le treillis. Les résultats de simulations obtenus avec et sans poursuite de la phase sont présentés et comparés dans le contexte du système AI

    The antimicrobial peptide Defensin cooperates with tumour necrosis factor to drive tumour cell death in Drosophila

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    Antimicrobial peptides (AMPs) are small cationic molecules best known as mediators of the innate defence against microbial infection. While in vitro and ex vivo evidence suggest AMPs’ capacity to kill cancer cells, in vivo demonstration of an anti-tumour role of endogenous AMPs is lacking. Using a Drosophila model of tumourigenesis, we demonstrate a role for the AMP Defensin in the control of tumour progression. Our results reveal that Tumour Necrosis Factor mediates exposure of phosphatidylserine (PS), which makes tumour cells selectively sensitive to the action of Defensin remotely secreted from tracheal and fat tissues. Defensin binds tumour cells in PS-enriched areas, provoking cell death and tumour regression. Altogether, our results provide the first in vivo demonstration for a role of an endogenous AMP as an anti-cancer agent, as well as a mechanism that explains tumour cell sensitivity to the action of AMPs

    Local control of intestinal stem cell homeostasis by enteroendocrine cells in the adult <i>Drosophila</i> midgut

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    Background: Enteroendocrine cells populate gastrointestinal tissues and are known to translate local cues into systemic responses through the release of hormones into the bloodstream.&lt;p&gt;&lt;/p&gt; Results: Here we report a novel function of enteroendocrine cells acting as local regulators of intestinal stem cell (ISC) proliferation through modulation of the mesenchymal stem cell niche in the &lt;i&gt;Drosophila&lt;/i&gt; midgut. This paracrine signaling acts to constrain ISC proliferation within the epithelial compartment. Mechanistically, midgut enteroendocrine cells secrete the neuroendocrine hormone Bursicon, which acts—beyond its known roles in development—as a paracrine factor on the visceral muscle (VM). Bursicon binding to its receptor, DLGR2, the ortholog of mammalian leucine-rich repeat-containing G protein-coupled receptors (LGR4-6), represses the production of the VM-derived EGF-like growth factor Vein through activation of cAMP.&lt;p&gt;&lt;/p&gt; Conclusions: We therefore identify a novel paradigm in the regulation of ISC quiescence involving the conserved ligand/receptor Bursicon/DLGR2 and a previously unrecognized tissue-intrinsic role of enteroendocrine cells.&lt;p&gt;&lt;/p&gt

    Ship localization using AIS signals received by satellite

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    This paper addresses the problem of ship localization by using the messages received by satellites and transmitted by the automatic identification system (AIS). In particular, one considers the localization of ships that do not transmit their actual position in AIS signals. The proposed localization method is based on the least squares algorithm and uses the differences of times of arrival and the carrier frequencies of the messages received by satellite. A modification of this algorithm is proposed to take into account the displacement model of the ships as additional measurements. This modification shows a significant localization improvement

    The Transcriptional Response of Drosophila melanogaster to Infection with the Sigma Virus (Rhabdoviridae)

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    Bacterial and fungal infections induce a potent immune response in Drosophila melanogaster, but it is unclear whether viral infections induce an antiviral immune response. Using microarrays, we examined the changes in gene expression in Drosophila that occur in response to infection with the sigma virus, a negative-stranded RNA virus (Rhabdoviridae) that occurs in wild populations of D. melanogaster. We detected many changes in gene expression in infected flies, but found no evidence for the activation of the Toll, IMD or Jak-STAT pathways, which control immune responses against bacteria and fungi. We identified a number of functional categories of genes, including serine proteases, ribosomal proteins and chorion proteins that were overrepresented among the differentially expressed genes. We also found that the sigma virus alters the expression of many more genes in males than in females. These data suggest that either Drosophila do not mount an immune response against the sigma virus, or that the immune response is not controlled by known immune pathways. If the latter is true, the genes that we identified as differentially expressed after infection are promising candidates for controlling the host's response to the sigma virus

    Critical Assessment of Metagenome Interpretation:A benchmark of metagenomics software

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    International audienceIn metagenome analysis, computational methods for assembly, taxonomic profilingand binning are key components facilitating downstream biological datainterpretation. However, a lack of consensus about benchmarking datasets andevaluation metrics complicates proper performance assessment. The CriticalAssessment of Metagenome Interpretation (CAMI) challenge has engaged the globaldeveloper community to benchmark their programs on datasets of unprecedentedcomplexity and realism. Benchmark metagenomes were generated from newlysequenced ~700 microorganisms and ~600 novel viruses and plasmids, includinggenomes with varying degrees of relatedness to each other and to publicly availableones and representing common experimental setups. Across all datasets, assemblyand genome binning programs performed well for species represented by individualgenomes, while performance was substantially affected by the presence of relatedstrains. Taxonomic profiling and binning programs were proficient at high taxonomicranks, with a notable performance decrease below the family level. Parametersettings substantially impacted performances, underscoring the importance ofprogram reproducibility. While highlighting current challenges in computationalmetagenomics, the CAMI results provide a roadmap for software selection to answerspecific research questions

    Genetic analyses of the QT interval and its components in over 250K individuals identifies new loci and pathways affecting ventricular depolarization and repolarization

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    Genetic analyses of the electrocardiographic QT interval and its components identify additional loci and pathways

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    The QT interval is an electrocardiographic measure representing the sum of ventricular depolarization and repolarization, estimated by QRS duration and JT interval, respectively. QT interval abnormalities are associated with potentially fatal ventricular arrhythmia. Using genome-wide multi-ancestry analyses (&gt;250,000 individuals) we identify 177, 156 and 121 independent loci for QT, JT and QRS, respectively, including a male-specific X-chromosome locus. Using gene-based rare-variant methods, we identify associations with Mendelian disease genes. Enrichments are observed in established pathways for QT and JT, and previously unreported genes indicated in insulin-receptor signalling and cardiac energy metabolism. In contrast for QRS, connective tissue components and processes for cell growth and extracellular matrix interactions are significantly enriched. We demonstrate polygenic risk score associations with atrial fibrillation, conduction disease and sudden cardiac death. Prioritization of druggable genes highlight potential therapeutic targets for arrhythmia. Together, these results substantially advance our understanding of the genetic architecture of ventricular depolarization and repolarization
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