Do Irrelevant Sounds Impair the Maintenance of All Characteristics of Speech in Memory?

Several studies have shown that maintaining in memory some attributes of speech, such as the content or pitch of an interlocutor's message, is markedly reduced in the presence of background sounds made of spectrotemporal variations. However, experimental paradigms showing this interference have only focused on one attribute of speech at a time, and thus differ from real-life situations in which several attributes have to be memorized and maintained simultaneously. It is possible that the interference is even greater in such a case and can occur for a broader range of background sounds. We developed a paradigm in which participants had to maintain the content, pitch and speaker size of auditorily presented speech information and used various auditory distractors to generate interference. We found that only distractors with spectrotemporal variations impaired the detection, which shows that similar interference mechanisms occur whether there are one or more speech attributes to maintain in memory. A high percentage of false alarms was observed with these distractors, suggesting that spectrotemporal variations not only weaken but also modify the information maintained in memory. Lastly, we found that participants were unaware of the interference. These results are similar to those observed in the visual modalit

Case Study of Non-Isolated MMC DC-DC Converter in HVDC Grids

Peer reviewedPublisher PD

Centronuclear myopathy in labrador retrievers: a recent founder mutation in the PTPLA gene has rapidly disseminated worldwide

Centronuclear myopathies (CNM) are inherited congenital disorders characterized by an excessive number of internalized nuclei. In humans, CNM results from ~70 mutations in three major genes from the myotubularin, dynamin and amphiphysin families. Analysis of animal models with altered expression of these genes revealed common defects in all forms of CNM, paving the way for unified pathogenic and therapeutic mechanisms. Despite these efforts, some CNM cases remain genetically unresolved. We previously identified an autosomal recessive form of CNM in French Labrador retrievers from an experimental pedigree, and showed that a loss-of-function mutation in the protein tyrosine phosphatase-like A (PTPLA) gene segregated with CNM. Around the world, client-owned Labrador retrievers with a similar clinical presentation and histopathological changes in muscle biopsies have been described. We hypothesized that these Labradors share the same PTPLA<sup>cnm</sup> mutation. Genotyping of an international panel of 7,426 Labradors led to the identification of PTPLA<sup>cnm</sup> carriers in 13 countries. Haplotype analysis demonstrated that the PTPLA<sup>cnm</sup> allele resulted from a single and recent mutational event that may have rapidly disseminated through the extensive use of popular sires. PTPLA-deficient Labradors will help define the integrated role of PTPLA in the existing CNM gene network. They will be valuable complementary large animal models to test innovative therapies in CNM

Antimatter and Matter Production in Heavy Ion Collisions at CERN (The NEWMASS Experiment NA52)

Besides the dedicated search for strangelets NA52 measures light (anti)particle and (anti)nuclei production over a wide range of rapidity. Compared to previous runs the statistics has been increased in the 1998 run by more than one order of magnitude for negatively charged objects at different spectrometer rigidities. Together with previous data taking at a rigidity of -20 GeV/c we obtained 10^6 antiprotons 10^3 antideuterons and two antihelium3 without centrality requirements. We measured nuclei and antinuclei (p,d,antiprotons, antideuterons) near midrapidity covering an impact parameter range of b=2-12 fm. Our results strongly indicate that nuclei and antinuclei are mainly produced via the coalescence mechanism. However the centrality dependence of the antibaryon to baryon ratios show that antibaryons are diminished due to annihilation and breakup reactions in the hadron dense environment. The volume of the particle source extracted from coalescence models agrees with results from pion interferometry for an expanding source. The chemical and thermal freeze-out of nuclei and antinuclei appear to coincide with each other and with the thermal freeze-out of hadrons.Comment: 12 pages, 8 figures, to appear in the proceedings of the conference on 'Fundamental Issues in Elementary Matter' Bad Honnef, Germany, Sept. 25-29, 200

Centrality dependence of K+ produced in Pb+Pb collisions at 158 GeV per nucleon

The NA52 collaboration searches for a discontinuous behaviour of charged kaons produced in Pb+Pb collisions at 158 A GeV as a function of the impact parameter, which could reveal a hadron to quark-gluon plasma (QGP) phase transition. The K+ yield is found to grow proportional to the number of participating ('wounded') nucleons N, above N=100. Previous NA52 data agree with the above finding and show a discontinuous behaviour in the kaon centrality dependence near N=100, marking the onset of strangeness enhancement -over e.g. p+A data at the same \sqrt{s}- in a chemically equilibrated phase.Comment: 2 pages, 2 figures, submitted to the XXXth International Conference on High Energy Physics, 27 July - 2 August, 2000, Osaka, Japa

HACD1, a regulator of membrane composition and fluidity, promotes myoblast fusion and skeletal muscle growth

The reduced diameter of skeletal myofibres is a hallmark of several congenital myopathies, yet the underlying cellular and molecular mechanisms remain elusive. In this study, we investigate the role of HACD1/PTPLA, which is involved in the elongation of the very long chain fatty acids, in muscle fibre formation. In humans and dogs, HACD1 deficiency leads to a congenital myopathy with fibre size disproportion associated with a generalized muscle weakness. Through analysis of HACD1-deficient Labradors, Hacd1-knockout mice, and Hacd1-deficient myoblasts, we provide evidence that HACD1 promotes myoblast fusion during muscle development and regeneration. We further demonstrate that in normal differentiating myoblasts, expression of the catalytically active HACD1 isoform, which is encoded by a muscle-enriched splice variant, yields decreased lysophosphatidylcholine content, a potent inhibitor of myoblast fusion, and increased concentrations of ≥C18 and monounsaturated fatty acids of phospholipids. These lipid modifications correlate with a reduction in plasma membrane rigidity. In conclusion, we propose that fusion impairment constitutes a novel, non-exclusive pathological mechanism operating in congenital myopathies and reveal that HACD1 is a key regulator of a lipid-dependent muscle fibre growth mechanism

Drivers for Rift Valley fever emergence in Mayotte: A Bayesian modelling approach

Rift Valley fever (RVF) is a major zoonotic and arboviral hemorrhagic fever. The conditions leading to RVF epidemics are still unclear, and the relative role of climatic and anthropogenic factors may vary between ecosystems. Here, we estimate the most likely scenario that led to RVF emergence on the island of Mayotte, following the 2006–2007 African epidemic. We developed the first mathematical model for RVF that accounts for climate, animal imports and livestock susceptibility, which is fitted to a 12-years dataset. RVF emergence was found to be triggered by the import of infectious animals, whilst transmissibility was approximated as a linear or exponential function of vegetation density. Model forecasts indicated a very low probability of virus endemicity in 2017, and therefore of re-emergence in a closed system (i.e. without import of infected animals). However, the very high proportion of naive animals reached in 2016 implies that the island remains vulnerable to the import of infectious animals. We recommend reinforcing surveillance in livestock, should RVF be reported is neighbouring territories. Our model should be tested elsewhere, with ecosystem-specific data