2,588 research outputs found

    Transparent Synchronous Dataflow

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    Dataflow programming is a popular and convenient programming paradigm in systems modelling, optimisation, and machine learning. It has a number of advantages, for instance the lacks of control flow allows computation to be carried out in parallel as well as in distributed machines. More recently the idea of dataflow graphs has also been brought into the design of various deep learning frameworks. They facilitate an easy and efficient implementation of automatic differentiation, which is the heart of modern deep learning paradigm. [abstract abridged

    Human Nerve Growth Factor Protects Common Marmosets against Autoimmune Encephalomyelitis by Switching the Balance of T Helper Cell Type 1 and 2 Cytokines within the Central Nervous System

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    Multiple sclerosis is a demyelinating disorder of the central nervous system (CNS), in which an immune attack directed against myelin constituents causes myelin destruction and death of oligodendrocytes, the myelin-producing cells. Here, the efficacy of nerve growth factor (NGF), a growth factor for neurons and oligodendrocytes, in promoting myelin repair was evaluated using the demyelinating model of experimental allergic encephalomyelitis (EAE) in the common marmoset. Surprisingly, we found that NGF delayed the onset of clinical EAE and, pathologically, prevented the full development of EAE lesions. We demonstrate by immunocytochemistry that NGF exerts its antiinflammatory effect by downregulating the production of interferon γ by T cells infiltrating the CNS, and upregulating the production of interleukin 10 by glial cells in both inflammatory lesions of EAE and normal-appearing CNS white matter. Thus, NGF, currently under investigation in human clinical trials as a neuronal trophic factor, may be an attractive candidate for therapy of autoimmune demyelinating disorders

    Gas turbine combustor

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    A gas turbine engine has a combustor module including an annular combustor having a liner assembly that defines an annular combustion chamber having a length, L. The liner assembly includes a radially inner liner, a radially outer liner that circumscribes the inner liner, and a bulkhead, having a height, H1, which extends between the respective forward ends of the inner liner and the outer liner. The combustor has an exit height, H3, at the respective aft ends of the inner liner and the outer liner interior. The annular combustor has a ratio H1/H3 having a value less than or equal to 1.7. The annular combustor may also have a ration L/H3 having a value less than or equal to 6.0

    Corticostriatal functional connectivity of bothersome tinnitus in single-sided deafness

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    Subjective tinnitus is an auditory phantom perceptual disorder without an objective biomarker. Bothersome tinnitus in single-sided deafness (SSD) is particularly challenging to treat because the deaf ear can no longer be stimulated by acoustic means. We contrasted an SSD cohort with bothersome tinnitus (TIN; N = 15) against an SSD cohort with no or non-bothersome tinnitus (NO TIN; N = 15) using resting-state functional magnetic resonance imaging (fMRI). All study participants had normal hearing in one ear and severe or profound hearing loss in the other. We evaluated corticostriatal functional connectivity differences by placing seeds in the caudate nucleus and Heschl’s Gyrus (HG) of both hemispheres. The TIN cohort showed increased functional connectivity between the left caudate and left HG, and left and right HG and the left caudate. Within the TIN cohort, functional connectivity between the right caudate and cuneus was correlated with the Tinnitus Functional Index (TFI) relaxation subscale. And, functional connectivity between the right caudate and superior lateral occipital cortex, and the right caudate and anterior supramarginal gyrus were correlated with the TFI control subscale. These findings support a striatal gating model of tinnitus and suggest tinnitus biomarkers to monitor treatment response and to target specific brain areas for innovative neuromodulation therapies

    Galaxy Zoo: Are Bars Responsible for the Feeding of Active Galactic Nuclei at 0.2 < z < 1.0?

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    We present a new study investigating whether active galactic nuclei (AGN) beyond the local universe are preferentially fed via large-scale bars. Our investigation combines data from Chandra and Galaxy Zoo: Hubble (GZH) in the AEGIS, COSMOS, and GOODS-S surveys to create samples of face-on, disc galaxies at 0.2 < z < 1.0. We use a novel method to robustly compare a sample of 120 AGN host galaxies, defined to have 10^42 erg/s < L_X < 10^44 erg/s, with inactive control galaxies matched in stellar mass, rest-frame colour, size, Sersic index, and redshift. Using the GZH bar classifications of each sample, we demonstrate that AGN hosts show no statistically significant enhancement in bar fraction or average bar likelihood compared to closely-matched inactive galaxies. In detail, we find that the AGN bar fraction cannot be enhanced above the control bar fraction by more than a factor of two, at 99.7% confidence. We similarly find no significant difference in the AGN fraction among barred and non-barred galaxies. Thus we find no compelling evidence that large-scale bars directly fuel AGN at 0.2<z<1.0. This result, coupled with previous results at z=0, implies that moderate-luminosity AGN have not been preferentially fed by large-scale bars since z=1. Furthermore, given the low bar fractions at z>1, our findings suggest that large-scale bars have likely never directly been a dominant fueling mechanism for supermassive black hole growth.Comment: 13 pages, 5 figures, 2 tables, accepted by MNRA

    Somatic Mutations of PIK3R1 Promote Gliomagenesis

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    The phosphoinositide 3-kinase (PI3K) pathway is targeted for frequent alteration in glioblastoma (GBM) and is one of the core GBM pathways defined by The Cancer Genome Atlas. Somatic mutations of PIK3R1 are observed in multiple tumor types, but the tumorigenic activity of these mutations has not been demonstrated in GBM. We show here that somatic mutations in the iSH2 domain of PIK3R1 act as oncogenic driver events. Specifically, introduction of a subset of the mutations identified in human GBM, in the nSH2 and iSH2 domains, increases signaling through the PI3K pathway and promotes tumorigenesis of primary normal human astrocytes in an orthotopic xenograft model. Furthermore, we show that cells that are dependent on mutant P85α-mediated PI3K signaling exhibit increased sensitivity to a small molecule inhibitor of AKT. Together, these results suggest that GBM patients whose tumors carry mutant PIK3R1 alleles may benefit from treatment with inhibitors of AKT
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