Deep Spiking Neural Network model for time-variant signals classification: a real-time speech recognition approach

Speech recognition has become an important task to improve the human-machine interface. Taking into account the limitations of current automatic speech recognition systems, like non-real time cloud-based solutions or power demand, recent interest for neural networks and bio-inspired systems has motivated the implementation of new techniques. Among them, a combination of spiking neural networks and neuromorphic auditory sensors offer an alternative to carry out the human-like speech processing task. In this approach, a spiking convolutional neural network model was implemented, in which the weights of connections were calculated by training a convolutional neural network with specific activation functions, using firing rate-based static images with the spiking information obtained from a neuromorphic cochlea. The system was trained and tested with a large dataset that contains ”left” and ”right” speech commands, achieving 89.90% accuracy. A novel spiking neural network model has been proposed to adapt the network that has been trained with static images to a non-static processing approach, making it possible to classify audio signals and time series in real time.Ministerio de Economía y Competitividad TEC2016-77785-

A Real-Time, Event Driven Neuromorphic System for Goal-Directed Attentional Selection

Computation with spiking neurons takes advantage of the abstraction of action potentials into streams of stereotypical events, which encode information through their timing. This approach both reduces power consumption and alleviates communication bottlenecks. A number of such spiking custom mixed-signal address event representation (AER) chips have been developed in recent years. In this paper, we present i) a flexible event-driven platform consisting of the integration of a visual AER sensor and the SpiNNaker system, a programmable massively parallel digital architecture oriented to the simulation of spiking neural networks; ii) the implementation of a neural network for feature-based attentional selection on this platfor

The Interaction of the Eta Carinae Primary Wind with a Century Old Slow Equatorial Ejecta

We argue that the asymmetric morphology of the blue and red shifted components of the outflow at hundreds of AU from the massive binary system Eta Carinae can be understood from the collision of the primary stellar wind with the slowly expanding dense equatorial gas. Recent high spatial observations of some forbidden lines, e.g. [Fe III] lambda4659, reveal the outflowing gas within about one arcsecond (2300 AU) from Eta Car. The distribution of the blue and red shifted components are not symmetric about the center, and they are quite different from each other. The morphologies of the blue and red shifted components correlate with the location of dense slowly moving equatorial gas (termed the Weigelt blob environment; WBE), that is thought to have been ejected during the 1887 - 1895 Lesser Eruption. In our model the division to the blue and red shifted components is caused by the postshock flow of the primary wind on the two sides of the equatorial plane after it collides with the WBE. The fast wind from the secondary star plays no role in our model for these components, and it is the freely expanding primary wind that collides with the WBE. Because the line of sight is inclined to the binary axis, the two components are not symmetric. We show that the postshock gas can also account for the observed intensity in the [Fe III] lambda4659 line.Comment: 15 pages, 3 figures. Accepted to New Astronom

A Perspective of Coagulation Dysfunction in Multiple Sclerosis and in Experimental Allergic Encephalomyelitis

A key role of both coagulation and vascular thrombosis has been reported since the first descriptions of multiple sclerosis (MS). Subsequently, the observation of a close concordance between perivascular fibrin(ogen) deposition and the occurrence of clinical signs in experimental allergic encephalomyelitis (EAE), an animal model of MS, led to numerous investigations focused on the role of thrombin and fibrin(ogen). Indeed, the activation of microglia, resident innate immune cells, occurs early after fibrinogen leakage in the pre-demyelinating lesion stage of EAE and MS. Thrombin has both neuroprotective and pro-apoptotic effects according to its concentration. After exposure to high concentrations of thrombin, astrocytes become reactive and lose their neuroprotective and supportive functions, microglia proliferate, and produce reactive oxygen species, IL-1β, and TNFα. Heparin inhibits the thrombin generation and suppresses EAE. Platelets play an important role too. Indeed, in the acute phase of the disease, they begin the inflammatory response in the central nervous system by producing of IL-1alpha and triggering and amplifying the immune response. Their depletion, on the contrary, ameliorates the course of EAE. Finally, it has been proven that the use of several anticoagulant agents can successfully improve EAE. Altogether, these studies highlight the role of the coagulation pathway in the pathophysiology of MS and suggest possible therapeutic targets that may complement existing treatments

ESCPE-1 mediates retrograde endosomal sorting of the SARS-CoV-2 host factor Neuropilin-1

Endosomal sorting maintains cellular homeostasis by recycling transmembrane proteins and associated proteins and lipids (termed “cargoes”) from the endosomal network to multiple subcellular destinations, including retrograde traffic to the trans-Golgi network (TGN). Viral and bacterial pathogens subvert retrograde trafficking machinery to facilitate infectivity. Here, we develop a proteomic screen to identify retrograde cargo proteins of the endosomal SNX-BAR sorting complex promoting exit 1 (ESCPE-1). Using this methodology, we identify Neuropilin-1 (NRP1), a recently characterized host factor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, as a cargo directly bound and trafficked by ESCPE-1. ESCPE-1 mediates retrograde trafficking of engineered nanoparticles functionalized with the NRP1-interacting peptide of the SARS-CoV-2 spike (S) protein. CRISPR-Cas9 deletion of ESCPE-1 subunits reduces SARS-CoV-2 infection levels in cell culture. ESCPE-1 sorting of NRP1 may therefore play a role in the intracellular membrane trafficking of NRP1-interacting viruses such as SARS-CoV-2.ISSN:0027-8424ISSN:1091-649

Neuropilin-1 is a host factor for SARS-CoV-2 infection

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), uses the viral spike (S) protein for host cell attachment and entry. The host protease furin cleaves the full-length precursor S glycoprotein into two associated polypeptides: S1 and S2. Cleavage of S generates a polybasic Arg-Arg-Ala-Arg carboxyl-terminal sequence on S1, which conforms to a C-end rule (CendR) motif that binds to cell surface neuropilin-1 (NRP1) and NRP2 receptors. We used x-ray crystallography and biochemical approaches to show that the S1 CendR motif directly bound NRP1. Blocking this interaction by RNA interference or selective inhibitors reduced SARS-CoV-2 entry and infectivity in cell culture. NRP1 thus serves as a host factor for SARS-CoV-2 infection and may potentially provide a therapeutic target for COVID-19. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the coronavirus responsible for the current coronavirus disease 2019 (COVID-19) pandemic (1, 2). A marked difference between the spike (S) protein of SARS-CoV-2 and SARS-CoV is the presence, in the former, of a polybasic sequence motif, Arg-Arg-Ala-Arg (RRAR), at the S1/S2 boundary. It provides a cleavage site for a host proprotein convertase, furin (3–5) (fig. S1A). The resulting two proteins, S1 and S2, remain noncovalently associated, with the serine protease TMPRSS2 further priming S2 (6). Furin-mediated processing increases infectivity and affects the tropism of SARS-CoV-2, whereas furin inhibition diminishes SARS-CoV-2 entry, and deletion of the polybasic site in the S protein reduces syncytia formation in cell culture (3–5, 7). The C terminus of the S1 protein generated by furin cleavage has an amino acid sequence (682RRAR685) that conforms to a [R/K]XX[R/K] motif, termed the “C-end rule” (CendR) (fig. S1B) (8). CendR peptides bind to neuropilin-1 (NRP1) and NRP2, transmembrane receptors that regulate pleiotropic biological processes, including axon guidance, angiogenesis, and vascular permeability (8–10). To explore the possibility that the SARS-CoV-2 S1 protein may associate with neuropilins, we generated a green fluorescent protein (GFP)–tagged S1 construct (GFP-S1) (fig. S1C). When expressed in human embryonic kidney 293T (HEK293T) cells engineered to express the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2), GFP-S1 immunoprecipitated endogenous NRP1 and ACE2 (Fig. 1A). We transiently coexpressed NRP1-mCherry and either GFP-S1 or GFP-S1 ΔRRAR (a deletion of the terminal 682RRAR685 residues) in HEK293T cells. NRP1 immunoprecipitated the S1 protein, and deletion of the CendR motif reduced this association (Fig. 1B). Comparable binding was also observed with mCherry-NRP2, a receptor with high homology to NRP1 (fig. S1, D and E). In both cases, residual binding was observed with the ΔRRAR mutant, indicating an additional CendR-independent association between neuropilins and the S1 protein