Conversion of Artificial Recurrent Neural Networks to Spiking Neural Networks for Low-power Neuromorphic Hardware

In recent years the field of neuromorphic low-power systems that consume orders of magnitude less power gained significant momentum. However, their wider use is still hindered by the lack of algorithms that can harness the strengths of such architectures. While neuromorphic adaptations of representation learning algorithms are now emerging, efficient processing of temporal sequences or variable length-inputs remain difficult. Recurrent neural networks (RNN) are widely used in machine learning to solve a variety of sequence learning tasks. In this work we present a train-and-constrain methodology that enables the mapping of machine learned (Elman) RNNs on a substrate of spiking neurons, while being compatible with the capabilities of current and near-future neuromorphic systems. This "train-and-constrain" method consists of first training RNNs using backpropagation through time, then discretizing the weights and finally converting them to spiking RNNs by matching the responses of artificial neurons with those of the spiking neurons. We demonstrate our approach by mapping a natural language processing task (question classification), where we demonstrate the entire mapping process of the recurrent layer of the network on IBM's Neurosynaptic System "TrueNorth", a spike-based digital neuromorphic hardware architecture. TrueNorth imposes specific constraints on connectivity, neural and synaptic parameters. To satisfy these constraints, it was necessary to discretize the synaptic weights and neural activities to 16 levels, and to limit fan-in to 64 inputs. We find that short synaptic delays are sufficient to implement the dynamical (temporal) aspect of the RNN in the question classification task. The hardware-constrained model achieved 74% accuracy in question classification while using less than 0.025% of the cores on one TrueNorth chip, resulting in an estimated power consumption of ~17 uW

Factorized Computation: What the Neocortex Can Tell Us About the Future of Computing

ISSN:1662-518

Strongly Correlated Quantum Fluids: Ultracold Quantum Gases, Quantum Chromodynamic Plasmas, and Holographic Duality

Strongly correlated quantum fluids are phases of matter that are intrinsically quantum mechanical, and that do not have a simple description in terms of weakly interacting quasi-particles. Two systems that have recently attracted a great deal of interest are the quark-gluon plasma, a plasma of strongly interacting quarks and gluons produced in relativistic heavy ion collisions, and ultracold atomic Fermi gases, very dilute clouds of atomic gases confined in optical or magnetic traps. These systems differ by more than 20 orders of magnitude in temperature, but they were shown to exhibit very similar hydrodynamic flow. In particular, both fluids exhibit a robustly low shear viscosity to entropy density ratio which is characteristic of quantum fluids described by holographic duality, a mapping from strongly correlated quantum field theories to weakly curved higher dimensional classical gravity. This review explores the connection between these fields, and it also serves as an introduction to the Focus Issue of New Journal of Physics on Strongly Correlated Quantum Fluids: from Ultracold Quantum Gases to QCD Plasmas. The presentation is made accessible to the general physics reader and includes discussions of the latest research developments in all three areas.Comment: 138 pages, 25 figures, review associated with New Journal of Physics special issue "Focus on Strongly Correlated Quantum Fluids: from Ultracold Quantum Gases to QCD Plasmas" (http://iopscience.iop.org/1367-2630/focus/Focus%20on%20Strongly%20Correlated%20Quantum%20Fluids%20-%20from%20Ultracold%20Quantum%20Gases%20to%20QCD%20Plasmas

A search for charged massive long-lived particles

We report on a search for charged massive long-lived particles (CMLLPs), based on 5.2 fb$^{-1}$ of integrated luminosity collected with the D0 detector at the Fermilab Tevatron $p\bar{p}$ collider. We search for events in which one or more particles are reconstructed as muons but have speed and ionization energy loss $(dE/dx)$ inconsistent with muons produced in beam collisions. CMLLPs are predicted in several theories of physics beyond the standard model. We exclude pair-produced long-lived gaugino-like charginos below 267 GeV and higgsino-like charginos below 217 GeV at 95% C.L., as well as long-lived scalar top quarks with mass below 285 GeV.Comment: submitted to Phys. Rev. Letter

Mechanism-Based Screen for G1/S Checkpoint Activators Identifies a Selective Activator of EIF2AK3/PERK Signalling

Human cancers often contain genetic alterations that disable G1/S checkpoint control and loss of this checkpoint is thought to critically contribute to cancer generation by permitting inappropriate proliferation and distorting fate-driven cell cycle exit. The identification of cell permeable small molecules that activate the G1/S checkpoint may therefore represent a broadly applicable and clinically effective strategy for the treatment of cancer. Here we describe the identification of several novel small molecules that trigger G1/S checkpoint activation and characterise the mechanism of action for one, CCT020312, in detail. Transcriptional profiling by cDNA microarray combined with reverse genetics revealed phosphorylation of the eukaryotic initiation factor 2-alpha (EIF2A) through the eukaryotic translation initiation factor 2-alpha kinase 3 (EIF2AK3/PERK) as the mechanism of action of this compound. While EIF2AK3/PERK activation classically follows endoplasmic reticulum (ER) stress signalling that sets off a range of different cellular responses, CCT020312 does not trigger these other cellular responses but instead selectively elicits EIF2AK3/PERK signalling. Phosphorylation of EIF2A by EIF2A kinases is a known means to block protein translation and hence restriction point transit in G1, but further supports apoptosis in specific contexts. Significantly, EIF2AK3/PERK signalling has previously been linked to the resistance of cancer cells to multiple anticancer chemotherapeutic agents, including drugs that target the ubiquitin/proteasome pathway and taxanes. Consistent with such findings CCT020312 sensitizes cancer cells with defective taxane-induced EIF2A phosphorylation to paclitaxel treatment. Our work therefore identifies CCT020312 as a novel small molecule chemical tool for the selective activation of EIF2A-mediated translation control with utility for proof-of-concept applications in EIF2A-centered therapeutic approaches, and as a chemical starting point for pathway selective agent development. We demonstrate that consistent with its mode of action CCT020312 is capable of delivering potent, and EIF2AK3 selective, proliferation control and can act as a sensitizer to chemotherapy-associated stresses as elicited by taxanes

Clinicopathologic Features Associated With Having Four or More Metastatic Axillary Nodes in Breast Cancer Patients With a Positive Sentinel Lymph Node

The survival benefit of a completion axillary lymph node dissection (ALND) in patients after removal of a metastatic sentinel lymph node (SLN) is uncertain and is under study in ongoing clinical trials. The completion ALND remains necessary, however, for the identification of cases with at least four metastatic lymph nodes, in which extended-field locoregional and/or postmastectomy radiation will be recommended. Our goal was evaluate clinicopathologic features that might serve as surrogates for determining which patients with a positive SLN are likely or unlikely to belong to this high-risk subset.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41409/1/10434_2006_Article_9251.pd

Feasibility studies for the measurement of time-like proton electromagnetic form factors from p¯ p→ μ+μ- at P ¯ ANDA at FAIR

This paper reports on Monte Carlo simulation results for future measurements of the moduli of time-like proton electromagnetic form factors, | GE| and | GM| , using the p¯ p→ μ+μ- reaction at P ¯ ANDA (FAIR). The electromagnetic form factors are fundamental quantities parameterizing the electric and magnetic structure of hadrons. This work estimates the statistical and total accuracy with which the form factors can be measured at P ¯ ANDA , using an analysis of simulated data within the PandaRoot software framework. The most crucial background channel is p¯ p→ π+π-, due to the very similar behavior of muons and pions in the detector. The suppression factors are evaluated for this and all other relevant background channels at different values of antiproton beam momentum. The signal/background separation is based on a multivariate analysis, using the Boosted Decision Trees method. An expected background subtraction is included in this study, based on realistic angular distributions of the background contribution. Systematic uncertainties are considered and the relative total uncertainties of the form factor measurements are presented

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Measurement of W and Z boson production cross sections

DO has measured the inclusive production cross section of W and Z bosons in a sample of 13 pb$^{-1}$ of data collected at the Fermilab Tevatron. The cross sections, multiplied by their leptonic branching fractions, for production in pbar-p collisions at sqrt{s}=1.8 TeV are sigma_W*B(W->e nu) = 2.36+-0.02+-0.08+-0.13 nb, sigma_W*B(W->mu nu) = 2.09+-0.06+-0.22+-0.11 nb, sigma_Z*B(Z->e+ e-) = 0.218+-0.008+-0.008+-0.012 nb, and sigma_Z*B(Z->mu+ mu-) = 0.178+-0.022+-0.021+-0.009 nb, where the first uncertainty is statistical and the second systematic; the third reflects the uncertainty in the integrated luminosity. For the combined electron and muon analyses, we find sigma_W*B(W->l mu)/sigma_Z*B(Z->l+ l-) = 10.90+-0.52. Assuming standard model couplings, we use this result to determine the width of the W boson, and obtain Gamma(W) = 2.044+-0.097 GeV.Comment: 46 pages with 17 embedded figures, submitted to PRD, Run 1a result