A Study of Deep Learning Robustness Against Computation Failures

For many types of integrated circuits, accepting larger failure rates in computations can be used to improve energy efficiency. We study the performance of faulty implementations of certain deep neural networks based on pessimistic and optimistic models of the effect of hardware faults. After identifying the impact of hyperparameters such as the number of layers on robustness, we study the ability of the network to compensate for computational failures through an increase of the network size. We show that some networks can achieve equivalent performance under faulty implementations, and quantify the required increase in computational complexity

Analyse du régime de conservation des milieux humides instauré par la Loi concernant la conservation des milieux humides et hydriques en vertu de son objectif d'aucune perte nette

En 2017, le Québec adopta la Loi concernant la conservation des milieux humides et hydriques. L’objectif principal de cette loi est d’instaurer un régime de conservation des milieux humides et hydriques visant le principe d’aucune perte nette. C’est dire que tout impact découlant d’un projet sur ces milieux devra être compensé. Considérant que la conservation et la restauration des milieux humides sont différentes de celles des milieux hydriques, cet essai s’intéresse exclusivement au premier type de milieux. Le gouvernement québécois désire les protéger, car ces derniers supportent une portion importante de la biodiversité du Québec. Ils remplissent également de nombreuses fonctions écosystémiques, notamment la protection contre les inondations et la recharge des nappes phréatiques. L’objectif de cet essai est l’analyse du régime de protection des milieux humides mis en place par la Loi concernant la conservation des milieux humides et hydriques en vertu de son objectif d’aucune perte nette. Pour se faire, une analyse approfondie des changements législatifs instaurés par la Loi concernant la conservation des milieux humides et hydriques est réalisée. Par la suite, de manière à soutenir l’analyse, trois autres modèles de conservation des milieux humides sont présentés. Il s’agit du modèle états-unien, ontarien ainsi que celui promu par l’Union internationale pour la conservation de la nature. L’analyse de ces trois modèles et celle de la littérature scientifique s’y intéressant permettent de soulever des points de vigie relatifs au nouveau régime de conservation des milieux humides. Tout d’abord, il semble incertain que le nouveau régime de conservation des milieux humides permette l’atteinte d’aucune perte nette. Plus spécifiquement, il est probable que ce dernier n’endigue point les pertes de biodiversité et de fonctions écosystémiques. Ensuite, l’analyse révèle que l’absence de lignes directrices orientant les efforts de conservation nuira sûrement à l’efficacité du nouveau régime. De plus, il semble nécessaire d’intégrer au processus de compensation les incertitudes relatives à la restauration d’habitats. Finalement, il est essentiel que le Québec applique plus rigoureusement la hiérarchie d’atténuation de manière à ce que la majorité des impacts touchant les milieux humides soit évitée. En conclusion, les changements mis en place par la Loi concernant la conservation des milieux humides et hydriques auront sans contredit des impacts positifs sur la conservation des milieux humides. Toutefois, dans sa forme actuelle, il semble incertain que la loi atteigne son objectif d’aucune perte nette

Energy homeostasis in leptin deficient Lep^(ob/ob) mice

Maintenance of reduced body weight is associated both with reduced energy expenditure per unit metabolic mass and increased hunger in mice and humans. Lowered circulating leptin concentration, due to decreased fat mass, provides a primary signal for this response. However, leptin deficient (Lepob/ob) mice (and leptin receptor deficient Zucker rats) reduce energy expenditure following weight reduction by a necessarily non-leptin dependent mechanisms. To identify these mechanisms, Lepob/ob mice were fed ad libitum (AL group; n = 21) or restricted to 3 kilocalories of chow per day (CR group, n = 21). After losing 20% of initial weight (in approximately 2 weeks), the CR mice were stabilized at 80% of initial body weight for two weeks by titrated refeeding, and then released from food restriction. CR mice conserved energy (-17% below predicted based on body mass and composition during the day; -52% at night); and, when released to ad libitum feeding, CR mice regained fat and lean mass (to AL levels) within 5 weeks. CR mice did so while their ad libitum caloric intake was equal to that of the AL animals. While calorically restricted, the CR mice had a significantly lower respiratory exchange ratio (RER = 0.89) compared to AL (0.94); after release to ad libitum feeding, RER was significantly higher (1.03) than in the AL group (0.93), consistent with their anabolic state. These results confirm that, in congenitally leptin deficient animals, leptin is not required for compensatory reduction in energy expenditure accompanying weight loss, but suggest that the hyperphagia of the weight-reduced state is leptin-dependent

Model-based verification of a security protocol for conditional access to services

peer reviewedWe use the formal language LOTOS to specify and verify the robustness of the Equicrypt protocol under design in the European OKAPI project for conditional access to multimedia services. We state some desired security properties and formalize them. We describe a generic intruder process and its modelling, and show that some properties are falsified in the presence of this intruder. The diagnostic sequences can be used almost directly to exhibit the scenarios of possible attacks on the protocol. Finally, we propose an improvement of the protocol which satisfies our properties

DMSO increases efficiency of genome editing at two non-coding loci

Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/CRISPR-associated protein-9 (Cas9) has become the tool of choice for genome editing. Despite the fact that it has evolved as a highly efficient means to edit/replace coding sequence, CRISPR/Cas9 efficiency for “clean” editing of non-coding DNA remains low. We set out to introduce a single base-pair substitution in two intronic SNPs at the FTO locus without altering nearby non-coding sequence. Substitution efficiency increased up to 10-fold by treatment of human embryonic stem cells (ESC) with non-toxic levels of DMSO (1%) before CRISPR/Cas9 delivery. Treatment with DMSO did not result in CRISPR/Cas9 off-target effects or compromise the chromosomal stability of the ESC. Twenty-four hour treatment of human ESC with DMSO before CRISPR/Cas9 delivery may prove a simple means to increase editing efficiency of non-coding DNA without incorporation of undesirable mutations

MKID development for SuperSpec: an on-chip, mm-wave, filter-bank spectrometer

SuperSpec is an ultra-compact spectrometer-on-a-chip for millimeter and submillimeter wavelength astronomy. Its very small size, wide spectral bandwidth, and highly multiplexed readout will enable construction of powerful multibeam spectrometers for high-redshift observations. The spectrometer consists of a horn-coupled microstrip feedline, a bank of narrow-band superconducting resonator filters that provide spectral selectivity, and Kinetic Inductance Detectors (KIDs) that detect the power admitted by each filter resonator. The design is realized using thin-film lithographic structures on a silicon wafer. The mm-wave microstrip feedline and spectral filters of the first prototype are designed to operate in the band from 195-310 GHz and are fabricated from niobium with at Tc of 9.2K. The KIDs are designed to operate at hundreds of MHz and are fabricated from titanium nitride with a Tc of 2K. Radiation incident on the horn travels along the mm-wave microstrip, passes through the frequency-selective filter, and is finally absorbed by the corresponding KID where it causes a measurable shift in the resonant frequency. In this proceedings, we present the design of the KIDs employed in SuperSpec and the results of initial laboratory testing of a prototype device. We will also briefly describe the ongoing development of a demonstration instrument that will consist of two 500-channel, R=700 spectrometers, one operating in the 1-mm atmospheric window and the other covering the 650 and 850 micron bands.Comment: As submitted, except that "in prep" references have been update

ILDR2: An Endoplasmic Reticulum Resident Molecule Mediating Hepatic Lipid Homeostasis

Ildr2, a modifier of diabetes susceptibility in obese mice, is expressed in most organs, including islets and hypothalamus, with reduced levels in livers of diabetes-susceptible B6.DBA mice congenic for a 1.8 Mb interval of Chromosome 1. In hepatoma and neuronal cells, ILDR2 is primarily located in the endoplasmic reticulum membrane. We used adenovirus vectors that express shRNA or are driven by the CMV promoter, respectively, to knockdown or overexpress Ildr2 in livers of wild type and ob/ob mice. Livers in knockdown mice were steatotic, with increased hepatic and circulating triglycerides and total cholesterol. Increased circulating VLDL, without reduction in triglyceride clearance suggests an effect of reduced hepatic ILDR2 on hepatic cholesterol clearance. In animals that overexpress Ildr2, hepatic triglyceride and total cholesterol levels were reduced, and strikingly so in ob/ob mice. There were no significant changes in body weight, energy expenditure or glucose/insulin homeostasis in knockdown or overexpressing mice. Knockdown mice showed reduced expression of genes mediating synthesis and oxidation of hepatic lipids, suggesting secondary suppression in response to increased hepatic lipid content. In Ildr2-overexpressing ob/ob mice, in association with reduced liver fat content, levels of transcripts related to neutral lipid synthesis and cholesterol were increased, suggesting “relief” of the secondary suppression imposed by lipid accumulation. Considering the fixed location of ILDR2 in the endoplasmic reticulum, we investigated the possible participation of ILDR2 in ER stress responses. In general, Ildr2 overexpression was associated with increases, and knockdown with decreases in levels of expression of molecular components of canonical ER stress pathways. We conclude that manipulation of Ildr2 expression in liver affects both lipid homeostasis and ER stress pathways. Given these reciprocal interactions, and the relatively extended time-course over which these studies were conducted, we cannot assign causal primacy to either the effects on hepatic lipid homeostasis or ER stress responses