Local-feature-based similarity measure for stochastic resonance in visual perception of spatially structured images

For images, stochastic resonance or useful-noise effects have previously been assessed with low-level pixel-based information measures. Such measures are not sensitive to coherent spatial structures usually existing in images. As a result, we show that such measures are not sufficient to properly account for stochastic resonance occurring in visual perception. We introduce higher-level similarity measures, inspired from visual perception, and based on local feature descriptors of scale invariant feature transform (SIFT) type. We demonstrate that such SIFT-based measures allow for an assessment of stochastic resonance that matches the visual perception of images with spatial structures. Constructive action of noise is registered in this way with both additive noise and multiplicative speckle noise. Speckle noise, with its grainy appearance, is particularly prone to introducing spurious spatial structures in images, and the stochastic resonance visually perceived and quantitatively assessed with SIFT-based measures is specially examined in this context

Automatic Detector of Abnormal EEG for Preterm Infants

Many of preterm babies suffer from neural disorders caused by birth complications. Hence, early prediction of neural disorders, in preterm infants, is extremely crucial for neuroprotective intervention. In this scope, the goal of this research was to propose an automatic way to study preterm babies Electroencephalograms (EEG). EEG were preprocessed and a time series of standard deviation was computed. These series were thresholded to detect Inter Burst Intervals (IBI). Features were extracted from bursts and IBI and were then classified as Abnormal or Normal using a Multiple Linear Regression. The method was successfully validated on a corpus of 100 infants with no early indication of brain injury. It was also implemented with a user-friendly interface using Java

An Aggregation Plateform for IoT-Based Healthcare: Illustration for Bioimpedancemetry, Temperature and Fatigue Level Monitoring

In this paper, we detail an in-home aggregation plateform for monitoring physiological parameters, and involving two objective physical sensors (bio-impedanceter and thermometer) and a subjective one (fatigue level perceived by the patient). This plateform uses modern IoT-related technologies such as embedded systems (Raspberry Pi and Arduino) and the MQTT communication protocol. Compared to many related works, monitoring is enterely achieved using a box as a central element, while the mobile device (tablet) is only used for controlling the acquisition procedure using a simple web browser, without any specific application. An example of a time stamped set of acquired data is shown, based on the in-home monitoring of healthy volunteers

A Multifunctional Interlayer for Solution Processed High Performance Indium Oxide Transistors

International audienceMultiple functionality of tungsten polyoxometalate (POM) has been achieved applying it as interfacial layer for solution processed high performance In 2 O 3 thin film transistors, which results in overall improvement of device performance. This approach not only reduces off-current of the device by more than two orders of magnitude, but also leads to a threshold voltage reduction, as well as significantly enhances the mobility through facilitated charge injection from the electrode to the active layer. Such a mechanism has been elucidated through morphological and spectroscopic studies

The V471A polymorphism in autophagy-related gene ATG7 modifies age at onset specifically in Italian Huntington disease patients

The cause of Huntington disease (HD) is a polyglutamine repeat expansion of more than 36 units in the huntingtin protein, which is inversely correlated with the age at onset of the disease. However, additional genetic factors are believed to modify the course and the age at onset of HD. Recently, we identified the V471A polymorphism in the autophagy-related gene ATG7, a key component of the autophagy pathway that plays an important role in HD pathogenesis, to be associated with the age at onset in a large group of European Huntington disease patients. To confirm this association in a second independent patient cohort, we analysed the ATG7 V471A polymorphism in additional 1,464 European HD patients of the “REGISTRY” cohort from the European Huntington Disease Network (EHDN). In the entire REGISTRY cohort we could not confirm a modifying effect of the ATG7 V471A polymorphism. However, analysing a modifying effect of ATG7 in these REGISTRY patients and in patients of our previous HD cohort according to their ethnic origin, we identified a significant effect of the ATG7 V471A polymorphism on the HD age at onset only in the Italian population (327 patients). In these Italian patients, the polymorphism is associated with a 6-years earlier disease onset and thus seems to have an aggravating effect. We could specify the role of ATG7 as a genetic modifier for HD particularly in the Italian population. This result affirms the modifying influence of the autophagic pathway on the course of HD, but also suggests population-specific modifying mechanisms in HD pathogenesis

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation