The disabled set sail

International audienceSailing is not an activity that can easily be done with a handicap. Sailors typically need mobility to steer a boat. An Arduino-compatible CAN architecture for sailing applications is set to change that

An Arduino compatible CAN Bus architecture for sailing applications

International audienceThis paper describes a Controller Area Network (CAN) Bus architecture based on Arduino compatible boards, to be used as an alternative communication system for robotic applications. This combines both, the robustness of CAN and the accessibility of Arduino software. The architecture is developed here to improve a Navigational Assistance System, which was initially created for disabled people. The system is composed of Arduino compatible boards, wired with various sensors and actuators, and communicating with an Human Machine Interface (HMI), directly accessible via a mobile phone or a tablet running on the open-source operating system Android. Information is transferred through the CAN bus architecture between multiple nodes (i.e. Arduino compatible boards) and the implementation of a CAN bootloader allows the reconfiguration of the nodes directly through the bus. The aim is to create a generic system able to work in various kinds of situations, adaptable to all kinds of users, including persons with all sorts of disabilities. This work will result in a demonstrator on a Miniji for the WRSC 2013 and an entirely joystick controlled boat for single handed sailing

Système d'assistance à la navigation handivoile

International audienceCe projet, fruit d'une collaboration entre l'ENSTA-Bretagne et l'entreprise Splashelec vise à développer une Interface Homme-Machine (IHM) qui facilite la navigation par le biais de capteurs et d'un boîtier de commandes embarqué sur le bateau. Il se concrétise par la création d'une interface graphique directement accessible via un téléphone mobile pour pallier le manque de mobilité du navigateur

On the role of NOS1 ex1f-VNTR in ADHD – allelic, subgroup, and meta-analysis

Attention deficit/hyperactivity disorder (ADHD) is a heritable neurodevelopmental disorder featuring complex genetics with common and rare variants contributing to disease risk. In a high proportion of cases, ADHD does not remit during adolescence but persists into adulthood. Several studies suggest that NOS1, encoding nitric oxide synthase I, producing the gaseous neurotransmitter NO, is a candidate gene for (adult) ADHD. We here extended our analysis by increasing the original sample, adding two further samples from Norway and Spain, and conducted subgroup and co-morbidity analysis. Our previous finding held true in the extended sample, and also meta-analysis demonstrated an association of NOS1 ex1fVNTR short alleles with adult ADHD (aADHD). Association was restricted to females, as was the case in the discovery sample. Subgroup analysis on the single allele level suggested that the repeat allele caused the association. Regarding subgroups, we found that NOS1 was associated with the hyperactive/impulsive ADHD subtype, but not to pure inattention. In terms of comorbidity, major depression, anxiety disorders, cluster C personality disorders and migraine were associated with short repeats, in particular the repeat allele. Also, short allele carriers had significantly lower IQ. Finally, we again demonstrated an influence of the repeat on gene expression in human post-mortem brain samples. These data validate the role of NOS-I in hyperactive/impulsive phenotypes and call for further studies into the neurobiological underpinnings of this association.PostprintPeer reviewe

Evolutionary Analysis of Mitogenomes from Parasitic and Free-Living Flatworms

Copyright: © 2015 Solà et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The attached file is the published version of the article

A conditionally replicating adenovirus with strict selectivity in killing cells expressing epidermal growth factor receptor

AbstractVirotherapy of cancer using oncolytic adenoviruses has shown promise in both preclinical and clinical settings. One important challenge to reach the full therapeutic potential of oncolytic adenoviruses is accomplishing efficient infection of cancer cells and avoiding uptake by normal tissue through tropism modification. Towards this goal, we constructed and characterized an oncolytic adenovirus, carrying mutated capsid proteins to abolish the promiscuous adenovirus native tropism and encoding a bispecific adapter molecule to target the virus to the epidermal growth factor receptor (EGFR). The new virus displayed a highly selective targeting profile, with reduced infection of EGFR-negative cells and efficient killing of EGFR-positive cancer cells including primary EGFR-positive osteosarcoma cells that are refractory to infection by conventional adenoviruses. Our method to modify adenovirus tropism might thus be useful to design new oncolytic adenoviruses for more effective treatment of cancer