An Ontological Approach to Inform HMI Designs for Minimizing Driver Distractions with ADAS

ADAS (Advanced Driver Assistance Systems) are in-vehicle systems designed to enhance driving safety and efficiency as well as comfort for drivers in the driving process. Recent studies have noticed that when Human Machine Interface (HMI) is not designed properly, an ADAS can cause distraction which would affect its usage and even lead to safety issues. Current understanding of these issues is limited to the context-dependent nature of such systems. This paper reports the development of a holistic conceptualisation of how drivers interact with ADAS and how such interaction could lead to potential distraction. This is done taking an ontological approach to contextualise the potential distraction, driving tasks and user interactions centred on the use of ADAS. Example scenarios are also given to demonstrate how the developed ontology can be used to deduce rules for identifying distraction from ADAS and informing future designs

Evolutionary approaches to neural control of rolling, walking, swimming and flying animats or robots

This article describes past and current research efforts in evolutionary robotics that have been carried out at the AnimatLab, Paris. Such approaches entail using an artificial selection process to automatically generate developmental programs for neural networks that control rolling, walking, swimming and flying animats or robots. Basically, they complement the underlying evolutionary process with a developmental procedure – in order hopefully to reduce the size of the genotypic space that is explored – and they occasionally call on an incremental approach, in order to capitalize upon solutions to simpler problems so as to devise solutions to more complex problems. This article successively outlines the historical background of our research, the evolutionary paradigm on which it relies, and the various results obtained so far. It also discusses the potentialities and limitations of the approach and indicates directions for future work

Effective countermeasure against poisoning by organophosphorus insecticides and nerve agents

The nerve agents soman, sarin, VX, and tabun are deadly organophosphorus (OP) compounds chemically related to OP insecticides. Most of their acute toxicity results from the irreversible inhibition of acetylcholinesterase (AChE), the enzyme that inactivates the neurotransmitter acetylcholine. The limitations of available therapies against OP poisoning are well recognized, and more effective antidotes are needed. Here, we demonstrate that galantamine, a reversible and centrally acting AChE inhibitor approved for treatment of mild to moderate Alzheimer’s disease, protects guinea pigs from the acute toxicity of lethal doses of the nerve agents soman and sarin, and of paraoxon, the active metabolite of the insecticide parathion. In combination with atropine, a single dose of galantamine administered before or soon after acute exposure to lethal doses of soman, sarin, or paraoxon effectively and safely counteracted their toxicity. Doses of galantamine needed to protect guinea pigs fully against the lethality of OPs were well tolerated. In preventing the lethality of nerve agents, galantamine was far more effective than pyridostigmine, a peripherally acting AChE inhibitor, and it was less toxic than huperzine, a centrally acting AChE inhibitor. Thus, a galantamine-based therapy emerges as an effective and safe countermeasure against OP poisoning

Deletion of a Cation Transporter Promotes Lysis in Streptococcus pneumoniae ▿ †

Streptococcus pneumoniae is a significant human pathogen which causes respiratory and serious invasive diseases. Mg2+ is essential for life, and its concentration varies throughout the human body. Magnesium uptake plays an important role in the virulence of many bacterial pathogens. To study the Mg2+ uptake of S. pneumoniae strain D39, a mutant was generated in SPD1383, a P-type ATPase with homology to the Salmonella Mg2+ transporter MgtA, which has also been shown to be a Ca2+ exporter in strain TIGR4. Under low-Ca2+ conditions, mutation led to a growth defect in complex medium and the gene was nearly essential for growth under low-Mg2+ conditions. Addition of Mg2+ restored the normal growth of the mutant in all cases, but the addition of other divalent cations had no effect. Addition of Ca2+, Mn2+, and Zn2+ in the presence of high Mg2+ concentrations inhibited restoration of growth. The mutant was unable to proliferate in blood, which was also alleviated by the addition of Mg2+. The protein was located in the membrane and produced in various S. pneumoniae strains and pathogenic streptococcal species. Surprisingly, mutation of the gene led to an elevated toxicity for endothelial cells. This was caused by an increased amount of pneumolysin in the medium, mediated by elevated lysis of the mutant. Thus, in this study, we uncovered a role for SPD1383 in Mg2+ uptake and hypothesize that the protein is a Mg2+/Ca2+ antiporter. Furthermore, a disturbance in Mg2+ homeostasis seems to promote lysis of S. pneumoniae