52 research outputs found

    Potential benefits of an adaptive forward collision warning system

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    Forward collision warning (FCW) systems can reduce rear-end vehicle collisions. However, if the presentation of warnings is perceived as mistimed, trust in the system is diminished and drivers become less likely to respond appropriately. In this driving simulator investigation, 45 drivers experienced two FCW systems: a non-adaptive and an adaptive FCW that adjusted the timing of its alarms according to each individual driver’s reaction time. Whilst all drivers benefited in terms of improved safety from both FCW systems, non-aggressive drivers (low sensation seeking, long followers) did not display a preference to the adaptive FCW over its non-adaptive equivalent. Furthermore, there was little evidence to suggest that the non-aggressive drivers’ performance differed with either system. Benefits of the adaptive system were demonstrated for aggressive drivers (high sensation seeking, short followers). Even though both systems reduced their likelihood of a crash to a similar extent, the aggressive drivers rated each FCW more poorly than their non-aggressive contemporaries. However, this group, with their greater risk of involvement in rear-end collisions, reported a preference for the adaptive system as they found it less irritating and stress-inducing. Achieving greater acceptance and hence likely use of a real system is fundamental to good quality FCW design

    Tissue graft rejection in mice

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    A liver-slice to kidney-bed grafting system was used to study the course of rejection of a specific tissue across various genetic barriers in inbred strains of mice. Rejection or survival, scored histologically at various times after grafting, demonstrated that multiple non H-2 differences cause rejection at least as rapidly as H-2 differences. Differences at the K end of the mouse major histocompatibility complex cause tissue rejection more rapidly than do differences at the D end of the complex. The latter differences cause chronic rejection similar to that found across several minor H locus barriers. The H-2 haplotype carried by the recipient or the strength of the H-2 antigens of the donor affect the survival time in liver tissue grafts. Studies employing this model system will contribute to the definition of different immunogenetic parameters affecting survival of various tissues in a genetically well-defined animal model.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46746/1/251_2005_Article_BF01576941.pd

    Large-scale discovery of novel genetic causes of developmental disorders

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    Despite three decades of successful, predominantly phenotype-driven discovery of the genetic causes of monogenic disorders1, up to half of children with severe developmental disorders of probable genetic origin remain without a genetic diagnosis. Particularly challenging are those disorders rare enough to have eluded recognition as a discrete clinical entity, those with highly variable clinical manifestations, and those that are difficult to distinguish from other, very similar, disorders. Here we demonstrate the power of using an unbiased genotype-driven approach2 to identify subsets of patients with similar disorders. By studying 1,133 children with severe, undiagnosed developmental disorders, and their parents, using a combination of exome sequencing3,4,5,6,7,8,9,10,11 and array-based detection of chromosomal rearrangements, we discovered 12 novel genes associated with developmental disorders. These newly implicated genes increase by 10% (from 28% to 31%) the proportion of children that could be diagnosed. Clustering of missense mutations in six of these newly implicated genes suggests that normal development is being perturbed by an activating or dominant-negative mechanism. Our findings demonstrate the value of adopting a comprehensive strategy, both genome-wide and nationwide, to elucidate the underlying causes of rare genetic disorders

    Consent in medicine Convergence and divergence in tradition

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    SIGLELD:83/30244(Consent) / BLDSC - British Library Document Supply CentreGBUnited Kingdo
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