1,789 research outputs found

    Inflammatory bowel disease psychological support pilot reduces inflammatory bowel disease symptoms and improves psychological wellbeing

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    This prospective service evaluation aimed to determine if integrated psychological support for patients with inflammatory bowel disease (IBD) enhanced outcomes. 75 patients were assessed and treated by a specialist liaison psychiatric service between 2015 and 2017; 43 received psychiatric intervention alone, 32 were referred for psychological intervention by clinical health psychologist; 26 completed this. Pre–post data (n=15 available) included global impression, quality of life, and psychiatric and IBD symptom scores. Referrer/patient satisfaction and cost-effectiveness were retrospectively calculated. Psychological intervention led to reductions in IBD symptoms (ΔSIBD; p=0.003), alongside improvements in depression scores (ΔPHQ-9, p=0.006) and global impression (ΔCGI; p=0.046). Patient/referrer satisfaction was very high. Indicative data comparing service utilisation 1 year before and after engagement found reductions in outpatient appointments and in imaging. This small study suggests consideration of increased access to integrated psychological support services to improve outcomes and gather further evidence of efficacy

    A Theory of Cheap Control in Embodied Systems

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    We present a framework for designing cheap control architectures for embodied agents. Our derivation is guided by the classical problem of universal approximation, whereby we explore the possibility of exploiting the agent's embodiment for a new and more efficient universal approximation of behaviors generated by sensorimotor control. This embodied universal approximation is compared with the classical non-embodied universal approximation. To exemplify our approach, we present a detailed quantitative case study for policy models defined in terms of conditional restricted Boltzmann machines. In contrast to non-embodied universal approximation, which requires an exponential number of parameters, in the embodied setting we are able to generate all possible behaviors with a drastically smaller model, thus obtaining cheap universal approximation. We test and corroborate the theory experimentally with a six-legged walking machine. The experiments show that the sufficient controller complexity predicted by our theory is tight, which means that the theory has direct practical implications. Keywords: cheap design, embodiment, sensorimotor loop, universal approximation, conditional restricted Boltzmann machineComment: 27 pages, 10 figure

    Simulating actuator energy consumption for trajectory optimisation

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    This work aims to construct a high-speed simulation tool which is used to quantify the dynamic actuator power consumption of an aircraft in flight, for use within trajectory optimisation packages. The purpose is to evaluate the energy penalties of the flight control actuation system as an aircraft manoeuvre along any arbitrary trajectory. The advantage is that the approximations include major transient properties which previous steady state techniques could not capture. The output can be used to provide feedback to a trajectory optimisation process to help it compute the aircraft level optimality of any given flight path. The tool features a six degree of freedom dynamic model of an aircraft which is combined with low frequency functional electro-mechanical actuator models in order to estimate the major transient power demands. The actuator models interact with the aircraft using an aerodynamic load estimator which generates load forces on the actuators that vary as a function of flight condition and control surface demands. A total energy control system is applied for longitudinal control and a total heading control system is implemented to manage the lateral motion. The outer loop is closed using a simple waypoint following guidance system with turn anticipation and variable turn radius control. To test the model, a simple trajectory analysis is undertaken which quantifies a heading change executed with four different turn rates. The tool shows that the actuation system requires 12.8 times more electrical energy when performing a 90° turn with a radius of 400 m compared to 1000 m. A second test is performed to verify the model’s ability to track a longer trajectory under windy conditions

    Genome-wide dissection of globally emergent multi-drug resistant serotype 19A Streptococcus pneumoniae

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    <p>Abstract</p> <p>Background</p> <p>Emergence of multi-drug resistant (MDR) serotype 19A Streptococcus pneumoniae (SPN) is well-documented but causal factors remain unclear. Canadian SPN isolates (1993-2008, n = 11,083) were serotyped and <it>in vitro </it>susceptibility tested. A subset of MDR 19A were multi-locus sequence typed (MLST) and representative isolates' whole genomes sequenced.</p> <p>Results</p> <p>MDR 19A increased in the post-PCV7 era while 19F, 6B, and 23F concurrently declined. MLST of MDR 19A (<it>n </it>= 97) revealed that sequence type (ST) 320 predominated. ST320 was unique amongst MDR 19A in that its minimum inhibitory concentration (MIC) values for penicillin, amoxicillin, ceftriaxone, and erythromycin were higher than for other ST present amongst post-PCV7 MDR 19A. DNA sequencing revealed that alleles at key drug resistance loci <it>pbp2a</it>, <it>pbp2x</it>, <it>pbp2b</it>, <it>ermB</it>, <it>mefA/E</it>, and <it>tetM </it>were conserved between pre-PCV7 ST 320 19F and post-PCV7 ST 320 19A most likely due to a capsule switch recombination event. A genome wide comparison of MDR 19A ST320 with MDR 19F ST320 identified 822 unique SNPs in 19A, 61 of which were present in antimicrobial resistance genes and 100 in virulence factors.</p> <p>Conclusions</p> <p>Our results suggest a complex genetic picture where high-level drug resistance, vaccine selection pressure, and SPN mutational events have created a "perfect storm" for the emergence of MDR 19A.</p

    In Vivo Imaging of Vesicular Monoamine Transporters in Human Brain Using [ 11 C]Tetrabenazine and Positron Emission Tomography

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    The pharmacokinetics of [ 11 CJtetrabenazine, a high-affinity radioligand for the monoamine vesicular transporter, were determined in living human brain using in vivo imaging by positron emission tomography (PET). The radiotracer showed high brain uptake and rapid washout from all brain regions with relatively slower clearance from regions of highest concentrations of monoamine vesicular transporters (striatum), resulting in clear differential visualization of these structures at short intervals after injection (10–20 min). As the first human PET imaging study of a vesicular neurotransmitter transporter, these experiments demonstrate that external imaging of vesicular transporters forms a new and valuable approach to the in vivo quantification of monoaminergic neurons, with potential application to the in vivo study of neurodegenerative disorders such as Parkinson's disease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65743/1/j.1471-4159.1993.tb03521.x.pd

    The Toll→NFκB Signaling Pathway Mediates the Neuropathological Effects of the Human Alzheimer's Aβ42 Polypeptide in Drosophila

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    Alzheimer's (AD) is a progressive neurodegenerative disease that afflicts a significant fraction of older individuals. Although a proteolytic product of the Amyloid precursor protein, the Αβ42 polypeptide, has been directly implicated in the disease, the genes and biological pathways that are deployed during the process of Αβ42 induced neurodegeneration are not well understood and remain controversial. To identify genes and pathways that mediated Αβ42 induced neurodegeneration we took advantage of a Drosophila model for AD disease in which ectopically expressed human Αβ42 polypeptide induces cell death and tissue degeneration in the compound eye. One of the genes identified in our genetic screen is Toll (Tl). It encodes the receptor for the highly conserved Tl→NFkB innate immunity/inflammatory pathway and is a fly homolog of the mammalian Interleukin-1 (Ilk-1) receptor. We found that Tl loss-of-function mutations dominantly suppress the neuropathological effects of the Αβ42 polypeptide while gain-of-function mutations that increase receptor activity dominantly enhance them. Furthermore, we present evidence demonstrating that Tl and key downstream components of the innate immunity/inflammatory pathway play a central role in mediating the neuropathological activities of Αβ42. We show that the deleterious effects of Αβ42 can be suppressed by genetic manipulations of the Tl→NFkB pathway that downregulate signal transduction. Conversely, manipulations that upregulate signal transduction exacerbate the deleterious effects of Aβ42. Since postmortem studies have shown that the Ilk-1→NFkB innate immunity pathway is substantially upregulated in the brains of AD patients, the demonstration that the Tl→NFkB signaling actively promotes the process of Αβ42 induced cell death and tissue degeneration in flies points to possible therapeutic targets and strategies
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