466 research outputs found

    Method and theory in the psychology of art

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    The unsatisfactory state of the psychology of art as a field of enquiry is analysed and two explanations are offered. The current state of psychology is also analysed and recommendations for change are made which should also improve the psychology of art, particularly in terms of effectiveness and relevance. This is followed by a detailed discussion of three major approaches to the subject, viz. Psycho-analysis, Gestalt psychology and experimental aesthetics. The empirical approach is further analysed in terms of the specific problems of aesthetic measurement. Certain procedures and kinds of measurement are strongly discouraged, whereas other forms are encouraged. The ideas of the preceding four chapters are integrated in chapter five within the frame-work of implicit aesthetic theories, which can structure both the individual's and a culture's encounter with art. In addition it can be used to structure the field of enquiry, particularly with reference to the model of aesthetic perception which is discussed in chapter five. In general, an enlightened empiricism is called for which is based on a model of man akin to that of 'the man in the street'. The psychology of art should deal directly with the phenomenal experience of real works of art. To this end introspection is regarded as an indispensible source of hypotheses which can be tested within an empirical framework. It is unlikely that problems in psychological aesthetics can be resolved except through multilevel, multi-disciplinary explanations. The next four chapters contain discussions of major topics in the psychology of art, viz. the structure of aesthetic reactions; the influences and determinants of aesthetic reactions; the development of aesthetic appreciation; and the problem of meaning in visual art. The final chapter presents a summary and overview.<p

    Parameterized Directed kk-Chinese Postman Problem and kk Arc-Disjoint Cycles Problem on Euler Digraphs

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    In the Directed kk-Chinese Postman Problem (kk-DCPP), we are given a connected weighted digraph GG and asked to find kk non-empty closed directed walks covering all arcs of GG such that the total weight of the walks is minimum. Gutin, Muciaccia and Yeo (Theor. Comput. Sci. 513 (2013) 124--128) asked for the parameterized complexity of kk-DCPP when kk is the parameter. We prove that the kk-DCPP is fixed-parameter tractable. We also consider a related problem of finding kk arc-disjoint directed cycles in an Euler digraph, parameterized by kk. Slivkins (ESA 2003) showed that this problem is W[1]-hard for general digraphs. Generalizing another result by Slivkins, we prove that the problem is fixed-parameter tractable for Euler digraphs. The corresponding problem on vertex-disjoint cycles in Euler digraphs remains W[1]-hard even for Euler digraphs

    Can clinical audits be enhanced by pathway simulation and machine learning? An example from the acute stroke pathway

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    OBJECTIVE: To evaluate the application of clinical pathway simulation in machine learning, using clinical audit data, in order to identify key drivers for improving use and speed of thrombolysis at individual hospitals

    Dopamine Augmented Rehabilitation in Stroke (DARS): a multicentre double-blind, randomised controlled trial of co-careldopa compared with placebo, in addition to routine NHS occupational and physical therapy, delivered early after stroke on functional recovery

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    BACKGROUND: Dopamine is a key modulator of striatal function and learning, and may improve motor recovery after stroke. Seven small trials of dopamine agonists after stroke have provided equivocal evidence of the clinical effectiveness of dopamine agonists in improving motor recovery. DESIGN: Dopamine Augmented Rehabilitation in Stroke was a multicentre, randomised, double-blind, placebo-controlled trial with stroke patients randomised to receive 6 weeks of co-careldopa (Sinemet®, Merck Sharp & Dohme Ltd) or placebo in combination with occupational and physical rehabilitation. METHODS: The primary outcome measure was the proportion of patients walking independently at 8 weeks [Rivermead Mobility Index (RMI) score of ≥ 7 points and ‘yes’ to item 7 on the RMI]. Secondary outcome measures assessed physical functioning, pain, cognition, mood, fatigue and carer burden at 8 weeks, 6 months and 12 months. RESULTS: Between May 2011 and March 2014, 593 patients (mean age 68.5 years) and 165 carers (mean age 59.7 years) were recruited from stroke rehabilitation units; 308 patients were randomised to co-careldopa and 285 to placebo at a median of 15 days following stroke onset. The study drug was to be taken 45–60 minutes before therapy, which included motor activities (mean 23.2 and 24.8 sessions in the co-careldopa and placebo groups, respectively). The mean number of investigational medicinal product doses taken was 20.6 in the co-careldopa group and 22.4 in the placebo group. Ability to walk independently was not improved at 8 weeks [40.6% (co-careldopa) vs. 44.6% (placebo); odds ratio 0.78, 95% confidence interval (CI) 0.53 to 1.15], 6 months [51.6% (co-careldopa) vs. 53.3% (placebo)] or 12 months [51.6% (co-careldopa) vs. 56.8% (placebo)]. There were no significant differences for Barthel Index, Nottingham Extended Activities of Daily Living, ABILHAND Manual Ability Measure or Modified Rankin Scale, pain or fatigue at any time point. Montreal Cognitive Assessment scores did not significantly differ; the majority of participants had cognitive impairment at baseline, which improved during 12 months’ follow-up. No difference was observed in General Health Questionnaire 12-item version scores between groups at 8 weeks and 12 months but, at 6 months, those in the co-careldopa group reported significantly better general health [mean difference (MD) –1.33, 95% CI –2.57 to –0.10]. Mortality at 12 months was not significantly different. Carers in the placebo group reported significantly greater burden at 6 months (MD 5.05, 95% CI 0.10 to 10.01) and 12 months (MD 7.52, 95% CI 1.87 to 13.18). CONCLUSION: Co-careldopa in addition to routine NHS occupational and physical therapy is not clinically effective or cost-effective in improving walking, physical functioning, mood or cognition following stroke. We recommend further research to develop imaging and clinical markers that would allow identification of promising drug therapies that would enhance motor therapy in improving walking ability and arm function. Further research is needed to compare strategies of giving drug therapy intermittently immediately prior to therapy sessions or as continuous background daily administration. LIMITATIONS: In total, 10.3% of patients were lost to follow-up at 8 weeks and < 10% of patients met the strict per-protocol definition. Despite this, the findings are robust and generalisable to patients with limited mobility in the first few weeks after stroke. TRIAL REGISTRATION: Current Controlled Trials ISRCTN99643613. FUNDING: This project was funded by the Efficacy and Mechanism Evaluation programme, a Medical Research Council and National Institute for Health Research partnership

    Efficacy and safety of co-careldopa as an add-on therapy to occupational and physical therapy in patients after stroke (DARS): a randomised, double-blind, placebo controlled trial

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    Background Dopamine is a key modulator of striatal function and learning and might improve motor recovery after stroke. Previous small trials of dopamine agonists after stroke provide equivocal evidence of effectiveness on improving motor recovery. We aimed to assess the safety and efficacy of co-careldopa plus routine occupational and physical therapy during early rehabilitation after stroke. Methods This double-blind, multicentre, randomised controlled trial of co-careldopa versus placebo in addition to routine NHS occupational and physical therapy was done at 51 UK NHS acute inpatient stroke rehabilitation services. We recruited patients with new or recurrent clinically diagnosed ischaemic or haemorrhagic (excluding subarachnoid haemorrhage) stroke 5–42 days before randomisation, who were unable to walk 10 m or more, had a score of less than 7 points on the Rivermead Mobility Index, were expected to need rehabilitation, and were able to access rehabilitation after discharge from hospital. Participants were assigned (1:1) using stratified random blocks to receive 6 weeks of oral co-careldopa or matched placebo in addition to routine NHS physiotherapy and occupational therapy. The initial two doses of co-careldopa were 62·5 mg (50 mg of levodopa and 12·5 mg of carbidopa) and the remaining doses were 125 mg (100 mg of levodopa and 25 mg of carbidopa). Participants were required to take a single oral tablet 45–60 min before physiotherapy or occupational therapy session. The primary outcome was ability to walk independently, defined as a Rivermead Mobility Index score of 7 or more, at 8 weeks. Primary and safety analyses were done in the intention-to-treat population. The trial is registered on the ISRCTN registry, number ISRCTN99643613.Findings Between May 30, 2011, and March 28, 2014, of 1574 patients found eligible, 593 (mean age 68·5 years) were randomly assigned to either the co-careldopa group (n=308) or to the placebo group (n=285), on an average 18 days after stroke onset. Primary outcome data were available for all 593 patients. We found no evidence that the ability to walk independently improved with co-careldopa (125 [41%] of 308 patients) compared with placebo (127 [45%] of 285 patients; odds ratio 0·78 [95% CI 0·53–1·15]) at 8 weeks. Mortality at 12 months did not differ between the two groups (22 [7%] vs 17 [6%]). Serious adverse events were largely similar between groups. Vomiting during therapy sessions, after taking the study drug, was the most frequent adverse event and was more frequent in the co-careldopa group than the placebo group (19 [6·2%] vs 9 [3·2%]).Interpretation Co-careldopa in addition to routine occupational and physical therapy does not seem to improve walking after stroke. Further research might identify subgroups of patients with stroke who could benefit from dopaminergic therapy at different doses or times after stroke with more intensive motor therap

    Morphological characteristics of motor neurons do not determine their relative susceptibility to degeneration in a mouse model of severe spinal muscular atrophy

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    Spinal muscular atrophy (SMA) is a leading genetic cause of infant mortality, resulting primarily from the degeneration and loss of lower motor neurons. Studies using mouse models of SMA have revealed widespread heterogeneity in the susceptibility of individual motor neurons to neurodegeneration, but the underlying reasons remain unclear. Data from related motor neuron diseases, such as amyotrophic lateral sclerosis (ALS), suggest that morphological properties of motor neurons may regulate susceptibility: in ALS larger motor units innervating fast-twitch muscles degenerate first. We therefore set out to determine whether intrinsic morphological characteristics of motor neurons influenced their relative vulnerability to SMA. Motor neuron vulnerability was mapped across 10 muscle groups in SMA mice. Neither the position of the muscle in the body, nor the fibre type of the muscle innervated, influenced susceptibility. Morphological properties of vulnerable and disease-resistant motor neurons were then determined from single motor units reconstructed in Thy.1-YFP-H mice. None of the parameters we investigated in healthy young adult mice - including motor unit size, motor unit arbor length, branching patterns, motor endplate size, developmental pruning and numbers of terminal Schwann cells at neuromuscular junctions - correlated with vulnerability. We conclude that morphological characteristics of motor neurons are not a major determinant of disease-susceptibility in SMA, in stark contrast to related forms of motor neuron disease such as ALS. This suggests that subtle molecular differences between motor neurons, or extrinsic factors arising from other cell types, are more likely to determine relative susceptibility in SMA

    Observations of the cold wake of Typhoon Fanapi (2010)

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    Author Posting. © American Geophysical Union, 2013. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geophysical Research Letters 40 (2013): 316–321, doi:10.1029/2012GL054282.Several tens of thousands of temperature profiles are used to investigate the thermal evolution of the cold wake of Typhoon Fanapi, 2010. Typhoon Fanapi formed a cold wake in the Western North Pacific Ocean on 18 September characterized by a mixed layer that was >2.5 °C cooler than the surrounding water, and extending to >80 m, twice as deep as the preexisting mixed layer. The initial cold wake became capped after 4 days as a warm, thin surface layer formed. The thickness of the capped wake, defined as the 26 °C–27 °C layer, decreased, approaching the background thickness of this layer with an e-folding time of 23 days, almost twice the e-folding lifetime of the Sea Surface Temperature (SST) cold wake (12 days). The wake was advected several hundreds of kilometers from the storm track by a preexisting mesoscale eddy. The observations reveal new intricacies of cold wake evolution and demonstrate the challenges of describing the thermal structure of the upper ocean using sea surface information alone.This work is primarily supported by the U.S. Office of Naval Research, with additional support from the National Science Foundation and the National Science Council, Taiwan

    Typhoon-ocean interaction in the western North Pacific : Part 1

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    Author Posting. © The Oceanography Society, 2011. This article is posted here by permission of The Oceanography Society for personal use, not for redistribution. The definitive version was published in Oceanography 24 no. 4 (2011): 24–31, doi:10.5670/oceanog.2011.91.The application of new technologies has allowed oceanographers and meteorologists to study the ocean beneath typhoons in detail. Recent studies in the western Pacific Ocean reveal new insights into the influence of the ocean on typhoon intensity.This work is supported by grants from the Office of Naval Research, N00014- 10-WX-20203 (Black), N00014-08-1- 0656 (Centurioni), N00014-08-1-0577 (D’Asaro), N00014-09-1-0816 (D’Asaro), N00014-10-WX-21335 (Harr), N00014-08-1-0614 (Jayne), N00014- 09-1-0133 (Lee), N00014-08-1-0560 (Lien), N00014-10-1-0313 (student support), N00014-08-1-0658 (Rainville), N00014-08-1-0560 (Sanford); the National Oceanic and Atmospheric Administration NA17RJ1231 (Centurioni); and the National Science Foundation OCE0549887 (D’Asaro)
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