210 research outputs found
Design as collective action
No full textIn this paper a model of the design process based on finite Markov processes is elaborated and extended in the context of a theory of collective action. The interpretation developed here is based on the notion that design is a process of social problem solving within a small group or collectivity, and specific comparisons between the Markov model and Coleman's (1966) theory of collective decisionmaking are thus possible. The paper is introduced by a brief summary of previous work in design methods, and previous presentations of the model by the author (Batty, 1974a; 1974b) are summarized. The main extension to this model involves disaggregating relationships within the design process into actor interests and control over factors or events, and this leads quite naturally to two associated Markov processes which are consistently and unambiguously related in the steady state. The model is then used to reinterpret Coleman's theory which is developed in terms of the value of control and power, and this leads to some oblique insights into the relationship between the two theories. To demonstrate the use of the model a problem of locating conservation areas in Waterloo County, Ontario, is simulated, with the emphasis on the speed of convergence of the process and the prior and posterior distributions of power in the system. A brief excursion into Monte Carlo simulation is presented to test whether or not the same results could be generated randomly; finally, conclusions for further research are drawn together.
The transcription and notation of Elizabeth Fry's journal 1780-1845
No full textThis thesis was submitted for the degree of Doctor of Philosophy and awarded by Brunel University.This thesis proposes to explain the production of Fry's journal and make available to researchers a full transcription of the autobiographical journal of Elizabeth Fry. This journal tells Fry's life story in an episodic diary format that encapsulates the last forty-eight years of her life. The justification for the production of the transcription and the motivation behind It: The thesis will investigate the importance of Fry's Journal in the evolution of the diary genre. It will justify the huge undertaking entailed in making a full transcription of Fry's journal and will discuss the condition of the journal books and their different locations. How these factors contributed to the delay in producing a transcription earlier will be considered. What motivated Fry to write her journal and what influenced her to continue the process unabated for all her adult life? The reasons Fry had originally given for her journal production changed as her journal evolved and her life priorities changed. I will investigate the destruction of Fry's early journal books and her reasoning behind such editorial interference and her motivation for keeping others. Finally this section will close with an analysis of Fry's journal in order to establish what class within the diary genre it belongs. Dyslexia and its effect on Fry's journal text and the editorial procedures adopted: This part of this thesis discusses the indicators of dyslexia within the journal text and their
effect on the journal's production. I explain the resulting methodology adopted to alleviate the destructive effect that dyslexia had on the journal text. I have limited the editorial interventions undertaken when producing the transcription as I wished to maintain the integrity of Fry's journal. The final part of the thesis evaluates Fry's journal by making a
comparison with a contemporary journal. The journal I used for comparison was written by
Deborah Darby, a woman who shared many of Fry's life experiences. This thesis will
establish Fry's journal as belonging to that elite group of great diarists that includes Pepys. The appendices: these consist of a short biography of Fry with a published work explaining her role in the founding of modern nursing. A glossary of Quakers and the Gurney family terminology and finally a bibliography and the first two books, from Fry's journal with notes
Motivational incentives and methylphenidate enhance electrophysiological correlates of error monitoring in children with attention deficit/hyperactivity disorder
No full textBackground
Children with attention deficit hyperactivity disorder (ADHD) are characterised by developmentally inappropriate levels of hyperactivity, impulsivity and/or inattention and are particularly impaired when performing tasks that require a high level of cognitive control. Methylphenidate (MPH) and motivational incentives may help improve cognitive control by enhancing the ability to monitor response accuracy and regulate performance accordingly.
Methods
Twenty-eight children with DSM-IV ADHD (combined type) aged 9–15 years and pairwise-matched typically developing children (CTRL) performed a go/no-go task in which the incentives attached to performance on no-go trials were manipulated. The ADHD group performed the task off and on their usual dose of MPH. CTRL children performed the task twice but were never medicated. EEG data were recorded simultaneously and two electrophysiological indices of error monitoring, the error-related negativity (ERN) and error positivity (Pe) were measured. Amplitudes of each ERP were compared between diagnostic groups (CTRL, ADHD), medication days (Off MPH, On MPH) and motivational conditions (baseline – low incentive, reward, response cost).
Results
Error rates were lower in the reward and response cost conditions compared with baseline across diagnostic groups and medication days. ERN and Pe amplitudes were significantly reduced in ADHD compared with CTRL, and were significantly enhanced by MPH. Incentives significantly increased ERN and Pe amplitudes in the ADHD group but had no effect in CTRL. The effects of incentives did not interact with the effects of MPH on either ERP. Effect sizes were computed and revealed larger effects of MPH than incentives on ERN and Pe amplitudes.
Conclusions
The findings reveal independent effects of motivational incentives and MPH on two electrophysiological markers of error monitoring in children with ADHD, suggesting that each may be important tools for enhancing or restoring cognitive control in these children
Building confidence about the academic journey
No full textWhile many research students may think they know the skills they need to develop to complete a doctoral degree, these may be entirely focused on the mechanical part of the process. For example, the need to read, research, gather information, conduct experiments or complete field work and write a thesis to defend the findings or thesis are all necessary for the journey. Yet many students may not be aware of the less tangible skills and knowledge that a research student must acquire, in terms of an awareness of, and adherence to, an academic culture. This chapter looks at the research journey as a master/apprentice model where both skills and culture are imparted to the student. Various tests must be passed along the way to prove the student has acquired the necessary academic proficiency to become a master or scholar. But they also must display the professional attributes, behaviour and codes of conduct required to become an academic. By recasting and explaining the steps of the research process, with its mandatory milestones in these terms, this chapter demystifies the process and explains the transformative steps and transferable skills that are required to achieve a doctorate. How, and where, to acquire these is also included
Task-related default mode network modulation and inhibitory control in ADHD: effects of motivation and methylphenidate
No full textBackground: Deficits characteristic of Attention Deficit/Hyperactivity Disorder (ADHD), including poor attention and inhibitory control, are at least partially alleviated by factors that increase engagement of attention, suggesting a hypodopaminergic reward deficit. Lapses of attention are associated with attenuated deactivation of the Default Mode Network (DMN), a distributed brain system normally deactivated during tasks requiring attention to the external world. Task-related DMN deactivation has been shown to be attenuated in ADHD relative to controls. We hypothesised that motivational incentives to balance speed against restraint would increase task engagement during an inhibitory control task, enhancing DMN deactivation in ADHD. We also hypothesised that methylphenidate, an indirect dopamine agonist, would tend to normalise abnormal patterns of DMN deactivation.
Method: We obtained functional magnetic resonance images from eighteen methylphenidate-responsive children with ADHD (DSM-IV combined subtype) and 18 pairwise-matched typically developing children aged 9-15 years while they performed a paced Go/No-go task. We manipulated motivational incentive to balance response speed against inhibitory control, and tested children with ADHD both on and off methylphenidate.
Results: When children with ADHD were off-methylphenidate and task incentive was low, event-related DMN deactivation was significantly attenuated compared to controls, but the two groups did not differ under high motivational incentives. The modulation of DMN deactivation by incentive in the children with ADHD, off- methylphenidate, was statistically significant, and significantly greater than in typically developing children. When children with ADHD were on-methylphenidate, motivational modulation of event-related DMN deactivation was abolished, and no attenuation relative to their typically developing peers was apparent in either motivational condition.
Conclusions: During an inhibitory control task, children with ADHD exhibit a raised motivational threshold at which task-relevant stimuli become sufficiently salient to deactivate the DMN. Treatment with methylphenidate normalises this threshold, rendering their pattern of task-related DMN deactivation indistinguishable from that of typically developing children
Socioeconomic status as a risk factor for dementia death:individual participant meta-analysis of 86 508 men and women from the UK
No full textLife-course socioeconomic factors may have a role in dementia aetiology but there is a current paucity of studies. Meta-analyses of individual participant data would considerably strengthen this evidence base
Harnessing genomics in the battle against antimicrobial resistance and neglected tropical diseases.
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Gene-silencing antisense oligomers inhibit Acinetobacter growth in vitro and in vivo
No full textBackground: Peptide-conjugated phosphorodiamidate morpholino oligomers (PPMOs) are synthetic DNA/RNA analogs that silence expression of specific genes. We studied whether PPMOs targeted to essential genes in Acinetobacter lwoffii and A. baumannii are active in vitro and in vivo. Methods: PPMOs were evaluated in vitro using MIC and viability assays, and in vivo using murine pulmonary infection models with intranasal PPMO treatment. Results: MICs of PPMOs ranged from 0.1 and 64 μM (~0.6 to 38 μg/ml). The most effective PPMO tested was (RXR)₄-AcpP, which is targeted to acpP. (RXR)₄-AcpP reduced viability of A. lwoffii and A. baumannii by > 10³ cfu/ml at 5 to 8 x MIC. Mice treated with 0.25 mg/kg or more of (RXR)₄-AcpP survived longer and had less inflammation and bacterial lung burden than mice treated with a scrambled-sequence PPMO or PBS. Treatment could be delayed after infection and still increase survival. Conclusions: PPMOs targeted to essential genes of A. lwoffii and A. baumannii were bactericidal and had MICs in a clinically relevant range. (RXR)₄-AcpP increased survival of mice infected with A. lwoffii or A. baumannii, even when initial treatment was delayed after infection. PPMOs could be a viable therapeutic approach in dealing with multidrug resistant Acinetobacter species.This article is published by Oxford University Press on behalf of the Infectious Diseases Society of America. This is a pre-copy-editing, author-produced PDF of an article accepted for publication in the Journal of Infectious Diseases following peer review. The definitive publisher-authenticated version, Geller, B. L., Marshall-Batty, K., Schnell, F. J., McKnight, M. M., Iversen, P. L., & Greenberg, D. E. (2013). Gene-Silencing Antisense Oligomers Inhibit Acinetobacter Growth In Vitro and In Vivo. Journal of Infectious Diseases, 208(10), 1553-1560. doi:10.1093/infdis/jit460, is available online at: http://jid.oxfordjournals.org/content/208/10/1553.full.pdf?keytype=ref&ijkey=qepbqtxt5pt.Keywords: antisense, infection, respiratory infection, phosphorodiamidate morpholino oligomer, lwoffii, baumannii, oligomer, MIC, Acinetobacter, PMO, morpholino, mous
Financial Incentives, Hospital Care, and Health Outcomes: Evidence from Fair Pricing Laws∗
No full textNOTE: Staff working papers in the Finance and Economics Discussion Series (FEDS) are preliminary materials circulated to stimulate discussion and critical comment. The analysis and conclusions set forth are those of the authors and do not indicate concurrence by other members of the research staff or the Board of Governors. References in publications to the Finance and Economics Discussion Series (other than acknowledgement) should be cleared with the author(s) to protect the tentative character of these papers
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