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Träfflista för sökning "WFRF:(Jones Ashley R.) ;srt2:(2010-2014)"

Search: WFRF:(Jones Ashley R.) > (2010-2014)

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2.
  • Söderström, Pär-Anders, et al. (author)
  • Spectroscopy of neutron-rich Dy-168,Dy-170 : Yrast band evolution close to the NpNn valence maximum
  • 2010
  • In: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 81:3, s. 034310-
  • Journal article (peer-reviewed)abstract
    • The yrast sequence of the neutron-rich dysprosium isotope Dy-168 has been studied using multinucleon transfer reactions following collisions between a 460-MeV Se-82 beam and an Er-170 target. The reaction products were identified using the PRISMA magnetic spectrometer and the gamma rays detected using the CLARA HPGe-detector array. The 2(+) and 4(+) members of the previously measured ground-state rotational band of Dy-168 have been confirmed and the yrast band extended up to 10(+). A tentative candidate for the 4(+) -> 2(+) transition in Dy-170 was also identified. The data on these nuclei and on the lighter even-even dysprosium isotopes are interpreted in terms of total Routhian surface calculations and the evolution of collectivity in the vicinity of the proton-neutron valence product maximum is discussed.
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3.
  • O'Brien, John T, et al. (author)
  • Clinical practice with anti-dementia drugs: a revised (second) consensus statement from the British Association for Psychopharmacology.
  • 2011
  • In: Journal of psychopharmacology (Oxford, England). - : SAGE Publications. - 1461-7285 .- 0269-8811. ; 25:8, s. 997-1019
  • Research review (peer-reviewed)abstract
    • The British Association for Psychopharmacology (BAP) coordinated a meeting of experts to review and revise its first (2006) Guidelines for clinical practice with anti-dementia drugs. As before, levels of evidence were rated using accepted standards which were then translated into grades of recommendation A to D, with A having the strongest evidence base (from randomized controlled trials) and D the weakest (case studies or expert opinion). Current clinical diagnostic criteria for dementia have sufficient accuracy to be applied in clinical practice (B) and brain imaging can improve diagnostic accuracy (B). Cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) are effective for mild to moderate Alzheimer's disease (A) and memantine for moderate to severe Alzheimer's disease (A). Until further evidence is available other drugs, including statins, anti-inflammatory drugs, vitamin E and Ginkgo biloba, cannot be recommended either for the treatment or prevention of Alzheimer's disease (A). Neither cholinesterase inhibitors nor memantine are effective in those with mild cognitive impairment (A). Cholinesterase inhibitors are not effective in frontotemporal dementia and may cause agitation (A), though selective serotonin reuptake inhibitors may help behavioural (but not cognitive) features (B). Cholinesterase inhibitors should be used for the treatment of people with Lewy body dementias (Parkinson's disease dementia and dementia with Lewy bodies (DLB)), especially for neuropsychiatric symptoms (A). Cholinesterase inhibitors and memantine can produce cognitive improvements in DLB (A). There is no clear evidence that any intervention can prevent or delay the onset of dementia. Although the consensus statement focuses on medication, psychological interventions can be effective in addition to pharmacotherapy, both for cognitive and non-cognitive symptoms. Many novel pharmacological approaches involving strategies to reduce amyloid and/or tau deposition are in progress. Although results of pivotal studies are awaited, results to date have been equivocal and no disease-modifying agents are either licensed or can be currently recommended for clinical use.
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4.
  • Abel, Olubunmi, et al. (author)
  • Development of a Smartphone App for a Genetics Website : The Amyotrophic Lateral Sclerosis Online Genetics Database (ALSoD)
  • 2013
  • In: JMIR mhealth and uhealth. - : JMIR Publications, Inc.. - 2291-5222. ; 1:2
  • Journal article (peer-reviewed)abstract
    • Background: The ALS Online Genetics Database (ALSoD) website holds mutation, geographical, and phenotype data on genes implicated in amyotrophic lateral sclerosis (ALS) and links to bioinformatics resources, publications, and tools for analysis. On average, there are 300 unique visits per day, suggesting a high demand from the research community. To enable wider access, we developed a mobile-friendly version of the website and a smartphone app. Objective: We sought to compare data traffic before and after implementation of a mobile version of the website to assess utility. Methods: We identified the most frequently viewed pages using Google Analytics and our in-house analytic monitoring. For these, we optimized the content layout of the screen, reduced image sizes, and summarized available information. We used the Microsoft. NET framework mobile detection property (HttpRequest. IsMobileDevice in the Request. Browser object in conjunction with HttpRequest. UserAgent), which returns a true value if the browser is a recognized mobile device. For app development, we used the Eclipse integrated development environment with Android plug-ins. We wrapped the mobile website version with the WebView object in Android. Simulators were downloaded to test and debug the applications. Results: The website automatically detects access from a mobile phone and redirects pages to fit the smaller screen. Because the amount of data stored on ALSoD is very large, the available information for display using smartphone access is deliberately restricted to improve usability. Visits to the website increased from 2231 to 2820, yielding a 26% increase from the pre-mobile to post-mobile period and an increase from 103 to 340 visits (230%) using mobile devices (including tablets). The smartphone app is currently available on BlackBerry and Android devices and will be available shortly on iOS as well. Conclusions: Further development of the ALSoD website has allowed access through smartphones and tablets, either through the website or directly through a mobile app, making genetic data stored on the database readily accessible to researchers and patients across multiple devices.
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5.
  • Fu, Yi-Ping, et al. (author)
  • The 19q12 Bladder Cancer GWAS Signal : Association with Cyclin E Function and Aggressive Disease
  • 2014
  • In: Cancer Research. - 0008-5472 .- 1538-7445. ; 74:20, s. 5808-5818
  • Journal article (peer-reviewed)abstract
    • A genome-wide association study (GWAS) of bladder cancer identified a genetic marker rs8102137 within the 19q12 region as a novel susceptibility variant. This marker is located upstream of the CCNE1 gene, which encodes cyclin E, a cell-cycle protein. We performed genetic fine-mapping analysis of the CCNE1 region using data from two bladder cancer GWAS (5,942 cases and 10,857 controls). We found that the original GWAS marker rs8102137 represents a group of 47 linked SNPs (with r(2) >= 0.7) associated with increased bladder cancer risk. From this group, we selected a functional promoter variant rs7257330, which showed strong allele-specific binding of nuclear proteins in several cell lines. In both GWASs, rs7257330 was associated only with aggressive bladder cancer, with a combined per-allele OR = 1.18 [95% confidence interval (CI), 1.09-1.27, P = 4.67 x 10(-5)] versus OR = 1.01 (95% CI, 0.93-1.10, P = 0.79) for nonaggressive disease, with P = 0.0015 for case-only analysis. Cyclin E protein expression analyzed in 265 bladder tumors was increased in aggressive tumors (P = 0.013) and, independently, with each rs7257330-A risk allele (P-trend = 0.024). Overexpression of recombinant cyclin E in cell lines caused significant acceleration of cell cycle. In conclusion, we defined the 19q12 signal as the first GWAS signal specific for aggressive bladder cancer. Molecular mechanisms of this genetic association may be related to cyclin E overexpression and alteration of cell cycle in carriers of CCNE1 risk variants. In combination with established bladder cancer risk factors and other somatic and germline genetic markers, the CCNE1 variants could be useful for inclusion into bladder cancer risk prediction models.
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