6,701 research outputs found

    Systematic and taxonomic issues concerning some East African bird species, notably those where treatment varies between authors

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    The taxonomy of various East African bird species is discussed. Fourteen of the non-passerines and forty-eight of the passerines listed in Britton (1980) are considered, with reference to treatments by various subsequent authors. Twenty-three species splits are recommended from the treatment in Britton (op. cit.), and one lump, the inclusion of Jackson’s Hornbill Tockus jacksoni as a race of T. deckeni

    Genome sequences of 12 isolates of the EU1 lineage of Phytophthora ramorum, a fungus-like pathogen that causes extensive damage and mortality to a wide range of trees and other plants

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    This is the author accepted manuscript. The final version is available from Elsevier via the DOI in this record.Here we present genome sequences for twelve isolates of the invasive pathogen Phytophthora ramorum EU1. The assembled genome sequences and raw sequence data are available via BioProject accession number PRJNA177509. These data will be useful in developing molecular tools for specific detection and identification of this pathogen.This work was supported in part by a grant funded jointly by the Biotechnology and Biological Sciences Research Council, the Department for Environment, Food and Rural Affairs, the Economic and Social Research Council, the Forestry Commission, the Natural Environment Research Council and the Scottish Government, under the Tree Health and Plant Biosecurity Initiative (BB/L012499/1). PAO was supported by a joint studentship from the Fera seedcorn programme and from the Defra Future-proofing Plant Health project (PH0441). We acknowledge funding for the joint studentship from the Fera seedcorn programme and from the Defra Future-proofing Plant Health project (PH0441)

    Mapping the methylation status of the miR-145 promoter in saphenous vein smooth muscle cells from individuals with type 2 diabetes

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    Type 2 diabetes mellitus prevalence is growing globally, and the leading cause of mortality in these patients is cardiovascular disease. Epigenetic mechanisms such as microRNAs (miRs) and DNA methylation may contribute to complications of type 2 diabetes mellitus. We discovered an aberrant type 2 diabetes mellitus–smooth muscle cell phenotype driven by persistent up-regulation of miR-145. This study aimed to determine whether elevated expression was due to changes in methylation at the miR-145 promoter. Smooth muscle cells were cultured from saphenous veins of 22 non-diabetic and 22 type 2 diabetes mellitus donors. DNA was extracted, bisulphite treated and pyrosequencing used to interrogate methylation at 11 CpG sites within the miR-145 promoter. Inter-patient variation was high irrespective of type 2 diabetes mellitus. Differential methylation trends were apparent between non-diabetic and type 2 diabetes mellitus–smooth muscle cells at most sites but were not statistically significant. Methylation at CpGs −112 and −106 was consistently lower than all other sites explored in non-diabetic and type 2 diabetes mellitus–smooth muscle cells. Finally, miR-145 expression per se was not correlated with methylation levels observed at any site. The persistent up-regulation of miR-145 observed in type 2 diabetes mellitus–smooth muscle cells is not related to methylation at the miR-145 promoter. Crucially, miR-145 methylation is highly variable between patients, serving as a cautionary note for future studies of this region in primary human cell types

    When the heart rules the head: ischaemic stroke and intracerebral haemorrhage complicating infective endocarditis

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    Sir William Osler meticulously described the clinical manifestations of infective endocarditis in 1885, concluding that: 'few diseases present greater difficulties in the way of diagnosis 
 which in many cases are practically insurmountable'. Even with modern investigation techniques, diagnosing infective endocarditis can be hugely challenging, yet is critically important in patients presenting with stroke (both cerebral infarction and intracranial haemorrhage), its commonest neurological complication. In ischaemic stroke, intravenous thrombolysis carries an unacceptably high risk of intracranial haemorrhage, while in intracerebral haemorrhage, mycotic aneurysms require urgent treatment to avoid rebleeding, and in all cases, prompt treatment with antibiotics and valve surgery may be life-saving. Here, we describe typical presentations of ischaemic stroke and intracerebral haemorrhage caused by infective endocarditis. We review the diagnostic challenges, the importance of rapid diagnosis, treatment options and controversies

    Additional Queen Square (QS) screening items improve the test accuracy of the Montreal Cognitive Assessment (MoCA) after acute stroke

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    BACKGROUND The Montreal Cognitive Assessment (MoCA) is a popular cognitive screening tool used in stroke, but lacks sensitivity for detecting impairment in stroke-relevant domains of processing speed, non-verbal memory and executive functions. Our aim was to assess whether the test accuracy of the MoCA can be improved with additional tailored screening items targeting these three domains. METHODS We included 196 patients admitted to an acute stroke unit at the National Hospital for Neurology and Neurosurgery, Queen Square (QS), London. Participants completed the MoCA as well as a series of additional QS-screening items designed to assess speed of processing, non-verbal memory and executive functions. Performance on the MoCA and QS screening items was compared with performance on “gold standard” neuropsychological assessment. RESULTS In our sample, 22% of patients were classified as “cognitively intact” on the traditional MoCA alone (≄ 25). However, when tested on the QS-screening items, 40% of these patients failed on speed of processing, 56% failed on non-verbal memory and 26% failed on executive functions. Compared with neuropsychological assessment, the QS-screening items had good sensitivity (QS-Speed: 0.85; QS-Vis: 0.71; QS-EF: 0.73) and modest specificity (QS-Speed: 0.59; QS-Vis: 0.39; QS-EF: 0.54), regardless of stroke lateralisation. CONCLUSION Additional screening items detected impairments in speed of processing, non-verbal memory and executive functions over and above those captured using the standard MoCA. The use of these QS-screening items improves the detection of post-stroke cognitive deficits in domains not adequately covered by the standard MoCA

    Insulin therapy and dietary adjustments to normalize glycaemia and prevent nocturnal hypoglycaemia after evening exercise in type 1 diabetes: a randomized controlled trial

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    Introduction Evening-time exercise is a frequent cause of severe hypoglycemia in type 1 diabetes, fear of which deters participation in regular exercise. Recommendations for normalizing glycemia around exercise consist of prandial adjustments to bolus insulin therapy and food composition, but this carries only short-lasting protection from hypoglycemia. Therefore, this study aimed to examine the impact of a combined basal-bolus insulin dose reduction and carbohydrate feeding strategy on glycemia and metabolic parameters following evening exercise in type 1 diabetes. Methods Ten male participants (glycated hemoglobin: 52.4±2.2 mmol/mol), treated with multiple daily injections, completed two randomized study-days, whereby administration of total daily basal insulin dose was unchanged (100%), or reduced by 20% (80%). Participants attended the laboratory at ∌08:00 h for a fasted blood sample, before returning in the evening. On arrival (∌17:00 h), participants consumed a carbohydrate meal and administered a 75% reduced rapid-acting insulin dose and 60 min later performed 45 min of treadmill running. At 60 min postexercise, participants consumed a low glycemic index (LGI) meal and administered a 50% reduced rapid-acting insulin dose, before returning home. At ∌23:00 h, participants consumed a LGI bedtime snack and returned to the laboratory the following morning (∌08:00 h) for a fasted blood sample. Venous blood samples were analyzed for glucose, glucoregulatory hormones, non-esterified fatty acids, ÎČ-hydroxybutyrate, interleukin 6, and tumor necrosis factor α. Interstitial glucose was monitored for 24 h pre-exercise and postexercise. Results Glycemia was similar until 6 h postexercise, with no hypoglycemic episodes. Beyond 6 h glucose levels fell during 100%, and nine participants experienced nocturnal hypoglycemia. Conversely, all participants during 80% were protected from nocturnal hypoglycemia, and remained protected for 24 h postexercise. All metabolic parameters were similar. Conclusions Reducing basal insulin dose with reduced prandial bolus insulin and LGI carbohydrate feeding provides protection from hypoglycemia during and for 24 h following evening exercise. This strategy is not associated with hyperglycemia, or adverse metabolic disturbances

    A Microsoft-Excel-based tool for running and critically appraising network meta-analyses--an overview and application of NetMetaXL.

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    This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.BACKGROUND: The use of network meta-analysis has increased dramatically in recent years. WinBUGS, a freely available Bayesian software package, has been the most widely used software package to conduct network meta-analyses. However, the learning curve for WinBUGS can be daunting, especially for new users. Furthermore, critical appraisal of network meta-analyses conducted in WinBUGS can be challenging given its limited data manipulation capabilities and the fact that generation of graphical output from network meta-analyses often relies on different software packages than the analyses themselves. METHODS: We developed a freely available Microsoft-Excel-based tool called NetMetaXL, programmed in Visual Basic for Applications, which provides an interface for conducting a Bayesian network meta-analysis using WinBUGS from within Microsoft Excel. . This tool allows the user to easily prepare and enter data, set model assumptions, and run the network meta-analysis, with results being automatically displayed in an Excel spreadsheet. It also contains macros that use NetMetaXL's interface to generate evidence network diagrams, forest plots, league tables of pairwise comparisons, probability plots (rankograms), and inconsistency plots within Microsoft Excel. All figures generated are publication quality, thereby increasing the efficiency of knowledge transfer and manuscript preparation. RESULTS: We demonstrate the application of NetMetaXL using data from a network meta-analysis published previously which compares combined resynchronization and implantable defibrillator therapy in left ventricular dysfunction. We replicate results from the previous publication while demonstrating result summaries generated by the software. CONCLUSIONS: Use of the freely available NetMetaXL successfully demonstrated its ability to make running network meta-analyses more accessible to novice WinBUGS users by allowing analyses to be conducted entirely within Microsoft Excel. NetMetaXL also allows for more efficient and transparent critical appraisal of network meta-analyses, enhanced standardization of reporting, and integration with health economic evaluations which are frequently Excel-based.CC is a recipient of a Vanier Canada Graduate Scholarship from the Canadian Institutes of Health Research (funding reference number—CGV 121171) and is a trainee on the Canadian Institutes of Health Research Drug Safety and Effectiveness Network team grant (funding reference number—116573). BH is funded by a New Investigator award from the Canadian Institutes of Health Research and the Drug Safety and Effectiveness Network. This research was partly supported by funding from CADTH as part of a project to develop Excel-based tools to support the conduct of health technology assessments. This research was also supported by Cornerstone Research Group

    Degradation of a quantum directional reference frame as a random walk

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    We investigate if the degradation of a quantum directional reference frame through repeated use can be modeled as a classical direction undergoing a random walk on a sphere. We demonstrate that the behaviour of the fidelity for a degrading quantum directional reference frame, defined as the average probability of correctly determining the orientation of a test system, can be fit precisely using such a model. Physically, the mechanism for the random walk is the uncontrollable back-action on the reference frame due to its use in a measurement of the direction of another system. However, we find that the magnitude of the step size of this random walk is not given by our classical model and must be determined from the full quantum description.Comment: 5 pages, no figures. Comments are welcome. v2: several changes to clarify the key results. v3: journal reference added, acknowledgements and references update

    Characterising hyperinsulinaemia induced insulin resistance in human skeletal muscle cells

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    Hyperinsulinaemia potentially contributes to insulin resistance in metabolic tissues, such as skeletal muscle. The purpose of these experiments was to characterise glucose uptake, insulin signalling and relevant gene expression in primary human skeletal muscle-derived cells (HMDCs), in response to prolonged insulin exposure (PIE) as a model of hyperinsulinaemia-induced insulin resistance. Differentiated HMDCs from healthy human donors were cultured with or without insulin (100 nM) for 3 days followed by an acute insulin stimulation. HMDCs exposed to PIE were characterised by impaired insulin-stimulated glucose uptake, blunted IRS-1 phosphorylation (Tyr612) and Akt (Ser473) phosphorylation in response to an acute insulin stimulation. Glucose transporter 1 (GLUT1), but not GLUT4, mRNA and protein increased following PIE. The mRNA expression of metabolic (PDK4) and inflammatory markers (TNF-α) was reduced by PIE but did not change lipid (SREBP1 and CD36) or mitochondrial (UCP3) markers. These experiments provide further characterisation of the effects of PIE as a model of hyperinsulinaemia-induced insulin resistance in HMDCs

    Corrigendum: Solar cycles or random processes? Evaluating solar variability in Holocene climate records

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    This is the final version of the article. Available from Springer Nature via the DOI in this record.The article to which this is the corrigendum is in ORE at http://hdl.handle.net/10871/21766A coding error in the Monte Carlo procedure for the determination of critical values in running correlation analysis (presented in Supplementary Data S8) has been brought to the attention of the authors.[...
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