3,985 research outputs found

    A remarkable recurrent nova in M 31: The predicted 2014 outburst in X-rays with Swift

    Get PDF
    The M 31 nova M31N 2008-12a was recently found to be a recurrent nova (RN) with a recurrence time of about 1 year. This is by far the fastest recurrence time scale of any known RNe. Our optical monitoring programme detected the predicted 2014 outburst of M31N 2008-12a in early October. We immediately initiated an X-ray/UV monitoring campaign with Swift to study the multiwavelength evolution of the outburst. We monitored M31N 2008-12a with daily Swift observations for 20 days after discovery, covering the entire supersoft X-ray source (SSS) phase. We detected SSS emission around day six after outburst. The SSS state lasted for approximately two weeks until about day 19. M31N 2008-12a was a bright X-ray source with a high blackbody temperature. The X-ray properties of this outburst were very similar to the 2013 eruption. Combined X-ray spectra show a fast rise and decline of the effective blackbody temperature. The short-term X-ray light curve showed strong, aperiodic variability which decreased significantly after about day 14. Overall, the X-ray properties of M31N 2008-12a are consistent with the average population properties of M 31 novae. The optical and X-ray light curves can be scaled uniformly to show similar time scales as those of the Galactic RNe U Sco or RS Oph. The SSS evolution time scales and effective temperatures are consistent with a high-mass WD. We predict the next outburst of M31N 2008-12a to occur in autumn 2015

    Proceedings of the Salford Postgraduate Annual Research Conference (SPARC) 2011

    Get PDF
    These proceedings bring together a selection of papers from the 2011 Salford Postgraduate Annual Research Conference(SPARC). It includes papers from PhD students in the arts and social sciences, business, computing, science and engineering, education, environment, built environment and health sciences. Contributions from Salford researchers are published here alongside papers from students at the Universities of Anglia Ruskin, Birmingham City, Chester,De Montfort, Exeter, Leeds, Liverpool, Liverpool John Moores and Manchester

    Elevated hemostasis markers after pneumonia increases one-year risk of all-cause and cardiovascular deaths

    Get PDF
    Background: Acceleration of chronic diseases, particularly cardiovascular disease, may increase long-term mortality after community-acquired pneumonia (CAP), but underlying mechanisms are unknown. Persistence of the prothrombotic state that occurs during an acute infection may increase risk of subsequent atherothrombosis in patients with pre-existing cardiovascular disease and increase subsequent risk of death. We hypothesized that circulating hemostasis markers activated during CAP persist at hospital discharge, when patients appear to have recovered clinically, and are associated with higher mortality, particularly due to cardiovascular causes. Methods: In a cohort of survivors of CAP hospitalization from 28 US sites, we measured D-Dimer, thrombin-antithrombin complexes [TAT], Factor IX, antithrombin, and plasminogen activator inhibitor-1 at hospital discharge, and determined 1-year all-cause and cardiovascular mortality. Results: Of 893 subjects, most did not have severe pneumonia (70.6% never developed severe sepsis) and only 13.4% required intensive care unit admission. At discharge, 88.4% of subjects had normal vital signs and appeared to have clinically recovered. D-dimer and TAT levels were elevated at discharge in 78.8% and 30.1% of all subjects, and in 51.3% and 25.3% of those without severe sepsis. Higher D-dimer and TAT levels were associated with higher risk of all-cause mortality (range of hazard ratios were 1.66-1.17, p = 0.0001 and 1.46-1.04, p = 0.001 after adjusting for demographics and comorbid illnesses) and cardiovascular mortality (p = 0.009 and 0.003 in competing risk analyses). Conclusions: Elevations of TAT and D-dimer levels are common at hospital discharge in patients who appeared to have recovered clinically from pneumonia and are associated with higher risk of subsequent deaths, particularly due to cardiovascular disease. © 2011 Yende et al

    Applications of Laboratory Technology in the Evaluation of the Risk of Rabies Transmissions by Biting Dogs and Cats

    Get PDF
    While rabies is not a common disease in domestic animal species of the United States, potential exposures to rabies in the form of bites are very common and increasing. A nationwide study conducted among general hospitals shows that 1 percent of emergency room visits are for animal bites, of which 80-90 percent are inflicted by the dog (Callaham 1980). This figure is conservative, as the study did not include pediatric hospitals, the bite of victims that progress only to a physician\u27s office, or those that receive no medical care at all. In Missouri alone, this study would infer about 1500 dog bites per year reaching only the general hospital. The number of dog and other animal bites across the country is unknown but may safely be assumed to be staggering in magnitude

    RNA-DNA differences are rarer in proto-oncogenes than in tumor suppressor genes

    Get PDF
    It has long been assumed that DNA sequences and corresponding RNA transcripts are almost identical; a recent discovery, however, revealed widespread RNA-DNA differences (RDDs), which represent a largely unexplored aspect of human genome variation. It has been speculated that RDDs can affect disease susceptibility and manifestations; however, almost nothing is known about how RDDs are related to disease. Here, we show that RDDs are rarer in proto-oncogenes than in tumor suppressor genes; the number of RDDs in coding exons, but not in 3′UTR and 5′UTR, is significantly lower in the former than the latter, and this trend is especially pronounced in non-synonymous RDDs, i.e., those cause amino acid changes. A potential mechanism is that, unlike proto-oncogenes, the requirement of tumor suppressor genes to have both alleles affected to cause tumor ‘buffers' these genes to tolerate more RDDs

    Do Bar-Headed Geese Train for High Altitude Flights?

    Get PDF
    This is the author accepted manuscript. The final version is available from OUP via the DOI in this recordSYNOPSIS: Exercise at high altitude is extremely challenging, largely due to hypobaric hypoxia (low oxygen levels brought about by low air pressure). In humans, the maximal rate of oxygen consumption decreases with increasing altitude, supporting progressively poorer performance. Bar-headed geese (Anser indicus) are renowned high altitude migrants and, although they appear to minimize altitude during migration where possible, they must fly over the Tibetan Plateau (mean altitude 4800 m) for much of their annual migration. This requires considerable cardiovascular effort, but no study has assessed the extent to which bar-headed geese may train prior to migration for long distances, or for high altitudes. Using implanted loggers that recorded heart rate, acceleration, pressure, and temperature, we found no evidence of training for migration in bar-headed geese. Geese showed no significant change in summed activity per day or maximal activity per day. There was also no significant change in maximum heart rate per day or minimum resting heart rate, which may be evidence of an increase in cardiac stroke volume if all other variables were to remain the same. We discuss the strategies used by bar-headed geese in the context of training undertaken by human mountaineers when preparing for high altitude, noting the differences between their respective cardiovascular physiology.This work was supported by the UK Biotechnology and Biological Sciences Research Council [BBSRC; BB/FO15615/1 to C.M.B. and P.J.B.]. Authors were supported by a Natural Sciences and Engineering Research Council of Canada (NSERC) award [W.K.M.], and the FAO through the Animal Health Service EMPRES surveillance program

    Antibiotic use and the risk of rheumatoid arthritis: a population-based case-control study

    Get PDF
    Background: Antibiotic-induced disturbances of the human microbiota have been implicated in the development of chronic autoimmune conditions. This study aimed to assess whether antibiotic use is associated with the onset of rheumatoid arthritis (RA). Methods: A nested case-control study was conducted utilising data from the primary care Clinical Practice Research Datalink (CPRD). Patients with an incident diagnosis of RA were identified (1995–2017). Each case was matched on age, gender, and general practice to ≥ 5 controls without RA. Conditional logistic regression was used to examine previous antibiotic prescriptions and RA onset after controlling for confounding factors. Results: We identified 22,677 cases of RA, matched to 90,013 controls, with a median follow-up of 10 years before RA diagnosis. The odds of developing RA were 60% higher in those exposed to antibiotics than in those not exposed (OR 1.60; 95% CI 1.51–1.68). A dose- or frequency-dependent association was observed between the number of previous antibiotic prescriptions and RA. All classes of antibiotics were associated with higher odds of RA, with bactericidal antibiotics carrying higher risk than bacteriostatic (45% vs. 31%). Those with antibiotic-treated upper respiratory tract (URT) infections were more likely to be RA cases. However, this was not observed for URT infections not treated with antibiotics. Antifungal (OR = 1.27; 95% CI 1.20–1.35) and antiviral (OR = 1.19; 95% CI 1.14–1.24) prescriptions were also associated with increased odds of RA. Conclusion: Antibiotic prescriptions are associated with a higher risk of RA. This may be due to microbiota disturbances or underlying infections driving risk. Further research is needed to explore these mechanisms

    Prevalence, sources, and predictors of soy consumption in breast cancer

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>A number of components in soy appear to have anticancer properties, including the isoflavones, genistein and daidzein. The use of soy by women with breast cancer is now being questioned because of the estrogen-like effects of isoflavones and possible interactions with tamoxifen. Clinicians providing nutrition counseling to these women are concerned because the availability of soy foods has increased dramatically in the past few years. The goal of this study was to quantify the intake of isoflavones in women with breast cancer.</p> <p>Methods</p> <p>A cross-sectional study of 100 women with breast cancer treated at Cancer Treatment Centers of America<sup>® </sup>between 09/03 and 02/04. Each patient completed a soy food frequency questionnaire (FFQ) that was scored by Fred Hutchinson Cancer Research Center. Demographic and clinical predictors of soy intake were evaluated using one-way non-parametric Mann Whitney test and non-parametric spearman's rank correlation.</p> <p>Results</p> <p>Mean age was 50.5 years (std. dev. = 9.4; range 31–70) and mean BMI was 27.3 kg/m<sup>2 </sup>(std. dev. = 6.75; range 17–59). Genistein and Daidzein consumption was limited to 65 patients with a mean intake of 11.6 mg/day (std. dev. = 21.9; range 0–97.4) and 7.6 mg/day (std. dev. = 14.1; range 0–68.9) respectively. Soy milk (37%) and pills containing soy, isoflavones, or "natural" estrogen (24%) were the two biggest contributors to isoflavone intake.</p> <p>Conclusion</p> <p>Our study suggests that the isoflavone intake of breast cancer patients at our hospital was quite variable. Thirty-five patients reported no soy intake. The mean daily intake of 11.6 mg genistein and 7.4 mg daidzein, is the equivalent of less than 1/4 cup of tofu per day. This amount is higher than what has been previously reported in non-Asian American women.</p

    A new vicious cycle involving glutamate excitotoxicity, oxidative stress and mitochondrial dynamics

    Get PDF
    Glutamate excitotoxicity leads to fragmented mitochondria in neurodegenerative diseases, mediated by nitric oxide and S-nitrosylation of dynamin-related protein 1, a mitochondrial outer membrane fission protein. Optic atrophy gene 1 (OPA1) is an inner membrane protein important for mitochondrial fusion. Autosomal dominant optic atrophy (ADOA), caused by mutations in OPA1, is a neurodegenerative disease affecting mainly retinal ganglion cells (RGCs). Here, we showed that OPA1 deficiency in an ADOA model influences N-methyl-D-aspartate (NMDA) receptor expression, which is involved in glutamate excitotoxicity and oxidative stress. Opa1enu/+ mice show a slow progressive loss of RGCs, activation of astroglia and microglia, and pronounced mitochondrial fission in optic nerve heads as found by electron tomography. Expression of NMDA receptors (NR1, 2A, and 2B) in the retina of Opa1enu/+ mice was significantly increased as determined by western blot and immunohistochemistry. Superoxide dismutase 2 (SOD2) expression was significantly decreased, the apoptotic pathway was activated as Bax was increased, and phosphorylated Bad and BcL-xL were decreased. Our results conclusively demonstrate that not only glutamate excitotoxicity and/or oxidative stress alters mitochondrial fission/fusion, but that an imbalance in mitochondrial fission/fusion in turn leads to NMDA receptor upregulation and oxidative stress. Therefore, we propose a new vicious cycle involved in neurodegeneration that includes glutamate excitotoxicity, oxidative stress, and mitochondrial dynamics
    • …
    corecore