542 research outputs found

    Schizophrenia is associated with excess multiple physical-health comorbidities but low levels of recorded cardiovascular disease in primary care: cross-sectional study

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    <b>Objective</b> To assess the nature and extent of physical-health comorbidities in people with schizophrenia and related psychoses compared with controls. <p></p> <b>Design </b>Cross-sectional study. <p></p> <b>Setting </b>314 primary care practices in Scotland. <p></p> <b>Participants </b>9677 people with a primary care record of schizophrenia or a related psychosis and 1 414 701 controls. Main outcome measures Primary care records of 32 common chronic physical-health conditions and combinations of one, two and three or more physical-health comorbidities adjusted for age, gender and deprivation status. <p></p> <b>Results</b> Compared with controls, people with schizophrenia were significantly more likely to have one physical-health comorbidity (OR 1.21, 95% CI 1.16 to 1.27), two physical-health comorbidities (OR 1.37, 95% CI 1.29 to 1.44) and three or more physical-health comorbidities (OR 1.19, 95% CI 1.12 to 1.27). Rates were highest for viral hepatitis (OR 3.98, 95% CI 2.81 to 5.64), constipation (OR 3.24, 95% CI 3.00 to 4.49) and Parkinson's disease (OR 3.07, 95% CI 2.42 to 3.88) but people with schizophrenia had lower recorded rates of cardiovascular disease, including atrial fibrillation (OR 0.62, 95% CI 0.51 to 0.73), hypertension (OR 0.71, 95% CI 0.67 to 0.76), coronary heart disease (OR 0.75, 95% CI 0.61 to 0.71) and peripheral vascular disease (OR 0.83, 95% CI 0.71 to 0.97).<p></p> <b>Conclusions </b>People with schizophrenia have a wide range of comorbid and multiple physical-health conditions but are less likely than people without schizophrenia to have a primary care record of cardiovascular disease. This suggests a systematic under-recognition and undertreatment of cardiovascular disease in people with schizophrenia, which might contribute to substantial premature mortality observed within this patient group. <p></p&gt

    Observations of Low Frequency Solar Radio Bursts from the Rosse Solar-Terrestrial Observatory

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    The Rosse Solar-Terrestrial Observatory (RSTO; www.rosseobservatory.ie) was established at Birr Castle, Co. Offaly, Ireland (53 05'38.9", 7 55'12.7") in 2010 to study solar radio bursts and the response of the Earth's ionosphere and geomagnetic field. To date, three Compound Astronomical Low-cost Low-frequency Instrument for Spectroscopy and Transportable Observatory (CALLISTO) spectrometers have been installed, with the capability of observing in the frequency range 10-870 MHz. The receivers are fed simultaneously by biconical and log-periodic antennas. Nominally, frequency spectra in the range 10-400 MHz are obtained with 4 sweeps per second over 600 channels. Here, we describe the RSTO solar radio spectrometer set-up, and present dynamic spectra of a sample of Type II, III and IV radio bursts. In particular, we describe fine-scale structure observed in Type II bursts, including band splitting and rapidly varying herringbone features

    Activation of α7 nicotinic receptors improves phencyclidine-induced deficits in cognitive tasks in rats: Implications for therapy of cognitive dysfunction in schizophrenia

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    YesRationale: Nicotinic α7 acetylcholine receptors (nAChRs) have been highlighted as a target for cognitive enhancement in schizophrenia. Aim: To investigate whether the deficits induced by sub-chronic phencyclidine (PCP) in reversal learning and novel object recognition could be attenuated by the selective α7 nAChR full agonist, PNU-282987. Methods: Adult female hooded-Lister rats received sub-chronic PCP (2 mg/kg) or vehicle i.p. twice daily for seven days, followed by 7-days washout. In cohort 1, PCP-treated rats then received PNU-282987 (5, 10, 20 mg/kg; s.c.) or vehicle and were tested in the reversal learning task. In cohort 2, PCP-treated rats received PNU-282987 (10 mg/kg; s.c.) or saline for 15 days and were tested in the novel object recognition test on day 1 and on day 15, to test for tolerance. Results: Sub-chronic PCP produced significant deficits in both cognitive tasks (P<0.01-0.001). PNU-282987 attenuated the PCP-induced deficits in reversal learning at 10 mg/kg (P<0.01) and 20 mg/kg (P<0.001), and in novel object recognition at 10 mg/kg on day 1 (P<0.01) and on day 15 (P<0.001). Conclusions: These data show that PNU-282987 has efficacy to reverse PCP-induced deficits in two paradigms of relevance to schizophrenia. Results further suggest that 15 day daily dosing of PNU-282987 (10 mg/kg s.c.) does not cause tolerance in rat. This study suggests that activation of α7 nAChRs, may represent a suitable strategy for improving cognitive deficits of relevance to schizophrenia.SL McLean was supported by a joint University of Bradford–GSK postgraduate studentship

    ‘Engage the World’: examining conflicts of engagement in public museums

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    Public engagement has become a central theme in the mission statements of many cultural institutions, and in scholarly research into museums and heritage. Engagement has emerged as the go-to-it-word for generating, improving or repairing relations between museums and society at large. But engagement is frequently an unexamined term that might embed assumptions and ignore power relationships. This article describes and examines the implications of conflicting and misleading uses of ‘engagement’ in relation to institutional dealings with contested questions about culture and heritage. It considers the development of an exhibition on the Dead Sea Scrolls by the Royal Ontario Museum, Toronto in 2009 within the new institutional goal to ‘Engage the World’. The chapter analyses the motivations, processes and decisions deployed by management and staff to ‘Engage the World’, and the degree to which the museum was able to re-think its strategies of public engagement, especially in relation to subjects,issues and publics that were more controversial in nature

    Targeting malaria parasites with novel derivatives of azithromycin

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    Introduction: The spread of artemisinin resistant Plasmodium falciparum parasites is of global concern and highlights the need to identify new antimalarials for future treatments. Azithromycin, a macrolide antibiotic used clinically against malaria, kills parasites via two mechanisms: ‘delayed death’ by inhibiting the bacterium-like ribosomes of the apicoplast, and ‘quick-killing’ that kills rapidly across the entire blood stage development. Methods: Here, 22 azithromycin analogues were explored for delayed death and quick-killing activities against P. falciparum (the most virulent human malaria) and P. knowlesi (a monkey parasite that frequently infects humans). Results: Seventeen analogues showed improved quick-killing against both Plasmodium species, with up to 38 to 20-fold higher potency over azithromycin after less than 48 or 28 hours of treatment for P. falciparum and P. knowlesi, respectively. Quick-killing analogues maintained activity throughout the blood stage lifecycle, including ring stages of P. falciparum parasites (5-fold more selective against P. falciparum than human cells. Isopentenyl pyrophosphate supplemented parasites that lacked an apicoplast were equally sensitive to quick-killing analogues, confirming that the quick killing activity of these drugs was not directed at the apicoplast. Further, activity against the related apicoplast containing parasite Toxoplasma gondii and the gram-positive bacterium Streptococcus pneumoniae did not show improvement over azithromycin, highlighting the specific improvement in antimalarial quick-killing activity. Metabolomic profiling of parasites subjected to the most potent compound showed a build-up of non-haemoglobin derived peptides that was similar to chloroquine, while also exhibiting accumulation of haemoglobin-derived peptides that was absent for chloroquine treatment. Discussion: The azithromycin analogues characterised in this study expand the structural diversity over previously reported quick-killing compounds and provide new starting points to develop azithromycin analogues with quickkilling antimalarial activity.Amy L. Burns, Brad E. Sleebs, Maria Gancheva, Kimberley T. McLean, Ghizal Siddiqui, Henrietta Venter, James G. Beeson, Ryan O, Handley, Darren J. Creek, Shutao Ma, Sonja Frölich, Christopher D. Goodman, Geoffrey I. McFadden, and Danny W. Wilso

    Observation of the Ξc+\Xi_c^+ Charmed Baryon Decays to Σ+Kπ+\Sigma^+ K^-\pi^+, Σ+Kˉ0\Sigma^+ \bar{K}^{*0}, and ΛKπ+π+\Lambda K^-\pi^+\pi^+

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    We have observed two new decay modes of the charmed baryon Ξc+\Xi_c^+ into Σ+Kπ+\Sigma^+ K^-\pi^+ and Σ+Kˉ0\Sigma^+ \bar{K}^{*0} using data collected with the CLEO II detector. We also present the first measurement of the branching fraction for the previously observed decay mode Ξc+ΛKπ+π+\Xi_c^+\to\Lambda K^-\pi^+\pi^+. The branching fractions for these three modes relative to Ξc+Ξπ+π+\Xi_c^+\to\Xi^-\pi^+\pi^+ are measured to be 1.18±0.26±0.171.18 \pm 0.26 \pm 0.17, 0.92±0.27±0.140.92 \pm 0.27 \pm 0.14, and 0.58±0.16±0.070.58 \pm 0.16 \pm 0.07, respectively.Comment: 12 page uuencoded postscript file, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    Study of the B^0 Semileptonic Decay Spectrum at the Upsilon(4S) Resonance

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    We have made a first measurement of the lepton momentum spectrum in a sample of events enriched in neutral B's through a partial reconstruction of B0 --> D*- l+ nu. This spectrum, measured with 2.38 fb**-1 of data collected at the Upsilon(4S) resonance by the CLEO II detector, is compared directly to the inclusive lepton spectrum from all Upsilon(4S) events in the same data set. These two spectra are consistent with having the same shape above 1.5 GeV/c. From the two spectra and two other CLEO measurements, we obtain the B0 and B+ semileptonic branching fractions, b0 and b+, their ratio, and the production ratio f+-/f00 of B+ and B0 pairs at the Upsilon(4S). We report b+/b0=0.950 (+0.117-0.080) +- 0.091, b0 = (10.78 +- 0.60 +- 0.69)%, and b+ = (10.25 +- 0.57 +- 0.65)%. b+/b0 is equivalent to the ratio of charged to neutral B lifetimes, tau+/tau0.Comment: 14 page, postscript file also available at http://w4.lns.cornell.edu/public/CLN
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