131 research outputs found

    The Young and Bright Type Ia Supernova ASASSN-14lp: Discovery, Early-Time Observations, First-Light Time, Distance to NGC 4666, and Progenitor Constraints

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    On 2014 Dec. 9.61, the All-Sky Automated Survey for SuperNovae (ASAS-SN or "Assassin") discovered ASASSN-14lp just 2\sim2 days after first light using a global array of 14-cm diameter telescopes. ASASSN-14lp went on to become a bright supernova (V=11.94V = 11.94 mag), second only to SN 2014J for the year. We present prediscovery photometry (with a detection less than a day after first light) and ultraviolet through near-infrared photometric and spectroscopic data covering the rise and fall of ASASSN-14lp for more than 100 days. We find that ASASSN-14lp had a broad light curve (Δm15(B)=0.796±0.001stat\Delta m_{15}(B) = 0.796 \pm 0.001_{\textrm{stat}}), a BB-band maximum at 2457015.823±0.030stat2457015.823 \pm 0.030_{\textrm{stat}}, a rise time of 16.940.11+0.1116.94^{+ 0.11 }_{- 0.11 } days, and moderate host--galaxy extinction (E(BV)host=0.329±0.001statE(B-V)_{\textrm{host}} = 0.329 \pm 0.001_{\textrm{stat}}). Using ASASSN-14lp we derive a distance modulus for NGC 4666 of μ=30.834±0.003stat±0.16syst\mu = 30.834 \pm 0.003_{\textrm{stat}} \pm 0.16_{\textrm{syst}} corresponding to a distance of 14.68±0.02stat±1.15syst14.68 \pm 0.02_{\textrm{stat}} \pm 1.15_{\textrm{syst}} Mpc. However, a tip of the red giant branch distance to the host galaxy should be measured to allow ASASSN-14lp to be added to the calibrating sample of Type Ia supernovae. Finally, using our early-time photometric and spectroscopic data along with our derived light curve properties, we rule out red giant secondaries with limits on the radius of a non-degenerate companion as small as 0.34R0.34 \rm{R}_\odot for favorable viewing angles and estimates of the explosion time

    PROMISING THE DREAM: changing destination image of London through the effect of website place

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    Drawing on theories of place identity and social identity, this study aims to fill a gap in place identity studies regarding the effect of a place website on the destination image of customers/visitors/tourists. The research addresses three questions: (1) what are the main impacts of tourists’ attitude on place identity and the place website, (2) what are the factors that influence destination image, and (3) what are the main impacts of a favorable destination image? The favorability of a destination image is reflected by the extent to which visitors positively regard that place website. Results reveal the importance of the destination image in enhancing the intention to revisit and recommend. Also, visitors’ satisfaction impacts on their intention to revisit and recommend the place. Significant implications for place managers and researchers are highlighted

    Ghrelin

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    This work was supported by grants from the NIH (DP2DK105570-01 and 2P30DK046200 to MLA, DK21397 to HJG, K01DK098319 to KMH, K01MH091222 to LH, DK093848 to RJS, R01DK082590 to LS, R01DK097550 to JT, RO1 DK 076037 to MOT, R01DA024680 and R01MH085298 to JMZ, R01AG019230 and R01AG029740 to RGS) The Wellcome Trust (MK), Science Foundation Ireland (12/YI/B2480 to CWL), the Alexander von Humboldt Foundation (MHT), the Deutsches Zentrum für Diabetesforschung (MHT), the Helmholtz Alliance ICEMED e Imaging and Curing Environmental Metabolic Diseases, through the Initiative and Networking Fund of the Helmholtz Association (MHT), and the Helmholtz cross-program topic “Metabolic Dysfunction” (MHT). Allan Geliebter was sponsored by NIH grants R01DK80153; R01DK074046; R03DK068603; P30DK26687

    Systematic review: conservative treatments for secondary lymphedema

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    <p>Abstract</p> <p>Background</p> <p>Several conservative (i.e., nonpharmacologic, nonsurgical) treatments exist for secondary lymphedema. The optimal treatment is unknown. We examined the effectiveness of conservative treatments for secondary lymphedema, as well as harms related to these treatments.</p> <p>Methods</p> <p>We searched MEDLINE<sup>®</sup>, EMBASE<sup>®</sup>, Cochrane Central Register of Controlled Trials<sup>®</sup>, AMED, and CINAHL from 1990 to January 19, 2010. We obtained English- and non-English-language randomized controlled trials or observational studies (with comparison groups) that reported primary effectiveness data on conservative treatments for secondary lymphedema. For English-language studies, we extracted data in tabular form and summarized the tables descriptively. For non-English-language studies, we summarized the results descriptively and discussed similarities with the English-language studies.</p> <p>Results</p> <p>Thirty-six English-language and eight non-English-language studies were included in the review. Most of these studies involved upper-limb lymphedema secondary to breast cancer. Despite lymphedema's chronicity, lengths of follow-up in most studies were under 6 months. Many trial reports contained inadequate descriptions of randomization, blinding, and methods to assess harms. Most observational studies did not control for confounding. Many studies showed that active treatments reduced the size of lymphatic limbs, although extensive between-study heterogeneity in areas such as treatment comparisons and protocols, and outcome measures, prevented us from assessing whether any one treatment was superior. This heterogeneity also precluded us from statistically pooling results. Harms were rare (< 1% incidence) and mostly minor (e.g., headache, arm pain).</p> <p>Conclusions</p> <p>The literature contains no evidence to suggest the most effective treatment for secondary lymphedema. Harms are few and unlikely to cause major clinical problems.</p

    IL-22 Is Produced by Innate Lymphoid Cells and Limits Inflammation in Allergic Airway Disease

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    Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production of CCL17 (TARC), IL-5 and IL-13 in the lung. Mice treated with IL-22 before antigen challenge displayed reduced expression of CCL17 and IL-13 and significant amelioration of airway constriction and inflammation. We conclude that innate IL-22 limits airway inflammation, tissue damage and clinical decline in allergic lung disease

    Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

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    The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

    ES-62 protects against collagen-induced arthritis by resetting interleukin-22 towards resolution of inflammation in the joints

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    Objective. The parasitic worm–derived immunomodulator ES-62 protects against disease in the mouse collagen-induced arthritis (CIA) model of rheumatoid arthritis (RA) by suppressing pathogenic interleukin-17 (IL-17) responses. The Th17 associated cytokine IL-22 also appears to have a pathogenic role in autoimmune arthritis, particularly in promoting proinflammatory responses by synovial fibroblasts and osteoclastogenesis. The present study was undertaken to investigate whether the protection against joint damage afforded by ES-62 also reflects suppression of IL-22. Methods. The role(s) of IL-22 was assessed by investigating the effects of neutralizing anti–IL-22 antibodies and recombinant IL-22 (rIL-22) on proinflammatory cytokine production, synovial fibroblast responses,and joint damage in mice with CIA, with versus without exposure to ES-62. Results. Neutralization of IL-22 during the initiation phase abrogated CIA, while administration of rIL-22 enhanced synovial fibroblast responses and exacerbated joint pathology. In contrast, after disease onset anti–IL-22 did not suppress progression, whereas administration of rIL-22 promoted resolution of inflammation. Consistent with these late antiinflammatory effects, the protection afforded by ES-62 was associated with elevated levels of IL-22 in the serum and joints that reflected a desensitization of the synovial fibroblast responses. Moreover, neutralization of IL-22 during the late effector stage of disease prevented ES-62–mediated desensitization of synovial fibroblast responses and protection against CIA. Conclusion. IL-22 plays a dual role in CIA, being pathogenic during the initiation phase while acting to resolve inflammation and joint damage during established disease. Harnessing of the tissue repair properties of IL-22 by ES-62 highlights the potential for joint-targeted therapeutic modulation of synovial fibroblast responses and consequent protection against bone damage in RA
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