54 research outputs found

    A Systematic Study of Mid-Infrared Emission from Core-Collapse Supernovae with Spirits

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    The American Astronomical Society. All rights reserved.We present a systematic study of mid-infrared emission from 141 nearby supernovae (SNe) observed with Spitzer/IRAC as part of the ongoing SPIRITS survey. We detect 8 Type Ia and 36 core-collapse SNe. All Type Ia/Ibc SNe become undetectable within three years of explosion, whereas 22 ± 11% of Type II SNe continue to be detected. Five Type II SNe are detected even two decades after discovery (SN 1974E, 1979C, 1980K, 1986J, and 1993J). Warm dust luminosity, temperature, and a lower limit on mass are obtained by fitting the two IRAC bands, assuming an optically thin dust shell. We derive warm dust masses between 10-6 and 10-2 M o and dust color temperatures between 200 and 1280 K. This observed warm dust could be pre-existing or newly created, but in either case represents a lower limit to the dust mass because cooler dust may be present. We present three case studies of extreme SNe. SN 2011ja (II-P) was over-luminous ([4.5] = -15.6 mag) at 900 days post explosion with increasing hot dust mass, suggesting either an episode of dust formation or intensifying circumstellar material (CSM) interactions heating up pre-existing dust. SN 2014bi (II-P) showed a factor of 10 decrease in dust mass over one month, suggesting either dust destruction or reduced dust heating. The IR luminosity of SN 2014C (Ib) stayed constant over 800 days, possibly due to strong CSM interaction with an H-rich shell, which is rare among stripped-envelope SNe. The observations suggest that this CSM shell originated from an LBV-like eruption roughly 100 years pre-explosion. The observed diversity demonstrates the power of mid-IR observations of a large sample of SNe. © 2017

    Natural solution to antibiotic resistance: bacteriophages ‘The Living Drugs’

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    International Society of Sports Nutrition Position Stand: Nutritional recommendations for single-stage ultra-marathon; training and racing

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    Background. In this Position Statement, the International Society of Sports Nutrition (ISSN) provides an objective and critical review of the literature pertinent to nutritional considerations for training and racing in single-stage ultra-marathon. Recommendations for Training. i) Ultra-marathon runners should aim to meet the caloric demands of training by following an individualized and periodized strategy, comprising a varied, food-first approach; ii) Athletes should plan and implement their nutrition strategy with sufficient time to permit adaptations that enhance fat oxidative capacity; iii) The evidence overwhelmingly supports the inclusion of a moderate-to-high carbohydrate diet (i.e., ~60% of energy intake, 5 – 8 g⸱kg−1·d−1) to mitigate the negative effects of chronic, training-induced glycogen depletion; iv) Limiting carbohydrate intake before selected low-intensity sessions, and/or moderating daily carbohydrate intake, may enhance mitochondrial function and fat oxidative capacity. Nevertheless, this approach may compromise performance during high-intensity efforts; v) Protein intakes of ~1.6 g·kg−1·d−1 are necessary to maintain lean mass and support recovery from training, but amounts up to 2.5 g⸱kg−1·d−1 may be warranted during demanding training when calorie requirements are greater; Recommendations for Racing. vi) To attenuate caloric deficits, runners should aim to consume 150 - 400 kcal⸱h−1 (carbohydrate, 30 – 50 g⸱h−1; protein, 5 – 10 g⸱h−1) from a variety of calorie-dense foods. Consideration must be given to food palatability, individual tolerance, and the increased preference for savory foods in longer races; vii) Fluid volumes of 450 – 750 mL⸱h−1 (~150 – 250 mL every 20 min) are recommended during racing. To minimize the likelihood of hyponatraemia, electrolytes (mainly sodium) may be needed in concentrations greater than that provided by most commercial products (i.e., >575 mg·L−1 sodium). Fluid and electrolyte requirements will be elevated when running in hot and/or humid conditions; viii) Evidence supports progressive gut-training and/or low-FODMAP diets (fermentable oligosaccharide, disaccharide, monosaccharide and polyol) to alleviate symptoms of gastrointestinal distress during racing; ix) The evidence in support of ketogenic diets and/or ketone esters to improve ultra-marathon performance is lacking, with further research warranted; x) Evidence supports the strategic use of caffeine to sustain performance in the latter stages of racing, particularly when sleep deprivation may compromise athlete safety

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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