2,401 research outputs found

    Radii of 88 M subdwarfs and updated radius relations for low-metallicity M-dwarf stars

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    M subdwarfs are low-metallicity M dwarfs that typically inhabit the halo population of the Galaxy. Metallicity controls the opacity of stellar atmospheres; in metal-poor stars, hydrostatic equilibrium is reached at a smaller radius, leading to smaller radii for a given effective temperature. We compile a sample of 88 stars that span spectral classes K7 to M6 and include stars with metallicity classes from solar-metallicity dwarf stars to the lowest metallicity ultra subdwarfs to test how metallicity changes the stellar radius. We fit models to Palomar Double Spectrograph (DBSP) optical spectra to derive effective temperatures (T_ eff) and we measure bolometric luminosities (L_ bol) by combining broad wavelength-coverage photometry with Gaia parallaxes. Radii are then computed by combining the T_ eff and L_ bol using the Stefan–Boltzman law. We find that for a given temperature, ultra subdwarfs can be as much as five times smaller than their solar-metallicity counterparts. We present color-radius and color-surface brightness relations that extend down to [Fe/H] of −2.0 dex, in order to aid the radius determination of M subdwarfs, which will be especially important for the WFIRST exoplanetary microlensing survey.Published versio

    OXA-66 structure and oligomerisation of OXAAb enzymes

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    The OXA β-lactamases are responsible for hydrolysing β-lactam antibiotics and contribute to the multidrug-resistant phenotype of several major human pathogens. The OXAAb enzymes are intrinsic to Acinetobacter baumannii and can confer resistance to carbapenem antibiotics. Here we determined the structure of the most prevalent OXAAb enzyme, OXA-66. The structure of OXA-66 was solved at a resolution of 2.1 Å and found to be very similar to the structure of OXA-51, the only other OXAAb enzyme that has had its structure solved. Our data contained one molecule per asymmetric unit, and analysis of positions responsible for dimer formation in other OXA enzymes suggest that OXA-66 likely exists as a monomer

    A 192×128 Time Correlated SPAD Image Sensor in 40-nm CMOS Technology

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    A 192 X 128 pixel single photon avalanche diode (SPAD) time-resolved single photon counting (TCSPC) image sensor is implemented in STMicroelectronics 40-nm CMOS technology. The 13% fill factor, 18.4\,\,\mu \text {m} \times 9.2\,\,\mu \text{m} pixel contains a 33-ps resolution, 135-ns full scale, 12-bit time-to-digital converter (TDC) with 0.9-LSB differential and 5.64-LSB integral nonlinearity (DNL/INL). The sensor achieves a mean 219-ps full-width half-maximum (FWHM) impulse response function (IRF) and is operable at up to 18.6 kframes/s through 64 parallelized serial outputs. Cylindrical microlenses with a concentration factor of 3.25 increase the fill factor to 42%. The median dark count rate (DCR) is 25 Hz at 1.5-V excess bias. A digital calibration scheme integrated into a column of the imager allows off-chip digital process, voltage, and temperature (PVT) compensation of every frame on the fly. Fluorescence lifetime imaging microscopy (FLIM) results are presented

    Using gene expression data to identify certain gastro-intestinal diseases

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    BACKGROUND: Inflammatory bowel diseases, ulcerative colitis and Crohn’s disease are considered to be of autoimmune origin, but the etiology of irritable bowel syndrome remains elusive. Furthermore, classifying patients into irritable bowel syndrome and inflammatory bowel diseases can be difficult without invasive testing and holds important treatment implications. Our aim was to assess the ability of gene expression profiling in blood to differentiate among these subject groups. METHODS: Transcript levels of a total of 45 genes in blood were determined by quantitative real-time polymerase chain reaction (RT-PCR). We applied three separate analytic approaches; one utilized a scoring system derived from combinations of ratios of expression levels of two genes and two different support vector machines. RESULTS: All methods discriminated different subject cohorts, irritable bowel syndrome from control, inflammatory bowel disease from control, irritable bowel syndrome from inflammatory bowel disease, and ulcerative colitis from Crohn’s disease, with high degrees of sensitivity and specificity. CONCLUSIONS: These results suggest these approaches may provide clinically useful prediction of the presence of these gastro-intestinal diseases and syndromes

    Discovery of Middle Pleistocene fossil and stone tool-bearing deposits at Groot Kloof, Ghaap escarpment, Northern Cape province

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    We report the discovery of a major fossil-bearing and archaeological complex of karstic deposits at Groot Kloof in the escarpment of the Ghaap Plateau, around 100 km southwest of Taung. The region is known for open fluvial and lacustrine sites sampling Lower and Middle Pleistocene tool types and the long, but discontinuous sequence ofWonderwerk Cave. Research at Groot Kloof has concentrated on two of four localities. One locality has yielded fossils from the Florisian Land Mammal Age and lithics that may sample a late Early Stone Age/early Middle Stone Age type industry. The second locality has been dated using U-Th to 248 <U>+</U> 37 kyr ago for fossil-bearing tufa, and normal magnetic polarity for various tufa and breccia. The occurrence of fossils embedded within tufa rather than infilling a cavity is unusual. Small pockets of Later Stone Age artefact-bearing breccia and rock art also occur. The significance of Groot Kloof is underscored by current debate about the emergence of modern humans in which the appearance of modern behaviour is posited to have occurred inthis and other regions during this part of the Middle Pleistocene

    Could an integrated model of health and social care after critical illness reduce socioeconomic disparities in outcomes? A Bayesian analysis

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    Background There is limited evidence to understand what impact, if any, recovery services might have for patients across the socioeconomic spectrum after critical illness. We analysed data from a multicentre critical care recovery programme to understand the impact of this programme across the socioeconomic spectrum. Methods The setting for this pre-planned secondary analysis was a critical care rehabilitation programme—Intensive Care Syndrome: Promoting Independence and Return to Employment. Data were collected from five hospital sites running this programme. We utilised a Bayesian approach to analysis and explore any possible effect of the InS:PIRE intervention on Health-Related Quality of Life (HRQoL) across the socioeconomic gradient. A Bayesian quantile, non-linear mixed effects regression model, using a compound symmetry covariance structure, accounting for multiple timepoints was utilised. The Scottish Index of Multiple Deprivation (SIMD) was used to measure socioeconomic status and HRQoL was measured using the EQ-5D-5L. Results In the initial baseline cohort of 182 patients, 55% of patients were male, the median age was 58 yr (inter-quartile range: 50–66 yr) and 129 (79%) patients had two or more comorbidities at ICU admission. Using the neutral prior, there was an overall probability of intervention benefit of 100% (β=0.71, 95% credible interval: 0.34–1.09) over 12 months to those in the SIMD≤3 cohort, and an 98.6% (β=−1.38, 95% credible interval: −2.62 to −0.16) probability of greater benefit (i.e. a steeper increase in improvement) at 12 months in the SIMD≤3 vs SIMD≥4 cohort in the EQ-visual analogue scale. Conclusions Using multicentre data, this re-analysis suggests, but does not prove, that an integrated health and social care intervention is likely to improve outcomes across the socioeconomic gradient after critical illness, with a potentially greater benefit for those from deprived communities. Future research designed to prospectively analyse how critical care recovery programmes could potentially improve outcomes across the socioeconomic gradient is warranted

    Development of an invasively monitored porcine model of acetaminophen-induced acute liver failure

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    Background: The development of effective therapies for acute liver failure (ALF) is limited by our knowledge of the pathophysiology of this condition, and the lack of suitable large animal models of acetaminophen toxicity. Our aim was to develop a reproducible invasively-monitored porcine model of acetaminophen-induced ALF. Method: 35kg pigs were maintained under general anaesthesia and invasively monitored. Control pigs received a saline infusion, whereas ALF pigs received acetaminophen intravenously for 12 hours to maintain blood concentrations between 200-300 mg/l. Animals surviving 28 hours were euthanased. Results: Cytochrome p450 levels in phenobarbital pre-treated animals were significantly higher than non pre-treated animals (300 vs 100 pmol/mg protein). Control pigs (n=4) survived 28-hour anaesthesia without incident. Of nine pigs that received acetaminophen, four survived 20 hours and two survived 28 hours. Injured animals developed hypotension (mean arterial pressure; 40.8+/-5.9 vs 59+/-2.0 mmHg), increased cardiac output (7.26+/-1.86 vs 3.30+/-0.40 l/min) and decreased systemic vascular resistance (8.48+/-2.75 vs 16.2+/-1.76 mPa/s/m3). Dyspnoea developed as liver injury progressed and the increased pulmonary vascular resistance (636+/-95 vs 301+/-26.9 mPa/s/m3) observed may reflect the development of respiratory distress syndrome. Liver damage was confirmed by deterioration in pH (7.23+/-0.05 vs 7.45+/-0.02) and prothrombin time (36+/-2 vs 8.9+/-0.3 seconds) compared with controls. Factor V and VII levels were reduced to 9.3 and 15.5% of starting values in injured animals. A marked increase in serum AST (471.5+/-210 vs 42+/-8.14) coincided with a marked reduction in serum albumin (11.5+/-1.71 vs 25+/-1 g/dL) in injured animals. Animals displayed evidence of renal impairment; mean creatinine levels 280.2+/-36.5 vs 131.6+/-9.33 mumol/l. Liver histology revealed evidence of severe centrilobular necrosis with coagulative necrosis. Marked renal tubular necrosis was also seen. Methaemoglobin levels did not rise >5%. Intracranial hypertension was not seen (ICP monitoring), but there was biochemical evidence of encephalopathy by the reduction of Fischer's ratio from 5.6 +/- 1.1 to 0.45 +/- 0.06. Conclusion: We have developed a reproducible large animal model of acetaminophen-induced liver failure, which allows in-depth investigation of the pathophysiological basis of this condition. Furthermore, this represents an important large animal model for testing artificial liver support systems
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