2,475 research outputs found

    Cometary ion drift energy and temperature at comet 67P-Churyumov/Gerasimeko

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    The Ion Composition Analyzer (ICA) on the Rosetta spacecraft observed both the solar wind and the cometary ionosphere around comet 67P/Churyumov-Gerasimenko for nearly two years. However, observations of low energy cometary ions were affected by a highly negative spacecraft potential, and the ICA ion density estimates were often much lower than plasma densities found by other instruments. Since the low energy cometary ions are often the highest density population in the plasma environment, it is nonetheless desirable to understand their properties. To do so, we select ICA data with densities comparable to those of Rosetta's Langmuir Probe (LAP)/Mutual Impedance Probe throughout the mission. We then correct the cometary ion energy distribution of each energy-angle scan for spacecraft potential and fit a drifting Maxwell-Boltzmann distribution, which gives an estimate of the drift energy and temperature for 3521 scans. The resulting drift energy is generally between 11--18 eV and the temperature between 0.5--1 eV. The drift energy shows good agreement with published ion flow speeds from LAP during the same time period and is much higher than the cometary neutral speed. We see additional higher energy cometary ions in the spectra closest to perihelion, which can either be a second Maxwellian or a kappa distribution. The energy and temperature are negatively correlated with heliocentric distance, but the slope of the change is small. It cannot be quantitatively determined whether this trend is primarily due to heliocentric distance or spacecraft distance to the comet, which increased with decreasing heliocentric distance.Comment: 9 pages, 10 figure

    Euclid: Fast two-point correlation function covariance through linear construction

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    We present a method for fast evaluation of the covariance matrix for a two-point galaxy correlation function (2PCF) measured with the Landy-Szalay estimator. The standard way of evaluating the covariance matrix consists in running the estimator on a large number of mock catalogs, and evaluating their sample covariance. With large random catalog sizes (random-to-data objects' ratio M >> 1) the computational cost of the standard method is dominated by that of counting the data-random and random-random pairs, while the uncertainty of the estimate is dominated by that of data-data pairs. We present a method called Linear Construction (LC), where the covariance is estimated for small random catalogs with a size of M = 1 and M = 2, and the covariance for arbitrary M is constructed as a linear combination of the two. We show that the LC covariance estimate is unbiased. We validated the method with PINOCCHIO simulations in the range r = 20-200 h(-1) Mpc. With M = 50 and with 2h(-1) Mpc bins, the theoretical speedup of the method is a factor of 14. We discuss the impact on the precision matrix and parameter estimation, and present a formula for the covariance of covariance.Peer reviewe

    Diabetes and Prostate Cancer Screening in Black and White Men

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    PURPOSE: Prior studies conducted primarily among white men find a reduced risk of prostate cancer associated with time since developing diabetes. While biologic explanations are plausible, the association may in part arise from more frequent prostate cancer screening among those with a diabetes diagnosis. The purpose of the present study was to investigate the association between diabetes and prostate cancer screening. METHODS: We examined differences in prostate cancer screening (prostate-specific antigen and/or digital rectal examination) testing practices after a diabetes diagnosis among lower-income persons living in the southeastern United States and enrolled in the Southern Community Cohort Study between 2002 and 2009. Baseline in-person interviews collected information on history of diabetes and prostate cancer screening from 18,809 black and 6,404 white men aged 40-79 years. RESULTS: After adjustment for confounding, diabetic black [odds ratio (OR) 1.12, 95 % confidence interval (CI) 1.01-1.25] and white (OR 1.25, 95 % CI 1.03-1.51) men were more likely to undergo recent prostate cancer screening compared to non-diabetic men of the same race. The increased risk for prostate cancer screening, however, occurred primarily within the first 12 months after diabetes diagnosis. CONCLUSIONS: Our results suggest that a diabetes diagnosis modestly increases the likelihood of having a prostate cancer screening test for both black and white men. The prevalence of screening was higher nearer to the time of diabetes diagnosis, which may contribute to an early increase in prostate cancer detection followed by lower prostate cancer detection after an extended time

    Progressive Structural Defects in Canine Centronuclear Myopathy Indicate a Role for HACD1 in Maintaining Skeletal Muscle Membrane Systems

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    Mutations in HACD1/PTPLA cause recessive congenital myopathies in humans and dogs. Hydroxyacyl-coA dehydratases are required for elongation of very long chain fatty acids, and HACD1 has a role in early myogenesis, but the functions of this striated muscle-specific enzyme in more differentiated skeletal muscle remain unknown. Canine HACD1 deficiency is histopathologically classified as a centronuclear myopathy (CNM). We investigated the hypothesis that muscle from HACD1-deficient dogs has membrane abnormalities in common with CNMs with different genetic causes. We found progressive changes in tubuloreticular and sarcolemmal membranes and mislocalized triads and mitochondria in skeletal muscle from animals deficient in HACD1. Furthermore, comparable membranous abnormalities in cultured HACD1-deficient myotubes provide additional evidence that these defects are a primary consequence of altered HACD1 expression. Our novel findings, including T-tubule dilatation and disorganization, associated with defects in this additional CNM-associated gene provide a definitive pathophysiologic link with these disorders, confirm that dogs deficient in HACD1 are relevant models, and strengthen the evidence for a unifying pathogenesis in CNMs via defective membrane trafficking and excitation-contraction coupling in muscle. These results build on previous work by determining further functional roles of HACD1 in muscle and provide new insight into the pathology and pathogenetic mechanisms of HACD1 CNM. Consequently, alterations in membrane properties associated with HACD1 mutations should be investigated in humans with related phenotypes
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