202 research outputs found
Purification of non-infectious ganglioside preparations from scrapie-infected brain tissue.
Inactivation of the scrapie agent in a scaled-down procedure for the purification of gangliosides from brain tissue.
Measurement of the time-dependent CP asymmetry in B0 -> J/ψ KS0 decays
This Letter reports a measurement of the CP violation observables SJ/ψK0S and CJ/ψK0S in the decay channel B0→J/ψK0S performed with 1.0 fb−1 of pp collisions at s√=7 TeV collected by the LHCb experiment. The fit to the data yields SJ/ψK0S=0.73±0.07(stat)±0.04(syst) and CJ/ψK0S=0.03±0.09(stat)±0.01(syst). Both values are consistent with the current world averages and within
expectations from the Standard Model
Systemic amyloidosis in England: an epidemiological study.
Epidemiological studies of systemic amyloidosis are scarce and the burden of disease in England has not previously been estimated. In 1999, the National Health Service commissioned the National Amyloidosis Centre (NAC) to provide a national clinical service for all patients with amyloidosis. Data for all individuals referred to the NAC is held on a comprehensive central database, and these were compared with English death certificate data for amyloidosis from 2000 to 2008, obtained from the Office of National Statistics. Amyloidosis was stated on death certificates of 2543 individuals, representing 0·58/1000 recorded deaths. During the same period, 1143 amyloidosis patients followed at the NAC died, 903 (79%) of whom had amyloidosis recorded on their death certificates. The estimated minimum incidence of systemic amyloidosis in the English population in 2008, based on new referrals to the NAC, was 0·4/100 000 population. The incidence peaked at age 60-79 years. Systemic AL amyloidosis was the most common type with an estimated minimum incidence of 0·3/100 000 population. Although there are various limitations to this study, the available data suggest the incidence of systemic amyloidosis in England exceeds 0·8/100 000 of the population
The doubling of stellar black hole nuclei
It is strongly believed that Andromeda's double nucleus signals a disc of stars revolving around its central supermassive black hole on eccentric Keplerian orbits with nearly aligned apsides. A self-consistent stellar dynamical origin for such apparently long-lived alignment has so far been lacking, with indications that cluster self-gravity is capable of sustaining such lopsided configurations if and when stimulated by external perturbations. Here, we present results of N-body simulations which show unstable counter-rotating stellar clusters around supermassive black holes saturating into uniformly precessing lopsided nuclei. The double nucleus in our featured experiment decomposes naturally into a thick eccentric disc of apo-apse aligned stars which is embedded in a lighter triaxial cluster. The eccentric disc reproduces key features of Keplerian disc models of Andromeda's double nucleus; the triaxial cluster has a distinctive kinematic signature which is evident in Hubble Space Telescope observations of Andromeda's double nucleus, and has been difficult to reproduce withKeplerian discs alone. Our simulations demonstrate how the combination of an eccentric disc and a triaxial cluster arises naturally when a star cluster accreted over a preexisting and counter-rotating disc of stars drives disc and cluster into a mutually destabilizing dance. Such accretion events are inherent to standard galaxy formation scenarios. They are here shown to double stellar black hole nuclei as they feed them. © 2013 The Authors Published by Oxford University Press on behalf of the Royal Astronomical Society.Alexander T, 2005, PHYS REP, V419, P65, DOI 10.1016-j.physrep.2005.08.002; Bacon R, 2001, ASTRON ASTROPHYS, V371, P409, DOI 10.1051-0004-6361:20010317; Bender R, 2005, ASTROPHYS J, V631, P280, DOI 10.1086-432434; Chang P, 2007, ASTROPHYS J, V668, P236, DOI 10.1086-521018; DRESSLER A, 1988, ASTROPHYS J, V324, P701, DOI 10.1086-165930; Emsellem E, 1997, ASTRON ASTROPHYS, V323, P674; Fujii M, 2010, ASTROPHYS J LETT, V716, pL80, DOI 10.1088-2041-8205-716-1-L80; Gerhard O, 2001, ASTROPHYS J, V546, pL39, DOI 10.1086-318054; Gultekin K, 2011, ASTROPHYS J, V741, DOI 10.1088-0004-637X-741-1-38; Hopkins PF, 2010, MON NOT R ASTRON SOC, V407, P1529, DOI 10.1111-j.1365-2966.2010.17064.x; Hopkins PF, 2010, MON NOT R ASTRON SOC, V405, pL41, DOI 10.1111-j.1745-3933.2010.00855.x; Jacobs V, 2001, ASTROPHYS J, V555, pL25, DOI 10.1086-321728; Jog CJ, 2009, PHYS REP, V471, P75, DOI 10.1016-j.physrep.2008.12.002; Kim SS, 2003, ASTROPHYS J, V597, P312, DOI 10.1086-378347; Kormendy J., 2004, CARNEGIE OBSERVATORI, V1, P1; KORMENDY J, 1988, ASTROPHYS J, V325, P128, DOI 10.1086-165988; Kormendy J, 1999, ASTROPHYS J, V522, P772, DOI 10.1086-307665; LAUER TR, 1993, ASTRON J, V106, P1436, DOI 10.1086-116737; Lauer TR, 1996, ASTROPHYS J, V471, pL79, DOI 10.1086-310344; Lauer TR, 2005, ASTRON J, V129, P2138, DOI 10.1086-429565; LIGHT ES, 1974, ASTROPHYS J, V194, P257, DOI 10.1086-153241; Magorrian J, 1998, ASTRON J, V115, P2285, DOI 10.1086-300353; Magorrian J, 1999, MON NOT R ASTRON SOC, V309, P447, DOI 10.1046-j.1365-8711.1999.02853.x; Naoz S., 2011, AAS DIVISION EXTREME, V2, P605; Peiris HV, 2003, ASTROPHYS J, V599, P237, DOI 10.1086-378638; Quillen AC, 2003, ASTRON J, V125, P2998, DOI 10.1086-375307; Salow RM, 2001, ASTROPHYS J, V551, pL49, DOI 10.1086-319834; Sambhus N, 2002, ASTRON ASTROPHYS, V388, P766, DOI 10.1051-0004-6361:20020298; Silk J., 2011, ARXIV E PRINTS; Springel V, 2005, MON NOT R ASTRON SOC, V364, P1105, DOI 10.1111-j.1365-2966.2005.09655.x; Sridhar S, 1997, MON NOT R ASTRON SOC, V292, P657; Sridhar S, 2010, MON NOT R ASTRON SOC, V404, P527, DOI 10.1111-j.1365-2966.2010.16306.x; Touma JR, 2002, MON NOT R ASTRON SOC, V333, P583, DOI 10.1046-j.1365-8711.2002.05437.x; Touma JR, 2009, MON NOT R ASTRON SOC, V394, P1085, DOI 10.1111-j.1365-2966.2009.14409.x; Tremaine S, 2001, ASTRON J, V121, P1776, DOI 10.1086-319398; TREMAINE S, 1995, ASTRON J, V110, P628, DOI 10.1086-117548; TREMAINE SD, 1975, ASTROPHYS J, V196, P407, DOI 10.1086-15342222
Dietary zinc and the control of Streptococcus pneumoniae infection
© 2019 Eijkelkamp et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Human zinc deficiency increases susceptibility to bacterial infection. Although zinc supplementation therapies can reduce the impact of disease, the molecular basis for protection remains unclear. Streptococcus pneumoniae is a major cause of bacterial pneumonia, which is prevalent in regions of zinc deficiency. We report that dietary zinc levels dictate the outcome of S. pneumoniae infection in a murine model. Dietary zinc restriction impacts murine tissue zinc levels with distribution post-infection altered, and S. pneumoniae virulence and infection enhanced. Although the activation and infiltration of murine phagocytic cells was not affected by zinc restriction, their efficacy of bacterial control was compromised. S. pneumoniae was shown to be highly sensitive to zinc intoxication, with this process impaired in zinc restricted mice and isolated phagocytic cells. Collectively, these data show how dietary zinc deficiency increases sensitivity to S. pneumoniae infection while revealing a role for zinc as a component of host antimicrobial defences
A Case Study of the Population Ecology of a Topmouth Gudgeon (Pseudorasbora parva) Population in the UK and the Implication for Native Fish Communities
1. The topmouth gudgeon Pseudorasbora parva is a small Asian cyprinid species that has proved invasive throughout many European countries. Following an initial introduction into the wild in 1996, the species is now proving invasive in the UK, with at least 25 infested waters in England and Wales, of which 10 are known to have direct connection to a major river catchment.
2. To demonstrate the threat of P. parva to fisheries in the UK, a case study is presented on a lake located in the Lake District of England where the species was introduced in 2000. The species rapidly established a breeding population that, by 2003, was the dominant species in size classes <70 mm. In 2004, they were the only species in the lake that produced young-of-the-year.
3. Individual P. parva adopted the reproductive tactics of early maturity, multiple spawning, male dominance and male nest guarding; sexual dimorphism was manifested in larger body size of males. These traits were in contrast to the resident, native species of the lake, including roach Rutilus rutilus and gudgeon Gobio gobio, which adopted traits of later maturity and single spawning.
4. This case study, therefore, revealed relatively rapid establishment of a P. parva population, their subsequent numerical dominance of the fish community, and the impediment of the recruitment of native fish. The implications for UK fisheries are concerning: should P. parva continue to disperse and individuals adopt similar traits as those in this case study, there may be few waters immune from their invasion, numerical dominance and subsequent impacts
Identification of heart rate-associated loci and their effects on cardiac conduction and rhythm disorders
Elevated resting heart rate is associated with greater risk of cardiovascular disease and mortality. In a 2-stage meta-analysis of genome-wide association studies in up to 181,171 individuals, we identified 14 new loci associated with heart rate and confirmed associations with all 7 previously established loci. Experimental downregulation of gene expression in Drosophila melanogaster and Danio rerio identified 20 genes at 11 loci that are relevant for heart rate regulation and highlight a role for genes involved in signal transmission, embryonic cardiac development and the pathophysiology of dilated cardiomyopathy, congenital heart failure and/or sudden cardiac death. In addition, genetic susceptibility to increased heart rate is associated with altered cardiac conduction and reduced risk of sick sinus syndrome, and both heart rate-increasing and heart rate-decreasing variants associate with risk of atrial fibrillation. Our findings provide fresh insights into the mechanisms regulating heart rate and identify new therapeutic targets
Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways
To newly identify loci for age at natural menopause, we carried out a meta-analysis of 22 genome-wide association studies (GWAS) in 38,968 women of European descent, with replication in up to 14,435 women. In addition to four known loci, we identified 13 loci newly associated with age at natural menopause (at P < 5 × 10(-8)). Candidate genes located at these newly associated loci include genes implicated in DNA repair (EXO1, HELQ, UIMC1, FAM175A, FANCI, TLK1, POLG and PRIM1) and immune function (IL11, NLRP11 and PRRC2A (also known as BAT2)). Gene-set enrichment pathway analyses using the full GWAS data set identified exoDNase, NF-κB signaling and mitochondrial dysfunction as biological processes related to timing of menopause
Hundreds of variants clustered in genomic loci and biological pathways affect human height
Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits(1), but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait(2,3). The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P<0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways
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