317 research outputs found

    Probing Satellite Quenching With Galaxy Clustering

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    Satellites within simulated massive clusters are significantly spatially correlated with each other, even when those satellites are not gravitationally bound to each other. This correlation is produced by satellites that entered their hosts relatively recently, and is undetectable for satellites that have resided in their hosts for multiple dynamical timescales. Therefore, a measurement of clustering statistics of cluster satellites may be used to determine the typical accretion redshifts of those satellites into their observed hosts. We argue that such measurements may be used to determine the fraction of satellite galaxies that were quenched by their current hosts, thereby discriminating among models for quenching of star formation in satellite galaxies.Comment: 7 page

    Extracting information from the exteriors of dark matter halos

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    While significant amounts of time has been spent studying dark matter halos, the environment around halos and the impact this environment has on structures that pass through it has not been investigated in nearly as much detail. In this thesis we perform several different studies all related to extracting information from the exteriors of dark matter halos. We study subhalos in clusters and the region outside of their virial radii, finding that there is additional matter correlated with recently accreted subhalos. We also find that recently accreted subhalos have stronger correlations with other subhalos than subhalos accreted long ago. We argue that this could distinguish between different theories of what causes star formation to be quenched in high-density environments like clusters. We also demonstrate that the caustic feature seen in the density profile of the exteriors of clusters is indeed related to the splashback radius. In addition, we investigate the possibility of observing matter that has been stripped by tidal interactions as galaxies enter clusters. We find that we can indeed detect tidal tails when using full 3D data but cannot do so when we only have access to projected data. Finally, we study the impact that future accretion has on galaxy-sized halos located near cluster-sized halos. We find that there is indeed a drop in the accretion rate of future subhalos even outside of the virial radius of the cluster, but the exact radius where this drop begins is sensitive to the smoothing scale we use for the local density

    Origin of intermittent accretion-powered X-ray oscillations in neutron stars with millisecond spin periods

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    We have shown previously that many of the properties of persistent accretion-powered millisecond pulsars can be understood if their X-ray emitting areas are near their spin axes and move as the accretion rate and structure of the inner disk vary. Here we show that this "nearly aligned moving spot model" may also explain the intermittent accretion-powered pulsations that have been detected in three weakly magnetic accreting neutron stars. We show that movement of the emitting area from very close to the spin axis to about 10 degrees away can increase the fractional rms amplitude from less than about 0.5 percent, which is usually undetectable with current instruments, to a few percent, which is easily detectable. The second harmonic of the spin frequency usually would not be detected, in agreement with observations. The model produces intermittently detectable oscillations for a range of emitting area sizes and beaming patterns, stellar masses and radii, and viewing directions. Intermittent oscillations are more likely in stars that are more compact. In addition to explaining the sudden appearance of accretion-powered millisecond oscillations in some neutron stars with millisecond spin periods, the model explains why accretion-powered millisecond oscillations are relatively rare and predicts that the persistent accretion-powered millisecond oscillations of other stars may become undetectable for brief intervals. It suggests why millisecond oscillations are frequently detected during the X-ray bursts of some neutron stars but not others and suggests mechanisms that could explain the occasional temporal association of intermittent accretion-powered oscillations with thermonuclear X-ray bursts.Comment: 5 pages, 1 figure; includes additional discussion and updated references; accepted for publication in ApJ

    Multidimensional treatment foster care for preschoolers: early findings of an implementation in the Netherlands

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    Multidimensional Treatment Foster Care (MTFC) has been shown to be an evidence based alternative to residential rearing and an effective method to improve behavior and attachment of preschool foster children in the US. This preliminary study investigated an application of MTFC for preschoolers (MTFC-P) in the Netherlands focusing on behavioral outcomes in course of the intervention. To examine the following hypothesis: β€œthe time in the MTFC-P intervention predicts a decline in problem behavior, as this is the desired outcome for children assigned to MTFC-P”, we assessed the daily occurrence of 38 problem behaviors via telephone interviews. Repeated measures revealed significant reduced problem behavior in course of the program. MTFC-P promises to be a treatment model suitable for high-risk foster children, that is transferable across centres and countries

    An Unexpected Function of the Prader-Willi Syndrome Imprinting Center in Maternal Imprinting in Mice

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    Genomic imprinting is a phenomenon that some genes are expressed differentially according to the parent of origin. Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are neurobehavioral disorders caused by deficiency of imprinted gene expression from paternal and maternal chromosome 15q11–q13, respectively. Imprinted genes at the PWS/AS domain are regulated through a bipartite imprinting center, the PWS-IC and AS-IC. The PWS-IC activates paternal-specific gene expression and is responsible for the paternal imprint, whereas the AS-IC functions in the maternal imprint by allele-specific repression of the PWS-IC to prevent the paternal imprinting program. Although mouse chromosome 7C has a conserved PWS/AS imprinted domain, the mouse equivalent of the human AS-IC element has not yet been identified. Here, we suggest another dimension that the PWS-IC also functions in maternal imprinting by negatively regulating the paternally expressed imprinted genes in mice, in contrast to its known function as a positive regulator for paternal-specific gene expression. Using a mouse model carrying a 4.8-kb deletion at the PWS-IC, we demonstrated that maternal transmission of the PWS-IC deletion resulted in a maternal imprinting defect with activation of the paternally expressed imprinted genes and decreased expression of the maternally expressed imprinted gene on the maternal chromosome, accompanied by alteration of the maternal epigenotype toward a paternal state spread over the PWS/AS domain. The functional significance of this acquired paternal pattern of gene expression was demonstrated by the ability to complement PWS phenotypes by maternal inheritance of the PWS-IC deletion, which is in stark contrast to paternal inheritance of the PWS-IC deletion that resulted in the PWS phenotypes. Importantly, low levels of expression of the paternally expressed imprinted genes are sufficient to rescue postnatal lethality and growth retardation in two PWS mouse models. These findings open the opportunity for a novel approach to the treatment of PWS

    Emerging Infectious Disease leads to Rapid Population Decline of Common British Birds

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    Emerging infectious diseases are increasingly cited as threats to wildlife, livestock and humans alike. They can threaten geographically isolated or critically endangered wildlife populations; however, relatively few studies have clearly demonstrated the extent to which emerging diseases can impact populations of common wildlife species. Here, we report the impact of an emerging protozoal disease on British populations of greenfinch Carduelis chloris and chaffinch Fringilla coelebs, two of the most common birds in Britain. Morphological and molecular analyses showed this to be due to Trichomonas gallinae. Trichomonosis emerged as a novel fatal disease of finches in Britain in 2005 and rapidly became epidemic within greenfinch, and to a lesser extent chaffinch, populations in 2006. By 2007, breeding populations of greenfinches and chaffinches in the geographic region of highest disease incidence had decreased by 35% and 21% respectively, representing mortality in excess of half a million birds. In contrast, declines were less pronounced or absent in these species in regions where the disease was found in intermediate or low incidence. Also, populations of dunnock Prunella modularis, which similarly feeds in gardens, but in which T. gallinae was rarely recorded, did not decline. This is the first trichomonosis epidemic reported in the scientific literature to negatively impact populations of free-ranging non-columbiform species, and such levels of mortality and decline due to an emerging infectious disease are unprecedented in British wild bird populations. This disease emergence event demonstrates the potential for a protozoan parasite to jump avian host taxonomic groups with dramatic effect over a short time period

    Factors Associated With Referring Close Contacts to an App With Individually-Tailored Vaccine Information

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    Background: Infants too young to be fully vaccinated are vulnerable to potentially deadly influenza and pertussis infections. The cocooning strategy limits this risk by vaccinating those likely to interact with the infant and mother during this vulnerable time, such as close friends and family members. Distribution of accurate and accessible vaccine information through existing social networks could be an important tool in increasing vaccine confidence and coverage. Methods: We surveyed 1095 pregnant women from diverse prenatal care practices in Georgia and Colorado. These women were surveyed through a mobile app to assess vaccine intentions, attitudes, beliefs, norms, and levels of trust, and then presented brief individually-tailored educational videos about maternal and infant vaccines and the cocooning strategy. They were then given the opportunity to refer up to six contacts to enroll in the app and receive similar vaccine education. Results: Twenty-eight percent of these women referred at least one contact, with an average of 2.67 contacts per referring woman. Most referrals (93%) were partners, parents, siblings, relatives, or close friends. Attitudinal constructs significantly associated with increased likelihood of referring contacts included: intention to receive maternal influenza vaccine, perceived safety of maternal Tdap vaccine, perceived efficacy of maternal influenza vaccine, perceived susceptibility to and severity of influenza during pregnancy, and trust in vaccine information from the Centers for Disease Control and Prevention (CDC) and academic institutions. Uncertainty about infant vaccine intentions was associated with decreased likelihood of referring contacts. Conclusions: Pregnant women who valued vaccination and trusted vaccine information from academic institutions were more likely to refer an educational app about vaccines than those who did not. Further research is needed to determine the potential impact of this strategy on vaccine coverage when implemented on a large scale. Trial Registration: The survey informing this article was part of a randomized controlled trial funded by the National Institutes of Health [clinicaltrials.gov registration number NCT02898688]

    Sarcolemma-localized nNOS is required to maintain activity after mild exercise

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    Many neuromuscular conditions are characterized by an exaggerated exercise- induced fatigue response that is disproportionate to activity level. This fatigue is not necessarily correlated with greater central or peripheral fatigue in patients(1), and some patients experience severe fatigue without any demonstrable somatic disease(2). Except in myopathies that are due to specific metabolic defects, the mechanism underlying this type of fatigue remains unknown(2). With no treatment available, this form of inactivity is a major determinant of disability(3). Here we show, using mouse models, that this exaggerated fatigue response is distinct from a loss in specific force production by muscle, and that sarcolemma-localized signalling by neuronal nitric oxide synthase ( nNOS) in skeletal muscle is required to maintain activity after mild exercise. We show that nNOS- null mice do not have muscle pathology and have no loss of muscle- specific force after exercise but do display this exaggerated fatigue response to mild exercise. In mouse models of nNOS mislocalization from the sarcolemma, prolonged inactivity was only relieved by pharmacologically enhancing the cGMP signal that results from muscle nNOS activation during the nitric oxide signalling response to mild exercise. Our findings suggest that the mechanism underlying the exaggerated fatigue response to mild exercise is a lack of contraction- induced signalling from sarcolemma- localized nNOS, which decreases cGMP- mediated vasomodulation in the vessels that supply active muscle after mild exercise. Sarcolemmal nNOS staining was decreased in patient biopsies from a large number of distinct myopathies, suggesting a common mechanism of fatigue. Our results suggest that patients with an exaggerated fatigue response to mild exercise would show clinical improvement in response to treatment strategies aimed at improving exercise- induced signalling.Paul D. Wellstone Muscular Dystrophy Cooperative Research Center Grant ; University of Iowa Cardiovascular Interdisciplinary Research ; National Research Service Award ; National Institute of Arthritis and Musculoskeletal and Skin Diseases ; National Institutes of Health ; Senator Paul D. Wellstone Fellowship ; Muscular Dystrophy Association Development Grant ; Howard Hughes Medical InstituteWe thank M. Anderson and M. Henry for comments, and M. M. Kilburg, K. Uppal, B. J. Steinmann and S. Watkins and members of the Campbell laboratory for scientific contributions. This work was supported in part by a Paul D. Wellstone Muscular Dystrophy Cooperative Research Center Grant. Y.M.K. was supported by grants from the University of Iowa Cardiovascular Interdisciplinary Research/ National Research Service Award (NRSA) Fellowship, from an individual NRSA Fellowship from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, from the National Institutes of Health (NIH), and from a Senator Paul D. Wellstone Fellowship. E.P.R. was supported by a Muscular Dystrophy Association Development Grant. R.M.W. was supported by the NIH. K.P.C. is an investigator of the Howard Hughes Medical Institute.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62850/1/nature07414.pd
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