163 research outputs found

    Behavioral Differences Between Two Recently Sympatric Paper Wasps, the Native \u3ci\u3ePolistes Fuscatus\u3c/i\u3e and the Invasive \u3ci\u3ePolistes Dominulus\u3c/i\u3e

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    Polistes dominulus (Christ), an old world paper wasp, was introduced into the eastern United States in the 1970s and has been rapidly spreading westward. Recently, it has displaced the native Polistes fuscatus (F.) in at least some areas of Michigan. In order to understand why P. dominulus has been so successful, several behavioral attributes were compared between P. dominulus and P. fuscatus at a Michigan field site that contained colonies of both species nest- ing semi-naturally in plywood nestboxes. Preworker colonies of P. dominulus had a significantly greater tendency to store nectar (and had significantly higher proportions of cells with nectar) than preworker colonies of P. fuscatus. This finding may explain the higher survivorship of P. dominulus foundresses reported in a previous study. P. dominulus also had a significantly greater tendency to build vertical nests and had significantly more pedicels per comb and per cell than P. fuscatus. These findings suggest that compared to P. fuscatus, P. dominulus may have more flexibility in the positioning of its combs and, because of a possibly stronger attachment of the comb to a substrate, may be less susceptible to bird predation. The higher winter survivorship reported for P. fuscatus over P. dominulus in a previous study does not appear to be due to differences in the proportions of gynes stranded on their nests late in the fall. Finally, behavioral evidence from videography was consistent with previous reports that P. dominulus is not replacing P. fuscatus through direct agonistic interactions

    Behavioral Differences Between Two Recently Sympatric Paper Wasps, the Native \u3ci\u3ePolistes Fuscatus\u3c/i\u3e and the Invasive \u3ci\u3ePolistes Dominulus\u3c/i\u3e

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    Polistes dominulus (Christ), an old world paper wasp, was introduced into the eastern United States in the 1970s and has been rapidly spreading westward. Recently, it has displaced the native Polistes fuscatus (F.) in at least some areas of Michigan. In order to understand why P. dominulus has been so successful, several behavioral attributes were compared between P. dominulus and P. fuscatus at a Michigan field site that contained colonies of both species nest- ing semi-naturally in plywood nestboxes. Preworker colonies of P. dominulus had a significantly greater tendency to store nectar (and had significantly higher proportions of cells with nectar) than preworker colonies of P. fuscatus. This finding may explain the higher survivorship of P. dominulus foundresses reported in a previous study. P. dominulus also had a significantly greater tendency to build vertical nests and had significantly more pedicels per comb and per cell than P. fuscatus. These findings suggest that compared to P. fuscatus, P. dominulus may have more flexibility in the positioning of its combs and, because of a possibly stronger attachment of the comb to a substrate, may be less susceptible to bird predation. The higher winter survivorship reported for P. fuscatus over P. dominulus in a previous study does not appear to be due to differences in the proportions of gynes stranded on their nests late in the fall. Finally, behavioral evidence from videography was consistent with previous reports that P. dominulus is not replacing P. fuscatus through direct agonistic interactions

    BLAST: Correlations in the Cosmic Far-Infrared Background at 250, 350, and 500 microns Reveal Clustering of Star-Forming Galaxies

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    We detect correlations in the cosmic far-infrared background due to the clustering of star-forming galaxies in observations made with the Balloon-borne Large Aperture Submillimeter Telescope, BLAST, at 250, 350, and 500 microns. We perform jackknife and other tests to confirm the reality of the signal. The measured correlations are well fit by a power law over scales of 5-25 arcminutes, with Delta I/I = 15.1 +/- 1.7%. We adopt a specific model for submillimeter sources in which the contribution to clustering comes from sources in the redshift ranges 1.3 <= z <= 2.2, 1.5 <= z <= 2.7, and 1.7 <= z <= 3.2, at 250, 350, and 500 microns, respectively. With these distributions, our measurement of the power spectrum, P(k_theta), corresponds to linear bias parameters, b = 3.8 +/- 0.6, 3.9 +/- 0.6 and 4.4 +/- 0.7, respectively. We further interpret the results in terms of the halo model, and find that at the smaller scales, the simplest halo model fails to fit our results. One way to improve the fit is to increase the radius at which dark matter halos are artificially truncated in the model, which is equivalent to having some star-forming galaxies at z >= 1 located in the outskirts of groups and clusters. In the context of this model we find a minimum halo mass required to host a galaxy is log (M_min / M_sun) = 11.5 (+0.4/-0.1), and we derive effective biases $b_eff = 2.2 +/- 0.2, 2.4 +/- 0.2, and 2.6 +/- 0.2, and effective masses log (M_eff / M_sun) = 12.9 +/- 0.3, 12.8 +/- 0.2, and 12.7 +/- 0.2, at 250, 350, and 500 microns, corresponding to spatial correlation lengths of r_0 = 4.9, 5.0, and 5.2 +/- 0.7 h^-1 Mpc, respectively. Finally, we discuss implications for clustering measurement strategies with Herschel and Planck.Comment: Accepted for publication in the Astrophysical Journal. Maps and other results available at http://blastexperiment.info

    The ClinGen Epilepsy Gene Curation Expert Panel—Bridging the divide between clinical domain knowledge and formal gene curation criteria

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    The field of epilepsy genetics is advancing rapidly and epilepsy is emerging as a frequent indication for diagnostic genetic testing. Within the larger ClinGen framework, the ClinGen Epilepsy Gene Curation Expert Panel is tasked with connecting two increasingly separate fields: the domain of traditional clinical epileptology, with its own established language and classification criteria, and the rapidly evolving area of diagnostic genetic testing that adheres to formal criteria for gene and variant curation. We identify critical components unique to the epilepsy gene curation effort, including: (a) precise phenotype definitions within existing disease and phenotype ontologies; (b) consideration of when epilepsy should be curated as a distinct disease entity; (c) strategies for gene selection; and (d) emerging rules for evaluating functional models for seizure disorders. Given that de novo variants play a prominent role in many of the epilepsies, sufficient genetic evidence is often awarded early in the curation process. Therefore, the emphasis of gene curation is frequently shifted toward an iterative precuration process to better capture phenotypic associations. We demonstrate that within the spectrum of neurodevelopmental disorders, gene curation for epilepsy-associated genes is feasible and suggest epilepsy-specific conventions, laying the groundwork for a curation process of all major epilepsy-associated genes

    A Single Peroxisomal Targeting Signal Mediates Matrix Protein Import in Diatoms

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    Peroxisomes are single membrane bound compartments. They are thought to be present in almost all eukaryotic cells, although the bulk of our knowledge about peroxisomes has been generated from only a handful of model organisms. Peroxisomal matrix proteins are synthesized cytosolically and posttranslationally imported into the peroxisomal matrix. The import is generally thought to be mediated by two different targeting signals. These are respectively recognized by the two import receptor proteins Pex5 and Pex7, which facilitate transport across the peroxisomal membrane. Here, we show the first in vivo localization studies of peroxisomes in a representative organism of the ecologically relevant group of diatoms using fluorescence and transmission electron microscopy. By expression of various homologous and heterologous fusion proteins we demonstrate that targeting of Phaeodactylum tricornutum peroxisomal matrix proteins is mediated only by PTS1 targeting signals, also for proteins that are in other systems imported via a PTS2 mode of action. Additional in silico analyses suggest this surprising finding may also apply to further diatoms. Our data suggest that loss of the PTS2 peroxisomal import signal is not reserved to Caenorhabditis elegans as a single exception, but has also occurred in evolutionary divergent organisms. Obviously, targeting switching from PTS2 to PTS1 across different major eukaryotic groups might have occurred for different reasons. Thus, our findings question the widespread assumption that import of peroxisomal matrix proteins is generally mediated by two different targeting signals. Our results implicate that there apparently must have been an event causing the loss of one targeting signal even in the group of diatoms. Different possibilities are discussed that indicate multiple reasons for the detected targeting switching from PTS2 to PTS1

    Adult Neurogenesis Transiently Generates Oxidative Stress

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    An increasing body of evidence suggests that alterations in neurogenesis and oxidative stress are associated with a wide variety of CNS diseases, including Alzheimer’s disease, schizophrenia and Parkinson’s disease, as well as routine loss of function accompanying aging. Interestingly, the association between neurogenesis and the production of reactive oxidative species (ROS) remains largely unexamined. The adult CNS harbors two regions of persistent lifelong neurogenesis: the subventricular zone and the dentate gyrus (DG). These regions contain populations of quiescent neural stem cells (NSCs) that generate mature progeny via rapidly-dividing progenitor cells. We hypothesized that the energetic demands of highly proliferative progenitors generates localized oxidative stress that contributes to ROS-mediated damage within the neuropoietic microenvironment. In vivo examination of germinal niches in adult rodents revealed increases in oxidized DNA and lipid markers, particularly in the subgranular zone (SGZ) of the dentate gyrus. To further pinpoint the cell types responsible for oxidative stress, we employed an in vitro cell culture model allowing for the synchronous terminal differentiation of primary hippocampal NSCs. Inducing differentiation in primary NSCs resulted in an immediate increase in total mitochondria number and overall ROS production, suggesting oxidative stress is generated during a transient window of elevated neurogenesis accompanying normal neurogenesis. To confirm these findings in vivo, we identified a set of oxidation-responsive genes, which respond to antioxidant administration and are significantly elevated in genetic- and exercise-induced model of hyperactive hippocampal neurogenesis. While no direct evidence exists coupling neurogenesis-associated stress to CNS disease, our data suggest that oxidative stress is produced as a result of routine adult neurogenesis

    Lupus-related single nucleotide polymorphisms and risk of diffuse large B-cell lymphoma

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    Objective: Determinants of the increased risk of diffuse large B-cell lymphoma (DLBCL) in SLE are unclear. Using data from a recent lymphoma genome-wide association study (GWAS), we assessed whether certain lupus-related single nucleotide polymorphisms (SNPs) were also associated with DLBCL. Methods: GWAS data on European Caucasians from the International Lymphoma Epidemiology Consortium (InterLymph) provided a total of 3857 DLBCL cases and 7666 general-population controls. Data were pooled in a random-effects meta-analysis. Results: Among the 28 SLE-related SNPs investigated, the two most convincingly associated with risk of DLBCL included the CD40 SLE risk allele rs4810485 on chromosome 20q13 (OR per risk allele=1.09, 95% CI 1.02 to 1.16, p=0.0134), and the HLA SLE risk allele rs1270942 on chromosome 6p21.33 (OR per risk allele=1.17, 95% CI 1.01 to 1.36, p=0.0362). Of additional possible interest were rs2205960 and rs12537284. The rs2205960 SNP, related to a cytokine of the tumour necrosis factor superfamily TNFSF4, was associated with an OR per risk allele of 1.07, 95% CI 1.00 to 1.16, p=0.0549. The OR for the rs12537284 (chromosome 7q32, IRF5 gene) risk allele was 1.08, 95% CI 0.99 to 1.18, p=0.0765. Conclusions: These data suggest several plausible genetic links between DLBCL and SLE

    Genetically predicted longer telomere length is associated with increased risk of B-cell lymphoma subtypes

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    Evidence from a small number of studies suggests that longer telomere length measured in peripheral leukocytes is associated with an increased risk of non-Hodgkin lymphoma (NHL). However, these studies may be biased by reverse causation, confounded by unmeasured environmental exposures and might miss time points for which prospective telomere measurement would best reveal a relationship between telomere length and NHL risk. We performed an analysis of genetically inferred telomere length and NHL risk in a study of 10 102 NHL cases of the four most common B-cell histologic types and 9562 controls using a genetic risk score (GRS) comprising nine telomere length-associated single-nucleotide polymorphisms. This approach uses existing genotype data and estimates telomere length by weighing the number of telomere length-associated variant alleles an individual carries with the published change in kb of telomere length. The analysis of the telomere length GRS resulted in an association between longer telomere length and increased NHL risk [four B-cell histologic types combined; odds ratio (OR) = 1.49, 95% CI 1.22–1.82, P-value = 8.5 × 10−5]. Subtype-specific analyses indicated that chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/SLL) was the principal NHL subtype contributing to this association (OR = 2.60, 95% CI 1.93–3.51, P-value = 4.0 × 10−10). Significant interactions were observed across strata of sex for CLL/SLL and marginal zone lymphoma subtypes as well as age for the follicular lymphoma subtype. Our results indicate that a genetic background that favors longer telomere length may increase NHL risk, particularly risk of CLL/SLL, and are consistent with earlier studies relating longer telomere length with increased NHL risk

    ENIGMA and global neuroscience: A decade of large-scale studies of the brain in health and disease across more than 40 countries

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    This review summarizes the last decade of work by the ENIGMA (Enhancing NeuroImaging Genetics through Meta Analysis) Consortium, a global alliance of over 1400 scientists across 43 countries, studying the human brain in health and disease. Building on large-scale genetic studies that discovered the first robustly replicated genetic loci associated with brain metrics, ENIGMA has diversified into over 50 working groups (WGs), pooling worldwide data and expertise to answer fundamental questions in neuroscience, psychiatry, neurology, and genetics. Most ENIGMA WGs focus on specific psychiatric and neurological conditions, other WGs study normal variation due to sex and gender differences, or development and aging; still other WGs develop methodological pipelines and tools to facilitate harmonized analyses of "big data" (i.e., genetic and epigenetic data, multimodal MRI, and electroencephalography data). These international efforts have yielded the largest neuroimaging studies to date in schizophrenia, bipolar disorder, major depressive disorder, post-traumatic stress disorder, substance use disorders, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, autism spectrum disorders, epilepsy, and 22q11.2 deletion syndrome. More recent ENIGMA WGs have formed to study anxiety disorders, suicidal thoughts and behavior, sleep and insomnia, eating disorders, irritability, brain injury, antisocial personality and conduct disorder, and dissociative identity disorder. Here, we summarize the first decade of ENIGMA's activities and ongoing projects, and describe the successes and challenges encountered along the way. We highlight the advantages of collaborative large-scale coordinated data analyses for testing reproducibility and robustness of findings, offering the opportunity to identify brain systems involved in clinical syndromes across diverse samples and associated genetic, environmental, demographic, cognitive, and psychosocial factors
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