339 research outputs found

    Coping With Human-Cat Interactions Beyond the Limits of Domesticity: Moral Pluralism in the Management of Cats and Wildlife

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    Although human interactions with cats are often even typically analyzed in the context of domesticity, with a focus on what sorts of interactions might make both people and cats “happy at home,” a large number of cats in the world live, for one reason or another, beyond the bounds of domesticity. Human interactions with these more or less free-living cats raise deeply controversial questions about how both the cats and the people they interact with should be sensibly managed, and about the moral imperatives that ought to guide the management of their interactions through the laws and public policies regulating both human interactions with pets and with wildlife. We review the geography of human interactions with cats living beyond the bounds of domesticity. We acknowledge the contributions made to ideas about how to manage cats by the animal protection movement. We review the tensions that have emerged over time between advocates for the eradication of free-living cats, because of the impacts they have on native wildlife species, and those who have imagined alternatives to eradication, most notably one or another variant of trap-neuter-return (TNR). The conflict over how best to deal with cats living beyond the bounds of domesticity and their wildlife impacts raises the prospect of stalemate, and we canvass and critique possibilities for moving beyond that stalemate.</jats:p

    Discovery of a single male Aedes aegypti (L.) in Merseyside, England

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    © The Author(s). 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. The file attached is the published (publishers PDF) version of the article

    Anthropogenic habitat disturbance and food availability affect the abundance of an endangered primate: a regional approach

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    Anthropogenic habitat disturbances are causing large-scale declines in animal abundance. For many species, information on the drivers of decline is lacking or restricted to single sites, despite calls for regional approaches. In this study, we determined the effect of different types of habitat disturbance (natural or anthropogenic) and ecological factors on Geoffroy’s spider monkey (Ateles geoffroyi) abundance using a regional approach. We selected this study species because of its high degree of social flexibility and its endangered status. We surveyed 4 sites in the Yucatan Peninsula and recorded the number of individual monkeys encountered along 72 line-transect segments each measuring 500 m. Habitat disturbance variables were obtained from open-access databases and included distance to roads, presence and number of hurricanes, forest loss, and presence of forest fires. Ecological factors were based on data collected during vegetation surveys and included number and basal area of feeding tree species, and canopy height. We ran generalized linear mixed models and found that monkey abundance was negatively affected by forest loss but positively affected by the basal area of feeding trees. We, therefore, suggest that a combination of anthropogenic and ecological factors affects spider monkey abundance. Spider monkey’s high degree of social flexibility may be a mechanism allowing them to adjust to changes in their environment when canopy connectivity is not lost. Our results provide policy and conservation decision makers with key information to develop regional conservation plans. Additionally, our methods can be used to identify the factors that affect the abundance of other mammal species. © 2020, Deutsche Gesellschaft für Säugetierkunde

    Simultaneous Analysis of All SNPs in Genome-Wide and Re-Sequencing Association Studies

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    Testing one SNP at a time does not fully realise the potential of genome-wide association studies to identify multiple causal variants, which is a plausible scenario for many complex diseases. We show that simultaneous analysis of the entire set of SNPs from a genome-wide study to identify the subset that best predicts disease outcome is now feasible, thanks to developments in stochastic search methods. We used a Bayesian-inspired penalised maximum likelihood approach in which every SNP can be considered for additive, dominant, and recessive contributions to disease risk. Posterior mode estimates were obtained for regression coefficients that were each assigned a prior with a sharp mode at zero. A non-zero coefficient estimate was interpreted as corresponding to a significant SNP. We investigated two prior distributions and show that the normal-exponential-gamma prior leads to improved SNP selection in comparison with single-SNP tests. We also derived an explicit approximation for type-I error that avoids the need to use permutation procedures. As well as genome-wide analyses, our method is well-suited to fine mapping with very dense SNP sets obtained from re-sequencing and/or imputation. It can accommodate quantitative as well as case-control phenotypes, covariate adjustment, and can be extended to search for interactions. Here, we demonstrate the power and empirical type-I error of our approach using simulated case-control data sets of up to 500 K SNPs, a real genome-wide data set of 300 K SNPs, and a sequence-based dataset, each of which can be analysed in a few hours on a desktop workstation

    Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

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    It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers

    Search for the Decays B^0 -> D^{(*)+} D^{(*)-}

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    Using the CLEO-II data set we have searched for the Cabibbo-suppressed decays B^0 -> D^{(*)+} D^{(*)-}. For the decay B^0 -> D^{*+} D^{*-}, we observe one candidate signal event, with an expected background of 0.022 +/- 0.011 events. This yield corresponds to a branching fraction of Br(B^0 -> D^{*+} D^{*-}) = (5.3^{+7.1}_{-3.7}(stat) +/- 1.0(syst)) x 10^{-4} and an upper limit of Br(B^0 -> D^{*+} D^{*-}) D^{*\pm} D^\mp and B^0 -> D^+ D^-, no significant excess of signal above the expected background level is seen, and we calculate the 90% CL upper limits on the branching fractions to be Br(B^0 -> D^{*\pm} D^\mp) D^+ D^-) < 1.2 x 10^{-3}.Comment: 12 page postscript file also available through http://w4.lns.cornell.edu/public/CLNS, submitted to Physical Review Letter

    ΛΛˉ\Lambda\bar{\Lambda} Production in Two-Photon Interactions at CLEO

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    Using the CLEO detector at the Cornell e+ee^+e^- storage ring, CESR, we study the two-photon production of ΛΛˉ\Lambda \bar{\Lambda}, making the first observation of γγΛΛˉ\gamma \gamma \to \Lambda \bar{\Lambda}. We present the cross-section for γγΛΛˉ \gamma \gamma \to \Lambda \bar{\Lambda} as a function of the γγ\gamma \gamma center of mass energy and compare it to that predicted by the quark-diquark model.Comment: 10 pages, postscript file also available through http://w4.lns.cornell.edu/public/CLN

    Observation of the Decay Ds+ωπ+D_{s}^{+}\to \omega\pi^{+}

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    Using e+e- annihilation data collected by the CLEO~II detector at CESR, we have observed the decay Ds+ to omega pi+. This final state may be produced through the annihilation decay of the Ds+, or through final state interactions. We find a branching ratio of [Gamma(Ds+ to omega pi+)/Gamma(Ds+ to eta pi+)]=0.16+-0.04+-0.03, where the first error is statistical and the second is systematic.Comment: 9 pages, postscript file also available through http://w4.lns.cornell.edu/public/CLN
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