611 research outputs found

    Female teat size is a reliable indicator of annual breeding success in European badgers: Genetic validation

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    Assessing which females have bred successfully is a central requirement in many ecological field studies, providing an estimate of the effective female population size. Researchers have applied teat measurements previously to assess whether females, in a variety of mammalian species, have bred; however, this technique has not been validated genetically. Furthermore, several analytical techniques are available to classify individuals, but their misclassification rates have not been compared. We used 22 microsatellite loci to assign maternity, with 95% confidence, within a high-density population of European badgers Meles meles, as plural and subterranean breeding means that maternity cannot be inferred from behavioural observations. The teat lengths and diameters of 136 females, measured May–July 1994–2005, from social groups in which all offspring were assigned a mother, were reliable indicators of recent breeding success. A Generalised Linear Mixed Model (GLMM) classified both breeding and non-breeding females with lower error rates than discriminant analyses and crude teat-size criteria. The GLMM model logit probability = −20 + 1.8 month + 1.6 mean teat length + 1.0 mean teat diameter can be applied quickly in the field to assess the probability with which a female badger should be assigned maternity. This is a low-cost measure which, after validation, could be used in other badger or mammalian populations to assess the breeding success of females. This may be a particularly useful welfare tool for veterinary practitioners, especially during badger culls

    Derivation of a Protein Risk Score for Cardiovascular Disease Among a Multiracial and Multiethnic HIV+ Cohort

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    Background Cardiovascular disease risk prediction models underestimate CVD risk in people living with HIV (PLWH). Our goal is to derive a risk score based on protein biomarkers that could be used to predict CVD in PLWH. Methods and Results In a matched case-control study, we analyzed normalized protein expression data for participants enrolled in 1 of 4 trials conducted by INSIGHT (International Network for Strategic Initiatives in Global HIV Trials). We used dimension reduction, variable selection and resampling methods, and multivariable conditional logistic regression models to determine candidate protein biomarkers and to generate a protein score for predicting CVD in PLWH. We internally validated our findings using bootstrap. A protein score that was derived from 8 proteins (including HGF [hepatocyte growth factor] and interleukin-6) was found to be associated with an increased risk of CVD after adjustment for CVD and HIV factors (odds ratio: 2.17 [95% CI: 1.58-2.99]). The protein score improved CVD prediction when compared with predicting CVD risk using the individual proteins that comprised the protein score. Individuals with a protein score above the median score were 3.10 (95% CI, 1.83-5.41) times more likely to develop CVD than those with a protein score below the median score. Conclusions A panel of blood biomarkers may help identify PLWH at a high risk for developing CVD. If validated, such a score could be used in conjunction with established factors to identify CVD at-risk individuals who might benefit from aggressive risk reduction, ultimately shedding light on CVD pathogenesis in PLWH

    Botanical Monography in the Anthropocene

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    Unprecedented changes in the Earth's biota are prompting urgent efforts to describe and conserve plant diversity. For centuries, botanical monographs — comprehensive systematic treatments of a family or genus — have been the gold standard for disseminating scientific information to accelerate research. The lack of a monograph compounds the risk that undiscovered species become extinct before they can be studied and conserved. Progress towards estimating the Tree of Life and digital information resources now bring even the most ambitious monographs within reach. Here, we recommend best practices to complete monographs urgently, especially for tropical plant groups under imminent threat or with expected socioeconomic benefits. We also highlight the renewed relevance and potential impact of monographies for the understanding, sustainable use, and conservation of biodiversity.Fil: Grace, Olwen M.. Royal Botanic Gardens, Kew; Reino UnidoFil: Pérez-Escobar, Oscar A.. Royal Botanic Gardens, Kew; Reino UnidoFil: Lucas, Eve J.. Royal Botanic Gardens, Kew; Reino UnidoFil: Vorontsova, Maria S.. Royal Botanic Gardens, Kew; Reino UnidoFil: Lewis, Gwilym P.. Royal Botanic Gardens, Kew; Reino UnidoFil: Walker, Barnaby E.. Royal Botanic Gardens, Kew; Reino UnidoFil: Lohmann, Lúcia G.. Universidade de Sao Paulo; BrasilFil: Knapp, Sandra. Natural History Museum; Reino UnidoFil: Wilkie, Peter. Royal Botanic Gardens; Reino UnidoFil: Sarkinen, Tiina. Royal Botanic Gardens; Reino UnidoFil: Darbyshire, Iain. Royal Botanic Gardens; Reino UnidoFil: Lughadha, Eimear Nic. Royal Botanic Gardens; Reino UnidoFil: Monro, Alexandre. Royal Botanic Gardens; Reino UnidoFil: Woudstra, Yannick. Universidad de Copenhagen; Dinamarca. Royal Botanic Gardens; Reino UnidoFil: Demissew, Sebsebe. Addis Ababa University; EtiopíaFil: Muasya, A. Muthama. University Of Cape Town; SudáfricaFil: Díaz, Sandra Myrna. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto Multidisciplinario de Biología Vegetal. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas Físicas y Naturales. Instituto Multidisciplinario de Biología Vegetal; ArgentinaFil: Baker, William J.. Royal Botanic Gardens, Kew; Reino UnidoFil: Antonelli, Alexandre. University of Oxford; Reino Unido. University Goteborg; Sueci

    Human Proteome Project Mass Spectrometry Data Interpretation Guidelines 3.0

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    The Human Proteome Organization’s (HUPO) Human Proteome Project (HPP) developed Mass Spectrometry (MS) Data Interpretation Guidelines that have been applied since 2016. These guidelines have helped ensure that the emerging draft of the complete human proteome is highly accurate and with low numbers of false-positive protein identifications. Here, we describe an update to these guidelines based on consensus-reaching discussions with the wider HPP community over the past year. The revised 3.0 guidelines address several major and minor identified gaps. We have added guidelines for emerging data independent acquisition (DIA) MS workflows and for use of the new Universal Spectrum Identifier (USI) system being developed by the HUPO Proteomics Standards Initiative (PSI). In addition, we discuss updates to the standard HPP pipeline for collecting MS evidence for all proteins in the HPP, including refinements to minimum evidence. We present a new plan for incorporating MassIVE-KB into the HPP pipeline for the next (HPP 2020) cycle in order to obtain more comprehensive coverage of public MS data sets. The main checklist has been reorganized under headings and subitems, and related guidelines have been grouped. In sum, Version 2.1 of the HPP MS Data Interpretation Guidelines has served well, and this timely update to version 3.0 will aid the HPP as it approaches its goal of collecting and curating MS evidence of translation and expression for all predicted ∼20 000 human proteins encoded by the human genome.This work was funded in part by the National Institutes of Health grants R01GM087221 (EWD/RLM), R24GM127667 (EWD), U54EB020406 (EWD), R01HL133135 (RLM), U19AG02312 (RLM), U54ES017885 (GSO), U24CA210967-01 (GSO), R01LM013115 (NB) and P41GM103484 (NB); National Science Foundation grants ABI-1759980 (NB), DBI-1933311 (EWD), and IOS-1922871 (EWD); Canadian Institutes of Health Research 148408 (CMO); Korean Ministry of Health and Welfare HI13C2098 (YKP); French Ministry of Higher Education, Research and Innovation, ProFI project, ANR-10-INBS-08 (YV); also in part by the National Eye Institute (NEI), National Human Genome Research Institute (NHGRI), National Heart, Lung, and Blood Institute (NHLBI), National Institute of Allergy and Infectious Diseases (NIAID), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institute of General Medical Sciences (NIGMS), and National Institute of Mental Health (NIMH) of the National Institutes of Health under Award Number U24HG007822 (SO) (the content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health)

    Non-cell autonomous influence of the astrocyte system xc− on hypoglycaemic neuronal cell death

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    Despite longstanding evidence that hypoglycaemic neuronal injury is mediated by glutamate excitotoxicity, the cellular and molecular mechanisms involved remain incompletely defined. Here, we demonstrate that the excitotoxic neuronal death that follows GD (glucose deprivation) is initiated by glutamate extruded from astrocytes via system xc− – an amino acid transporter that imports l-cystine and exports l-glutamate. Specifically, we find that depriving mixed cortical cell cultures of glucose for up to 8 h injures neurons, but not astrocytes. Neuronal death is prevented by ionotropic glutamate receptor antagonism and is partially sensitive to tetanus toxin. Removal of amino acids during the deprivation period prevents – whereas addition of l-cystine restores – GD-induced neuronal death, implicating the cystine/glutamate antiporter, system xc−. Indeed, drugs known to inhibit system xc− ameliorate GD-induced neuronal death. Further, a dramatic reduction in neuronal death is observed in chimaeric cultures consisting of neurons derived from WT (wild-type) mice plated on top of astrocytes derived from sut mice, which harbour a naturally occurring null mutation in the gene (Slc7a11) that encodes the substrate-specific light chain of system xc− (xCT). Finally, enhancement of astrocytic system xc− expression and function via IL-1β (interleukin-1β) exposure potentiates hypoglycaemic neuronal death, the process of which is prevented by removal of l-cystine and/or addition of system xc− inhibitors. Thus, under the conditions of GD, our studies demonstrate that astrocytes, via system xc−, have a direct, non-cell autonomous effect on cortical neuron survival
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