161 research outputs found

    Do intraspecific or interspecific interactions determine responses to predators feeding on a shared size‐structured prey community?

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    Summary Coexistence of predators that share the same prey is common. This is still the case in size‐structured predator communities where predators consume prey species of different sizes (interspecific prey responses) or consume different size classes of the same species of prey (intraspecific prey responses). A mechanism has recently been proposed to explain coexistence between predators that differ in size but share the same prey species, emergent facilitation, which is dependent on strong intraspecific responses from one or more prey species. Under emergent facilitation, predators can depend on each other for invasion, persistence or success in a size‐structured prey community. Experimental evidence for intraspecific size‐structured responses in prey populations remains rare, and further questions remain about direct interactions between predators that could prevent or limit any positive effects between predators [e.g. intraguild predation (IGP)]. Here, we provide a community‐wide experiment on emergent facilitation including natural predators. We investigate both the direct interactions between two predators that differ in body size (fish vs. invertebrate predator), and the indirect interaction between them via their shared prey community (zooplankton). Our evidence supports the most likely expectation of interactions between differently sized predators that IGP rates are high, and interspecific interactions in the shared prey community dominate the response to predation (i.e. predator‐mediated competition). The question of whether emergent facilitation occurs frequently in nature requires more empirical and theoretical attention, specifically to address the likelihood that its pre‐conditions may co‐occur with high rates of IGP. </jats:p

    Microscopic theory of single-electron tunneling through molecular-assembled metallic nanoparticles

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    We present a microscopic theory of single-electron tunneling through metallic nanoparticles connected to the electrodes through molecular bridges. It combines the theory of electron transport through molecular junctions with the description of the charging dynamics on the nanoparticles. We apply the theory to study single-electron tunneling through a gold nanoparticle connected to the gold electrodes through two representative benzene-based molecules. We calculate the background charge on the nanoparticle induced by the charge transfer between the nanoparticle and linker molecules, the capacitance and resistance of molecular junction using a first-principles based Non-Equilibrium Green's Function theory. We demonstrate the variety of transport characteristics that can be achieved through ``engineering'' of the metal-molecule interaction.Comment: To appear in Phys. Rev.

    Variation in market access decisions for cell and gene therapies across the United States, Canada, and Europe

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    Transformative cell and gene therapies have now launched worldwide, and many potentially curative cell and gene therapies are in development, offering the prospect of significant health gains for patients. Access to these therapies depend on decisions made by health technology assessment (HTA) and payer organizations. We sought to describe the emerging cell and gene therapies market access landscape by analyzing 17 US commercial payer medical policies, and HTA reports from five European countries and Canada. We found that some US health plans applied coverage restrictions more often than others (four plans applied restrictions in all decisions, while four plans applied restrictions in < 30% of decisions). The European and Canadian HTA bodies recommend access to fewer therapies than US health plans, reflecting a more stringent approach in the context of limited evidence and high scientific uncertainty that is commonly associated with these treatments. Our findings suggest that patient access to approved cell and gene therapies is restricted in all regions studied, though the nature of these restrictions differs between US health plans and the European/Canada HTA recommendations. Payers, HTA groups, pharmaceutical companies, and other stakeholders should collaborate to more clearly define the “uncertainties” and develop market access policies that balance benefits of early access with ongoing data collection to close evidence gaps over time

    The missing pieces for better future predictions in subarctic ecosystems: a TornetrÀsk case study

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    Arctic and subarctic ecosystems are experiencing substantial changes in hydrology, vegetation, permafrost conditions, and carbon cycling, in response to climatic change and other anthropogenic drivers, and these changes are likely to continue over this century. The total magnitude of these changes results from multiple interactions among these drivers. Field measurements can address the overall responses to different changing drivers, but are less capable of quantifying the interactions among them. Currently, a comprehensive assessment of the drivers of ecosystem changes, and the magnitude of their direct and indirect impacts on subarctic ecosystems, is missing. The TornetrÀsk area, in the Swedish subarctic, has an unrivalled history of environmental observation over 100 years, and is one of the most studied sites in the Arctic. In this study, we summarize and rank the drivers of ecosystem change in the TornetrÀsk area, and propose research priorities identified, by expert assessment, to improve predictions of ecosystem changes. The research priorities identified include understanding impacts on ecosystems brought on by altered frequency and intensity of winter warming events, evapotranspiration rates, rainfall, duration of snow cover and lake-ice, changed soil moisture, and droughts. This case study can help us understand the ongoing ecosystem changes occurring in the TornetrÀsk area, and contribute to improve predictions of future ecosystem changes at a larger scale. This understanding will provide the basis for the future mitigation and adaptation plans needed in a changing climate

    Age-related changes in neural functional connectivity and its behavioral relevance

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    <p>Abstract</p> <p>Background</p> <p>Resting-state recordings are characterized by widely distributed networks of coherent brain activations. Disturbances of the default network - a set of regions that are deactivated by cognitive tasks and activated during passive states - have been detected in age-related disorders such as Alzheimer's or Parkinson's disease but alterations in the course of healthy aging still need to be explored.</p> <p>Results</p> <p>Using magnetoencephalography (MEG), the present study investigated how age-related functional resting-state brain connectivity links to cognitive performance in healthy aging in fifty-three participants ranging in age from 18 to 89 years. A beamforming technique was used to reconstruct the brain activity in source space and the interregional coupling was investigated using partial directed coherence (PDC). We found significant age-related alterations of functional resting-state connectivity. These are mainly characterized by reduced information input into the posterior cingulum/precuneus region together with an enhanced information flow to the medial temporal lobe. Furthermore, higher inflow in the medial temporal lobe subsystem was associated with weaker cognitive performance whereas stronger inflow in the posterior cluster was related to better cognitive performance.</p> <p>Conclusion</p> <p>This is the first study to show age-related alterations in subsystems of the resting state network that are furthermore associated with cognitive performance.</p

    Genomic Prevalence of Heterochromatic H3K9me2 and Transcription Do Not Discriminate Pluripotent from Terminally Differentiated Cells

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    Cellular differentiation entails reprogramming of the transcriptome from a pluripotent to a unipotent fate. This process was suggested to coincide with a global increase of repressive heterochromatin, which results in a reduction of transcriptional plasticity and potential. Here we report the dynamics of the transcriptome and an abundant heterochromatic histone modification, dimethylation of histone H3 at lysine 9 (H3K9me2), during neuronal differentiation of embryonic stem cells. In contrast to the prevailing model, we find H3K9me2 to occupy over 50% of chromosomal regions already in stem cells. Marked are most genomic regions that are devoid of transcription and a subgroup of histone modifications. Importantly, no global increase occurs during differentiation, but discrete local changes of H3K9me2 particularly at genic regions can be detected. Mirroring the cell fate change, many genes show altered expression upon differentiation. Quantitative sequencing of transcripts demonstrates however that the total number of active genes is equal between stem cells and several tested differentiated cell types. Together, these findings reveal high prevalence of a heterochromatic mark in stem cells and challenge the model of low abundance of epigenetic repression and resulting global basal level transcription in stem cells. This suggests that cellular differentiation entails local rather than global changes in epigenetic repression and transcriptional activity

    Diagnostic Accuracy of S100B Urinary Testing at Birth in Full-Term Asphyxiated Newborns to Predict Neonatal Death

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    BACKGROUND: Neonatal death in full-term infants who suffer from perinatal asphyxia (PA) is a major subject of investigation, since few tools exist to predict patients at risk of ominous outcome. We studied the possibility that urine S100B measurement may identify which PA-affected infants are at risk of early postnatal death. METHODOLOGY/PRINCIPAL FINDINGS: In a cross-sectional study between January 1, 2001 and December 1, 2006 we measured S100B protein in urine collected from term infants (n = 132), 60 of whom suffered PA. According to their outcome at 7 days, infants with PA were subsequently classified either as asphyxiated infants complicated by hypoxic ischemic encephalopathy with no ominous outcome (HIE Group; n = 48), or as newborns who died within the first post-natal week (Ominous Outcome Group; n = 12). Routine laboratory variables, cerebral ultrasound, neurological patterns and urine concentrations of S100B protein were determined at first urination and after 24, 48 and 96 hours. The severity of illness in the first 24 hours after birth was measured using the Score for Neonatal Acute Physiology-Perinatal Extension (SNAP-PE). Urine S100B levels were higher from the first urination in the ominous outcome group than in healthy or HIE Groups (p<0.001 for all), and progressively increased. Multiple logistic regression analysis showed a significant correlation between S100B concentrations and the occurrence of neonatal death. At a cut-off >1.0 microg/L S100B had a sensitivity/specificity of 100% for predicting neonatal death. CONCLUSIONS/SIGNIFICANCE: Increased S100B protein urine levels in term newborns suffering PA seem to suggest a higher risk of neonatal death for these infants

    Acute phase response in two consecutive experimentally induced E. coli intramammary infections in dairy cows

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    <p>Abstract</p> <p>Background</p> <p>Acute phase proteins haptoglobin (Hp), serum amyloid A (SAA) and lipopolysaccharide binding protein (LBP) have suggested to be suitable inflammatory markers for bovine mastitis. The aim of the study was to investigate acute phase markers along with clinical parameters in two consecutive intramammary challenges with <it>Escherichia coli </it>and to evaluate the possible carry-over effect when same animals are used in an experimental model.</p> <p>Methods</p> <p>Mastitis was induced with a dose of 1500 cfu of <it>E. coli </it>in one quarter of six cows and inoculation repeated in another quarter after an interval of 14 days. Concentrations of acute phase proteins haptoglobin (Hp), serum amyloid A (SAA) and lipopolysaccharide binding protein (LBP) were determined in serum and milk.</p> <p>Results</p> <p>In both challenges all cows became infected and developed clinical mastitis within 12 hours of inoculation. Clinical disease and acute phase response was generally milder in the second challenge. Concentrations of SAA in milk started to increase 12 hours after inoculation and peaked at 60 hours after the first challenge and at 44 hours after the second challenge. Concentrations of SAA in serum increased more slowly and peaked at the same times as in milk; concentrations in serum were about one third of those in milk. Hp started to increase in milk similarly and peaked at 36–44 hours. In serum, the concentration of Hp peaked at 60–68 hours and was twice as high as in milk. LBP concentrations in milk and serum started to increase after 12 hours and peaked at 36 hours, being higher in milk. The concentrations of acute phase proteins in serum and milk in the <it>E. coli </it>infection model were much higher than those recorded in experiments using Gram-positive pathogens, indicating the severe inflammation induced by <it>E. coli</it>.</p> <p>Conclusion</p> <p>Acute phase proteins would be useful parameters as mastitis indicators and to assess the severity of mastitis. If repeated experimental intramammary induction of the same animals with <it>E. coli </it>is used in cross-over studies, the interval between challenges should be longer than 2 weeks, due to the carry-over effect from the first infection.</p
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