639 research outputs found

    Fire history reconstruction in grassland ecosystems: amount of charcoal reflects local area burned

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    Citation: Leys, B., Brewer, S. C., McConaghy, S., Mueller, J., & McLauchlan, K. K. (2015). Fire history reconstruction in grassland ecosystems: amount of charcoal reflects local area burned. Environmental Research Letters, 10(11), 114009. https://doi.org/10.1088/1748-9326/10/11/114009Fire is one of the most prevalent disturbances in the Earth system, and its past characteristics can be reconstructed using charcoal particles preserved in depositional environments. Although researchers know that fires produce charcoal particles, interpretation of the quantity or composition of charcoal particles in terms of fire source remains poorly understood. In this study, we used a unique four-year dataset of charcoal deposited in traps from a native tallgrass prairie in mid-North America to test which environmental factors were linked to charcoal measurements on three spatial scales. We investigated small and large charcoal particles commonly used as a proxy of fire activity at different spatial scales, and charcoal morphotypes representing different types of fuel. We found that small (125–250 μ m) and large (250 μ m–1 mm) particles of charcoal are well-correlated (Spearman correlation = 0.88) and likely reflect the same spatial scale of fire activity in a system with both herbaceous and woody fuels. There was no significant relationship between charcoal pieces and fire parameters <500 m from the traps. Moreover, local area burned (<5 km distance radius from traps) explained the total charcoal amount, and regional burning (200 km radius distance from traps) explained the ratio of non arboreal to total charcoal (NA/ T ratio). Charcoal variables, including total charcoal count and NA/ T ratio, did not correlate with other fire parameters, vegetation cover, landscape, or climate variables. Thus, in long-term studies that involve fire history reconstructions, total charcoal particles, even of a small size (125–250 μ m), could be an indicator of local area burned. Further studies may determine relationships among amount of charcoal recorded, fire intensity, vegetation cover, and climatic parameters

    Solar-like oscillations in the G2 subgiant beta Hydri from dual-site observations

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    We have observed oscillations in the nearby G2 subgiant star beta Hyi using high-precision velocity observations obtained over more than a week with the HARPS and UCLES spectrographs. The oscillation frequencies show a regular comb structure, as expected for solar-like oscillations, but with several l=1 modes being strongly affected by avoided crossings. The data, combined with those we obtained five years earlier, allow us to identify 28 oscillation modes. By scaling the large frequency separation from the Sun, we measure the mean density of beta Hyi to an accuracy of 0.6%. The amplitudes of the oscillations are about 2.5 times solar and the mode lifetime is 2.3 d. A detailed comparison of the mixed l=1 modes with theoretical models should allow a precise estimate of the age of the star.Comment: 13 pages, 14 figures, accepted by ApJ. Fixed minor typo (ref to Fig 14

    Murine Gut Microbiota Is Defined by Host Genetics and Modulates Variation of Metabolic Traits

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    The gastrointestinal tract harbors a complex and diverse microbiota that has an important role in host metabolism. Microbial diversity is influenced by a combination of environmental and host genetic factors and is associated with several polygenic diseases. In this study we combined next-generation sequencing, genetic mapping, and a set of physiological traits of the BXD mouse population to explore genetic factors that explain differences in gut microbiota and its impact on metabolic traits. Molecular profiling of the gut microbiota revealed important quantitative differences in microbial composition among BXD strains. These differences in gut microbial composition are influenced by host-genetics, which is complex and involves many loci. Linkage analysis defined Quantitative Trait Loci (QTLs) restricted to a particular taxon, branch or that influenced the variation of taxa across phyla. Gene expression within the gastrointestinal tract and sequence analysis of the parental genomes in the QTL regions uncovered candidate genes with potential to alter gut immunological profiles and impact the balance between gut microbial communities. A QTL region on Chr 4 that overlaps several interferon genes modulates the population of Bacteroides, and potentially Bacteroidetes and Firmicutes–the predominant BXD gut phyla. Irak4, a signaling molecule in the Toll-like receptor pathways is a candidate for the QTL on Chr15 that modulates Rikenellaceae, whereas Tgfb3, a cytokine modulating the barrier function of the intestine and tolerance to commensal bacteria, overlaps a QTL on Chr 12 that influence Prevotellaceae. Relationships between gut microflora, morphological and metabolic traits were uncovered, some potentially a result of common genetic sources of variation

    Murine Gut Microbiota Is Defined by Host Genetics and Modulates Variation of Metabolic Traits

    Get PDF
    The gastrointestinal tract harbors a complex and diverse microbiota that has an important role in host metabolism. Microbial diversity is influenced by a combination of environmental and host genetic factors and is associated with several polygenic diseases. In this study we combined next-generation sequencing, genetic mapping, and a set of physiological traits of the BXD mouse population to explore genetic factors that explain differences in gut microbiota and its impact on metabolic traits. Molecular profiling of the gut microbiota revealed important quantitative differences in microbial composition among BXD strains. These differences in gut microbial composition are influenced by host-genetics, which is complex and involves many loci. Linkage analysis defined Quantitative Trait Loci (QTLs) restricted to a particular taxon, branch or that influenced the variation of taxa across phyla. Gene expression within the gastrointestinal tract and sequence analysis of the parental genomes in the QTL regions uncovered candidate genes with potential to alter gut immunological profiles and impact the balance between gut microbial communities. A QTL region on Chr 4 that overlaps several interferon genes modulates the population of Bacteroides, and potentially Bacteroidetes and Firmicutes–the predominant BXD gut phyla. Irak4, a signaling molecule in the Toll-like receptor pathways is a candidate for the QTL on Chr15 that modulates Rikenellaceae, whereas Tgfb3, a cytokine modulating the barrier function of the intestine and tolerance to commensal bacteria, overlaps a QTL on Chr 12 that influence Prevotellaceae. Relationships between gut microflora, morphological and metabolic traits were uncovered, some potentially a result of common genetic sources of variation

    HES5 silencing is an early and recurrent change in prostate tumourigenesis.

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    Prostate cancer is the most common cancer in men, resulting in over 10 000 deaths/year in the UK. Sequencing and copy number analysis of primary tumours has revealed heterogeneity within tumours and an absence of recurrent founder mutations, consistent with non-genetic disease initiating events. Using methylation profiling in a series of multi-focal prostate tumours, we identify promoter methylation of the transcription factor HES5 as an early event in prostate tumourigenesis. We confirm that this epigenetic alteration occurs in 86-97% of cases in two independent prostate cancer cohorts (n=49 and n=39 tumour-normal pairs). Treatment of prostate cancer cells with the demethylating agent 5-aza-2'-deoxycytidine increased HES5 expression and downregulated its transcriptional target HES6, consistent with functional silencing of the HES5 gene in prostate cancer. Finally, we identify and test a transcriptional module involving the AR, ERG, HES1 and HES6 and propose a model for the impact of HES5 silencing on tumourigenesis as a starting point for future functional studies.The authors are grateful to study volunteers for their participation and staff at the Welcome Trust Clinical Research Facility, Addenbrooke’s Clinical Research Centre, Cambridge. They also thank the NIHR Cambridge Biomedical Research Centre, the DOH HTA (ProtecT grant), and the NCRI/MRC (ProMPT grant) for help with the bio-repository, The University of Cambridge, Hutchison Whampoa Limited and Cancer Research UK for funding. They are grateful to the CRUK Cambridge Institute Genomics and Bioinformatics Core Facilities. Cross-validation of HES5 methylation includes the use of data generated by the TCGA Research Network.This is the final version of the article. It was originally published in the Endocrine-Related Cancer, April 1, 2015 22 131-144 doi: 10.1530/ERC-14-0454

    Ability-based view in action: a software corporation study

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    This research investigates antecedents, developments and consequences of dynamic capabilities in an organization. It contributes by searching theoretical and empirical answers to the questions: (a) What are the antecedents which can provide an organization with dynamic and ordinary capabilities?; (b) How do these antecedents contribute to create capabilities in an organization?; (c) How do they affect an organization's competitive advantage?; (d) Can we assess and measure the antecedents and consequences to an organization? From a first (theoretical) perspective, this paper searches answers to the first, second and third questions by reviewing concepts of an ability-based view of organizations that involves the abilities of cognition, intelligence, autonomy, learning and knowledge management, and which contributes to explain the dynamic behavior of the firm in the pursuit of competitive advantage. From a second (empirical) perspective, this paper reinforces and delivers findings to the second, third and fourth questions by presenting a case study that evidences the ability-based view in action in a software corporation, where it contributes by investigating: (a) the development of organizational capabilities; (b) the effects of the new capabilities on the organization; and (c) the assessment and measurement of the abilities and consequences

    Endothelial NADPH oxidase-2 promotes interstitial cardiac fibrosis and diastolic dysfunction through proinflammatory effects and endothelial-mesenchymal transition

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    OBJECTIVES: This study sought to investigate the effect of endothelial dysfunction on the development of cardiac hypertrophy and fibrosis. BACKGROUND: Endothelial dysfunction accompanies cardiac hypertrophy and fibrosis, but its contribution to these conditions is unclear. Increased nicotinamide adenine dinucleotide phosphate oxidase-2 (NOX2) activation causes endothelial dysfunction. METHODS: Transgenic mice with endothelial-specific NOX2 overexpression (TG mice) and wild-type littermates received long-term angiotensin II (AngII) infusion (1.1 mg/kg/day, 2 weeks) to induce hypertrophy and fibrosis. RESULTS: TG mice had systolic hypertension and hypertrophy similar to those seen in wild-type mice but developed greater cardiac fibrosis and evidence of isolated left ventricular diastolic dysfunction (p < 0.05). TG myocardium had more inflammatory cells and VCAM-1-positive vessels than did wild-type myocardium after AngII treatment (both p < 0.05). TG microvascular endothelial cells (ECs) treated with AngII recruited 2-fold more leukocytes than did wild-type ECs in an in vitro adhesion assay (p < 0.05). However, inflammatory cell NOX2 per se was not essential for the profibrotic effects of AngII. TG showed a higher level of endothelial-mesenchymal transition (EMT) than did wild-type mice after AngII infusion. In cultured ECs treated with AngII, NOX2 enhanced EMT as assessed by the relative expression of fibroblast versus endothelial-specific markers. CONCLUSIONS: AngII-induced endothelial NOX2 activation has profound profibrotic effects in the heart in vivo that lead to a diastolic dysfunction phenotype. Endothelial NOX2 enhances EMT and has proinflammatory effects. This may be an important mechanism underlying cardiac fibrosis and diastolic dysfunction during increased renin-angiotensin activation
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