3,884 research outputs found

    Effects of Ponderosa Pine Ecological Restoration on Forest Soils and Understory Vegetation in Northern Arizona

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    The human exclusion of wildfire and overgrazing by livestock since settlement have caused dramatic changes in ponderosa pine (Pinus ponderosa Dougl ex Laws) forest ecosystems. These changes include increased numbers of tree stems, reduced understory cover and diversity, and the introduction of invasive, non-native understory species. This study evaluated the coverage and species composition of understory vegetation present in the “cool-season” (late spring and early summer) in a ponderosa pine forest on grazed and ungrazed plots that had undergone restoration treatments on three different soil/geologic parent material types near Flagstaff, Arizona, twelve years after tree thinning and grazing exclosure treatments were applied. Several measured soil properties, such as soil respiration and temperature, were also evaluated in this study. Species richness of “cool-season” vegetation was influenced more by grazing practices than restoration treatments. Differences could be less or greater when vegetation that is active later in the season is measured. Vegetative cover was significantly influenced by restoration treatments (9.3% cover under open canopies and 6.5% under dense canopies), probably due to differences in competition for light and other resources (i.e. soil moisture and nutrients). Unlike finding by Abella et al. (2015), who studied “warm-season” vegetation, “cool-season” understory cover was not influenced by soil parent material type in this study, which might suggest that differences in understory cover due to soil properties are only seen shortly after restoration treatments are applied, or the time of year vegetation is evaluated may play a role in the differences seen. Soil respiration was highest on limestone soil parent material type (3.3 g C-CO2 m-2 day-1), and soil temperature was lowest under closed canopy treatments (15°C)

    Effect of component variations on the gate fidelity in linear optical networks

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    We investigate the effect of variations in beam-splitter transmissions and path-length differences in the nonlinear sign gate that is used for linear optical quantum computing. We identify two implementations of the gate and show that the sensitivity to variations in their components differs significantly between them. Therefore, circuits that require a precision implementation will generally benefit from additional circuit analysis of component variations to identify the most practical implementation. We suggest possible routes to efficient circuit analysis in terms of quantum parameter estimation

    Comparison of microbial signatures between paired faecal and rectal biopsy samples from healthy volunteers using next-generation sequencing and culturomics

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    Acknowledgements We are indebted to our volunteers for providing the faecal and biopsy samples without which this study would not have been possible. We thank the members of the Rowett Gut Health research team for discussions and advice. The authors thank the Centre for Genome Enabled Biology and Medicine for Illumina sequencing and useful discussions. Funding This work was supported by funding from Probi AB (Grant Ref: RG14104). The Rowett Institute (University of Aberdeen) receives financial support from the Scottish Government Rural and Environmental Sciences and Analytical Services (RESAS).Peer reviewedPublisher PD

    Daily Fermented Whey Consumption Alters the Fecal Short-Chain Fatty Acid Profile in Healthy Adults

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    FUNDING: This study was funded by A.Vogel Bioforce AG, Roggwil, Switzerland. NS was co-funded by the School of Medicine, Medical Sciences and Nutrition (University of Aberdeen) and A.Vogel Bioforce AG. The Rowett Institute (University of Aberdeen) receives financial support from the Scottish Government Rural and Environmental Sciences and Analytical Services (RESAS). ACKNOWLEDGMENTS: We thank all the volunteers which contributed their time and efforts into enrolling and completing the trial. Further, we are grateful for the staff at the Human Nutrition Unit and Analytical Services at the Rowett Institute for supporting the research and assisting when needed. We would like to thank Brennan Martin at the Center for Genome Enabled Biology of Medicine for his assistance in DNA sequencingPeer reviewedPublisher PD

    Exendin-4 stimulates autophagy in pancreatic β-cells via the RAPGEF/EPAC-Ca PPP3/calcineurin-TFEB axis

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    Macroautophagy/autophagy is critical for the regulation of pancreatic β-cell mass and its deregulation has been implicated in the pathogenesis of type 2 diabetes (T2D). We have previously shown that treatment of pancreatic β-cells with the GLP1R (glucagon like peptide 1 receptor) agonist exendin-4 stimulates autophagic flux in a setting of chronic nutrient excess. The aim of this study was to identify the underlying pathways contributing to enhanced autophagic flux.Pancreatic β-cells (INS-1E),mouse and human islets were treated with glucolipotoxic stress (0.5 mM palmitate and 25 mM glucose) in the presence of exendin-4. Consistent with our previous work, exendin-4 stimulated autophagic flux. Using chemical inhibitors and siRNA knockdown, we identified RAPGEF4/EPAC2 (Rap guanine nucleotide exchange factor 4) and downstream calcium signaling to be essential for regulation of autophagic flux by exendin-4. This pathway was independent of AMPK and MTOR signaling. Further analysis identified PPP3/calcineurin and its downstream regulator TFEB (transcription factor EB) as key proteins mediating exendin-4 induced autophagy. Importantly, inhibition of this pathway prevented exendin-4-mediated cell survival and overexpression of TFEB mimicked the cell protective effects of exendin-4 in INS-1E and human islets. Moreover, treatment of db/db mice with exendin-4 for 21 days increased the expression of lysosomal markers within the pancreatic islets. Collectively our data identify the RAPGEF4/EPAC2-calcium-PPP3/calcineurin-TFEB axis as a key mediator of autophagic flux, lysosomal function and cell survival in pancreatic β-cells. Pharmacological modulation of this axis may offer a novel therapeutic target for the treatment of T2D.Abbreviations: AKT1/protein kinase B: AKT serine/threonine kinase 1; AMPK: 5' AMP-activated protein kinase; CAMKK: calcium/calmodulin-dependent protein kinase kinase; cAMP: cyclic adenosine monophosphate; CASP3: caspase 3; CREB: cAMP response element-binding protein; CTSD: cathepsin D; Ex4: exendin-4(1-39); GLP-1: glucagon like peptide 1; GLP1R: glucagon like peptide 1 receptor; GLT: glucolipotoxicity; INS: insulin; MTOR: mechanistic target of rapamycin kinase; NFAT: nuclear factor of activated T-cells; PPP3/calcineurin: protein phosphatase 3; PRKA/PKA: protein kinase cAMP activated; RAPGEF3/EPAC1: Rap guanine nucleotide exchange factor 3; RAPGEF4/EPAC2: Rap guanine nucleotide exchange factor 4; SQSTM1/p62: sequestosome 1; T2D: type 2 diabetes; TFEB: transcription factor EB

    Systems, interactions and macrotheory

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    A significant proportion of early HCI research was guided by one very clear vision: that the existing theory base in psychology and cognitive science could be developed to yield engineering tools for use in the interdisciplinary context of HCI design. While interface technologies and heuristic methods for behavioral evaluation have rapidly advanced in both capability and breadth of application, progress toward deeper theory has been modest, and some now believe it to be unnecessary. A case is presented for developing new forms of theory, based around generic “systems of interactors.” An overlapping, layered structure of macro- and microtheories could then serve an explanatory role, and could also bind together contributions from the different disciplines. Novel routes to formalizing and applying such theories provide a host of interesting and tractable problems for future basic research in HCI
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