133 research outputs found

    Constructing a Predator Exclusionary Fence to Protect Hawaiian Petrels (Pterodroma sandwichensis) at Hawai῾i Volcanoes National Park

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    Reports were scanned in black and white at a resolution of 600 dots per inch and were converted to text using Adobe Paper Capture Plug-in.Remnant nesting colonies of endangered Hawaiian Petrels, or ‘Ua’u (Pterodroma sandwichensis), on Mauna Loa, Hawai’i Island, are primarily threatened by feral cats. At Hawai῾i Volcanoes National Park, trapping success has been variable due several challenges, including the difficulty of accessing remote, subalpine (9,000’) sites. To create a core area free from cat predation, the park, with support from multiple partners, constructed a five mile barrier fence encircling 640 acres of the richest known concentration of subalpine Hawaiian Petrel nests on Mauna Loa. We report on key fence design elements, pilot studies, step by step construction details, concurrent and subsequent monitoring, and lessons learned throughout the project for the benefit of other managers considering exclusionary fencing

    Nod2 Suppresses Borrelia burgdorferi Mediated Murine Lyme Arthritis and Carditis through the Induction of Tolerance

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    The internalization of Borrelia burgdorferi, the causative agent of Lyme disease, by phagocytes is essential for an effective activation of the immune response to this pathogen. The intracellular, cytosolic receptor Nod2 has been shown to play varying roles in either enhancing or attenuating inflammation in response to different infectious agents. We examined the role of Nod2 in responses to B. burgdorferi. In vitro stimulation of Nod2 deficient bone marrow derived macrophages (BMDM) resulted in decreased induction of multiple cytokines, interferons and interferon regulated genes compared with wild-type cells. However, B. burgdorferi infection of Nod2 deficient mice resulted in increased rather than decreased arthritis and carditis compared to control mice. We explored multiple potential mechanisms for the paradoxical response in in vivo versus in vitro systems and found that prolonged stimulation with a Nod2 ligand, muramyl dipeptide (MDP), resulted in tolerance to stimulation by B. burgdorferi. This tolerance was lost with stimulation of Nod2 deficient cells that cannot respond to MDP. Cytokine patterns in the tolerance model closely paralleled cytokine profiles in infected Nod2 deficient mice. We propose a model where Nod2 has an enhancing role in activating inflammation in early infection, but moderates inflammation after prolonged exposure to the organism through induction of tolerance

    Effect of yarn cross-sectional shape on resin flow through inter-yarn gaps in textile reinforcements

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    Axial flow through gaps between aligned straight yarns with realistic cross-sectional shapes, described by power-ellipses, was analysed numerically. At a given fibre volume fraction, equivalent gap permeabilities have a maximum at minimum size of elongated tapering parts of the gap cross-section and a ratio of gap width to height near 1. When the yarn spacing is given in addition to the fibre volume fraction, calculated maximum and minimum values for the equivalent permeability of inter-yarn gaps, which occur at near-rectangular and lenticular cross-sections, differ by factors of up to 3.3. Novel approximations for the shape factor and the hydraulic diameter in Poiseuille flow were derived as a function of the fibre volume fraction, the yarn cross-sectional aspect ratio and the exponent describing the shape of the power-elliptical yarn cross-section. This allows the equivalent gap permeability to be predicted with good accuracy for any fibre volume fraction and yarn cross-section

    Rapid Evaluation in Whole Blood Culture of Regimens for XDR-TB Containing PNU-100480 (Sutezolid), TMC207, PA-824, SQ109, and Pyrazinamide

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    There presently is no rapid method to assess the bactericidal activity of new regimens for tuberculosis. This study examined PNU-100480, TMC207, PA-824, SQ109, and pyrazinamide, singly and in various combinations, against intracellular M. tuberculosis, using whole blood culture (WBA). The addition of 1,25-dihydroxy vitamin D facilitated detection of the activity of TMC207 in the 3-day cultures. Pyrazinamide failed to show significant activity against a PZA-resistant strain (M. bovis BCG), and was not further considered. Low, mid, and high therapeutic concentrations of each remaining drug were tested individually and in a paired checkerboard fashion. Observed bactericidal activity was compared to that predicted by the sum of the effects of individual drugs. Combinations of PNU-100480, TMC207, and SQ109 were fully additive, whereas those including PA-824 were less than additive or antagonistic. The cumulative activities of 2, 3, and 4 drug combinations were predicted based on the observed concentration-activity relationship, published pharmacokinetic data, and, for PNU-100480, published WBA data after oral dosing. The most active regimens, including PNU-100480, TMC207, and SQ109, were predicted to have cumulative activity comparable to standard TB therapy. Further testing of regimens including these compounds is warranted. Measurement of whole blood bactericidal activity can accelerate the development of novel TB regimens

    Metallized Plastic Current Collectors

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    Metallized plastic current collectors are an innovation patented by the Soteria Battery Innovation Group with the promise of isolating active material involved in an internal short by vaporizing and isolating the short from the rest of the cell electrode jellyroll or stack. Partnering with NREL, UCL, Coulometrics, and Soteria, NASA is leading a research effort into demonstrating the merits and understanding the phenomena of this safety innovation using prototype 18650 cylindrical cells vs control cells with standard metal foil current collectors. Cells with and without the plastic collector, with and without the on-demand internal short circuit device, and with polymer or cellulose separators were made. Safety evaluations were done with driving cells into thermal runaway (TR) with thermal and nail penetration triggers while inside our TR calorimeter and with ultra high speed X-ray videography provided at Synchrotrons. Preliminary results suggests that the thermally unstable plastic current collector innovation has great promise for preventing TR or reducing the severity of the TR output

    Human Integrin α3β1 Regulates TLR2 Recognition of Lipopeptides from Endosomal Compartments

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    Toll-like receptor (TLR)-2/TLR1 heterodimers recognize bacterial lipopeptides and initiate the production of inflammatory mediators. Adaptors and co-receptors that mediate this process, as well as the mechanisms by which these adaptors and co-receptors function, are still being discovered.Using shRNA, blocking antibodies, and fluorescent microscopy, we show that U937 macrophage responses to the TLR2/1 ligand, Pam(3)CSK(4), are dependent upon an integrin, α(3)β(1). The mechanism for integrin α(3)β(1) involvement in TLR2/1 signaling is through its role in endocytosis of lipopeptides. Using inhibitors of endosomal acidification/maturation and physical tethering of the ligand, we show that the endocytosis of Pam(3)CSK(4) is necessary for the complete TLR2/1-mediated pro-inflammatory cytokine response. We also show that TLR2/1 signaling from the endosome results in the induction of different inflammatory mediators than TLR2/1 signaling from the plasma membrane.Here we identify integrin α(3)β(1) as a novel regulator for the recognition of bacterial lipopeptides. We demonstrate that induction of a specific subset of cytokines is dependent upon integrin α(3)β(1)-mediated endocytosis of the ligand. In addition, we address an ongoing controversy regarding endosomal recognition of bacterial lipopeptides by demonstrating that TLR2/1 signals from within endosomal compartments as well as the plasma membrane, and that downstream responses may differ depending upon receptor localization. We propose that the regulation of endosomal TLR2/1 signaling by integrin α(3)β(1) serves as a mechanism for modulating inflammatory responses

    Nod2 Suppresses Borrelia burgdorferi Mediated Murine Lyme Arthritis and Carditis through the Induction of Tolerance

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    The internalization of Borrelia burgdorferi, the causative agent of Lyme disease, by phagocytes is essential for an effective activation of the immune response to this pathogen. The intracellular, cytosolic receptor Nod2 has been shown to play varying roles in either enhancing or attenuating inflammation in response to different infectious agents. We examined the role of Nod2 in responses to B. burgdorferi. In vitro stimulation of Nod2 deficient bone marrow derived macrophages (BMDM) resulted in decreased induction of multiple cytokines, interferons and interferon regulated genes compared with wild-type cells. However, B. burgdorferi infection of Nod2 deficient mice resulted in increased rather than decreased arthritis and carditis compared to control mice. We explored multiple potential mechanisms for the paradoxical response in in vivo versus in vitro systems and found that prolonged stimulation with a Nod2 ligand, muramyl dipeptide (MDP), resulted in tolerance to stimulation by B. burgdorferi. This tolerance was lost with stimulation of Nod2 deficient cells that cannot respond to MDP. Cytokine patterns in the tolerance model closely paralleled cytokine profiles in infected Nod2 deficient mice. We propose a model where Nod2 has an enhancing role in activating inflammation in early infection, but moderates inflammation after prolonged exposure to the organism through induction of tolerance

    Update on neutrophil function in severe inflammation

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    Neutrophils are main players in the effector phase of the host defense against micro-organisms and have a major role in the innate immune response. Neutrophils show phenotypic heterogeneity and functional flexibility, which highlight their importance in regulation of immune function. However, neutrophils can play a dual role and besides their antimicrobial function, deregulation of neutrophils and their hyperactivity can lead to tissue damage in severe inflammation or trauma. Neutrophils also have an important role in the modulation of the immune system in response to severe injury and trauma. In this review we will provide an overview of the current understanding of neutrophil subpopulations and their function during and post-infection and discuss the possible mechanisms of immune modulation by neutrophils in severe inflammation
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