518 research outputs found

    The effect of precipitation and application rate on dicyandiamide persistence and efficiency in two Irish grassland soils

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    peer-reviewedThe nitrification inhibitor dicyandiamide (DCD) has had variable success in reducing nitrate (NO3-) leaching and nitrous oxide (N2O) emissions from soils receiving nitrogen (N) fertilisers. Factors such as soil type, temperature and moisture have been linked to the variable efficacy of DCD. Since DCD is water soluble it can be leached from the rooting zone where it is intended to inhibit nitrification. Intact soil columns (15 cm diameter by 35 cm long) were taken from luvic gleysol and haplic cambisol grassland sites and placed in growth chambers. DCD was applied at 15 or 30 kg DCD ha-1, with high or low precipitation. Leaching of DCD, mineral N and the residual soil DCD concentrations were determined over eight weeks High precipitation increased DCD in leachate and decreased recovery in soil. A soil x DCD rate interaction was detected for the DCD unaccounted (proxy for degraded DCD). In the cambisol degradation of DCD was high (circa 81%) and unaffected by DCD rate. In contrast DCD degradation in the gleysol was lower and differentially affected by rate, 67 and 46% for the 15 and 30 kg ha-1 treatments, respectively. Differences DCD degradation rates between soils may be related to differences in organic matter content and associated microbiological activity. Variable degradation rates of DCD in soil, unrelated to temperature or moisture, may contribute to varying DCD efficacy. Soil properties should be considered when tailoring DCD strategies for improving nitrogen use efficiency and crop yields, through the reduction of reactive nitrogen loss.This research was financially supported under the National Development Plan, through the Research Stimulus Fund, administered by the Department of Agriculture, Food and the Marine under grants 07519 and 07545

    The effect of cattle slurry in combination with nitrate and the nitrification inhibitor dicyandiamide on in situ nitrous oxide and dinitrogen emissions

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    peer-reviewedA field study was conducted to determine the effect of the nitrification inhibitor dicyandiamide (DCD) on N2O and N2 emissions after cattle slurry (CS) application in the presence of nitrate (NO3) fertiliser on seven different occasions (between March 2009 and March 2011). N2O emissions from CS in the presence of NO3 fertiliser were very high (0.4–8.7% of applied N) over a 20-day period, under mild moist conditions. Emissions were significantly larger from the CS treatment compared to an NH4+-N source, supplying the same rate of N as in the slurry. This study supports the view that organic fertilisers should not be applied at the same time as nitrate-based fertilisers, as significant increases in N2O emissions occur. The average N2O mole fraction (N2O/(N2O + N2)) over all seven application dates was 0.34 for CSNO3 compared to 0.24 for the NH4ClNO3 treatment, indicating the dominance of N2 emissions. The rate of nitrification in CSNO3 was slower than in NH4ClNO3, and DCD was found to be an effective nitrification inhibitor in both treatments. However, as N2O emissions were found to be predominantly associated with the NO3 pool, the effect of DCD in lowering N2O emissions is limited in the presence of a NO3 fertiliser. To obtain the maximum cost-benefit of DCD in lowering N2O emissions, under mild moist conditions, it should not be applied to a nitrate containing fertiliser (e.g. ammonium nitrate or calcium ammonium nitrate), and therefore the application of DCD should be restricted to ammonium-based organic or synthetic fertilisers.This research was funded by the Irish National Development Plan, through the Research Stimulus Fund (RSF 07 519), administered by the Irish Department of Agriculture, Food and the Marine

    Allosteric Mechanism of Water Channel Gating by Ca2+–calmodulin

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    Calmodulin (CaM) is a universal regulatory protein that communicates the presence of calcium to its molecular targets and correspondingly modulates their function. This key signaling protein is important for controlling the activity of hundreds of membrane channels and transporters. However, our understanding of the structural mechanisms driving CaM regulation of full-length membrane proteins has remained elusive. In this study, we determined the pseudo-atomic structure of full-length mammalian aquaporin-0 (AQP0, Bos Taurus) in complex with CaM using electron microscopy to understand how this signaling protein modulates water channel function. Molecular dynamics and functional mutation studies reveal how CaM binding inhibits AQP0 water permeability by allosterically closing the cytoplasmic gate of AQP0. Our mechanistic model provides new insight, only possible in the context of the fully assembled channel, into how CaM regulates multimeric channels by facilitating cooperativity between adjacent subunits

    Drug hypersensitivity caused by alteration of the MHC-presented self-peptide repertoire

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    Idiosyncratic adverse drug reactions are unpredictable, dose independent and potentially life threatening; this makes them a major factor contributing to the cost and uncertainty of drug development. Clinical data suggest that many such reactions involve immune mechanisms, and genetic association studies have identified strong linkage between drug hypersensitivity reactions to several drugs and specific HLA alleles. One of the strongest such genetic associations found has been for the antiviral drug abacavir, which causes severe adverse reactions exclusively in patients expressing the HLA molecular variant B*57:01. Abacavir adverse reactions were recently shown to be driven by drug-specific activation of cytokine-producing, cytotoxic CD8+ T cells that required HLA-B*57:01 molecules for their function. However, the mechanism by which abacavir induces this pathologic T cell response remains unclear. Here we show that abacavir can bind within the F-pocket of the peptide-binding groove of HLA-B*57:01 thereby altering its specificity. This supports a novel explanation for HLA-linked idiosyncratic adverse drug reactions; namely that drugs can alter the repertoire of self-peptides presented to T cells thus causing the equivalent of an alloreactive T cell response. Indeed, we identified specific self-peptides that are presented only in the presence of abacavir, and that were recognized by T cells of hypersensitive patients. The assays we have established can be applied to test additional compounds with suspected HLA linked hypersensitivities in vitro. Where successful, these assays could speed up the discovery and mechanistic understanding of HLA linked hypersensitivities as well as guide the development of safer drugs
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