136 research outputs found

    Variability of the Norwegian Atlantic Current and associated eddy field from surface drifters

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    The Norwegian Atlantic Current (NwAC) and its eddy field are examined using data from surface drifters. The data set used spans nearly 20 years, from June 1991 to December 2009. The results are largely consistent with previous estimates, which were based on data from the first decade only. With our new data set, statistical analysis of the mean fields can be calculated with larger confidence. The two branches of the NwAC, one over the continental slope and a second further offshore, are clearly captured. The Norwegian Coastal Current is also resolved. In addition, we observe a semipermanent anticylonic eddy in the Lofoten Basin, a feature seen previously in hydrography and in models. The eddy kinetic energy (EKE) is intensified along the path of the NwAC, with the largest values occurring in the Lofoten Basin. The strongest currents, exceeding 100 cm s−1, occur west of Lofoten. Lateral diffusivities were computed in five domains and ranged from 1–5 × 107 cm2 s−1. The Lagrangian integral time and space scales are 1–2 days and 7–23 km, respectively. The data set allows studies of seasonal and interannual variations as well. The strongest seasonal signal is in the NwAC itself, as the mean flow strengthens by approximately 20% in winter. The EKE and diffusivities on the other hand do not exhibit consistent seasonality in the sampled regions. There are no consistent indications of changes in either the mean or fluctuating surface velocities between the 1990s and 2000s

    Weddell Sea Export Pathways from Surface Drifters

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    The complex export pathways that connect the surface waters of the Weddell Sea with the Antarctic Circumpolar Current influence water mass modification, nutrient fluxes, and ecosystem dynamics. To study this exchange, 40 surface drifters, equipped with temperature sensors, were released into the northwestern Weddell Sea’s continental shelf and slope frontal system in late January 2012. Comparison of the drifter trajectories with a similar deployment in early February 2007 provides insight into the interannual variability of the surface circulation in this region. Observed differences in the 2007 and 2012 drifter trajectories are related to a variable surface circulation responding to changes in wind stress curl over the Weddell Gyre. Differences between northwestern Weddell Sea properties in 2007 and 2012 include 1) an enhanced cyclonic wind stress forcing over the Weddell Gyre in 2012; 2) an acceleration of the Antarctic Slope Current (ASC) and an offshore shift of the primary drifter export pathway in 2012; and 3) a strengthening of the Coastal Current (CC) over the continental shelf in 2007. The relationship between wind stress forcing and surface circulation is reproduced over a longer time period in virtual drifter deployments advected by a remotely sensed surface velocity product. The mean offshore position and speed of the drifter trajectories are correlated with the wind stress curl over the Weddell Gyre, although with different temporal lags. The drifter observations are consistent with recent modeling studies suggesting that Weddell Sea boundary current variability can significantly impact the rate and source of exported surface waters to the Scotia Sea, a process that determines regional chlorophyll distributions

    Impact Forecasting to Support Emergency Management of Natural Hazards

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    Forecasting and early warning systems are important investments to protect lives, properties, and livelihood. While early warning systems are frequently used to predict the magnitude, location, and timing of potentially damaging events, these systems rarely provide impact estimates, such as the expected amount and distribution of physical damage, human consequences, disruption of services, or financial loss. Complementing early warning systems with impact forecasts has a twofold advantage: It would provide decision makers with richer information to take informed decisions about emergency measures and focus the attention of different disciplines on a common target. This would allow capitalizing on synergies between different disciplines and boosting the development of multihazard early warning systems. This review discusses the state of the art in impact forecasting for a wide range of natural hazards. We outline the added value of impact-based warnings compared to hazard forecasting for the emergency phase, indicate challenges and pitfalls, and synthesize the review results across hazard types most relevant for Europe

    Resident Cardiac Immune Cells and Expression of the Ectonucleotidase Enzymes CD39 and CD73 after Ischemic Injury

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    BACKGROUND: The ectoenzymes CD39 and CD73 are expressed by a broad range of immune cells and promote the extracellular degradation of nucleotides to anti-inflammatory adenosine. This study explored the abundance of CD73 and CD39 on circulating and resident cardiac leukocytes and coronary endothelial cells under control conditions and in response to inflammation following myocardial ischemia and reperfusion (I/R). METHODS AND RESULTS: A method was elaborated to permit FACS analysis of non-myocardial cells (resident leukocytes, coronary endothelium and CD31(-) CD45(-) cells) of the unstressed heart. Under control conditions the murine heart contained 2.3 × 10(3) resident leukocytes/mg tissue, the most prominent fraction being antigen-presenting mononuclear cells (CD11b(+) CD11c(+) F4/80(+) MHCII(+)) followed by B-cells, monocytes and T-cells. CD73 was highly expressed on circulating and resident cardiac lymphoid cells with little expression on myeloid cells, while the opposite was true for CD39. Cardiomyocytes and erythrocytes do not measurably express CD39/CD73 and CD39 dominates on coronary endothelium. Three days after I/R, CD73 was significantly upregulated on invading granulocytes (2.8-fold) and T-cells (1.5-fold). Compared with coronary endothelial cells, CD73 associated with leukocytes comprised 2/3 of the total cardiac CD73. CONCLUSION: Our study suggests that extracellular ATP formed during I/R is preferentially degraded by CD39 present on myeloid cells, while the formation of immunosuppressive adenosine is mainly catalysed by CD73 present on granulocytes and lymphoid cells. Upregulated CD73 on granulocytes and T-cells infiltrating the injured heart is consistent with the existence of an autocrine adenosinergic loop which may promote the healing process

    Features of adenosine metabolism of mouse heart

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    Adenosine metabolism and transport were evaluated in the isolated perfused mouse heart and compared with the well-established model of isolated perfused guinea pig heart. Coronary venous release of adenosine under well-oxygenated conditions in the mouse exceeds that in the guinea pig threefold when related to tissue mass. Total myocardial adenosine production rate under this condition was approximately 2 nmol/min per gramme and similar in both species. Coronary resistance vessels of mice are highly sensitive to exogenous adenosine, and the threshold for adenosine-induced vasodilation is approximately 30 nmol/l. Adenosine membrane transport was largely insensitive to nitrobenzyl-thioinosine (NBTI) in mouse heart, which is in contrast to guinea pig and several other species. This indicates the dominance of NBTI-insensitive transporters in mouse heart. For future studies, the assessment of cytosolic and extracellular adenosine metabolism and its relationship with coronary flow will require the use of more effective membrane transport blockers

    Ecto-5′-nucleotidase and intestinal ion secretion by enteropathogenic Escherichia coli

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    Enteropathogenic Escherichia coli (EPEC) triggers a large release of adenosine triphosphate (ATP) from host intestinal cells and the extracellular ATP is broken down to adenosine diphosphate (ADP), AMP, and adenosine. Adenosine is a potent secretagogue in the small and large intestine. We suspected that ecto-5′-nucleotidase (CD73, an intestinal enzyme) was a critical enzyme involved in the conversion of AMP to adenosine and in the pathogenesis of EPEC diarrhea. We developed a nonradioactive method for measuring ecto-5′-nucleotidase in cultured T84 cell monolayers based on the detection of phosphate release from 5′-AMP. EPEC infection triggered a release of ecto-5′-nucleotidase from the cell surface into the supernatant medium. EPEC-induced 5′-nucleotidase release was not correlated with host cell death but instead with activation of phosphatidylinositol-specific phospholipase C (PI-PLC). Ecto-5′-nucleotidase was susceptible to inhibition by zinc acetate and by α,β-methylene-adenosine diphosphate (α,β-methylene-ADP). In the Ussing chamber, these inhibitors could reverse the chloride secretory responses triggered by 5′-AMP. In addition, α,β-methylene-ADP and zinc blocked the ability of 5′-AMP to stimulate EPEC growth under nutrient-limited conditions in vitro. Ecto-5′-nucleotidase appears to be the major enzyme responsible for generation of adenosine from adenine nucleotides in the T84 cell line, and inhibitors of ecto-5′-nucleotidase, such as α,β-methylene-ADP and zinc, might be useful for treatment of the watery diarrhea produced by EPEC infection

    Autoimmunity in CD73/Ecto-5′-Nucleotidase Deficient Mice Induces Renal Injury

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    Extracellular adenosine formed by 5′-ectonucleotidase (CD73) is involved in tubulo-glomerular feedback in the kidney but is also known to be an important immune modulator. Since CD73−/−mutant mice exhibit a vascular proinflammatory phenotype, we asked whether long term lack of CD73 causes inflammation related kidney pathologies. CD73−/−mice (13 weeks old) showed significantly increased low molecule proteinuria compared to C57BL6 wild type controls (4.8≥0.52 vs. 2.9±0.54 mg/24 h, p<0.03). Total proteinuria increased to 5.97±0.78 vs. 2.55±0.35 mg/24 h at 30 weeks (p<0.01) whereas creatinine clearance decreased (0.161±0.02 vs. 0.224±0.02 ml/min). We observed autoimmune inflammation in CD73−/−mice with glomerulitis and peritubular capillaritis, showing glomerular deposition of IgG and C3 and enhanced presence of CD11b, CD8, CD25 as well as GR-1-positive cells in the interstitium. Vascular inflammation was associated with enhanced serum levels of the cytokines IL-18 and TNF-α as well as VEGF and the chemokine MIP-2 (CXCL-2) in CD73−/−mice, whereas chemokines and cytokines in the kidney tissue were unaltered or reduced. In CD73−/−mice glomeruli, we found a reduced number of podocytes and endothelial fenestrations, increased capillaries per glomeruli, endotheliosis and enhanced tubular fibrosis. Our results show that adult CD73−/−mice exhibit spontaneous proteinuria and renal functional deterioration even without exogenous stress factors. We have identified an autoimmune inflammatory phenotype comprising the glomerular endothelium, leading to glomeruli inflammation and injury and to a cellular infiltrate of the renal interstitium. Thus, long term lack of CD73 reduced renal function and is associated with autoimmune inflammation
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