4 research outputs found

    Interdependence of Model Systematic Biases in the Tropical Atlantic and the Tropical Pacific

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    International audienceThe tropical climatology represented in simulations with General Circulation Models (GCMs) is affected by significant systematic biases despite the huge investments in model devlopment over the past 20 years. In this study, coupled seasonal hindcasts performed with EC-Earth and ECMWF System 4 are analyzed to understand the development of systematic biases in the tropical Atlantic and Pacific oceans. These models use similar atmosphere and ocean components (IFS and NEMO, respectively). We focus on hindcasts initialized in February and May. We discuss possible mechanisms for the evolution and origin of rapidly developing systematic biases over the tropical Atlantic during boreal spring. In addition, we look for evidence of the interrelation of systematic biases in the Atlantic and Pacific, and investigate if the errors in one ocean basin affect those in the other. We perform an upper-atmosphere wave analysis by Fourier filtering for certain ranges of temporal frequencies and zonal wavenumbers. Our results identicate common systematic biases in EC-Earth and System 4 purely attributable to the atmosphere component. Biases develop in the Atlantic basin independently of external influences, while a possible effect of such biases on the eastern Pacific is found

    Extracellular N-acetylaspartate depletion in traumatic brain injury

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    N-Acetylaspartate (NAA) is almost exclusively localized in neurons in the adult brain and is present in high concentration in the CNS. It can be measured by proton magnetic resonance spectroscopy and is seen as a marker of neuronal damage and death. NMR spectroscopy and animal models have shown NAA depletion to occur in various types of chronic and acute brain injury. We investigated 19 patients with traumatic brain injury (TBI). Microdialysis was utilized to recover NAA, lactate, pyruvate, glycerol and glutamate, at 12-h intervals. These markers were correlated with survival and a 6-month Glasgow Outcome Score. Eleven patients died and eight survived. A linear mixed model analysis showed a significant effect of outcome and of the interaction between time of injury and outcome on NAA levels (p = 0.009 and p = 0.004, respectively). Overall, extracellular NAA was 34% lower in non-survivors. A significant non-recoverable fall was observed in this group from day 4 onwards, with a concomitant rise in lactate–pyruvate ratio and glycerol. These results suggest that mitochondrial dysfunction is a significant contributor to poor outcome following TBI and propose extracellular NAA as a potential marker for monitoring interventions aimed at preserving mitochondrial function
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