Surface currents in the Alderney Race from high-frequency radar measurements and three-dimensional modelling.

Two weeks of high-frequency radar measurements collected at the Alderney Race are compared with the results of a three-dimensional fully coupled wave-current model. Spatial current measurements are rare in this site, otherwise well investigated through modelling. Thus, the radar measurements offer a unique opportunity to examine the spatial reliability of numerical results, and can help to improve our understanding of the complex currents in the area. Comparison of observed and modelled surface current velocities showed a good agreement between the methods, represented by root mean squared errors ranging from 14 to 40 cm s-1 and from 18 to 60 cm s-1 during neap and spring tides, respectively. Maximum errors were found in shallow regions with consistently high current velocities, represented by mean neap and spring magnitudes of 1.25 m s-1 and 2.7 m s-1, respectively. Part of the differences between modelled and observed surface currents in these areas are thought to derive from limitations in the k-epsilon turbulence model used to simulate vertical mixing, when the horizontal turbulent transport is high. In addition, radar radial currents showed increased variance over the same regions, and might also be contributing to the discrepancies found. Correlation analyses yielded magnitudes above 0.95 over the entire study area, with better agreement during spring than during neap tides, probably because of an increase in the phase lag between radar and model velocities during the latter. This article is part of the theme issue 'New insights on tidal dynamics and tidal energy harvesting in the Alderney Race'.

Glucose-induced up-regulation of CD36 mediates oxidative stress and microvascular endothelial cell dysfunction.

AIMS/HYPOTHESIS: Hyperglycaemia-induced oxidative stress is implicated in the pathogenesis of chronic diabetic complications. Glucose-mediated oxidation of LDL may result in increased oxidative stress and vascular endothelial cell dysfunction via interaction with a cell surface scavenger receptor, CD36. In this study, we investigated the role of CD36 in cultured microvascular endothelial cells (MVECs) and in the heart by using an animal model of chronic diabetes. METHODS: Cultured MVECs were subjected to varying glucose concentrations and assayed for alteration in CD36 gene expression and protein levels. To assess for oxidised LDL (ox-LDL) uptake, MVECs exposed to low and high glucose were treated with ox-LDL (80 microg/ml), a ligand for CD36. Haem oxygenase-1 (HO-1) and endothelin-1 (ET-1) induction, as well as oxidative stress were determined. The role of glucose-induced CD36 alteration in ox-LDL uptake was also assayed following post-transcriptional CD36 gene silencing. For in vivo studies, CD36 mRNA and oxidative DNA and protein damage were measured in heart tissues of 1-month-old diabetic Sprague-Dawley rats. RESULTS: We found that glucose increased CD36 mRNA and protein levels in MVECs. High levels of glucose also augmented ox-LDL uptake, in association with increasing HO-1 and ET-1 mRNA levels. CD36 gene silencing prevented glucose-induced CD36 alteration, reduced ox-LDL uptake, and prevented HO-1 and ET-1 up-regulation. Similar to in vitro studies, diabetic heart tissues exhibited increased CD36 mRNA levels and increased oxidative DNA and protein damage. CONCLUSIONS/INTERPRETATION: Our results provide evidence that up-regulation of CD36 may have a role in increasing oxidative stress in MVECs and the heart in chronic diabetes.

Bistramide A, a new toxin from the urochordata Lissoclinum bistratum Sluiter: isolation and preliminary characterization.

Two cases of human intoxication caused by the lyophilized powder of Lissoclinum bistratum Sluiter, a New Caledonian ascidian, are reported. The symptoms observed were caused by a substance designated bistramide A (C40H68N2O8) of hitherto unknown chemical structure. Preliminary toxicological investigations indicate that bistramide A may effect the central nervous system, leading to paresthesia and loss of muscle tone. A progressive decrease in cardiac rhythm was also observed in animals. Bistramide A (1.4 x 10(-6) M) did not alter the resting potential of frog heart and skeletal muscle but reduced the amplitude and duration of cardiac action potential and prolonged the interval between action potentials. Bistramide A also has a marked cytotoxic effect on cancer cells KB (IC50 = 4.5 x 10(-8) M) and P 388 (IC50 = 2.0 x 10(-8) M) and on normal endothelial cells (IC50 = 2.2 x 10(-8) M). However, it has not been possible to relate the cytotoxic property to the symptoms of intoxication. Bistramide A may originate from the urochordate itself or from symbiotic algae.