Simulation of wave damping during a cold front over the muddy Atchafalaya shelf

The Atchafalaya Shelf off the Louisiana coast in the United States is characterized by fine grained sediments dispersing into the shelf from the lower Atchafalaya River and Wax Lake outlets. Rapid seaward flushing of the sediment-laden river plumes, due to water level set-down during cold front passages forms a fluid mud layer close to the bottom, which effectively dampens the wave energy. In this study, the performance of a phase-averaged spectral wave model was skill assessed based on the wave data recorded close to the southern periphery of the mud zone during several days in March 2009. Separation of wave spectra into sea and swell partitions showed that the wave model overestimated the sea waves generated by northerly wind during the cold front passage. A non-stationary scheme was needed to solve the wave action balance equation to include the wind dynamics during the cold front passages over the study area. A recently developed mud-induced dissipation term was improved by modifying its algorithm for solving the implicit dispersion equation. The modified model became efficient enough to be used for non-stationary calculations. The thickness, density, kinematic viscosity of the mud layer, and its offshore extent were determined by trial and error. The mud-induced energy dissipation term enabled the model to reproduce the energy attenuation of short waves by the fluid mud. A high value of mud viscosity (0.01-0.1m /s) was required to obtain good agreement with in situ measurements when the maximum wave height occurred. However, the model using lower values of mud viscosity (0.001-0.01m /s) was more successful in reproducing the measured wave spectra from a few hours after the maximum wave activity. The simulation results also showed that presence of fluid mud with high value of mud viscosity hindered the wave growth in shallow water due to suppression of high frequency waves. © 2012 Elsevier Ltd. 2

Vascular relaxation, antihypertensive effect, and cardioprotection of a novel peptide agonist of the Mas receptor

Mas stimulation with angiotensin (Ang)-(1-7) produces cardioprotective effects and vasorelaxation. Using a computational discovery platform for predicting novel naturally occurring peptides that may activate G protein-coupled receptors, we discovered a novel Mas agonist peptide, CGEN-856S. An endothelium- and NO-dependent vasodilating effect was observed for CGEN-856S in thoracic aorta rings of rats (maximal value for the relaxant effect: 39.99+/-5.034%), which was similar to that produced by Ang-(1-7) (10(-10) to 10(-6) mol/L). In addition, the vasodilator activity of this peptide depended on a functional Mas receptor, because it was abolished in aorta rings of Mas-knockout mice. CGEN-856S appears to bind the Mas receptor at the same binding domain as Ang-(1-7), as suggested by the blocking of its vasorelaxant effect with the Ang-(1-7) analogue D-Ala(7)-Ang-(1-7), and by its competitive inhibition of Ang-(1-7) binding to Mas-transfected cells. The effect of CGEN-856S on reperfusion arrhythmias and cardiac function was studied on ischemia reperfusion of isolated rat hearts. We found that picomolar concentration of CGEN-856S (0.04 nmol/L) had an antiarrhythmogenic effect, as demonstrated by a reduction in the incidence and duration of reperfusion arrhythmias. Furthermore, acute infusion of CGEN-856S produced a shallow dose-dependent decrease in mean arterial pressure of conscious spontaneously hypertensive rats. The maximum change during infusion was observed at the highest dose. Strikingly, blood pressure continued to drop in the postinfusion period. The results presented here indicate that the novel Mas agonist, CGEN-856S, might have a therapeutic value, because it induces vasorelaxing, antihypertensive, and cardioprotective effects