4 resultados para Stress driven interdiffusion

em CentAUR: Central Archive University of Reading - UK


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A one-dimensional water column model using the Mellor and Yamada level 2.5 parameterization of vertical turbulent fluxes is presented. The model equations are discretized with a mixed finite element scheme. Details of the finite element discrete equations are given and adaptive mesh refinement strategies are presented. The refinement criterion is an "a posteriori" error estimator based on stratification, shear and distance to surface. The model performances are assessed by studying the stress driven penetration of a turbulent layer into a stratified fluid. This example illustrates the ability of the presented model to follow some internal structures of the flow and paves the way for truly generalized vertical coordinates. (c) 2005 Elsevier Ltd. All rights reserved.

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The interaction between ocean surface waves and the overlying wind leads to a transfer of momentum across the air–sea interface. Atmospheric and oceanic models typically allow for momentum transfer to be directed only downward, from the atmosphere to the ocean. Recent observations have suggested that momentum can also be transferred upward when long wavelength waves, characteristic of remotely generated swell, propagate faster than the wind speed. The effect of upward momentum transfer on the marine atmospheric boundary layer is investigated here using idealized models that solve the momentum budget above the ocean surface. A variant of the classical Ekman model that accounts for the wave-induced stress demonstrates that, although the momentum flux due to the waves penetrates only a small fraction of the depth of the boundary layer, the wind profile is profoundly changed through its whole depth. When the upward momentum transfer from surface waves sufficiently exceeds the downward turbulent momentum flux, then the near-surface wind accelerates, resulting in a low-level wave-driven wind jet. This increases the Coriolis force in the boundary layer, and so the wind turns in the opposite direction to the classical Ekman layer. Calculations of the wave-induced stress due to a wave spectrum representative of fast-moving swell demonstrate upward momentum transfer that is dominated by contributions from waves in the vicinity of the peak in the swell spectrum. This is in contrast to wind-driven waves whose wave-induced stress is dominated by very short wavelength waves. Hence the role of swell can be characterized by the inverse wave age based on the wave phase speed corresponding to the peak in the spectrum. For a spectrum of waves, the total momentum flux is found to reverse sign and become upward, from waves to wind, when the inverse wave age drops below the range 0.15–0.2, which agrees reasonably well with previously published oceanic observations.

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Myostatin, a member of the TGF-beta family, has been identified as a powerful inhibitor of muscle growth. Absence or blockade of myostatin induces massive skeletal muscle hypertrophy that is widely attributed to proliferation of the population of muscle fiber-associated satellite cells that have been identified as the principle source of new muscle tissue during growth and regeneration. Postnatal blockade of myostatin has been proposed as a basis for therapeutic strategies to combat muscle loss in genetic and acquired myopathies. But this approach, according to the accepted mechanism, would raise the threat of premature exhaustion of the pool of satellite cells and eventual failure of muscle regeneration. Here, we show that hypertrophy in the absence of myostatin involves little or no input from satellite cells. Hypertrophic fibers contain no more myonuclei or satellite cells and myostatin had no significant effect on satellite cell proliferation in vitro, while expression of myostatin receptors dropped to the limits of detectability in postnatal satellite cells. Moreover, hypertrophy of dystrophic muscle arising from myostatin blockade was achieved without any apparent enhancement of contribution of myonuclei from satellite cells. These findings contradict the accepted model of myostatin-based control of size of postnatal muscle and reorient fundamental investigations away from the mechanisms that control satellite cell proliferation and toward those that increase myonuclear domain, by modulating synthesis and turnover of structural muscle fiber proteins. It predicts too that any benefits of myostatin blockade in chronic myopathies are unlikely to impose any extra stress on the satellite cells.

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This study describes the turbulent processes in the upper ocean boundary layer forced by a constant surface stress in the absence of the Coriolis force using large-eddy simulation. The boundary layer that develops has a two-layer structure, a well-mixed layer above a stratified shear layer. The depth of the mixed layer is approximately constant, whereas the depth of the shear layer increases with time. The turbulent momentum flux varies approximately linearly from the surface to the base of the shear layer. There is a maximum in the production of turbulence through shear at the base of the mixed layer. The magnitude of the shear production increases with time. The increase is mainly a result of the increase in the turbulent momentum flux at the base of the mixed layer due to the increase in the depth of the boundary layer. The length scale for the shear turbulence is the boundary layer depth. A simple scaling is proposed for the magnitude of the shear production that depends on the surface forcing and the average mixed layer current. The scaling can be interpreted in terms of the divergence of a mean kinetic energy flux. A simple bulk model of the boundary layer is developed to obtain equations describing the variation of the mixed layer and boundary layer depths with time. The model shows that the rate at which the boundary layer deepens does not depend on the stratification of the thermocline. The bulk model shows that the variation in the mixed layer depth is small as long as the surface buoyancy flux is small.