31 research outputs found
Forced Stratified Turbulence: Successive Transitions with Reynolds Number
Numerical simulations are made for forced turbulence at a sequence of
increasing values of Reynolds number, R, keeping fixed a strongly stable,
volume-mean density stratification. At smaller values of R, the turbulent
velocity is mainly horizontal, and the momentum balance is approximately
cyclostrophic and hydrostatic. This is a regime dominated by so-called pancake
vortices, with only a weak excitation of internal gravity waves and large
values of the local Richardson number, Ri, everywhere. At higher values of R
there are successive transitions to (a) overturning motions with local
reversals in the density stratification and small or negative values of Ri; (b)
growth of a horizontally uniform vertical shear flow component; and (c) growth
of a large-scale vertical flow component. Throughout these transitions, pancake
vortices continue to dominate the large-scale part of the turbulence, and the
gravity wave component remains weak except at small scales.Comment: 8 pages, 5 figures (submitted to Phys. Rev. E
Acoustic Mapping Velocimetry (AMV) for in-situ bedload transport estimation
Despite the importance of sediment transport processes in large rivers, the measurement of sed-iment transport rate in the in-situ, especially bedload, is difficult, costly and time consuming using conven-tional methods. In this paper, a novel indirect bedload estimation methodology is presented that is based on the Acoustic Mapping Velocimetry (AMV). AMV is a combination of acoustic and imaging techniques that provides 2D bedform velocity maps. As such, it can only be used if bedload is represented by bedform migra-tion. This paper illustrates the applicability of the bedload estimation method using as test case a section of the Ohio River in the United States. Repeated measurements of the bathymetry provided by multi-beam echo sounder serve as input data for AMV. Cross-sectional distributions of bedload transport rates obtained with AMV are compared with the estimates provided by another non-intrusive technique, ISSDOTv2, developed by the US Army Corps of Engineers. The good agreement between the results with the two different methods is encouraging and suggests further field tests covering a wider range of hydro-morphological situations
The protrusive phase and full development of integrin-dependent adhesions in colon epithelial cells require FAK- and ERK-mediated actin spike formation: Deregulation in cancer cells
Integrins play an important role in tumour progression by influencing cellular responses and matrix-dependent adhesion. However, the regulation of matrix-dependent adhesion assembly in epithelial cells is poorly understood. We have investigated the integrin and signalling requirements of cell-matrix adhesion assembly in colon carcinoma cells after plating on fibronectin. Adhesion assembly in these, and in the adenoma cells from which they were derived, was largely dependent on alpha v beta 6 integrin and required phosphorylation of FAK on tyrosine-397. The rate of fibronectin-induced adhesion assembly and the expression of both alpha v beta 6 integrin and FAK were increased during the adenoma-to-carcinoma transition. The matrix-dependent adhesion assembly process, particularly the final stages of complex protrusion that is required for optimal cell spreading, required the activity of extracellular signal-regulated kinase (ERK). Furthermore, phosphorylated ERK was targeted to newly forming cell--matrix adhesions in the carcinoma cells but not the adenoma cells, and inhibition of FAK--tyrosine-397 phosphorylation or MEK suppressed the appearance of phosphorylated ERK at peripheral sites. In addition, inhibition of MEK--ERK activation blocked the formation of peripheral actin microspikes that were necessary for the protrusive phase of cell-matrix adhesion assembly. Thus, MEK--ERK--dependent peripheral actin re-organization is required for the full development of integrin-induced adhesions and this pathway is stimulated in an in vitro model of colon cancer progression