[1] U-tube measurements of instantaneous velocities, concentrations, and fluxes for a well-sorted, medium-sized sand in oscillatory sheet flow are analyzed. The experiments involved two velocity-asymmetric flows, the same two flows with an opposing current of 0.4 m/s, and a mixed skewed-asymmetric flow, all with a velocity amplitude of 1.2 m/s and flow period of 7 s. We find that the net positive transport rate beneath velocityasymmetric oscillatory flow results from large, but opposing sand fluxes during the positive and negative flow phase. With an increase in velocity asymmetry and, in particular, velocity skewness, the difference in the magnitude of the fluxes in the two half cycles increases, leading to larger net transport rates. This trend is consistent with the observed increase in skewness of the oscillatory bed shear stress. Phase-lag effects, whereby sand stirred during the negative flow phase has not settled by the time of the negative-to-positive flow reversal and is subsequently transported during the positive flow phase, are notable but of minor importance to the net transport rate compared to earlier experiments with finer sands. In the vertical, the oscillatory flux is positive above the noflow bed. Within the sheet flow pick-up layer, the oscillatory flux is negative and similar in magnitude to the positive flux induced by the residual flow. The 0.4 m/s opposing current causes more sand to be picked up during the negative than during the positive flow phase. Above the no-flow bed the resulting negative oscillatory flux is comparable in magnitude to the current-related flux.

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Prenatal malnutrition is responsible for the onset of alterations in renal Na(+) transport in the adult offspring. Here we investigated the molecular mechanisms by which increased formation of reactive oxygen species during prenatal malnutrition affects the pathways that couple angiotensin II (Ang II) receptors (AT(1)R and AT(2)R) to kidney Na(+)-ATPase in adulthood, and how maternal treatment with α-tocopherol can prevent alterations in the main regulatory cascade of the pump. The experiments were carried out on the adult progeny of control and malnourished dams during pregnancy that did or did not receive α-tocopherol during lactation. Malnutrition during pregnancy increased maternal hepatic and adult offspring renal malondialdehyde levels, which returned to control after supplementation with α-tocopherol. In the adult offspring, placental malnutrition programmed: decrease in Na(+)-ATPase activity, loss of the physiological stimulation of this pump by Ang II, up-regulation of AT(1)R and AT(2)R, decrease in membrane PKC activity, selective decrease of the PKCε isoform expression, and increase in PKA activity with no change in PKA α-catalytic subunit expression. These alterations were reprogrammed to normal levels by α-tocopherol during lactation. The influence of α-tocopherol on the signaling machinery in adult offspring indicates selective non-antioxidant effects at the gene transcription and protein synthesis levels.