Flow measurements near a Reynolds ridge

The Reynolds ridge is a well-known phenomenon first observed in 1854 by Henry David Thoreau. It was then rediscovered by Langton in 1872, but Reynolds was the first to recognize that the surface tension difference was the physical mechanism behind its formation and saw the equality between the case of a spreading film and that of a stagnant film met by oncoming flow. However, it wasn't until McCutchen in 1970 that the prediction of a boundary layer forming beneath the film was introduced as the cause of the surface deformation rise ahead of the film due to the retardation of the flow. The first quantitative theory of the ridge was formed by Harper and Dixon (1974), who stated that the surface tension gradient balances the viscous shear stress generated in the boundary layer. Experimental studies of the ridge so far include Schlieren visualizations by Sellin (1968) as well as by Scott (1982) who measured the surface slope across the ridge and found good comparisons between the theoretical results of Harper and Dixon. Finally, it was Scott who recognized that even at very low levels of surface contamination the Reynolds ridge is found to exist

Amplitude measurements of Faraday waves

A light reflection technique is used to measure quantitatively the surface elevation of Faraday waves. The performed measurements cover a wide parameter range of driving frequencies and sample viscosities. In the capillary wave regime the bifurcation diagrams exhibit a frequency independent scaling proportional to the wavelength. We also provide numerical simulations of the full Navier-Stokes equations, which are in quantitative agreement up to supercritical drive amplitudes of 20%. The validity of an existing perturbation analysis is found to be limited to 2.5% overcriticaly.Comment: 7 figure

Distinct cytokine profiles of circulating mononuclear cells stimulated with Staphylococcus aureus enterotoxin A in vitro during early and late episodes of chronic osteomyelitis

We investigated the cytokine profile of peripheral mononuclear cells from chronic osteomyelitis (OST) patients following in vitro stimulation with staphylococcal enterotoxin A (SEA). We demonstrate that stimulation with SEA induced prominent lymphocyte proliferation and high levels of tumour necrosis factor (TNF)-α, interleukin (IL)-4 and IL-10 secretion in both OST and non-infected individuals (NI). Even though stimulation with SEA had no impact on IL-6 production in either patient group, the baseline level of IL-6 production by cells from OST patients was always significantly less than that produced by cells from NI. After classifying the osteomyelitic episodes based on the time after the last reactivation event as "early" (1-4 months) or "late" osteomyelitis (5-12 months), we found that increased levels of TNF-α and IL-4 in combination with decreased levels of IL-6 were observed in the early episodes. By contrast, increased levels of IL-10, IL-2 and IL-6 were hallmarks of late episodes. Our data demonstrate that early osteomyelitic episodes are accompanied by an increased frequency of "high producers" of TNF-α and IL-4, whereas late events are characterised by increased frequencies of "high producers" of IL-10, IL-6 and IL-2. These findings demonstrate the distinct cytokine profiles in chronic osteomyelitis, with a distinct regulation of IL-6 production during early and late episodes