Three-dimensional foam flow resolved by fast X-ray tomographic microscopy

Thanks to ultra fast and high resolution X-ray tomography, we managed to capture the evolution of the local structure of the bubble network of a 3D foam flowing around a sphere. As for the 2D foam flow around a circular obstacle, we observed an axisymmetric velocity field with a recirculation zone, and indications of a negative wake downstream the obstacle. The bubble deformations, quantified by a shape tensor, are smaller than in 2D, due to a purely 3D feature: the azimuthal bubble shape variation. Moreover, we were able to detect plastic rearrangements, characterized by the neighbor-swapping of four bubbles. Their spatial structure suggest that rearrangements are triggered when films faces get smaller than a characteristic area.Comment: 5 pages, 5 figure

Two-dimensional flow of foam around an obstacle: force measurements

A Stokes experiment for foams is proposed. It consists in a two-dimensional flow of a foam, confined between a water subphase and a top plate, around a fixed circular obstacle. We present systematic measurements of the drag exerted by the flowing foam on the obstacle, \emph{versus} various separately controlled parameters: flow rate, bubble volume, bulk viscosity, obstacle size, shape and boundary conditions. We separate the drag into two contributions, an elastic one (yield drag) at vanishing flow rate, and a fluid one (viscous coefficient) increasing with flow rate. We quantify the influence of each control parameter on the drag. The results exhibit in particular a power-law dependence of the drag as a function of the bulk viscosity and the flow rate with two different exponents. Moreover, we show that the drag decreases with bubble size, and increases proportionally to the obstacle size. We quantify the effect of shape through a dimensioned drag coefficient, and we show that the effect of boundary conditions is small.Comment: 26 pages, 13 figures, resubmitted version to Phys. Rev.

Structure-dependent mobility of a dry aqueous foam flowing along two parallel channels

The velocity of a two-dimensional aqueous foam has been measured as it flows through two parallel channels, at a constant overall volumetric flow rate. The flux distribution between the two channels is studied as a function of the ratio of their widths. A peculiar dependence of the velocity ratio on the width ratio is observed when the foam structure in the narrower channel is either single staircase or bamboo. In particular, discontinuities in the velocity ratios are observed at the transitions between double and single staircase and between single staircase and bamboo. A theoretical model accounting for the viscous dissipation at the solid wall and the capillary pressure across a film pinned at the channel outlet predicts the observed non-monotonic evolution of the velocity ratio as a function of the width ratio. It also predicts quantitatively the intermittent temporal evolution of the velocity in the narrower channel when it is so narrow that film pinning at its outlet repeatedly brings the flow to a near stop

Flow of foam through a convergent channel

International audienceWe study experimentally the flow of a foam confined as a bubble monolayer between two plates through a convergent channel. We quantify the velocity, the distribution and orientation of plastic events, and the elastic stress, using image analysis. We use two different soap solutions: a sodium dodecyl sulfate (SDS) solution, with a negligible wall friction between the bubbles and the confining plates, and a mixture containing a fatty acid, giving a large wall friction. We show that for SDS solutions, the velocity profile obeys a self-similar form which results from the superposition of plastic events, and the elastic deformation is uniform. For the other solution, the velocity field differs and the elastic deformation increases towards the exit of the channel. We discuss and quantify the role of wall friction on the velocity profile, the elastic deformation, and the rate of plastic events

Distribution of Peanut Clump Virus (PCV), a virus with high symptom variability.

In 1974, Peanut Clump disease was present only in two very localized places in West Africa: Area of Bambey in Senegal and one agricultural research station in Burkina Faso. Following a number of surveys made in the 80s up to 1991, Peanut Clump Virus (PCV) was detected in Côte d'Ivoire, Mali, Niger and Benin. In Senegal, the virus is now widely distributed from the Senegal river to the frontier of Gambia. Transmission of PCV through seeds is partly responsible for the increased spread of the disease. Abundance of PCV in agricultural research stations, or in seed-gardens shows the importance of seed transmission. Existence of infected soils is another factor of dissemination of the virus. Symptoms induced by PCV in a given variety of groundnut vary from classical stunting with small dark green leaves, to normal sized plants with different light leaf symptoms such as line pattern, specking and a great variety of other foliar symptoms. Therefore, PCV is very difficult to diagnose in the field

Identification of excreted iron superoxide dismutase for the diagnosis of Phtytomonas

An excreted iron superoxide dismutase (FeSODe) of pI 3.6 with a molecular weight of 28-30 kDa was detected in the in vitro culture of Phytomonas isolated from Euphorbia characias (SODeCHA) and from Lycopersicon esculentum (SODeTOM), in Grace's medium without serum. These FeSODe excreted into the medium had immunogenic capacity: the positivity of the anti-SODeCHA serum persisted to a dilution of 1/30,000, and for the anti-SODeTOM to 1/10,000 by Western blot. In addition, cross reaction was detected between the anti-SODe serum of Phytomonas isolated from E. characias against SODeTOM, and the anti-SODe serum from L. esculentum with SODeCHA. This characteristic offers the possibility of its use to diagnose plant trypanosomatids. The validation of the test was confirmed by experimental inoculation of tomato fruits with Phytomonas isolated from L. esculentum. At 7, 10, 15, and 21 days post infection, it was possible to detect the presence of the parasites with the anti-SODe serum of Phytomonas isolated from L. esculentum at a dilution of 1/250. These serological results were confirmed by visualization of the parasites by optical microscopy. The data of this study confirm that the SOD is sufficient to identify a trypanosomatid isolated from plants as belonging to the genus Phytomonas.Finacial support: ATP 2002/03: Circulation of Trypanosomatidae Project (CIRAD, France), grant BIO-2000-1429 (University of Granada, Spain)

Th1 Disabled Function in Response to TLR4 Stimulation of Monocyte-Derived DC from Patients Chronically-Infected by Hepatitis C Virus

Background: Lack of protective antibodies and inefficient cytotoxic responses are characteristics of chronic hepatitis C infection. A defect in dendritic cell (DC) function has thus been suspected, but this remains a controversial issue. Methods and Findings: Here we show that monocyte-derived DC (MoDC) from chronically-infected patients can mature in response to TLR1/2, TLR2/6 or TLR3 ligands. In contrast, when stimulated with the TLR4 ligand LPS, MoDC from patients show a profound defect in inducing IFNc secretion by allogeneic T cells. This defect is not due to defective phenotypic maturation or to the presence of HCV-RNA in DC or monocytes but is correlated to reduced IL-12 secretion by DC. Restoration of DC ability to stimulate IFNc secretion can be obtained by blocking MEK activation in DC, indicating that MEK/ ERK pathway is involved in the Th1 defect of MoDC. Monocytes from HCV patients present increased spontaneous secretion of cytokines and chemokines, especially MIP-1b. Addition of MIP-1b on healthy monocytes during differentiation results in DC that have Th1 defect characteristic of MoDC from HCV patients, suggesting that MIP-1b secretion by HCV monocytes participates in the Th1 defect of DC. Conclusions: Our data indicate that monocytes from HCV patients are activated in vivo. This interferes with their differentiation into DC, leading to deficient TLR4 signaling in these cells that are enable to induce a Th1 response. Thi