Rate Dependence and Role of Disorder in Linearly Sheared Two-Dimensional Foams

The shear flow of two dimensional foams is probed as a function of shear rate and disorder. Disordered foams exhibit strongly rate dependent velocity profiles, whereas ordered foams show rate independence. Both behaviors are captured quantitatively in a simple model based on the balance of the time-averaged drag forces in the foam, which are found to exhibit power-law scaling with the foam velocity and strain rate. Disorder modifies the scaling of the averaged inter-bubble drag forces, which in turn causes the observed rate dependence in disordered foams.Comment: 4 Figures, 4 page

Representations of integers by certain positive definite binary quadratic forms

We prove part of a conjecture of Borwein and Choi concerning an estimate on the square of the number of solutions to n=x^2+Ny^2 for a squarefree integer N.Comment: 8 pages, submitte

Couette Flow of Two-Dimensional Foams

We experimentally investigate flow of quasi two-dimensional disordered foams in Couette geometries, both for foams squeezed below a top plate and for freely floating foams. With the top-plate, the flows are strongly localized and rate dependent. For the freely floating foams the flow profiles become essentially rate-independent, the local and global rheology do not match, and in particular the foam flows in regions where the stress is below the global yield stress. We attribute this to nonlocal effects and show that the "fluidity" model recently introduced by Goyon {\em et al.} ({\em Nature}, {\bf 454} (2008)) captures the essential features of flow both with and without a top plate.Comment: 6 pages, 5 figures, revised versio

Flow in linearly sheared two dimensional foams: from bubble to bulk scale

We probe the flow of two dimensional foams, consisting of a monolayer of bubbles sandwiched between a liquid bath and glass plate, as a function of driving rate, packing fraction and degree of disorder. First, we find that bidisperse, disordered foams exhibit strongly rate dependent and inhomogeneous (shear banded) velocity profiles, while monodisperse, ordered foams are also shear banded, but essentially rate independent. Second, we introduce a simple model based on balancing the averaged drag forces between the bubbles and the top plate and the averaged bubble-bubble drag forces. This model captures the observed rate dependent flows, and the rate independent flows. Third, we perform independent rheological measurements, both for ordered and disordered systems, and find these to be fully consistent with the scaling forms of the drag forces assumed in the simple model, and we see that disorder modifies the scaling. Fourth, we vary the packing fraction $\phi$ of the foam over a substantial range, and find that the flow profiles become increasingly shear banded when the foam is made wetter. Surprisingly, our model describes flow profiles and rate dependence over the whole range of packing fractions with the same power law exponents -- only a dimensionless number $k$ which measures the ratio of the pre-factors of the viscous drag laws is seen to vary with packing fraction. We find that $k \sim (\phi-\phi_c)^{-1}$, where $\phi_c \approx 0.84$, corresponding to the 2d jamming density, and suggest that this scaling follows from the geometry of the deformed facets between bubbles in contact. Overall, our work suggests a route to rationalize aspects of the ubiquitous Herschel-Bulkley (power law) rheology observed in a wide range of disordered materials.Comment: 16 pages, 14 figures, submitted to Phys. Rev. E. High quality version available at: http://www.physics.leidenuniv.nl/sections/cm/gr

Mononuclear cell transcriptome changes associated with dimethyl fumarate in MS.

ObjectiveTo identify short-term changes in gene expression in peripheral blood mononuclear cells (PBMCs) associated with treatment response to dimethyl fumarate (DMF, Tecfidera) in patients with relapsing-remitting MS (RRMS).MethodsBlood samples were collected from 24 patients with RRMS (median Expanded Disability Status Scale score, 2.0; range 1-7) at baseline, 6 weeks, and 15 months after the initiation of treatment with DMF (BG-12; Tecfidera). Seven healthy controls were also recruited, and blood samples were collected over the same time intervals. PBMCs were extracted from blood samples and sequenced using next-generation RNA sequencing. Treatment responders were defined using the composite outcome measure "no evidence of disease activity" (NEDA-4). Time-course and cross-sectional differential expression analyses were performed to identify transcriptomic markers of treatment response.ResultsTreatment responders (NEDA-4 positive, 8/24) over the 15-month period had 478 differentially expressed genes (DEGs) 6 weeks after the start of treatment. These were enriched for nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and inhibition of nuclear factor κB (NFκB) pathway transcripts. For patients who showed signs of disease activity, there were no DEGs at 6 weeks relative to their (untreated) baseline. Contrasting transcriptomes expressed at 6 weeks with those at 15 months of treatment, 0 and 1,264 DEGs were found in the responder and nonresponder groups, respectively. Transcripts in the nonresponder group (NEDA-4 negative, 18/24) were enriched for T-cell signaling genes.ConclusionShort-term PBMC transcriptome changes reflecting activation of the Nrf2 and inhibition of NFκB pathways distinguish patients who subsequently show a medium-term treatment response with DMF. Relative stabilization of gene expression patterns may accompany treatment-associated suppression of disease activity

Packing geometry and statistics of force networks in granular media

Article / Letter to editorLeiden Instituut Onderzoek Natuurkund

In-vitro activation of complement system by lactic acidosis in newborn and adults.

INTRODUCTION: Complement activation occurs secondary to a variety of external stimuli. Lactic acidosis has been previously shown to activate the complement factors C3a and C5a. In the present investigation we examined the differential effect of lactic acidosis on anaphylatoxin levels in cord and adult blood. Furthermore we aimed to determine if the entire complement cascade could be activated by lactic acidosis. METHODS: Cord and adult blood samples (n = 20 each) were collected and incubated for one hour in either untreated condition or with the addition of lactate in two concentrations (5.5 mmol/l vs. 22 mmol/l). Following incubation, levels of C3a, C5a and sC5b-9, and blood gas parameters were determined. RESULTS: Anaphylatoxin (C3a and C5a) and sC5b-9 levels increased with the addition of lactate in a dose-dependent manner in cord and adult blood (C3a: 1 h, 5.5 mmo/l, 22 mmol/l: 418/498/622 microg/l in cord blood; 1010/1056/1381 microg/l in adult blood, p<0,05; similar results were found for C5a and sC5b-9). CONCLUSION: Lactic acidosis leads to an activation of the entire complement system in neonates and in adults. This activation is dose-dependent and more pronounced in adults as compared to neonates

Sources and sinks separating domains of left- and right-traveling waves: Experiment versus amplitude equations

In many pattern forming systems that exhibit traveling waves, sources and sinks occur which separate patches of oppositely traveling waves. We show that simple qualitative features of their dynamics can be compared to predictions from coupled amplitude equations. In heated wire convection experiments, we find a discrepancy between the observed multiplicity of sources and theoretical predictions. The expression for the observed motion of sinks is incompatible with any amplitude equation description.Comment: 4 pages, RevTeX, 3 figur