Shear-thickening of a non-colloidal suspension with a viscoelastic matrix

In this work we study the rheology of a non-colloidal suspension of rigid spherical particles interacting with a viscoelastic matrix. Three-dimensional numerical simulations under shear flow are performed using the smoothed particle hydrodynamics method and compared with experimental data available in the literature using different constant- viscosity elastic Boger fluids. The rheological properties of the Boger matrices are matched in simulation under viscometric flow conditions. Suspension rheology under dilute to semi-concentrated conditions (i.e. up to solid volume fraction φ = 0.3) is explored. It is found that at small Deborah numbers (based on the macroscopic imposed shear rate), relative suspension viscosities ηr exhibit a plateau at every concentration investigated. By increasing the Deborah number De shear-thickening is observed which is related to the extensional-thickening of the underlying viscoelastic matrix. Under dilute conditions (φ = 0.05) numerical results for ηr agree quantitatively with experimental data both in the De- and φ-dependencies. Even under dilute conditions, simulations of full many-particle systems with no ’a priori’ specification of their spatial distribution need to be considered to recover precisely experimental values. By increasing the solid volume fraction towards φ = 0.3, despite the fact that the trend is well captured, the agreement remains qualitative with discrepancies arising in the absolute values of ηr obtained from simulations and experiments but also with large deviations existing among different experiments. With regard to the specific mechanism of elastic thickening, the microstructural analysis shows that elastic thickening correlates well with the averaged viscoelastic dissipation function θ_elast, requiring a scaling as θ_elasti ∼De^α with α > 2 to take place. Locally, despite the fact that regions of large polymer stretching (and viscoelastic dissipation) can occur everywhere in the domain, flow regions uniquely responsible of the elastic thickening are well correlated to areas with significant extensional component

Relationships between traditional and fundamental dough-testing methods

Two fundamental test systems were used to evaluate the visco-elastic properties of doughs from wheat samples of three varieties grown at four distinct sites. For comparison, tests were also performed with traditional equipment, namely the Mixograph, an extension tester and a Farinograph-type small-scale recording mixer. Uniaxial dough elongation (with an Instron) produced results similar to the conventional extension tester, except that results were provided in fundamental units (Pascals), the critical value recorded being the elongational stress at maximum strain. Stress relaxation measurements were performed following a small initial shear strain. With this method, it was possible to distinguish between the viscosity and the elastic components of dough visco-elasticity. In all the tests the extra dough-strength properties were evident for the variety (Guardian) that had the 5 + 10 glutenin subunits, in contrast to the other two with the 2 + 12 combination of subunits

Discovery and functional prioritization of Parkinson's disease candidate genes from large-scale whole exome sequencing.

BACKGROUND: Whole-exome sequencing (WES) has been successful in identifying genes that cause familial Parkinson's disease (PD). However, until now this approach has not been deployed to study large cohorts of unrelated participants. To discover rare PD susceptibility variants, we performed WES in 1148 unrelated cases and 503 control participants. Candidate genes were subsequently validated for functions relevant to PD based on parallel RNA-interference (RNAi) screens in human cell culture and Drosophila and C. elegans models. RESULTS: Assuming autosomal recessive inheritance, we identify 27 genes that have homozygous or compound heterozygous loss-of-function variants in PD cases. Definitive replication and confirmation of these findings were hindered by potential heterogeneity and by the rarity of the implicated alleles. We therefore looked for potential genetic interactions with established PD mechanisms. Following RNAi-mediated knockdown, 15 of the genes modulated mitochondrial dynamics in human neuronal cultures and four candidates enhanced α-synuclein-induced neurodegeneration in Drosophila. Based on complementary analyses in independent human datasets, five functionally validated genes-GPATCH2L, UHRF1BP1L, PTPRH, ARSB, and VPS13C-also showed evidence consistent with genetic replication. CONCLUSIONS: By integrating human genetic and functional evidence, we identify several PD susceptibility gene candidates for further investigation. Our approach highlights a powerful experimental strategy with broad applicability for future studies of disorders with complex genetic etiologies