A LES-Langevin model for turbulence

We propose a new model of turbulence for use in large-eddy simulations (LES). The turbulent force, represented here by the turbulent Lamb vector, is divided in two contributions. The contribution including only subfilter fields is deterministically modeled through a classical eddy-viscosity. The other contribution including both filtered and subfilter scales is dynamically computed as solution of a generalized (stochastic) Langevin equation. This equation is derived using Rapid Distortion Theory (RDT) applied to the subfilter scales. The general friction operator therefore includes both advection and stretching by the resolved scale. The stochastic noise is derived as the sum of a contribution from the energy cascade and a contribution from the pressure. The LES model is thus made of an equation for the resolved scale, including the turbulent force, and a generalized Langevin equation integrated on a twice-finer grid. The model is validated by comparison to DNS and is tested against classical LES models for isotropic homogeneous turbulence, based on eddy viscosity. We show that even in this situation, where no walls are present, our inclusion of backscatter through the Langevin equation results in a better description of the flow.Comment: 18 pages, 14 figures, to appear in Eur. Phys. J.

Thrombopoietin-Increased DNA-PK-Dependent DNA Repair Limits Hematopoietic STEM and Progenitor CELL Mutagenesis in Response to Irradiation

54th Annual Meeting and Exposition of the American-Society-of-Hematology (ASH), Atlanta, GA, DEC 08-11, 2012International audienceno abstrac

Thrombopoietin increases dna repair and limits hematopoietic stem cell long-term injury and mutagenesis in response to dna damage

ISEH 41st Annual Scientific Meeting of the Society-for-Hematology-and-Stem-Cells, Amsterdam, NETHERLANDS, AUG 23-26, 2012International audienceno abstrac

Maternal and fetal microchimerism in granulocytes

Cell trafficking during pregnancy may result in durable microchimerism, both fetal microchimerism in the mother and maternal microchimerism in her children. Whether microchimerism is continuously replenished has not been well-described. To address this question, we isolated granulocytes, cells with relatively short half-lives, from peripheral blood of healthy women. CD66b-positive cells were isolated by fluorescence activated cell sorting and a panel of polymorphism-specific quantitative pCR assays was employed to investigate fetal and maternal microchimerism. Overall 33% (10/30) of study subjects had at least one source of microchimerism in CD66b+ cells. Interestingly, maternal microchimerism was more common than fetal microchimerism, 40% vs. 15%, respectively (p = 0.05) and was present at higher levels (p = 0.03). The identification of maternal and fetal origin CD66b+ cells is strong evidence for an active microchimeric hematopoietic stem and progenitor cell niche. Furthermore, microchimeric CD66b+ cells could have an impact on innate and adaptive immune responses