On a projection method for piecewise-constant pressure nonconforming finite elements

We present a study of the incremental projection method to solve incompressible unsteady Stokes equations based on a low degree nonconforming finite element approximation in space, with, in particular, a piecewise constant approximation for the pressure. The numerical method falls in the class of algebraic projection methods. We provide an error analysis in the case of Dirichlet boundary conditions, which confirms that the splitting error is second order in time. In addition, we show that pressure artificial boundary conditions are present in the discrete pressure elliptic operator, even if this operator is obtained by a splitting performed at the discrete level; however, these boundary conditions are imposed in the finite volume (weak) sense and the optimal order of approximation in space is still achieved, even for open boundary conditions

Analysis of a projection method for low-order non-conforming finite elements

International audienceWe present a study of the incremental projection method to solve incompressible unsteady Stokes equations based on a low degree non-conforming finite element approximation in space, with, in particular, a piecewise constant approximation for the pressure. The numerical method falls in the class of algebraic projection methods. We provide an error analysis in the case of Dirichlet boundary conditions, which confirms that the splitting error is second-order in time. In addition, we show that pressure artificial boundary conditions are present in the discrete pressure elliptic operator, even if this operator is obtained by a splitting performed at the discrete level; however, these boundary conditions are imposed in the finite volume (weak) sense and the optimal order of approximation in space is still achieved, even for open boundary conditions

Specific transcriptional responses induced by 8-methoxypsoralen and UVA in yeast

Treatment of eukaryotic cells with 8-methoxypsoralen plus UVA irradiation (8-MOP/UVA) induces pyrimidine monoadducts and interstrand crosslinks and initiates a cascade of events leading to cytotoxic, mutagenic and carcinogenic responses. Transcriptional activation plays an important part in these responses. Our previous study in Saccharomyces cerevisiae showed that the repair of these lesions involves the transient formation of DNA double-strand breaks and the enhanced expression of landmark DNA damage response genes such as RAD51, RNR2 and DUN1, as well as the Mec1/Rad53 kinase signaling cascade. We have now used DNA microarrays to examine genome-wide transcriptional changes produced after induction of 8-MOP/UVA photolesions. We found that 128 genes were strongly induced and 29 genes strongly repressed. Modifications in gene expression concern numerous biological processes. Compared to other genotoxic treatments, c. 42% of the response genes were specific to 8-MOP/UVA treatment. In addition to common DNA damage response genes and genes induced by environmental stresses, a large fraction of 8-MOP/UVA response genes correspond to membrane-related functions

Impact of Technology Spreading on MEMS design Robustness

International audienc

Editorial: Knocking on neuroimmunology’s doors: an entrechat concerning the immune system balance and its cell metabolism orchestration

ISSN:1664-322

MicroRNAs regulate T-cell production of interleukin-9 and identify hypoxia-inducible factor-2a as an important regulator of T helper 9 and regularoty T-cell differentiation

MicroRNAs (miRNAs) regulate many aspects of helper T cell (Th) development and function. Here we found that they are required for the suppression of interleukin‐9 (IL‐9) expression in Th9 cells and other Th subsets. Two highly related miRNAs (miR‐15b and miR‐16) that we previously found to play an important role in regulatory T (Treg) cell differentiation were capable of suppressing IL‐9 expression when they were over‐expressed in Th9 cells. We used these miRNAs as tools to identify novel regulators of IL‐9 expression and found that they could regulate the expression of Epas1, which encodes hypoxia‐inducible factor (HIF)‐2α. HIF proteins regulate metabolic pathway usage that is important in determining appropriate Th differentiation. The related protein, HIF‐1α enhances Th17 differentiation and inhibits Treg cell differentiation. Here we found that HIF‐2α was required for IL‐9 expression in Th9 cells, but its expression was not sufficient in other Th subsets. Furthermore, HIF‐2α suppressed Treg cell differentiation like HIF‐1α, demonstrating both similar and distinct roles of the HIF proteins in Th differentiation and adding a further dimension to their function. Ironically, even though miR‐15b and miR‐16 suppressed HIF‐2α expression in Treg cells, inhibiting their function in Treg cells did not lead to an increase in IL‐9 expression. Therefore, the physiologically relevant miRNAs that regulate IL‐9 expression in Treg cells and other subsets remain unknown. Nevertheless, the analysis of miR‐15b and miR‐16 function led to the discovery of the importance of HIF‐2α so this work demonstrated the utility of studying miRNA function to identify novel regulatory pathways in helper T‐cell development

Результаты российского проспективного обсервационного исследования СПЕКТР

ПРОСПЕКТИВНЫЕ ИССЛЕДОВАНИЯНАСЕЛЕНИЯ ГРУПП ИЗУЧЕНИЕВЕНОЗНАЯ НЕДОСТАТОЧНОСТЬКРОВЕНОСНЫХ СОСУДОВ БОЛЕЗН

Perinatal Bisphenol A Exposure in C57B6/129svj Male Mice: Potential Altered Cytokine/Chemokine Production in Adulthood

Pregnant mice (n = 3) were exposed to BPA by intraperitoneal injection, from gestation day 9.5 until end of lactation. Male offspring were evaluated for cytokine production at 20 wk-of-age. One pregnant control mouse produced no males, precluding statistical analysis. However, recurring shifts in cytokines were suggested in the adult BPA offspring. Serum showed a numeric increase in 16 of 21 basal cytokine levels. ConA-stimulated splenocytes showed a numeric increase in 17 of 21 cytokines, and LPS-stimulated splenocytes an increase in 18 of 21 cytokines. The cytokine profile was one of TH1 up-regulation more than TH2, and with skewing toward TH17 responses

Loss of the Lupus Autoantigen Ro52/Trim21 Induces Tissue Inflammation and Systemic Autoimmunity by Disregulating the IL-23–Th17 Pathway

Ro52/Trim21 is targeted as an autoantigen in systemic lupus erythematosus and Sjögren's syndrome. Polymorphisms in the Ro52 gene have been linked to these autoimmune conditions, but the molecular mechanism by which Ro52 may promote development of systemic autoimmune diseases has not been explored. To address this issue, we generated Ro52-null mice ($Ro52^{−/−}$), which appear phenotypically normal if left unmanipulated. However, $Ro52^{−/−}$ mice develop severe dermatitis extending from the site of tissue injury induced by ear tags. The affected mice further develop several signs of systemic lupus with hypergammaglobulinemia, autoantibodies to DNA, proteinuria, and kidney pathology. Ro52, which was recently identified as an E3 ligase, mediates ubiquitination of several members of the interferon regulatory factor (IRF) family, and the Ro52-deficient mice have an enhanced production of proinflammatory cytokines that are regulated by the IRF transcription factors, including cytokines involved in the Th17 pathway (interleukin [IL] 6, IL-12/IL-23p40, and IL-17). Loss of IL-23/IL-17 by genetic deletion of IL-23/p19 in the $Ro52^{−/−}$ mice conferred protection from skin disease and systemic autoimmunity. These data reveal that the lupus-associated Ro52 protein is an important negative regulator of proinflammatory cytokine production, and they provide a mechanism by which a defective Ro52 function can lead to tissue inflammation and systemic autoimmunity through the IL-23–Th17 pathway