Locally Resonant Metagrating by Elastic Impedance Modulation

The optical and acoustic metagratings have addressed the limitations of low-efficiency wave manipulation and high-complexity fabrication of metamaterials and metasurfaces. In this research, we introduce the concept of elastic metagrating and present the theoretical and experimental demonstration of locally resonant elastic metagrating (LREM). Remarkably, the LREM, with dimensions two orders of magnitude smaller than the relevant wavelength, overcomes the size limitations of conventional metagratings and offers a unique design paradigm for highly efficient wave manipulation with an extremely compact structure in elastic wave systems. Based on a distinctive elastic impedance engineering with hybridization of intrinsic evanescent waves, the proposed LREM achieves wide-angle perfect absorption. This tackles a fundamental challenge faced by all elastic metastructures designed for wave manipulation, which consists in the unavoidable vibration modes in finite structures hindering their implementations in real-world applications

DCAF1 controls T-cell function via p53-dependent and -independent mechanisms

On activation, naive T cells grow in size and enter cell cycle to mount immune response. How the fundamental processes of T-cell growth and cell cycle entry are regulated is poorly understood. Here we report that DCAF1 (Ddb1–cullin4-associated-factor 1) is essential for these processes. The deletion of DCAF1 in T cells impairs their peripheral homeostasis. DCAF1 is upregulated on T-cell receptor activation and critical for activation-induced T-cell growth, cell cycle entry and proliferation. In addition, DCAF1 is required for T-cell expansion and function during anti-viral and autoimmune responses in vivo. DCAF1 deletion leads to a drastic stabilization of p53 protein, which can be attributed to a requirement of DCAF1 for MDM2-mediated p53 poly-ubiquitination. Importantly, p53 deletion rescues the cell cycle entry defect but not the growth defect of DCAF1-deficient cells. Therefore, DCAF1 is vital for T-cell function through p53-dependent and -independent mechanisms

Altered microRNA expression profile with miR-146a upregulation in CD4+ T cells from patients with rheumatoid arthritis

Introduction: Increasing evidence indicates that microRNAs (miRNAs) play a critical role in the pathogenesis of inflammatory diseases. The aim of the study was to investigate the expression pattern and function of miRNAs in CD4 + T cells from patients with rheumatoid arthritis (RA).Methods: The expression profile of miRNAs in CD4 + T cells from synovial fluid (SF) and peripheral blood of 33 RA patients was determined by microarray assay and validated by qRT-PCR analysis. The correlation between altered expression of miRNAs and cytokine levels was determined by linear regression analysis. The role of miR-146a overexpression in regulating T cell apoptosis was evaluated by flow cytometry. A genome-wide gene expression analysis was further performed to identify miR-146a-regulated genes in T cells.Results: miRNA expression profile analysis revealed that miR-146a expression was significantly upregulated while miR-363 and miR-498 were downregulated in CD4 + T cells of RA patients. The level of miR-146a expression was positively correlated with levels of tumor necrosis factor-alpha (TNF-α), and in vitro studies showed TNF-α upregulated miR-146a expression in T cells. Moreover, miR-146a overexpression was found to suppress Jurkat T cell apoptosis. Finally, transcriptome analysis of miR-146a overexpression in T cells identified Fas associated factor 1 (FAF1) as a miR-146a-regulated gene, which was critically involved in modulating T cell apoptosis.Conclusions: We have detected increased miR-146a in CD4 + T cells of RA patients and its close correlation with TNF-α levels. Our findings that miR-146a overexpression suppresses T cell apoptosis indicate a role of miR-146a in RA pathogenesis and provide potential novel therapeutic targets. © 2010 Li et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.published_or_final_versio

ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics

BACKGROUND: Thiamine (vitamin B1) deficiency (TD) causes mild impairment of oxidative metabolism and region-selective neuronal loss in the central nervous system (CNS). TD in animals has been used to model aging-associated neurodegeneration in the brain. The mechanisms of TD-induced neuron death are complex, and it is likely multiple mechanisms interplay and contribute to the action of TD. In this study, we demonstrated that TD significantly increased intracellular calcium concentrations [Ca2+]i in cultured cortical neurons. RESULTS: TD drastically potentiated AMPA-triggered calcium influx and inhibited pre-mRNA editing of GluR2, a Ca2+-permeable subtype of AMPA receptors. The Ca2+ permeability of GluR2 is regulated by RNA editing at the Q/R site. Edited GluR2 (R) subunits form Ca2+-impermeable channels, whereas unedited GluR2 (Q) channels are permeable to Ca2+ flow. TD inhibited Q/R editing of GluR2 and increased the ratio of unedited GluR2. The Q/R editing of GluR2 is mediated by adenosine deaminase acting on RNA 2 (ADAR2). TD selectively decreased ADAR2 expression and its self-editing ability without affecting ADAR1 in cultured neurons and in the brain tissue. Over-expression of ADAR2 reduced AMPA-mediated rise of [Ca2+]i and protected cortical neurons against TD-induced cytotoxicity, whereas down-regulation of ADAR2 increased AMPA-elicited Ca2+ influx and exacerbated TD-induced death of cortical neurons. CONCLUSIONS: Our findings suggest that TD-induced neuronal damage may be mediated by the modulation of ADAR2-dependent RNA Editing of GluR2

Development of a High-Density Genetic Map Based on Specific Length Amplified Fragment Sequencing and Its Application in Quantitative Trait Loci Analysis for Yield-Related Traits in Cultivated Peanut

High-density genetic maps (HDGMs) are very useful for genomic studies and quantitative trait loci (QTL) mapping. However, the low frequency of DNA polymorphisms in peanut has limited the quantity of available markers and hindered the construction of a HDGM. This study generated a peanut genetic map with the highest number of high-quality SNPs based on specific locus amplified fragment sequencing (SLAF-seq) technology and a newly constructed RIL population (“ZH16” × “sd-H1”). The constructed HDGM included 3,630 SNP markers belonging to 2,636 bins on 20 linkage groups (LGs), and it covers 2,098.14 cM in length, with an average marker distance of 0.58 cM. This HDGM was applied for the following collinear comparison, scaffold anchoring and analysis of genomic characterization including recombination rates and segregation distortion in peanut. For QTL mapping of investigated 14 yield-related traits, a total of 62 QTLs were detected on 12 chromosomes across 3 environments, and the co-localization of QTLs was observed for these traits which were significantly correlated on phenotype. Two stable co-located QTLs for seed- and pod-related traits were significantly identified in the chromosomal end of B06 and B07, respectively. The construction of HDGM and QTL analysis for yield-related traits in this study provide useful information for fine mapping and functional analysis of genes as well as molecular marker-assisted breeding

Transcriptional Activation of OsDERF1 in OsERF3 and OsAP2-39 Negatively Modulates Ethylene Synthesis and Drought Tolerance in Rice

The phytohormone ethylene is a key signaling molecule that regulates a variety of developmental processes and stress responses in plants. Transcriptional modulation is a pivotal process controlling ethylene synthesis, which further triggers the expression of stress-related genes and plant adaptation to stresses; however, it is unclear how this process is transcriptionally modulated in rice. In the present research, we report the transcriptional regulation of a novel rice ethylene response factor (ERF) in ethylene synthesis and drought tolerance. Through analysis of transcriptional data, one of the drought-responsive ERF genes, OsDERF1, was identified for its activation in response to drought, ethylene and abscisic acid. Transgenic plants overexpressing OsDERF1 (OE) led to reduced tolerance to drought stress in rice at seedling stage, while knockdown of OsDERF1 (RI) expression conferred enhanced tolerance at seedling and tillering stages. This regulation was supported by negative modulation in osmotic adjustment response. To elucidate the molecular basis of drought tolerance, we identified the target genes of OsDERF1 using the Affymetrix GeneChip, including the activation of cluster stress-related negative regulators such as ERF repressors. Biochemical and molecular approaches showed that OsDERF1 at least directly interacted with the GCC box in the promoters of ERF repressors OsERF3 and OsAP2-39. Further investigations showed that OE seedlings had reduced expression (while RI lines showed enhanced expression) of ethylene synthesis genes, thereby resulting in changes in ethylene production. Moreover, overexpression of OsERF3/OsAP2-39 suppressed ethylene synthesis. In addition, application of ACC recovered the drought-sensitive phenotype in the lines overexpressing OsERF3, showing that ethylene production contributed to drought response in rice. Thus our data reveal that a novel ERF transcriptional cascade modulates drought response through controlling the ethylene synthesis, deepening our understanding of the regulation of ERF proteins in ethylene related drought response

Reversing SKI-SMAD4-mediated suppression is essential for TH17 cell differentiation

T helper 17 (TH17) cells are critically involved in host defence, inflammation, and autoimmunity. Transforming growth factor β (TGFβ) is instrumental in TH17 cell differentiation by cooperating with interleukin-6 (refs 6, 7). Yet, the mechanism by which TGFβ enables TH17 cell differentiation remains elusive. Here we reveal that TGFβ enables TH17 cell differentiation by reversing SKI-SMAD4-mediated suppression of the expression of the retinoic acid receptor (RAR)-related orphan receptor γt (RORγt). We found that, unlike wild-type T cells, SMAD4-deficient T cells differentiate into TH17 cells in the absence of TGFβ signalling in a RORγt-dependent manner. Ectopic SMAD4 expression suppresses RORγt expression and TH17 cell differentiation of SMAD4-deficient T cells. However, TGFβ neutralizes SMAD4-mediated suppression without affecting SMAD4 binding to the Rorc locus. Proteomic analysis revealed that SMAD4 interacts with SKI, a transcriptional repressor that is degraded upon TGFβ stimulation. SKI controls histone acetylation and deacetylation of the Rorc locus and TH17 cell differentiation via SMAD4: ectopic SKI expression inhibits H3K9 acetylation of the Rorc locus, Rorc expression, and TH17 cell differentiation in a SMAD4-dependent manner. Therefore, TGFβ-induced disruption of SKI reverses SKI-SMAD4-mediated suppression of RORγt to enable TH17 cell differentiation. This study reveals a critical mechanism by which TGFβ controls TH17 cell differentiation and uncovers the SKI-SMAD4 axis as a potential therapeutic target for treating TH17-related diseases

L’expérience scolaire des enfants de réfugiés syriens au cours de l’exil : du transit à la réinstallation

Cadre de la recherche : Cet article est basé sur une enquête ethnographique menée auprès d’une dizaine de familles de réfugiés syriens arrivées à Strasbourg après 2011. Objectifs : On explicite les parcours scolaires des enfants, de la Syrie à la France en passant par les pays de transit (Liban, Turquie), afin de montrer les contraintes d’une scolarisation pendant l’exil, ainsi que les différentes formes de mobilisations familiales pour l’accès aux droits et la réussite scolaire de ces enfants. Méthodologie : Cette enquête de terrain ethnographique mobilise des méthodes qualitatives telles que l’«   observation participante  » et le recueil de «   récits de vie  » . Résultats : Les contraintes scolaires rencontrées dans les pays de transit sont liées aux limites de l’accès aux droits. Ces dernières créent des ruptures et placent les enfants en situation de retard scolaire au moment de leur arrivée en France. Les obstacles posés par les retards accumulés, la langue et les contenus enseignés conduisent parfois à des impasses. Malgré les difficultés, les familles sont aussi des actrices qui mobilisent différentes ressources pour assurer une poursuite de la scolarité à leurs enfants. Conclusion : Les contraintes successives pendant l’exil amènent à s’interroger sur les institutions scolaires qui évaluent et catégorisent les élèves en oubliant leurs parcours. Que pourrions-nous envisager afin d’assurer une égalité de traitement entre des enfants ayant des parcours différents   ? Contribution : Partant des nombreuses recherches existantes qui traitent des contraintes scolaires des enfants réfugiés d’un point de vue institutionnel, cette recherche explore la famille de l’intérieur afin de montrer le point de vue de ses membres. Elle relie la dimension institutionnelle à la dimension familiale et individuelle.Research framework: This article is based on an ethnographic survey conducted with a dozen Syrian refugee families who arrived in Strasbourg after 2011. Objectives: We explain the children’s educational pathways, from Syria to France via transit countries (Lebanon, Turkey), in order to show the constraints of schooling during exile, as well as the different forms of family mobilization for access to rights and academic success for these children. Methodology: This ethnographic study mobilizes qualitative methods such as “participant observation” and the collection of “life stories”. Results: The educational constraints encountered in transit countries are linked to the limits of access to rights. These create gaps and put children behind in their schooling when they arrive in France. The obstacles posed by accumulated delays, the language and the contents taught sometimes lead to dead ends. Despite the difficulties, families are also actors who mobilize different resources to ensure that their children continue their education. Conclusion: The successive constraints during exile lead to questions about educational institutions that evaluate and categorize students while forgetting their background. What could we consider in order to ensure equal treatment between children with different backgrounds? Contribution: Starting from the numerous existing studies that deal with the educational constraints of refugee children from an institutional point of view, this research explores the family from the inside to show the point of view of its members. It links the institutional dimension to the family and individual dimension.Marco de la investigación : Este artículo se basa en una investigación etnográfica realizada entre una docena de familias de refugiados sirios que llegaron a Estrasburgo después de 2011. Objetivo : El objetivo es explicitar los itinerarios de escolarización de los niños, desde Siria hasta Francia, pasando por los países de tránsito (Líbano, Turquía), con el fin de mostrar las limitaciones de la escolarización durante el exilio, así como las diferentes formas de movilización familiar para el acceso a los derechos y el éxito escolar de estos niños. Metodología : Este estudio etnográfico de campo utiliza métodos cualitativos como la "observación participante" y la recopilación de "historias de vida". Resultados : Las dificultades de escolarización identificadas en los países de tránsito están relacionadas con los límites de acceso a los derechos, que crean rupturas y colocan a los niños en una situación de retraso educativo en el momento de su llegada a Francia. Los obstáculos que suponen los retrasos acumulados, el idioma y los contenidos que se enseñan conducen a veces a callejones sin salida. A pesar de las dificultades, las familias también son actores que movilizan diferentes recursos para que estos niños continúen su educación. Conclusiones : Las sucesivas limitaciones durante el exilio llevan a cuestionar las instituciones escolares que evalúan y clasifican a los alumnos, olvidando su trayecto. ¿Qué se podría hacer para garantizar la igualdad de tratamiento entre los criterios de un sistema normalizado y la diversidad de orígenes de los niños? Contribución : Partiendo de la amplia investigación existente que aborda las limitaciones educativas de los niños refugiados desde una perspectiva institucional, esta investigación explora el interior de la familia para mostrar sus perspectivas. DE esa forma, se vincula la dimensión institucional con la dimensión familiar e individual

Multiple invasion trajectories induce niche dynamics inconsistency and increase risk uncertainty of a plant invader

Abstract Our knowledge of how niche dynamic patterns respond to invasion trajectories and influence invasion risk prediction is elusive for the majority of notorious invaders, hindering scientific understanding, biosecurity planning and practice, and management implementation of biological invasions. We used Mikania micrantha, one of the world's worst invasive alien species (IAS), to test the hypothesis that multiple invasion trajectories could induce niche dynamics inconsistency and increase risk uncertainty of IAS. We compiled a robust database of M. micrantha occurrence across its native range in Central and South America and invaded range in China. This database was used to clarify different invaded ranges and invasion trajectories of M. micrantha in China. Principal components analysis of climatic variables associated with the database was used to explore the niche dynamic patterns associated with multiple invasion trajectories of M. micrantha. Maximum entropy algorithm was used to predict the high‐risk area of M. micrantha invasion using occurrence datasets for invaded ranges where niches remained conservative, and to detect area changes with the inclusion of occurrence datasets for invaded ranges where niche shifts occurred. M. micrantha invasion occurred in three geographically distinct regions, with conservative climate niches in southern and southeastern China and climatic niche shifts in southwestern China. A high‐risk area for M. micrantha invasion spanned multiple provinces and cities and expanded considerably with the inclusion of the occurrence dataset for southwestern China. Our findings contribute to the theoretical understanding of invasion mechanisms and the practical optimization of biosecurity planning and implementation