La fondation de l’Empire ottoman chez Kemal Tahir et Tarik Bugra entre mythe et réalité historique

En traitant majoritairement du déclin de l’Empire ottoman et de l’épopée républicaine, le roman turc du début du XXe siècle se fait amplement l’écho de la vision officielle de l’État kémaliste moderniste et occidentaliste. Mais au fil du temps, conscients qu’il est vital pour une société de connaître son histoire, des écrivains se repenchent sur le passé ottoman. Dans Devlet Ana (1967) et Osmancık (1983), Kemal Tahir et Tarık Buğra prennent pour sujet le début de la fondation d’un ordre étatique par les tribus turkmènes aux XIIIe et XIVe siècles. Vision marxiste pour l’un, plus spiritualiste pour l’autre, tous deux s’attachent à mettre en lumière les aspects positifs qui ont présidé à la fondation de l’Empire ottoman (défense des valeurs humaines, modèle de droit et de justice) et se rejoignent dans une même défense de l’identité nationale.One of the prominent themes of Turkish literature of the 20th century adresses the decline of the Ottoman Empire and the emergence of the Republic. This largely echoes the official view of the western orientated Kemalistic government. Gradually, some writers became conscious of the vital necessity for the country to embrace its history, and started to examine their ottoman past.In Devlet Ana (1967) and in Osmancık (1983), Kemal Tahir and Tarık Buğra took as a subject the beginning of the foundation of a State by the tribes of Turkmen in the 13th and 14th centuries. Despite a marxist vision on one side and a spiritual view on the other, both of them were attached to putting emphasis on the positive aspects of the ottoman Empire’s foundation ( the defense of human values and the model of law and order) ; they both came together to stand up for the defense of a national identity

Future challenges on focused fluid migration in sedimentary basins: insight from field data, laboratory experiments and numerical simulations

In a present context of sustainable energy and hazard mitigation, understanding fluid migration in sedimentary basins – large subsea provinces of fine saturated sands and clays – is a crucial challenge. Such migration leads to gas or liquid expulsion at the seafloor, which may be the signature of deep hydrocarbon reservoirs, or precursors to violent subsea fluid releases. If the former may orient future exploitation, the latter represent strong hazards for anthropic activities such as offshore production, CO$_2$ storage, transoceanic telecom fibers or deep-sea mining. However, at present, the dynamics of fluid migration in sedimentary layers, in particular the upper 500 m, still remains unknown in spite of its strong influence on fluid distribution at the seafloor. Understanding the mechanisms controlling fluid migration and release requires the combination of accurate field data, laboratory experiments and numerical simulations. Each technique shall lead to the understanding of the fluid structures, the mechanisms at stake, and deep insights into fundamental processes ranging from the grain scale to the kilometers-long natural pipes in the sedimentary layers. Here we review the present available techniques, advances and challenges still open for the geosciences, physics, and computer science communities

Le sommeil chez l'enfant, comment le respecter de manière appropriée en milieu collectif ?

Ce travail a pour but d’aider les professionnelles de l’enfance à respecter le sommeil de l’enfant de la naissance à trois ans. Étant considéré comme un élément important pour un développement harmonieux, le sommeil doit être respecté dans la mesure du possible. Son évolution est constante et spécifique à différentes tranches d’âge. De plus, chaque individu possède son propre rythme ainsi que son cycle de sommeil. Pour cela, il est essentiel de prendre connaissance de la théorie et conscientiser qu’elle diffère selon les âges. Les professionnelles doivent collaborer de manière constructive avec les parents ainsi qu’entre elles afin de pouvoir identifier les besoins de l’enfant. Il est essentiel de connaître la théorie pour procurer à l’enfant un sommeil approprié en milieu collectif

Live cell division dynamics monitoring in 3D large spheroid tumor models using light sheet microscopy

<p>Abstract</p> <p>Background</p> <p>Multicellular tumor spheroids are models of increasing interest for cancer and cell biology studies. They allow considering cellular interactions in exploring cell cycle and cell division mechanisms. However, 3D imaging of cell division in living spheroids is technically challenging and has never been reported.</p> <p>Results</p> <p>Here, we report a major breakthrough based on the engineering of multicellular tumor spheroids expressing an histone H2B fluorescent nuclear reporter protein, and specifically designed sample holders to monitor live cell division dynamics in 3D large spheroids using an home-made selective-plane illumination microscope.</p> <p>Conclusions</p> <p>As illustrated using the antimitotic drug, paclitaxel, this technological advance paves the way for studies of the dynamics of cell divion processes in 3D and more generally for the investigation of tumor cell population biology in integrated system as the spheroid model.</p

Increased levels of circulating microparticles in primary Sjögren's syndrome, systemic lupus erythematosus and rheumatoid arthritis and relation with disease activity

INTRODUCTION: Cell stimulation leads to the shedding of phosphatidylserine (PS)-rich microparticles (MPs). Because autoimmune diseases (AIDs) are characterized by cell activation, we investigated level of circulating MPs as a possible biomarker in primary Sjögren's syndrome (pSS), systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). METHODS: We measured plasma levels of total, platelet and leukocyte MPs by prothrombinase capture assay and flow cytometry in 43 patients with pSS, 20 with SLE and 24 with RA and in 44 healthy controls (HCs). Secretory phospholipase A2 (sPLA2) activity was assessed by fluorometry. Soluble CD40 ligand (sCD40L) and soluble P-selectin (sCD62P), reflecting platelet activation, were measured by ELISA. RESULTS: Patients with pSS showed increased plasma level of total MPs (mean +/- SEM 8.49 +/- 1.14 nM PS equivalent (Eq), P < 0.0001), as did patients with RA (7.23 +/- 1.05 n PS Eq, P = 0.004) and SLE (7.3 +/- 1.25 nM PS Eq, P = 0.0004), as compared with HCs (4.13 +/- 0.2 nM PS Eq). Patients with AIDs all showed increased level of platelet MPs (P < 0.0001), but only those with pSS showed increased level of leukocyte MPs (P < 0.0001). Results by capture assay and flow cytometry were correlated. In patients with high disease activity according to extra-glandular complications (pSS), DAS28 (RA) or SLEDAI (SLE) compared with low-activity patients, the MP level was only slightly increased in comparison with those having a low disease activity. Platelet MP level was inversely correlated with anti-DNA antibody level in SLE (r = -0.65; P = 0.003) and serum beta2 microglobulin level in pSS (r = -0.37; P < 0.03). The levels of total and platelet MPs were inversely correlated with sPLA2 activity (r = -0.37, P = 0.0007; r = -0.36, P = 0.002, respectively). sCD40L and sCD62P concentrations were significantly higher in pSS than in HC (P </= 0.006). CONCLUSIONS: Plasma MP level is elevated in pSS, as well as in SLE and RA, and could be used as a biomarker reflecting systemic cell activation. Level of leukocyte-derived MPs is increased in pSS only. The MP level is low in case of more severe AID, probably because of high secretory phospholipase A2 (sPLA2) activity, which leads to consumption of MPs. Increase of platelet-derived MPs, sCD40L and sCD62P, highlights platelet activation in pSS

Structural Biology of Human H3K9 Methyltransferases

SET domain methyltransferases deposit methyl marks on specific histone tail lysine residues and play a major role in epigenetic regulation of gene transcription. We solved the structures of the catalytic domains of GLP, G9a, Suv39H2 and PRDM2, four of the eight known human H3K9 methyltransferases in their apo conformation or in complex with the methyl donating cofactor, and peptide substrates. We analyzed the structural determinants for methylation state specificity, and designed a G9a mutant able to tri-methylate H3K9. We show that the I-SET domain acts as a rigid docking platform, while induced-fit of the Post-SET domain is necessary to achieve a catalytically competent conformation. We also propose a model where long-range electrostatics bring enzyme and histone substrate together, while the presence of an arginine upstream of the target lysine is critical for binding and specificity. Enhanced version: This article can also be viewed as an enhanced version in which the text of the article is integrated with interactive 3D representations and animated transitions. Please note that a web plugin is required to access this enhanced functionality. Instructions for the installation and use of the web plugin are available i

Complement component C4 structural variation and quantitative traits contribute to sex-biased vulnerability in systemic sclerosis

Altres ajuts: Fondo Europeo de Desarrollo Regional (FEDER), "A way of making Europe".Copy number (CN) polymorphisms of complement C4 play distinct roles in many conditions, including immune-mediated diseases. We investigated the association of C4 CN with systemic sclerosis (SSc) risk. Imputed total C4, C4A, C4B, and HERV-K CN were analyzed in 26,633 individuals and validated in an independent cohort. Our results showed that higher C4 CN confers protection to SSc, and deviations from CN parity of C4A and C4B augmented risk. The protection contributed per copy of C4A and C4B differed by sex. Stronger protection was afforded by C4A in men and by C4B in women. C4 CN correlated well with its gene expression and serum protein levels, and less C4 was detected for both in SSc patients. Conditioned analysis suggests that C4 genetics strongly contributes to the SSc association within the major histocompatibility complex locus and highlights classical alleles and amino acid variants of HLA-DRB1 and HLA-DPB1 as C4-independent signals

Integrative epigenomics in Sjögren´s syndrome reveals novel pathways and a strong interaction between the HLA, autoantibodies and the interferon signature

Primary Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by lymphocytic infiltration and damage of exocrine salivary and lacrimal glands. The etiology of SS is complex with environmental triggers and genetic factors involved. By conducting an integrated multi-omics study, we confirmed a vast coordinated hypomethylation and overexpression effects in IFN-related genes, what is known as the IFN signature. Stratified and conditional analyses suggest a strong interaction between SS-associated HLA genetic variation and the presence of Anti-Ro/SSA autoantibodies in driving the IFN epigenetic signature and determining SS. We report a novel epigenetic signature characterized by increased DNA methylation levels in a large number of genes enriched in pathways such as collagen metabolism and extracellular matrix organization. We identified potential new genetic variants associated with SS that might mediate their risk by altering DNA methylation or gene expression patterns, as well as disease-interacting genetic variants that exhibit regulatory function only in the SS population. Our study sheds new light on the interaction between genetics, autoantibody profiles, DNA methylation and gene expression in SS, and contributes to elucidate the genetic architecture of gene regulation in an autoimmune population

Systèmes de contrôle de constitutionnalité par voie incidente et protection des personnes en situation de vulnérabilité

Répondant à l’appel à projets « QPC 2020 » du Conseil constitutionnel, le travail de recherche collectif – dont les résultats sont publiés dans cet ouvrage – entend évaluer l’efficacité de la question prioritaire de constitutionnalité sous l’angle particulier de la protection des personnes en situation de vulnérabilité et selon une approche de droit comparé. La recherche a ainsi eu pour ambition de dresser un bilan de la jurisprudence QPC du Conseil constitutionnel pour ce qui concerne la protection des personnes vulnérables, en la confrontant avec les procédures similaires existant dans deux pays voisins : l’Italie et l’Espagne. La protection effective des personnes qui en ont le plus besoin a semblé en effet être un point de vue particulièrement pertinent pour évaluer, de manière générale, l’efficacité du système de la QPC et pour vérifier s’il constitue un véritable progrès dans la défense des droits fondamentaux. Pour rendre compte de la manière la plus fidèle possible des résultats de cette recherche, l’ouvrage présente, dans une première partie, le rapport de synthèse adressé au Conseil constitutionnel par les porteurs du projet, dans lequel est réalisée la comparaison proprement dite ; puis, dans une seconde partie, les études nationales concernant la jurisprudence constitutionnelle des trois pays étudiés, élaborées par les chercheurs participants au projet scientifique

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead