Une identité imposée, une identité revendiquée

Les habitants du royaume de Grenade ont été identifiés en l’espace de dix ans de trois façons différentes : musulmans, mudéjars, et nouveaux-chrétiens ou nouveaux convertis. Avec le temps, et l’échec de l’évangélisation, on les dénommera morisques. Si le vocabulaire change, qu’en est-il des personnes ? Comment revendiquèrent-elles leur identité, qui ne cessait d’être ambiguë tout au long de ce siècle d’existence ? L’identité d’une personne peut évidemment s’étudier de différentes manières et à partir de sources toutes aussi diverses. Dans ce travail, nous nous pencherons sur ce que nous révèlent les protocoles notariaux, notamment les contrats de dots, où l’on peut voir l’identité familiale et sa transmission. Nous étudierons les noms de famille et leur mode de transmission au sein de la famille morisque. Y a-t-il eu adoption de l’identité chrétienne par les morisques ? Le mode de transmission du nom de famille suivait-il le modèle chrétien ? Les morisques revendiquaient-ils l’identité arabe ?The Kingdom of Granada’s inhabitants were identified in three different ways in a period of ten years : Muslims, Mudejars and New Christians or new converts. In the course of time and with the failure of the evangelization, they were called Moriscos, that is Catholics of Moorish descent. Vocabulary changes, but what about people ? How did they claim their identity that had not stopped changing all century long ? Obviously, personal identity can be studied in many ways and from equally different sources. For this work presented here, we will look into what Notarial Protocols show us, particularly the marriage dowries, where we can find family names and their transmission. We will study surnames and their way of transmission within a Moorish family. Had the Moriscos adopted the Christian identity ? Had the way of surname transmission followed the Christian model? Had the Moriscos claimed Arab identity 

Using plant litter decomposition as an indicator of ecosystem response to soil contamination

The inventory and remediation of contaminated sites have emerged as top environmental priorities worldwide. A large body of evidence has accumulated to show how soil contamination affects biological communities and ecological processes. This knowledge has yet to be used for the development of indicators of soil quality that are meaningful to end-users and are easy to implement in soil quality assessment schemes. In this study, we used quantifiable measures of litter decomposition, a key biophysical process, as indicators of the ecological impact of soil contamination by trace metals and hydrocarbons. We conducted a litterbag experiment with coarse and fine mesh bags to compare highly vs. minimally contaminated sites within eight locations representative of a wide array of environmental conditions and types of pollution. Contrary to the common assumption that soil contamination hampers soil functions, idiosyncratic responses were detected for litter decomposition rate and decomposer activity metrics. A negative relationship between detritivore and microbial responses to soil contamination indicates that wherever the activity of one group of decomposers is reduced, increase in activity of the other group may ensure litter decomposition to proceed at rate similar or higher than baseline rate. This finding may indicate that compensatory dynamics in soil communities is important in determining ecosystem stability against chemical stressors. As litter decomposition may inform on the capacity of terrestrial ecosystems to cope with soil contamination, it may be a useful complement to chemical soil analyses in routine soil quality assessment schemes

ICAM-1 PROMOTES THE ABNORMAL ENDOTHELIAL CELLPHENOTYPE IN CHRONIC THROMBOEMBOLIC PULMONARYHYPERTENSION

International audienceBACKGROUND - Pulmonary endothelial cells play a key role in the pathogenesis of ChronicThromboembolic Pulmonary Hypertension (CTEPH). Increased synthesis and/or release ofIntercellular Adhesion Molecule 1 (ICAM-1) by pulmonary endothelial cells of patients withCTEPH has been recently reported, suggesting a potential role for ICAM-1 in CTEPH.METHODS - We studied pulmonary endarterectomy specimens from 172 patients with CTEPHand pulmonary artery specimens from 97 controls undergoing lobectomy for low-stage cancerwithout metastasis.RESULTS - ICAM-1 was overexpressed in vitro in isolated and cultured endothelial cells fromendarterectomy specimens. Endothelial cell (EC) growth and apoptosis resistance weresignificantly higher in CTEPH specimens than in controls (P<0.001). Both abnormalities wereabolished by pharmacological inhibition of ICAM-1 synthesis or activity. Overexpression ofICAM-1 contributed to the acquisition and maintenance of abnormal EC growth and apoptosisresistance via phosphorylation of SRC, p38 and ERK1/2 and overproduction of Survivin.Regarding the ICAM-1 E469K polymorphism, the KE heterozygote genotype was significantlymore frequent in CTEPH than in controls, but was not associated with disease severity amongpatients with CTEPH.CONCLUSIONS - ICAM-1 contributes to maintaining the abnormal endothelial cell phenotypein CTEPH

Pyroséquençage pour le développement d'EST et de SNP aviaires

Le but du programme est de combler les déficits en marqueurs observés pour trois espèces aviaires : la caille, le canard et la poule. La stratégie choisie est l'obtention, à partir de plusieurs individus de lignées d'intérêt, de SNP (Single Nucleotide Polymorphism, polymorphisme d'un nucléotide) par une nouvelle technologie de séquençage à haut débit (séquenceur 454 GS-FLX, Roche). Nous séquençons des représentations réduites du génome, en sélectionnant d'une part des fragments de restriction d'ADN génomique - les mêmes chez tous les individus - et d'autre part les transcrits qui représentent globalement la partie du génome correspondant aux gènes exprimés. Ces expérimentations sont réalisées à partir d'échantillons d'ADN ou d'ARN issus d'individus de lignées à l'origine de croisements existants, pour chacune des trois espèces. Les données générées par plusieurs "runs" de séquence seront traitées in silico : contigage à haut débit, recherche de SNP, comparaison avec les banques de séquences connues...En plus de l'intérêt que représente la production d'un très grand nombre de SNP nouveaux, cette technologie devrait permettre de mieux séquencer les régions riches en (G+C) correspondant aux plus petits des microchromosomes pour lesquels il n'y a pas de séquence chez la poule. La comparaison des séquences des transcrits obtenues chez la caille et le canard avec la séquence du génome de la poule permettra d'établir une "cartographie virtuelle" des SNP obtenus, grâce à la grande conservation de synténie existant entre ces trois espèces

L'homocystéinémie chez les dyslipidémiques (étude de 274 patients)

LILLE2-BU Santé-Recherche (593502101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Ecological functioning of multicontaminated soils: a leaf litter decomposition experiment

International audienc

Abnormal pulmonary endothelial cells may underlie the enigmatic pathogenesis of chronic thromboembolic pulmonary hypertension

International audienceChronic thromboembolic pulmonary hypertension results from chronic mechanical obstruction of the pulmonary arteries after acute venous thromboembolism. However, the mechanisms that result in the progression from unresolved thrombus to fibrotic vascular remodeling are unknown. We hypothesized that pulmonary artery endothelial cells contribute to this phenomenon via paracrine growth factor and cytokine signaling

The beneficial effect of suramin on monocrotaline-induced pulmonary hypertension in rats.

BACKGROUND:Pulmonary hypertension (PH) is a progressive disorder characterized by an increase in pulmonary artery pressure and structural changes in the pulmonary vasculature. Several observations indicate that growth factors play a key role in PH by modulating pulmonary artery smooth muscle cell (PA-SMC) function. In rats, established monocrotaline-induced PH (MCT-PH) can be reversed by blocking platelet-derived growth factor receptors (PDGF-R), epidermal growth factor receptors (EGF-R), or fibroblast growth factor receptors (FGF-R). All these receptors belong to the receptor tyrosine kinase (RTK) family. METHODS AND RESULTS:We evaluated whether RTK blockade by the nonspecific growth factor inhibitor, suramin, reversed advanced MCT-PH in rats via its effects on growth-factor signaling pathways. We found that suramin inhibited RTK and ERK1/2 phosphorylation in cultured human PA-SMCs. Suramin inhibited PA-SMC proliferation induced by serum, PDGF, FGF2, or EGF in vitro and ex vivo. Treatment with suramin from day 1 to day 21 after monocrotaline injection attenuated PH development, as shown by lower values for pulmonary artery pressure, right ventricular hypertrophy, and distal vessel muscularization on day 21 compared to control rats. Treatment with suramin from day 21 to day 42 after monocrotaline injection reversed established PH, thereby normalizing the pulmonary artery pressure values and vessel structure. Suramin treatment suppressed PA-SMC proliferation and attenuated both the inflammatory response and the deposition of collagen. CONCLUSIONS:RTK blockade by suramin can prevent MCT-PH and reverse established MCT-PH in rats. This study suggests that an anti-RTK strategy that targets multiple RTKs could be useful in the treatment of pulmonary hypertension