74 research outputs found

    Lithosphere tearing along STEP faults and synkinematic formation of lherzolite and wehrlite in the shallow subcontinental mantle

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    Subduction-transform edge propagator (STEP) faults are the locus of continual lithospheric tearing at slab edges, resulting in sharp changes in the lithospheric and crustal thickness and triggering lateral and/or near-vertical mantle flow. However, the mechanisms at the lithospheric mantle scale are still poorly understood. Here, we present the microstructural study of olivine-rich lherzolite, harzburgite and wehrlite mantle xenoliths from the Oran volcanic field (Tell Atlas, northwest Algeria). This alkali volcanic field occurs along a major STEP fault responsible for the Miocene westward slab retreat in the westernmost Mediterranean. Mantle xenoliths provide a unique opportunity to investigate the microstructures in the mantle section of a STEP fault system. The microstructures of mantle xenoliths show a variable grain size ranging from coarse granular to fine-grained equigranular textures uncorrelated with lithology. The major element composition of the mantle peridotites provides temperature estimates in a wide range (790–1165 ÂșC) but in general, the coarse-grained and fine-grained peridotites suggest deeper and shallower provenance depth, respectively. Olivine grain size in the fine-grained peridotites depends on the size and volume fraction of the pyroxene grains, which is consistent with pinning of olivine grain growth by pyroxenes as second-phase particles. In the coarse-grained peridotites, well-developed olivine crystal-preferred orientation (CPO) is characterized by orthorhombic and [100]-fiber symmetries, and orthopyroxene has a coherent CPO with that of olivine, suggesting their coeval deformation by dislocation creep at high temperature. In the fine-grained microstructures, along with the weakening of the fabric strength, olivine CPO symmetry exhibits a shift towards [010] fiber and the [010] and [001] axes of orthopyroxene are generally distributed subparallel to those of olivine. These data are consistent with deformation of olivine in the presence of low amounts of melts and the precipitation of orthopyroxenes from a melt phase. The bulk CPO of clinopyroxene mimics that of orthopyroxene via a topotaxial relationship of the two pyroxenes. This observation points to a melt-related origin of most clinopyroxenes in the Oran mantle xenoliths.This research has been supported by the Agencia Estatal de InvestigaciĂłn (grant nos. CGL2016-75224-R, CGL2016-81085-R and CGL2015-67130-C2-1-R), the Junta de AndalucĂ­a research groups RNM-131 and RNM-148, and the International Lithosphere Program (grant no. CC4-MEDYNA)

    Food allergy enhances allergic asthma in mice

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    BackgroundAtopic march refers to the typical transition from a food allergy in early childhood to allergic asthma in older children and adults. However the precise interplay of events involving gut, skin and pulmonary inflammation in this process is not completely understood.ObjectivesTo develop a mouse model of mixed food and respiratory allergy mimicking the atopic march and better understand the impact of food allergies on asthma.MethodsFood allergy to ovalbumin (OVA) was induced through intra-peritoneal sensitization and intra-gastric challenge, and/or a respiratory allergy to house dust mite (HDM) was obtained through percutaneous sensitization and intra-nasal challenges with dermatophagoides farinae (Der f) extract. Digestive, respiratory and systemic parameters were analyzed.ResultsOVA-mediated gut allergy was associated with an increase in jejunum permeability, and a worsening of Der f-induced asthma with stronger airway hyperresponsiveness and pulmonary cell infiltration, notably eosinophils. There was overproduction of the pro-eosinophil chemokine RANTES in broncho-alveolar lavages associated with an enhanced Th2 cytokine secretion and increased total and Der f-specific IgE when the two allergies were present. Both AHR and lung inflammation increased after a second pulmonary challenge.ConclusionGut sensitization to OVA amplifies Der f-induced asthma in mice

    Les sociétés populaires à travers leurs procÚs-verbaux

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    Sous la RĂ©volution française, les sociĂ©tĂ©s populaires ont crĂ©Ă© et animĂ© des rĂ©seaux de sociabilitĂ© politique dont leurs procĂšs-verbaux sont des tĂ©moins. Ces dĂ©libĂ©rations sont des sources remarquables que la collection des "Documents inĂ©dits sur l’histoire de France", publiĂ©e sous l’égide du ComitĂ© des travaux historiques et scientifiques, permet de redĂ©couvrir. Les Ă©tudes rĂ©unies dans cet ouvrage nous invitent Ă  mieux comprendre le fonctionnement des sociĂ©tĂ©s populaires et Ă  mesurer l’importance de leurs archives pour l’histoire politique et sociale

    Maternal prebiotic supplementation impacts colitis development in offspring mice

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    Background and aimsMaternal diet plays a key role in preventing or contributing to the development of chronic diseases, such as obesity, allergy, and brain disorders. Supplementation of maternal diet with prebiotics has been shown to reduce the risk of food allergies and affect the intestinal permeability in offspring later in life. However, its role in modulating the development of other intestinal disorders, such as colitis, remains unknown. Therefore, we investigated the effects of prebiotic supplementation in pregnant mice on the occurrence of colitis in their offspring.Materials and methodsOffspring from mothers, who were administered prebiotic galacto-oligosaccharides and inulin during gestation or fed a control diet, were subjected to three cycles of dextran sulphate sodium (DSS) treatment to induce chronic colitis, and their intestinal function and disease activity were evaluated. Colonic remodelling, gut microbiota composition, and lipidomic and transcriptomic profiles were also assessed.ResultsDSS-treated offspring from prebiotic-fed mothers presented a higher disease score, increased weight loss, and increased faecal humidity than those from standard diet-fed mothers. DSS-treated offspring from prebiotic-fed mothers also showed increased number of colonic mucosal lymphocytes and macrophages than the control group, associated with the increased colonic concentrations of resolvin D5, protectin DX, and 14-hydroxydocosahexaenoic acid, and modulation of colonic gene expression. In addition, maternal prebiotic supplementation induced an overabundance of eight bacterial families and a decrease in the butyrate caecal concentration in DSS-treated offspring.ConclusionMaternal prebiotic exposure modified the microbiota composition and function, lipid content, and transcriptome of the colon of the offspring. These modifications did not protect against colitis, but rather sensitised the mice to colitis development

    Integrating multiple lines of evidence to assess the effects of maternal BMI on pregnancy and perinatal outcomes

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    Background: Higher maternal pre-pregnancy body mass index (BMI) is associated with adverse pregnancy and perinatal outcomes. However, whether these associations are causal remains unclear. Methods: We explored the relation of maternal pre-/early-pregnancy BMI with 20 pregnancy and perinatal outcomes by integrating evidence from three different approaches (i.e. multivariable regression, Mendelian randomisation, and paternal negative control analyses), including data from over 400,000 women. Results: All three analytical approaches supported associations of higher maternal BMI with lower odds of maternal anaemia, delivering a small-for-gestational-age baby and initiating breastfeeding, but higher odds of hypertensive disorders of pregnancy, gestational hypertension, preeclampsia, gestational diabetes, pre-labour membrane rupture, induction of labour, caesarean section, large-for-gestational age, high birthweight, low Apgar score at 1 min, and neonatal intensive care unit admission. For example, higher maternal BMI was associated with higher risk of gestational hypertension in multivariable regression (OR = 1.67; 95% CI = 1.63, 1.70 per standard unit in BMI) and Mendelian randomisation (OR = 1.59; 95% CI = 1.38, 1.83), which was not seen for paternal BMI (OR = 1.01; 95% CI = 0.98, 1.04). Findings did not support a relation between maternal BMI and perinatal depression. For other outcomes, evidence was inconclusive due to inconsistencies across the applied approaches or substantial imprecision in effect estimates from Mendelian randomisation. Conclusions: Our findings support a causal role for maternal pre-/early-pregnancy BMI on 14 out of 20 adverse pregnancy and perinatal outcomes. Pre-conception interventions to support women maintaining a healthy BMI may reduce the burden of obstetric and neonatal complications. Funding: Medical Research Council, British Heart Foundation, European Research Council, National Institutes of Health, National Institute for Health Research, Research Council of Norway, Wellcome Trust.</p

    DNA methylation signature of chronic low-grade inflammation and its role in cardio-respiratory diseases

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    We performed a multi-ethnic Epigenome Wide Association study on 22,774 individuals to describe the DNA methylation signature of chronic low-grade inflammation as measured by C-Reactive protein (CRP). We find 1,511 independent differentially methylated loci associated with CRP. These CpG sites show correlation structures across chromosomes, and are primarily situated in euchromatin, depleted in CpG islands. These genomic loci are predominantly situated in transcription factor binding sites and genomic enhancer regions. Mendelian randomization analysis suggests altered CpG methylation is a consequence of increased blood CRP levels. Mediation analysis reveals obesity and smoking as important underlying driving factors for changed CpG methylation. Finally, we find that an activated CpG signature significantly increases the risk for cardiometabolic diseases and COPD.publishedVersionPeer reviewe

    Abstracts from the Food Allergy and Anaphylaxis Meeting 2016

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    ETUDE DE LA CONTRIBUTION RELATIVE DU TCR, DU CD8 ET DES MOLECULES ACCESSOIRES DANS L'ACTIVATION ET LA SELECTION DES LYMPHOCYTES T CYTOTOXIQUES HUMAINS (DOCTORAT IMMUNOLOGIE)

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    NANTES-BU MĂ©decine pharmacie (441092101) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF
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