TRACKING THE P–T PATH OF PRECAMBRIAN ECLOGITE USING PSEUDOSECTION, Ti-IN-QUARTZ AND Zr-IN-RUTILE THERMOBAROMETRY

International audienceSveconorwegian eclogite occur as a nappe within the high-grade metamorphic region in southernSweden, which constitutes a window into the deepest part of this Precambrian mountain belt. Distinctmicrostructural domains (i.e., garnet core, garnet rim, and matrix) in a Fe-Ti-rich eclogite variety containabundant quartz, rutile and zircon.A pseudosection approach was first applied and compared to results from a combination of Zr-in-rutileand Ti-in-quartz. The pressure input used for both thermometers was first deduced for each microstructuraldomain from the pseudosection. For the garnet core, Zr-in-rutile yields temperatures of 700-715°C and Ti-inquartz~ 635°C at 7 kbar. For the garnet rim, temperatures of 760-790°C (Zr-in-rutile) and 740-890°C (Ti-inquartz)at 12-18 kbar were calculated. Matrix rutile recorded temperatures of ~ 810°C, while quartz recordedtemperatures up to ~ 890°C. Additionally, direct combination of Ti content in quartz and Zr content in rutileisopleths (i.e., independent from the pseudosection) yield a prograde path in nearly perfect agreement withthe one deduced from the pseudosection.The pseudosection shows that rutile was produced by continuous breakdown of ilmenite during the earlystages of prograde metamorphism, a reaction that ran to completion at ~ 730°C. Most rutile grains in garnetrim and matrix are interpreted to subsequently form by recrystallization of smaller matrix grains. However,they generally do not record the peak-P temperatures and instead range mostly between 775 and 815°C,interpreted as a result of more efficient recrystallization during a dehydration reaction (progressivereplacement of hornblende by clinopyroxene).This study illustrates that both Zr-in-rutile and Ti-in-quartz thermometry cannot only robustly constrain aprograde evolution, but when combined with a pseudosection model can also yield information onrecrystallization processes. In fact, the combination of these three methods provides an unrivalled tool forpetrologic interpretation.The variation in Ti concentration in quartz is small regardless of crystal size. This P–T path reach veryhigh temperatures (up to 875°C) with a high dP/dT ratio, both during prograde and retrograde histories. Thesteep P–T path, together with preservation of garnet growth zoning, symplectitic textures and the lack ofsignificant Ti diffusion in quartz is consistent with a short residence time at high-temperature, implyingunusual fast burial and exhumation of the eclogite-bearing nappe

PPAR-alpha is essential for microparticle-induced differentiation of bone marrow-derived endothelial progenitor cells and in vitro angiogenesis

Résumé publié dans : Fundamental & Clinical Pharmacology, 23 (S1). Oxford : Wiley-Blackwell, 2009. doi:10.1111/j.1472-8206.2009.00689.xNational audienc

Increased Oxidative Stress Induces Apoptosis in Human Cystic Fibrosis Cells

Oxidative stress results in deleterious cell function in pathologies associated with inflammation. Here, we investigated the generation of superoxide anion as well as the anti-oxidant defense systems related to the isoforms of superoxide dismutases (SOD) in cystic fibrosis (CF) cells. Pro-apoptotic agents induced apoptosis in CF but not in control cells that was reduced by treatment with SOD mimetic. These effects were associated with increased superoxide anion production, sensitive to the inhibition of IκB-α phosphorylation, in pancreatic but not tracheal CF cells, and reduced upon inhibition of either mitochondrial complex I or NADPH oxidase. CF cells exhibited reduced expression, but not activity, of both Mn-SOD and Cu/Zn-SOD when compared to control cells. Although, expression of EC-SOD was similar in normal and CF cells, its activity was reduced in CF cells. We provide evidence that high levels of oxidative stress are associated with increased apoptosis in CFTR-mutated cells, the sources being different depending on the cell type. These observations underscore a reduced anti-oxidant defense mechanism, at least in part, via diminished EC-SOD activity and regulation of Cu/Zn-SOD and Mn-SOD expressions. These data point to new therapeutic possibilities in targeting anti-oxidant pathways to reduce oxidative stress and apoptosis in CF cells

Circulating microparticles from pulmonary hypertensive rats are vectors of oxidative stress

Date du colloque : 04/2010National audienc

Microparticle release in remote ischemic conditioning mechanism

Remote ischemic conditioning (RCond) induced by short periods of ischemia and reperfusion of an organ or tissue before myocardial reperfusion is an attractive strategy of cardioprotection in the context of acute myocardial infarction. Nonetheless, its mechanism remains unknown. A humoral factor appears to be involved, although its identity is currently unknown. We hypothesized that the circulating microparticles (MPs) are the link between the remote tissue and the heart. MPs from rats and healthy humans undergoing RCond were characterized. In rats, RCond was induced by 10 min of limb ischemia. In humans, RCond was induced by three cycles of 5-min inflation and 5-min deflation of a blood-pressure cuff. In the second part of the study, rats underwent 40 min myocardial ischemia followed by 2 h reperfusion. Infarct size was measured and compared among three groups of rats: 1) myocardial infarction alone (MI) (n = 6); 2) MI + RCond started 20 min after coronary ligation (n = 6); and 3) MI + injection of RCond-derived rat MPs (MI + MPs) (n = 5). MPs from endothelial cells (CD54(+) and CD146(+) for rats and humans, respectively) and procoagulant MPs (Annexin V(+)) markedly increased after RCond, both in rats and humans. RCond reduced infarct size (24.4 ± 5.9% in MI + RCond vs. 54.6 ± 4.7% in MI alone; P < 0.01). Infarct size did not decrease in MI + MPs compared with MI alone (50.2 ± 6.4% vs. 54.6 ± 4.7%, not significantly different). RCond increased endothelium-derived and procoagulant MPs in both rats and humans. However, MP release did not appear to be a biological vector of RCond in our model

Cinq millénaires de métallurgie en montagne basque. Les apports d'une démarche intégrée alliant palynologie et géochimie isotopique du plomb

National audienceUne démarche intégrée alliant palynologie et géochimie isotopique du plomb a été engagée dans une tourbière du Pays Basque, au coeur d'une région reconnue comme étant un foyer métallurgique ancien. Elle permet de reconstituer l'histoire des activités minières et métallurgiques et d'en apprécier l'impact sur l'environnement forestier au cours des cinq derniers millénaires. Plusieurs phases d'activités ont été repérées entre le début du IIIè millénaire av. J.-C. et l'époque moderne (Bronze moyen, Bronze final, Antiquité, époque moderne). La plupart sont clairement associées à des indices polliniques de réduction du couvert forestier, toutefois il ressort que localement l'impact de la métallurgie au bois sur les forêts n'atteint son paroxysme qu'à partir des XVè-XVIè siècles

Nocturnal release of leukocyte-derived microparticles in males with obstructive sleep apnoea

Multiple pathophysiological mechanisms have been proposed to contribute to the increased cardiovascular morbidity in obstructive sleep apnoea (OSA), including autonomic dysfunction, inflammation, oxidative stress and endothelial dysfunction 1. Microparticles (MPs) are small membrane vesicles that are shed from circulating cells or from the components of the vessel wall in response to activation and apoptosis. There is growing evidence in support of a potential role of MPs in the field of cardiovascular diseases. Increased levels of MPs derived from various cell types are found in patients at risk of cardiovascular diseases 2. By modulating inflammation, coagulation, vasomotor reactivity and angiogenesis, MPs might directly contribute to cardiovascular diseases 2. Recent case–control studies suggest a potential involvement of MPs in OSA-associated cardiovascular morbidity 3–6. An increase in morning levels of MPs derived from activated leukocytes has been demonstrated in otherwise healthy male OSA patients with marked nocturnal desaturations 5. In vitro, nitric oxide (NO) production by endothelial cells incubated with MPs from OSA patients correlates negatively with circulating levels of activated leukocyte-derived MPs 5. Ex vivo, mice previously injected with MPs from OSA patients display endothelial dysfunction, reduced endothelial NO release and increased adhesion molecule expression 5

Circulating microparticles from patients with obstructive sleep apnea enhance vascular contraction: mandatory role of the endothelium

Obstructive sleep apnea (OSA) is characterized by repetitive apnea-hypopnea cycles during sleep associated with oxygen desaturation and sleep disruption. We evaluated the role of circulating microparticles (MPs) from patients with OSA in the regulation of vascular function. MPs from whole blood from patients with OSA or control subjects were injected i.v. into mice. Injection of MPs from patients with OSA induced ex vivo vascular hyperreactivity in aortas with functional endothelium but, in contrast, hyporeactivity in vessels without functional endothelium. Vascular hyperreactivity was blunted in the presence of a nitric oxide synthase inhibitor alone or combined with the cyclooxygenase inhibitor indomethacin. MPs from patients with OSA reduced endothelial nitric oxide synthase activity and nitric oxide production, increased aortic cyclooxygenase-1 and cyclooxygenase-2 expression, and increased thromboxane A(2) and prostacyclin production. Blockade of thromboxane A(2) receptor did not affect the serotonin response in arteries from OSA MP-treated mice. A superoxide dismutase mimetic reduced the vascular hyperreactivity induced by MPs from patients with OSA but had no effect on contraction in vessels from control and non-OSA MP-treated mice. These data provide evidence that circulating MPs from patients with OSA induce ex vivo vascular hyperreactivity with the obligatory role of the endothelium and subtle interactions between the nitric oxide and cyclooxygenase pathways and metabolites. These results highlight the participation of MPs in vascular dysfunction associated with OSA