Melting kinetics of granitic powder aggregates at 1175°C, 1 atm.

Melting experiments of pressed granitic powders (10% < 3.23 m, 50% < 31.63 m, 90% < 169.85 m) have been performed at 1175°C, 1 atm for different run durations (5, 10, 40 mn and 3, 24, 68 h). During partial melting, quartz and feldspars progressively decrease in abundance, the amount of melt produced increases sharply after 40 mn and leads to a strong decrease of the porosity of the powder (from 42% before heat-treatment to 10% after 68 h). In the 5 mn charge, thin glass films (1-2 m) appear cementing small particles grains and narrow glass channels are formed and trapped within both albite and K-feldspar. Newly-formed K-feldspars appear in the 10 and 40 mn charges. They are both texturally and compositionally distinctive from the original feldspars. All feldspars have totally disappeared after 3 h and quartz (up to 330 m) persists in the longest experiment (68 h). For durations longer than 40 mn, glass compositions are chemically zoned. They vary mainly between two end-members, one rich in normative feldspar components and poor in normative quartz and the other rich in normative quartz corresponding to areas close to the quartz interface. The melting reaction is governed by disequilibrium melting. Two melting regimes were identified: (1) a low melt fraction regime corresponding to heterogeneous nucleation of melt at the surface and within interiors of both albite and K-feldspar and (2) a high melt fraction regime kinetically controlled by diffusive mass transport within the melt layer. The lack of leucite implies that the melting relations of K-feldspar observed in this study are congruent. About 50 days are needed for the melting reaction to approach chemical equilibrium at 1175°C

Dynamic Crystallization of a Haplogranitic Melt - Application to Pegmatites

International audienceBoth equilibrium and dynamic crystallization experiments have been performed on a hydrous haplogranitic melt at 200 MPa to model nucleation and growth mechanisms and simulate pegmatite textures. The equilibrium results provide a reference frame (phase assemblages and compositions, liquidus and solidus temperatures and dependence with the melt H2O concentration) to parametrize the kinetic experiments. The seven H2O-saturated dynamic crystallization experiments followed a specific time-temperature path. After a pre-conditioning step at 800 °C, charges were cooled between 3.5 and 7 °C/min to 700, 660 and 600 °C corresponding to ΔT of 20, 60 and 120 °C. Dwell times ranged from 42 up to 1440h. Variable mineral assemblages and textures, and two types of polymineralic assemblages were obtained depending on ΔT and t. For ΔT = 120 °C, crystallization is sequential and includes graphic quartz-alkali feldspar intergrowths characteristic of pegmatite textures. The crystallization sequence reflects nucleation and growth of kinetically-favored metastable phases and solid solution compositions from the supercooled melt. Early alkali feldspars are more K-rich than expected at equilibrium and late albites more Na-rich. The K-rich graphic texture progressively evolves to a Na-rich intergrowth texture. Melts also follow a progressive though limited sodic evolution with time. At the interface of growing alkali feldspars, melts are enriched in SiO2 and depleted in Al2O3, Na2O and, to a lesser extent, K2O. H2O accumulates at the interface reaching concentration levels higher (by 1-2 wt%) than the saturation. Rejection of SiO2 and H2O at the interface controls the effective undercooling in the local melt and promotes rapid textural changes toward larger grain sizes at the front of graphic zones. Textural ripening takes place contemporaneously to sequential crystallization. Growth rates for quartz and alkali feldspar are tightly grouped, between 7.3 x 10-11 and 1.6 x 10-12 m s-1. Textures from the dynamic crystallization experiments closely resemble natural pegmatites but layered aplite units have not been reproduced. Our results confirm and strengthen the importance of liquidus undercooling to generate pegmatite textures

Effect of Induced Mild Hypothermia on Acid-Base Balance During Experimental Acute Sepsis in Rats

International audienceThe aim of this study was to determine the effect of induced mild hypothermia (34°C) on acid-base balance in septic rats. Twenty-eight male Sprague-Dawley rats median weight 306 g, range 251–333 g were used. After anesthesia and when the target temperature was reached (normothermia: 38°C or induced mild hypothermia: 34°C), sepsis was induced by cecal ligation and perforation. Measurements of cardiopulmonary parameters and blood samples were performed at T0h (occurring immediately after chirurgical procedures), T2h, T4h (at each temperature), and T6h (at 34°C only). Blood oxygen saturation, heart and respiratory rates, arterial blood pH, carbon dioxide partial pressure, sodium, potassium, chloride and calcium concentrations, hematocrit, blood lactate, tumor necrosis factor-α and interleukin-6 concentrations were measured on anesthetized rats. Other parameters such as bicarbonate concentration, hemoglobin concentration, base excess, and anion gap were estimated from measured parameters. Main results showed that an increase in both cytokines concentrations was observed in septic rats compared with sham rats. This increase was less marked at 34°C compared with 38°C. Moreover, sepsis induction led to a marked metabolic acidosis and hypothermia delayed this acidosis. Induced mild hypothermia delays the evolution of cytokines and metabolic acidosis during experimental sepsis

Does Induction Time of Mild Hypothermia Influence the Survival Duration of Septic Rats?

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Involvement of respiratory chain in the regulatory volume decrease process in turbot hepatocytes.

International audienceRegulatory volume decrease (RVD) constitutes a fundamental process that turbot (Scophthalmus maximus) hepatocytes are able to perform when exposed to hypo-osmotic stress. RVD is an integrative mechanism that involves various elements of the cellular machinery. Among others, ATP is an essential protagonist: released following hypo-osmotic shock, it acts as an auto/paracrine factor to trigger other signalling events. The origin of this ATP remains unclear and, to the best of our knowledge, no information exists about the role of mitochondrial respiration in RVD. Therefore, we propose to analyse the potential link between RVD and the respiratory chain, with a focus on ATP release and exocytosis. Using inhibitors of mitochondrial respiration, RVD was shown to be dependent on respiratory chain activity. However, we demonstrated an indirect role of mitochondrial respiration: ATP could be synthesized and then stored in intracellular vesicles until the moment cells release it to face hypo-osmotic swelling. However, the involvement of exocytosis in this process needs to be further investigated

Activation of the MAPKs ERK1/2 by cell swelling in turbot hepatocytes.

International audienceBACKGROUND INFORMATION: Activation of MAPKs (mitogen-activated protein kinases), in particular ERK1/2 (extracellular-signal-regulated kinase 1/2), has been reported to take place in a large variety of cell types after hypo-osmotic cell swelling. Depending on cell type, ERK1/2 phosphorylation can then serve or not the RVD (regulatory volume decrease) process. The present study investigates ERK1/2 activation after aniso-osmotic stimulations in turbot hepatocytes and the potential link between phosphorylation of these proteins and RVD. RESULTS: In turbot hepatocytes, Western-blot analysis shows that a hypo-osmotic shock from 320 to 240 mOsm kg(-1) induced a rapid increase in ERK1/2 phosphorylation, whereas a hyper-osmotic shock from 320 to 400 mOsm kg(-1) induced no significant change in the phosphorylation of these proteins. The hypo-osmotic-induced ERK1/2 phosphorylation was significantly prevented when hypo-osmotic shock was performed in the presence of the specific MEK (MAPK/ERK kinase) inhibitor PD98059 (100 microM). In these conditions, the RVD process was not altered, suggesting that ERK1/2 did not participate in this process in turbot hepatocytes. Moreover, the hypo-osmotic-induced activation of ERK1/2 was significantly prevented by breakdown of extracellular ATP by apyrase (10 units ml(-1)), by inhibition of purinergic P2 receptors by suramin (100 microM) or by calcium depletion using EGTA (1 mM) and thapsigargin (1 microM). CONCLUSIONS: In turbot hepatocytes, hypo-osmotic swelling but not hyper-osmotic shrinkage induced the activation of ERK1/2. However, these proteins do not seem to be involved in the RVD process. Their hypo-osmotic-induced activation is partially due to cascades of signalling events triggered by the binding of released ATP on purinergic P2 receptors and requires the presence of calcium

Volume regulation following hyposmotic shock in isolated turbot (Scophthalmus maximus) hepatocytes.

International audienceRegulatory volume decrease (RVD) following hyposmotic stimulation was studied in isolated turbot, Scophthalmus maximus, hepatocytes. Exposed to a reduced osmolality (from 320 to 240 mosm kg(-1)), cells first swelled and then exhibited a RVD. Volume regulation was significantly inhibited in presence of NPPB, 9-AC, acetazolamide, DIDS and barium. Taken together, these results could suggest that RVD operated via separate K+ and Cl- channels and probably Cl-/HCO3(-) exchanger in turbot hepatocytes. The K+/Cl- cotransporter could also be involved as furosemide and DIOA strongly inhibited the process whereas NEM, a K+/Cl- cotransporter activator, added under isosmotic conditions, led to cell shrinkage. RVD in turbot hepatocytes appeared also to depend on proteins p38 MAP kinase and tyrosine kinase but not on proteins ERK 1/2. Arachidonic acid and leukotrienes could also be involved since inhibition of synthesis of both these compounds by quinacrine and NDGA, respectively, inhibited the volume regulation. Likewise, Ca2+ has been proved to be an essential messenger as RVD was prevented in absence of Ca2+. Finally, this work provides bases for novel studies on cell volume regulation in marine teleosteans

Impacts of mixtures of herbicides on molecular and physiological responses of the European flounder Platichthys flesus

International audienceThe widespread use of pesticides results in a growing contamination of the aquatic environment. The effects of (1) a simple mixture of a glyphosate-based formulation and AMPA (Aminomethylphosphonic acid -- a primary metabolite of glyphosate) and of (2) a more complex mixture of herbicides (glyphosate/AMPA/mecoprop/acetochlor/2,4D) were explored on the molecular and physiological responses of the European flounder Platichthys flesus, considering a long-term and environmentally realistic contamination. Molecular responses were identified using suppression subtractive hybridization on liver samples: the level of gene transcription was significantly different between contaminated fishes vs control ones for 532 sequences, after a 62-day contamination. Among them, 222 sequences were identified by homology with data-based sequences; they encoded several metabolic pathways including: methionine and lipid metabolism, immunity, protein regulation, coagulation and energetic metabolism. Expression pattern of nine transcripts in the liver was confirmed by real-time PCR. The molecular study underlined that potential markers of liver injury were expressed for both mixtures, in particular betaine homocysteine methyl transferase and chemotaxin. Physiological responses were analysed considering blood parameters and condition factor; after the two months contamination period; no significant physiological difference was detected between contaminated and control fish