Contact metamorphic reactions and fluid–rock interactions related to magmatic sill intrusion in the Guaymas Basin

Igneous basaltic intrusions into young organic-rich sedimentary basins have a major impact not only on the carbon cycle but also on major and trace element transfers between deep and superficial geological reservoirs. The actively rifting Guaymas Basin in the Gulf of California, which was drilled by the International Ocean Discovery Program during Expedition 385, represents the nascent stage of an ocean characterized by siliceous organic-rich sediments (diatom ooze) intruded by a very dense network of basaltic sills. This study focuses on Site U1546 where the relatively high geothermal gradient (over 200 ∘C km−1) induces early diagenetic transformations in both pore waters and sediments, involving sulfide, carbonate and silica. Geochemical and mineralogical characterizations of the sediment at sill contacts indicate that sulfides and silica polymorphs are the main phases impacted by contact metamorphism, being evident by a transition from opal-CT to quartz and pyrite to pyrrhotite, respectively. Mass balance calculations have been used to estimate mass transfers in metamorphic aureoles. In the top contact aureole, predominantly isochemical metamorphism is reflected by the presence of authigenic quartz and disseminated 20–50 µm sized pyrrhotite crystals, filling primary interstitial space, and partial dissolution of detrital feldspar grains. In the bottom contact aureole, quartz and euhedral pyrrhotite crystals occur, which are up to 4 times larger than those at the top contact. Significant metamorphism of sediments is observed in the lower contact aureole, where plagioclase recrystallizes around the detrital feldspars and locally euhedral pyroxenes are included in patches of carbonate cement; this suggests precipitation from carbon-rich fluids at temperatures (T) higher than 300 ∘C. The lower contact aureole also is more enriched in CaO, Na2O, Fe2O3 and trace elements (Cu, As, Zn, etc.) compared to the upper contact. Based on these petrological investigations, a conceptual model of magma–sediment–fluid interaction is proposed distinguishing top and bottom contact processes. Initial contact metamorphism due to sill emplacement is characterized by dehydration reactions in sediments and crystallization of new minerals. It was followed by carbonate precipitation from the released fluids. At a final stage, the temperature re-equilibrated with the geothermal gradient and the rocks were further altered by hydrothermal fluids.</p

Alterations in MicroRNA Expression Contribute to Fatty Acid–Induced Pancreatic β-Cell Dysfunction

OBJECTIVE—Visceral obesity and elevated plasma free fatty acids are predisposing factors for type 2 diabetes. Chronic exposure to these lipids is detrimental for pancreatic β-cells, resulting in reduced insulin content, defective insulin secretion, and apoptosis. We investigated the involvement in this phenomenon of microRNAs (miRNAs), a class of noncoding RNAs regulating gene expression by sequence-specific inhibition of mRNA translation

A Novel Function of Noc2 in Agonist-Induced Intracellular Ca2+ Increase during Zymogen-Granule Exocytosis in Pancreatic Acinar Cells

Noc2, a putative Rab effector, contributes to secretory-granule exocytosis in neuroendocrine and exocrine cells. Here, using two-photon excitation live-cell imaging, we investigated its role in Ca2+-dependent zymogen granule (ZG) exocytosis in pancreatic acinar cells from wild-type (WT) and Noc2-knockout (KO) mice. Imaging of a KO acinar cell revealed an expanded granular area, indicating ZG accumulation. In our spatiotemporal analysis of the ZG exocytosis induced by agonist (cholecystokinin or acetylcholine) stimulation, the location and rate of progress of ZG exocytosis did not differ significantly between the two strains. ZG exocytosis from KO acinar cells was seldom observed at physiological concentrations of agonists, but was normal (vs. WT) at high concentrations. Flash photolysis of a caged calcium compound confirmed the integrity of the fusion step of ZG exocytosis in KO acinar cells. The decreased ZG exocytosis present at physiological concentrations of agonists raised the possibility of impaired elicitation of calcium spikes. When calcium spikes were evoked in KO acinar cells by a high agonist concentration: (a) they always started at the apical portion and traveled to the basal portion, and (b) calcium oscillations over the 10 µM level were observed, as in WT acinar cells. At physiological concentrations of agonists, however, sufficient calcium spikes were not observed, suggesting an impaired [Ca2+]i-increase mechanism in KO acinar cells. We propose that in pancreatic acinar cells, Noc2 is not indispensable for the membrane fusion of ZG per se, but instead performs a novel function favoring agonist-induced physiological [Ca2+]i increases

The GTPase RalA Regulates Different Steps of the Secretory Process in Pancreatic β-Cells

BACKGROUND: RalA and RalB are multifuntional GTPases involved in a variety of cellular processes including proliferation, oncogenic transformation and membrane trafficking. Here we investigated the mechanisms leading to activation of Ral proteins in pancreatic beta-cells and analyzed the impact on different steps of the insulin-secretory process. METHODOLOGY/PRINCIPAL FINDINGS: We found that RalA is the predominant isoform expressed in pancreatic islets and insulin-secreting cell lines. Silencing of this GTPase in INS-1E cells by RNA interference led to a decrease in secretagogue-induced insulin release. Real-time measurements by fluorescence resonance energy transfer revealed that RalA activation in response to secretagogues occurs within 3-5 min and reaches a plateau after 10-15 min. The activation of the GTPase is triggered by increases in intracellular Ca2+ and cAMP and is prevented by the L-type voltage-gated Ca2+ channel blocker Nifedipine and by the protein kinase A inhibitor H89. Defective insulin release in cells lacking RalA is associated with a decrease in the secretory granules docked at the plasma membrane detected by Total Internal Reflection Fluorescence microscopy and with a strong impairment in Phospholipase D1 activation in response to secretagogues. RalA was found to be activated by RalGDS and to be severely hampered upon silencing of this GDP/GTP exchange factor. Accordingly, INS-1E cells lacking RalGDS displayed a reduction in hormone secretion induced by secretagogues and in the number of insulin-containing granules docked at the plasma membrane. CONCLUSIONS/SIGNIFICANCE: Taken together, our data indicate that RalA activation elicited by the exchange factor RalGDS in response to a rise in intracellular Ca2+ and cAMP controls hormone release from pancreatic beta-cell by coordinating the execution of different events in the secretory pathway

Analysis of SEC9 Suppression Reveals a Relationship of SNARE Function to Cell Physiology

BACKGROUND:Growth and division of Saccharomyces cerevisiae is dependent on the action of SNARE proteins that are required for membrane fusion. SNAREs are regulated, through a poorly understood mechanism, to ensure membrane fusion at the correct time and place within a cell. Although fusion of secretory vesicles with the plasma membrane is important for yeast cell growth, the relationship between exocytic SNAREs and cell physiology has not been established. METHODOLOGY/PRINCIPAL FINDINGS:Using genetic analysis, we identified several influences on the function of exocytic SNAREs. Genetic disruption of the V-ATPase, but not vacuolar proteolysis, can suppress two different temperature-sensitive mutations in SEC9. Suppression is unlikely due to increased SNARE complex formation because increasing SNARE complex formation, through overexpression of SRO7, does not result in suppression. We also observed suppression of sec9 mutations by growth on alkaline media or on a non-fermentable carbon source, conditions associated with a reduced growth rate of wild-type cells and decreased SNARE complex formation. CONCLUSIONS/SIGNIFICANCE:Three main conclusions arise from our results. First, there is a genetic interaction between SEC9 and the V-ATPase, although it is unlikely that this interaction has functional significance with respect to membrane fusion or SNAREs. Second, Sro7p acts to promote SNARE complex formation. Finally, Sec9p function and SNARE complex formation are tightly coupled to the physiological state of the cell

Some Examples of Industrial Applications of Ultra-High Purity Steels

In the last decade, the evolution and control of steelmaking practice have enabled drastic reductions to be made in the impurity content of low alloy steels (mainly S, P, O, N and H) and the resulting superclean steel products have seen their in-service behaviour greatly improved. The following examples concerning CLI products are presented : 1 - The reduction of S content by a factor of more than ten and the control of O content have considerably reduced the Hydrogen Induced Cracking (HIC) sensitivity of the C-Mn steel grades for the storage of oil and gas in sour environments. 2 - Superclean Ni Cr Mo V steel grades for turbine rotors shafts have a very low sensitivity to lower nose temper embrittlement. 3 - Thick (>100 mm) plates or forgings in Mn Ni Mo steel grade used for nuclear pressure vessels welded by the electron beam process offer high toughness in fused areas when S + P are reduced to less than 30 ppm. 4 - Steel grades very close to pure iron have been developed to improve the performance of magnetic circuits in large accelerators

ICER induced by hyperglycemia represses the expression of genes essential for insulin exocytosis

The GTPases Rab3a and Rab27a and their effectors Granuphilin/Slp4 and Noc2 are essential regulators of neuroendocrine secretion. Chronic exposure of pancreatic β-cells to supraphysiological glucose levels decreased selectively the expression of these proteins. This glucotoxic effect was mimicked by cAMP-raising agents and blocked by PKA inhibitors. We demonstrate that the transcriptional repressor ICER, which is induced in a PKA-dependent manner by chronic hyperglycemia and cAMP-raising agents, is responsible for the decline of the four genes. ICER overexpression diminished the level of Granuphilin, Noc2, Rab3a and Rab27a by binding to cAMP responsive elements located in the promoters of these genes and inhibited exocytosis of β-cells in response to secretagogues. Moreover, the loss in the expression of the genes of the secretory machinery caused by glucose and cAMP-raising agents was prevented by an antisense construct that reduces ICER levels. We propose that induction of inappropriate ICER levels lead to defects in the secretory process of pancreatic β-cells possibly contributing, in conjunction with other known deleterious effects of hyperglycemia, to defective insulin release in type 2 diabetes