Understanding the kinetic behavior of a Mo-V-Te-Nb mixed oxide in the oxydehydrogenation of ethane

Two kinetic models based on Langmuir-Hinshelwood (LH) and Eley-Rideal (ER) mechanisms were developed to describe the oxydehydrogenation of ethane to yield ethylene over a Mo-V-Te-Nb catalyst. Obtained in a lab-scale fixed-bed reactor, experimental data at the steady-state were used to estimate the kinetic models parameters via a nonisothermal regression. Experiments were performed using an ethane, oxygen and nitrogen mixture as feedstock, spanning temperatures from 673 to 753 K, inlet partial pressures of oxygen and ethane between 5.0 and 22.0 kPa, and space-time from 10 to 70 g(cat) h(molethane)- (1). Ethylene, CO and CO2 were the only detected products, the selectivity for ethylene ranged from 76% to 96% for an ethane conversion interval 4-85%. A series of tests feeding ethylene instead of ethane were also performed at 713 K, varying inlet partial pressures and space-time in the same ranges as was done for ethane. Ethylene conversion was relatively low, 3-14%, the dominant product being CO with CO/CO2 ratios from 0.73 to 0.79. The LH mechanism was found to represent better the experimental data. The oxydehydrogenation of ethane was the reaction with the lowest activation energy, 108-115 kJ mol (1). Except for the conversion of ethane into CO2, deep oxidations were detected as very energetically demanding steps, 156-193 kJ mol (1). Competitive adsorption between reagents and products occurred in the two mechanisms particularly at relatively high reaction severity, water re-adsorption being weaker in comparison with COx re-adsorption. (C) 2014 Elsevier Ltd. All rights reserved.This work was financially supported by the Instituto Mexicano del Petroleo.Quintana-Solorzano, R.; Barragan-Rodriguez, G.; Armendariz-Herrera, H.; López Nieto, JM.; Valente, JS. (2014). Understanding the kinetic behavior of a Mo-V-Te-Nb mixed oxide in the oxydehydrogenation of ethane. Fuel. 138:15-26. doi:10.1016/j.fuel.2014.07.051152613

MicroRNAs regulate Ca2+ homeostasis in murine embryonic stem cells

MicroRNAs (miRNAs) are important regulators of embryonic stem cell (ESC) biology, and their study has identified key regulatory mechanisms. To find novel pathways regulated by miRNAs in ESCs, we undertook a bioinformatics analysis of gene pathways differently expressed in the absence of miRNAs due to the deletion of Dicer, which encodes an RNase that is essential for the synthesis of miRNAs. One pathway that stood out was Ca2+ signaling. Interestingly, we found that Dicer-/- ESCs had no difference in basal cytoplasmic Ca2+ levels but were hyperresponsive when Ca2+ import into the endoplasmic reticulum (ER) was blocked by thapsigargin. Remarkably, the increased Ca2+ response to thapsigargin in ESCs resulted in almost no increase in apoptosis and no differences in stress response pathways, despite the importance of miRNAs in the stress response of other cell types. The increased Ca2+ response in Dicer-/- ESCs was also observed during purinergic receptor activation, demonstrating a physiological role for the miRNA regulation of Ca2+ signaling pathways. In examining the mechanism of increased Ca2+ responsiveness to thapsigargin, neither store-operated Ca2+ entry nor Ca2+ clearance mechanisms from the cytoplasm appeared to be involved. Rather, it appeared to involve an increase in the expression of one isoform of the IP3 receptors (Itpr2). miRNA regulation of Itpr2 expression primarily appeared to be indirect, with transcriptional regulation playing a major role. Therefore, the miRNA regulation of Itpr2 expression offers a unique mechanism to regulate Ca2+ signaling pathways in the physiology of pluripotent stem cells

MicroRNAs control the apoptotic threshold in primed Pluripotent stem cells through regulation of BIM

Mammalian primed pluripotent stem cells have been shown to be highly susceptible to cell death stimuli due to their low apoptotic threshold, but how this threshold is regulated remains largely unknown. Here we identify microRNA (miRNA)-mediated regulation as a key mechanism controlling apoptosis in the post-implantation epiblast. Moreover, we found that three miRNA families, miR-20, miR-92, and miR-302, control the mitochondrial apoptotic machinery by fine-tuning the levels of expression of the proapoptotic protein BIM. These families therefore represent an essential buffer needed to maintain cell survival in stem cells that are primed for not only differentiation but also cell death

Study on the correlation between plasma electron temperature and penetration depth in laser welding processes

The plasma electron temperature has been estimated starting from the spectroscopic analysis of the optical emission of the laser-generated plasma plume during quite diverse stainless steel welding procedures (c.w. CO2 and pulsed Nd:YAG). Although the optical emissions present different spectral features, a discrete contribution of several iron lines can be highlighted in both types of welding. We have found that the electron temperature decreases as the laser power is enhanced, in static as well as dynamic conditions. Such a result could be useful to develop a closed loop control system of the weld penetration depth

MicroRNAs Regulate Ca2+ Homeostasis in Murine Embryonic Stem Cells

MicroRNAs (miRNAs) are important regulators of embryonic stem cell (ESC) biology, and their study has identified key regulatory mechanisms. To find novel pathways regulated by miRNAs in ESCs, we undertook a bioinformatics analysis of gene pathways differently expressed in the absence of miRNAs due to the deletion of Dicer, which encodes an RNase that is essential for the synthesis of miRNAs. One pathway that stood out was Ca2+ signaling. Interestingly, we found that Dicer−/− ESCs had no difference in basal cytoplasmic Ca2+ levels but were hyperresponsive when Ca2+ import into the endoplasmic reticulum (ER) was blocked by thapsigargin. Remarkably, the increased Ca2+ response to thapsigargin in ESCs resulted in almost no increase in apoptosis and no differences in stress response pathways, despite the importance of miRNAs in the stress response of other cell types. The increased Ca2+ response in Dicer−/− ESCs was also observed during purinergic receptor activation, demonstrating a physiological role for the miRNA regulation of Ca2+ signaling pathways. In examining the mechanism of increased Ca2+ responsiveness to thapsigargin, neither store-operated Ca2+ entry nor Ca2+ clearance mechanisms from the cytoplasm appeared to be involved. Rather, it appeared to involve an increase in the expression of one isoform of the IP3 receptors (Itpr2). miRNA regulation of Itpr2 expression primarily appeared to be indirect, with transcriptional regulation playing a major role. Therefore, the miRNA regulation of Itpr2 expression offers a unique mechanism to regulate Ca2+ signaling pathways in the physiology of pluripotent stem cells

Isochronism and tangent bifurcation of band edge modes in Hamiltonian lattices

In {\em Physica D} {\bf 91}, 223 (1996), results were obtained regarding the tangent bifurcation of the band edge modes ($q=0,\pi$) of nonlinear Hamiltonian lattices made of $N$ coupled oscillators. Introducing the concept of {\em partial isochronism} which characterises the way the frequency of a mode, $\omega$, depends on its energy, $\epsilon$, we generalize these results and show how the bifurcation energies of these modes are intimately connected to their degree of isochronism. In particular we prove that in a lattice of coupled purely isochronous oscillators ($\omega(\epsilon)$ strictly constant), the in-phase mode ($q=0$) never undergoes a tangent bifurcation whereas the out-of-phase mode ($q=\pi$) does, provided the strength of the nonlinearity in the coupling is sufficient. We derive a discrete nonlinear Schr\"odinger equation governing the slow modulations of small-amplitude band edge modes and show that its nonlinear exponent is proportional to the degree of isochronism of the corresponding orbits. This equation may be seen as a link between the tangent bifurcation of band edge modes and the possible emergence of localized modes such as discrete breathers.Comment: 23 pages, 1 figur

NiO diluted in high surface area TiO2 as efficient catalysts for the oxidative dehydrogenation of ethane

[EN] Catalysts consisting of NiO diluted in high surface area TiO2 can be as efficient in the oxidative dehydrogenation of ethane as the most selective NiO-promoted catalysts reported previously in the literature. By selecting the titania matrix and the NiO loading, yields to ethylene over 40% have been obtained. In the present article, three different titanium oxides (TiO2) have been employed as supports or diluters of nickel oxide and have been tested in the oxidative dehydrogenation of ethane to ethylene. All TiO2 used present anatase as the main crystalline phase and different surface areas of 11,55 and 85 m(2) g(-1). It has been observed that by selecting an appropriate nickel loading and the titanium oxide extremely high selectivity towards ethylene can be obtained. Thus, nickel oxide supported on TiO2 with high surface areas (i.e. 55 and 85 m(2) g(-1)) have resulted to give the best catalytic performance although the optimal nickel loading is different for each case. The optimal catalyst has been obtained for NiO-loadings up to 5-10 theoretical monolayers regardless of the TiO2 employed. Free TiO2 is inactive whereas unsupported NiO is active and unselective (forming mainly carbon dioxide) and, therefore, unmodified NiO particles have to be avoided in order to obtain the optimal catalytic performance. The use of low surface area titania (11 m(2) g(-1)) have led to the lowest selectivity to olefin due to the presence of an excess of free NiO particles. (C) 2017 Elsevier B.V. All rights reserved.The authors would like to acknowledge the DGICYT in Spain CTQ2012-37925-C03-2, CTQ2015-68951-C3-1-R, CTQ2015-68951-C3-3-R and SEV-2012-0267 Projects for financial support. D.D. also thanks Severo Ochoa Excellence fellowship (SVP-2014-068669). We also thank the University of Valencia (UV-INV-AE-16-484416 project) and SCSIE-UV for assistanceSanchis, R.; Delgado-Muñoz, D.; Agouram, S.; Soriano Rodríguez, MD.; Vázquez, MI.; Rodriguez-Castellon, E.; Solsona, B.... (2017). NiO diluted in high surface area TiO2 as efficient catalysts for the oxidative dehydrogenation of ethane. Applied Catalysis A General. 536:18-26. https://doi.org/10.1016/j.apcata.2017.02.012S182653

Phase transitions in tumor growth VI: Epithelial–Mesenchymal transition

Herewith we discuss a network model of the epithelial–mesenchymal transition (EMT) based on our previous proposed framework. The EMT appears as a “first order” phase transition process, analogous to the transitions observed in the chemical–physical field. Chiefly, EMT should be considered a transition characterized by a supercritical Andronov–Hopf bifurcation, with the emergence of limit cycle and, consequently, a cascade of saddle-foci Shilnikov's bifurcations. We eventually show that the entropy production rate is an EMT-dependent function and, as such, its formalism reminds the van der Waals equation.Fil: Guerra, A.. Universidad de La Habana; CubaFil: Rodriguez, D. J.. Universidad de La Habana; CubaFil: Montero, S.. Medical Sciences University Of Havana; CubaFil: Betancourt Mar, J. A.. Universidad de La Habana; CubaFil: Martín Pardo, Reinaldo Román. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Investigaciones en Tecnología Química. Universidad Nacional de San Luis. Facultad de Química, Bioquímica y Farmacia. Instituto de Investigaciones en Tecnología Química; Argentina. Mexican Institute Of Complex Systems. Tamaulipas; MéxicoFil: Silva Lamar, Eduardo. Universidad de La Habana; CubaFil: Bizzarri, María Julia. Universidad de La Habana; CubaFil: Cocho, G.. Universidad Nacional Autónoma de México; MéxicoFil: Mansilla, R.. Universidad Nacional Autónoma de México; MéxicoFil: Nieto Villar, José Manuel. Universidad de La Habana; Cub

Inhibition of PTP1B Restores IRS1-Mediated Hepatic Insulin Signaling in IRS2-Deficient Mice

[Objective]: Mice with complete deletion of insulin receptor substrate 2 (IRS2) develop hyperglycaemia, impaired hepatic insulin signaling and elevated gluconeogenesis, whereas mice deficient for protein tyrosine phosphatase (PTP) 1B display an opposing hepatic phenotype characterized by increased sensitivity to insulin. To define the relationship between these two signaling pathways in the regulation of liver metabolism, we used genetic and pharmacological approaches to study the effects of inhibiting PTP1B on hepatic insulin signaling and expression of gluconeogenic enzymes in IRS2−/− deficient mice. [Research design and methods]: We analyzed glucose homeostasis and insulin signaling in liver and isolated hepatocytes from IRS2−/− and IRS2−/−/PTP1B−/−. Additionally, hepatic insulin signaling was assessed in control and IRS2−/− mice treated with resveratrol, an anti-oxidant present in red wine. [Results]: In livers of hyperglycaemic IRS2−/− mice, the expression levels of PTP1B and its association with the insulin receptor (IR) were increased. The absence of PTP1B in the double mutant mice restored hepatic IRS1-mediated phosphatidylinositol (PI) 3-kinase/Akt/Foxo1 signaling. Moreover, resveratrol treatment of hyperglycaemic IRS2−/− mice decreased hepatic PTP1B mRNA and inhibited PTP1B activity, thereby restoring IRS1-mediated PI 3-kinase/Akt/Foxo1 signaling and peripheral insulin sensitivity. [Conclusions]: By regulating the phosphorylation state of IR, PTB1B determines sensitivity to insulin in liver and exerts a unique role in the interplay between IRS1 and IRS2 in the modulation of hepatic insulin action.This work was supported by Ministerio de Ciencia e Innovación Grants (Spain) BFU2008-02420, SAF2009- 08114 (to A.M.V.), BFU2008-04901-C03-03 (to M.R.), BFU2005-00084, and SAF2008-00011 (to D.J.B.) and the Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) (Instituto Salud Carlos III). A.G.-R. holds a postdoctoral contract from CIBERDEM.Peer reviewe

The Snail repressor recruits EZH2 to specific genomic sites through the enrollment of the lncRNA HOTAIR in epithelial-to-mesenchymal transition

The transcription factor Snail is a master regulator of cellular identity and epithelial-to-mesenchymal transition (EMT) directly repressing a broad repertoire of epithelial genes. How chromatin modifiers instrumental to its activity are recruited to Snail-specific binding sites is unclear. Here we report that the long non-coding RNA (lncRNA) HOTAIR (for HOX Transcript Antisense Intergenic RNA) mediates a physical interaction between Snail and enhancer of zeste homolog 2 (EZH2), an enzymatic subunit of the polycomb-repressive complex 2 and the main writer of chromatin-repressive marks. The Snail-repressive activity, here monitored on genes with a pivotal function in epithelial and hepatic morphogenesis, differentiation and cell-type identity, depends on the formation of a tripartite Snail/HOTAIR/EZH2 complex. These results demonstrate an lncRNA-mediated mechanism by which a transcriptional factor conveys a general chromatin modifier to specific genes, thereby allowing the execution of hepatocyte transdifferentiation; moreover, they highlight HOTAIR as a crucial player in the Snail-mediated EMT.Oncogene advance online publication, 25 July 2016; doi:10.1038/onc.2016.260