Efficient thermoelectric materials using nonmagnetic double perovskites with d0 / d6 band filling

Efficient thermoelectric materials should present large Seebeck coefficient, high electrical conductivity, and low thermal conductivity. An enhanced Seebeck coefficient can be obtained from materials where the Fermi level can be aligned with a large and narrow peak of the density of states, particularly when a substantial band valley degeneracy occurs. A high electrical conductivity comes as a consequence of large conductive hopping paths between the atoms of the material. Both physical quantities can be decoupled and optimized independently if their origins can be ascribed to different sets of bands. Based on these assumptions, double perovskites A2BB?O6 with d0/d6 filling for the B and B? metal cations, respectively, have been considered. They provide a desirable band structure with degenerate B-t2g / B?-eg bands above the Fermi level together with a low thermal conductivity. We have carried out first-principles simulations for various of these nonmagnetic double perovskites and showed that all of them present a large Seebeck coefficient (consequence of the localized and empty t2g states of the B cation), and large electrical conductivity due to the more spread unoccupied eg band of the B? cation. We have seen that if they can be optimally doped, they could show a figure of merit comparable or even higher than the best n-type thermoelectric oxides, such as SrTiO3. Different mechanisms to tune the band structure and enhance the thermoelectric figure of merit are explored, including epitaxial strain, hydrostatic pressure, chemical pressure, and external doping. A fully relaxed structure has also been studied, showing that a realistic calculation is necessary to make accurate predictions but also proving that the main trends shown throughout the paper remain unchanged. © 2016 American Physical Society.ACKNOWLEDGMENTS. P.V.A. and V.P. thank the Xunta de Galicia for financial support through project EM 2013/037. V.P., P.G.F., and J.J. acknowledge financial support from the Spanish Ministery of Economy and Competitiveness through the MINECO Grants No. MAT2013-44673-R (V.P.), No. FIS2012-37549-C05-04 (P.G.F. and J.J.), and No. FIS2015-64886-C5-2-P (P.G.F. andJ.J.). V.P. and P.G.F. also acknowledge funding from the Ramón y Cajal Fellowship RYC-2011-09024 and RYC-2013-12515, respectively

Crosstalk between Mitochondrial and Sarcoplasmic Reticulum Ca2+ Cycling Modulates Cardiac Pacemaker Cell Automaticity

Mitochondria dynamically buffer cytosolic Ca(2+) in cardiac ventricular cells and this affects the Ca(2+) load of the sarcoplasmic reticulum (SR). In sinoatrial-node cells (SANC) the SR generates periodic local, subsarcolemmal Ca(2+) releases (LCRs) that depend upon the SR load and are involved in SANC automaticity: LCRs activate an inward Na(+)-Ca(2+) exchange current to accelerate the diastolic depolarization, prompting the ensemble of surface membrane ion channels to generate the next action potential (AP).To determine if mitochondrial Ca(2+) (Ca(2+) (m)), cytosolic Ca(2+) (Ca(2+) (c))-SR-Ca(2+) crosstalk occurs in single rabbit SANC, and how this may relate to SANC normal automaticity.Inhibition of mitochondrial Ca(2+) influx into (Ru360) or Ca(2+) efflux from (CGP-37157) decreased [Ca(2+)](m) to 80 ± 8% control or increased [Ca(2+)](m) to 119 ± 7% control, respectively. Concurrent with inhibition of mitochondrial Ca(2+) influx or efflux, the SR Ca(2+) load, and LCR size, duration, amplitude and period (imaged via confocal linescan) significantly increased or decreased, respectively. Changes in total ensemble LCR Ca(2+) signal were highly correlated with the change in the SR Ca(2+) load (r(2) = 0.97). Changes in the spontaneous AP cycle length (Ru360, 111 ± 1% control; CGP-37157, 89 ± 2% control) in response to changes in [Ca(2+)](m) were predicted by concurrent changes in LCR period (r(2) = 0.84).A change in SANC Ca(2+) (m) flux translates into a change in the AP firing rate by effecting changes in Ca(2+) (c) and SR Ca(2+) loading, which affects the characteristics of spontaneous SR Ca(2+) release

Should science educators deal with the science/religion issue?

I begin by examining the natures of science and religion before looking at the ways in which they relate to one another. I then look at a number of case studies that centre on the relationships between science and religion, including attempts to find mechanisms for divine action in quantum theory and chaos theory, creationism, genetic engineering and the writings of Richard Dawkins. Finally, I consider some of the pedagogical issues that would need to be considered if the science/religion issue is to be addressed in the classroom. I conclude that there are increasing arguments in favour of science educators teaching about the science/religion issue. The principal reason for this is to help students better to learn science. However, such teaching makes greater demands on science educators than has generally been the case. Certain of these demands are identified and some specific suggestions are made as to how a science educator might deal with the science/religion issue. © 2008 Taylor & Francis

Ca²+/calmodulin-dependent protein kinase II (CaMKII) activity and sinoatrial nodal pacemaker cell energetics.

: Ca(2+)-activated basal adenylate cyclase (AC) in rabbit sinoatrial node cells (SANC) guarantees, via basal cAMP/PKA-calmodulin/CaMKII-dependent protein phosphorylation, the occurrence of rhythmic, sarcoplasmic-reticulum generated, sub-membrane Ca(2+) releases that prompt rhythmic, spontaneous action potentials (APs). This high-throughput signaling consumes ATP.We have previously demonstrated that basal AC-cAMP/PKA signaling directly, and Ca(2+) indirectly, regulate mitochondrial ATP production. While, clearly, Ca(2+)-calmodulin-CaMKII activity regulates ATP consumption, whether it has a role in the control of ATP production is unknown.We superfused single, isolated rabbit SANC at 37°C with physiological saline containing CaMKII inhibitors, (KN-93 or autocamtide-2 Related Inhibitory Peptide (AIP)), or a calmodulin inhibitor (W-7) and measured cytosolic Ca(2+), flavoprotein fluorescence and spontaneous AP firing rate. We measured cAMP, ATP and O2 consumption in cell suspensions. Graded reductions in basal CaMKII activity by KN-93 (0.5-3 µmol/L) or AIP (2-10 µmol/L) markedly slow the kinetics of intracellular Ca(2+) cycling, decrease the spontaneous AP firing rate, decrease cAMP, and reduce O2 consumption and flavoprotein fluorescence. In this context of graded reductions in ATP demand, however, ATP also becomes depleted, indicating reduced ATP production.CaMKII signaling, a crucial element of normal automaticity in rabbit SANC, is also involved in SANC bioenergetics

The “Funny” Current (I<sub>f</sub>) Inhibition by Ivabradine at Membrane Potentials Encompassing Spontaneous Depolarization in Pacemaker Cells

Recent clinical trials have shown that ivabradine (IVA), a drug that inhibits the funny current (<em>I<sub>f</sub></em>) in isolated sinoatrial nodal cells (SANC), decreases heart rate and reduces morbidity and mortality in patients with cardiovascular diseases. While IVA inhibits<em> I<sub>f</sub></em>, this effect has been reported at essentially unphysiological voltages,<em> i.e.</em>, those more negative than the spontaneous diastolic depolarization (DD) between action potentials (APs). We tested the relative potency of IVA to block <em>I<sub>f</sub></em> over a wide range of membrane potentials, including those that encompass DD governing to the SANC spontaneous firing rate. A clinically relevant IVA concentration of 3 μM to single, isolated rabbit SANC slowed the spontaneous AP firing rate by 15%. During voltage clamp the maximal <em>I<sub>f</sub> </em>was 18 ± 3 pA/pF (at −120 mV) and the maximal <em>I<sub>f</sub> </em>reduction by IVA was 60 ± 8% observed at −92 ± 4 mV. At the maximal diastolic depolarization (~−60 mV) <em>I<sub>f</sub> </em>amplitude was only −2.9 ± 0.4 pA/pF, and was reduced by only 41 ± 6% by IVA. Thus, <em>I<sub>f</sub></em> amplitude and its inhibition by IVA at physiologically relevant membrane potentials are substantially less than that at unphysiological (hyperpolarized) membrane potentials. This novel finding more accurately describes how IVA affects SANC function and is of direct relevance to numerical modeling of SANC automaticity

Average cells AP induced Ca²⁺ parameters in control (CON) and following introduction of W-7 (20 µmol/L; n = 6), *p<0.05 vs. drug control.

<p>Average cells AP induced Ca²⁺ parameters in control (CON) and following introduction of W-7 (20 µmol/L; n = 6), *p<0.05 vs. drug control.</p