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Synthesis of cork-derived ceria ecoceramic, an emerging porous catalyst, for enhancing solar thermochemical water splitting.

The recent implementation of the EU Emissions Trading Scheme (EU ETS) in January 2005 created new financial risks for emitting firms. To deal with these risks, options are traded since October 2006. Because the EU ETS is a new market, the relevant underlying model for option pricing is still a controversial issue. This article improves our understanding of this issue by characterizing the conditional and unconditional distributions of the realized volatility for the 2008 futures contract in the European Climate Exchange (ECX), which is valid during Phase II (2008-2012) of the EU ETS. The realized volatility measures from naive, kernel-based and subsampling estimators are used to obtain inferences about the distributional and dynamic properties of the ECX emissions futures volatility. The distribution of the daily realized volatility in logarithmic form is shown to be close to normal. The mixture-of-distributions hypothesis is strongly rejected, as the returns standardized using daily measures of volatility clearly departs from normality. A simplified HAR-RV model (Corsi, 2009) with only a weekly component, which reproduces long memory properties of the series, is then used to model the volatility dynamics. Finally, the predictive accuracy of the HAR-RV model is tested against GARCH specifications using one-step-ahead forecasts, which confirms the HAR-RV superior ability. Our conclusions indicate that (i) the standard Brownian motion is not an adequate tool for option pricing in the EU ETS, and (ii) a jump component should be included in the stochastic process to price options, thus providing more efficient tools for risk-management activities.

Optimisation-based Energy Management Strategies for hybrid and electric vehicles have to face some issues for real-time applications. In this study,an online adaptive optimisation-based strategy is used for an electric vehicle with a Hybrid Energy Storage System including supercapacitors and batteries. The SCs voltage limitations are taken into account by using a feedback control. Indeed the voltage limitation is a key point for safe operations in the vehicle. A comparison with a more classical optimisation-based method is performed by simulations on a normalised driving cycle. The results point out a more effective behaviour of the adaptive strategy.

The Nuclear Energy Agency organised its third workshop on ‘Science and values in radiological protection’ in November 2012 in Tokyo. One of the issues addressed, non-cancer effects, had also been addressed in the first two science and values workshops (Helsinki, Finland, 2008; Vaux-de-Cernay, France, 2009), but presented several new elements of relevance to International Commission on Radiological Protection discussions of the evolution of the system of radiological protection. Radiological protection science, both epidemiological and biological, now suggests that stroke and heart disease may well be caused by radiation exposure at doses of the order of 0.5 Gy or less. Further, it is possible that such detriments may be caused by either chronic or acute exposures. While significant uncertainties remain, the need to consider non-cancer detriment in risk assessment and in the development of protection strategies is now a significant scientific and ethical question. This paper will present the results of the Nuclear Energy Agency science and values workshop discussion of non-cancer risks, and of the questions and possible future directions raised during the workshop.

This paper extends recent work on interruption insurance for electric power by introducing onsite backup generation capacity as a supplementary form of interruption insurance. The basic model of interruption insurance as a mechanism for differential pricing is reviewed, the incentive for providing onsite backup generation capacity is demonstrated and the interaction between onsite backup generation and interruption insurance is analyzed. Two types of onsite backup, customer and utility owned, are discussed. It is shown that individuals’ economic incentives to install onsite backup generation dominate the utility’s incentive. Hence customer owned onsite backup decisions will pre-empt the utility’s plan to mitigate compensation payments by providing onsite backup generation.

Abstract The OECD/NEA Sandia Fuel Project provided unique thermal-hydraulic experimental data associated with Spent Fuel Pool (SFP) complete drain down. The study conducted at Sandia National Laboratories (SNL) was successfully completed (July 2009 to February 2013). The accident conditions of interest for the SFP were simulated in a full scale prototypic fashion (electrically heated, prototypic assemblies in a prototypic SFP rack) so that the experimental results closely represent actual fuel assembly responses. A major impetus for this work was to facilitate severe accident code validation and to reduce modeling uncertainties within the codes. Phase I focused on axial heating and burn propagation in a single PWR 17 × 17 assembly (i.e. “hot neighbors” configuration). Phase II addressed axial and radial heating and zirconium fire propagation including effects of fuel rod ballooning in a 1 × 4 assembly configuration (i.e. single, hot center assembly and four, “cooler neighbors”). This paper summarizes the comparative analysis regarding the final destructive ignition test of the phase I of the project. The objective of the benchmark is to evaluate and compare the predictive capabilities of computer codes concerning the ignition testing of PWR fuel assemblies. Nine institutions from eight different countries were involved in the benchmark calculations. The time to ignition and the maximum temperature are adequately captured by the calculations. It is believed that the benchmark constitutes an enlargement of the validation range for the codes to the conditions tested, thus enhancing the code applicability to other fuel assembly designs and configurations. The comparison of lumped parameter and CFD computer codes represents a further valuable achievement.

AbstractActivation of potassium (K+) currents plays a critical role in the control of programmed cell death. Because pituitary adenylate cyclase‐activating polypeptide (PACAP) has been shown to inhibit the apoptotic cascade in the cerebellar cortex during development, we have investigated the effect of PACAP on K+ currents in cultured cerebellar granule cells using the patch‐clamp technique in the whole‐cell configuration. Two types of outward K+ currents, a transient K+ current (IA) and a delayed rectifier K+ current (IK) were characterized using two different voltage protocols and specific inhibitors of K+ channels. Application of PACAP induced a reversible reduction of the IK amplitude, but did not affect IA, while the PACAP‐related peptide vasoactive intestinal polypeptide had no effect on either types of K+ currents. Repeated applications of PACAP induced gradual attenuation of the electrophysiological response. In the presence of guanosine 5′‐[γthio]triphosphate (GTPγS), PACAP provoked a marked and irreversible IK depression, whereas cell dialysis with guanosine 5′‐[βthio]diphosphate GDPβS totally abolished the effect of PACAP. Pre‐treatment of the cells with pertussis toxin did not modify the effect of PACAP on IK. In contrast, cholera toxin suppressed the PACAP‐induced inhibition of IK. Exposure of granule cells to dibutyryl cyclic adenosine monophosphate (dbcAMP) mimicked the inhibitory effect of PACAP on IK. Addition of the specific protein kinase A inhibitor H89 in the patch pipette solution prevented the reduction of IK induced by both PACAP and dbcAMP. PACAP provoked a sustained increase of the resting membrane potential in cerebellar granule cells cultured either in high or low KCl‐containing medium, and this long‐term depolarizing effect of PACAP was mimicked by the IK specific blocker tetraethylammonium chloride (TEA). In addition, pre‐incubation of granule cells with TEA suppressed the effect of PACAP on resting membrane potential. TEA mimicked the neuroprotective effect of PACAP against ethanol‐induced apoptotic cell death, and the increase of caspase‐3 activity observed after exposure of granule cells to ethanol was also significantly inhibited by TEA. Taken together, the present results demonstrate that, in rat cerebellar granule cells, PACAP reduces the delayed outward rectifier K+ current by activating a type 1 PACAP (PAC1) receptor coupled to the adenylyl cyclase/protein kinase A pathway through a cholera toxin‐sensitive Gs protein. Our data also show that PACAP and TEA induce long‐term depolarization of the resting membrane potential, promote cell survival and inhibit caspase‐3 activity, suggesting that PACAP‐evoked inhibition of IK contributes to the anti‐apoptotic effect of the peptide on cerebellar granule cells.