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An important accident management measure for controlling severe accident transients in Light Water Reactors is the injection of water to cool the degrading core. Flooding of the overheated core, which causes quenching of the fuel rods, is considered a worst-case scenario regarding hydrogen generation rates which should not exceed safety-relevant critical values. Within the frame of the QUENCH test-program the loss of coolant accidents with the following flooding of overheated core in Light Water Reactors is analysed using an experimental facility. The modelling of QUENCH-03 and QUENCH-06 experiments was performed with RELAP/SCDAPSIM computer code. The observed calculation results showed that thermal properties of shroud materials (heat losses through the shroud) and electrical power of fuel simulators are the main source of uncertainty in the calculations. The main idea of this article is modification of input parameters to receive the best agreement with the measurements for the selected QUENCH test. Modified input parameters are used in the input deck for another QUENCH test. The good agreement between calculation results and measurements of both QUENCH tests demonstrated the correctness of modified parameters and legitimacy with the real physical processes.

Bivalve culture systems are hierarchical, with culture units being nested within culture gear, which are nested within farms, and so on. The possibility that processes acting at the scale of individual culture units may interact with high-level processes has been overlooked in carrying capacity models, although basin-scale patterns are generated at the scale of culture units. Here I study the effect of increasing basin-scale loading on unit-scale optimal stocking density (OSD). I find a curvilinear relationship, with OSD decreasing with basin-scale loading. Clearly basin-scale models should incorporate culture-unit effects. This may be achieved by using experimental studies of the clearance rate of whole culture units to complement estimates of ecophysiological processes of individuals. Such culture-unit information, along with knowledge of associated local phytoplankton depletion at various current speeds and culture-unit stocking levels, may be used to generate submodels to be included in basin-scale models. To facilitate experimental testing of across-scale effects, I develop a simple food-regulated growth model combining density dependence at the scale of individual culture units and at the scale of basins.

Oxidant stress is strongly associated with cardiovascular disease, including pulmonary hypertension, but antioxidant therapies have so far proven ineffective. This is partly due to a lack of understanding of the key role played by reactive oxygen species (ROS) in physiological cell signalling, and partly to the complex interrelationships between generators of ROS (e.g. mitochondria and NADPH oxidases, NOX), cellular antioxidant systems and indeed Ca2+ signalling. At physiological levels ROS reversibly affect the function of numerous enzymes and transcription factors, most often via oxidation of specific protein thiols. Importantly, they also affect pathways that promote ROS generation by NOX or mitochondria (ROS-induced ROS release), which has an inherent propensity for positive feedback and uncontrolled oxidant production. The reason this does not occur under normal conditions reflects in part a high level of compartmentalisation of ROS signalling within the cell, akin to that for Ca2+. This article considers the physiological processes which regulate NOX and mitochondrial ROS production and degradation and their interactions with each other and Ca2+ signalling pathways, and discusses how loss of spatiotemporal constraints and activation of positive feedback pathways may impact on their dysregulation in pulmonary hypertension.

The production of hydrogen via electrochemical water splitting combined with fuel cells is a promising way to realize sustainable energy systems. Herein, we report a simple one-step, scalable glucose-blowing method to synthesize substrate-free porous molybdenum carbide nanoparticles coated with an N-doped porous carbon shell, termed Gb-Mo2C@PC. This catalyst exhibited a good hydrogen evolution reaction (HER) performance with overpotentials of 169 and 188 mV at a current density of 10 mA cm−2 and long-term stability in basic and acid electrolyte, respectively. The HER activity can be ascribed to the fact that the high surface area of its carbon shell can effectively prevent the aggregation of the Mo2C nanoparticles, and their uniform distribution favourably exposes abundant active sites. Moreover, the porous carbon shell coating can accelerate the charge transfer during the process of hydrogen generation and protect the Mo2C nanoparticles from corrosion. Furthermore, this strategy may provide a versatile route for the scaled-up production of cost-effective materials for electrochemical applications.

Mobile service providers often invest heavily on attracting new customers. If these new customers cannot be transformed into loyal ones, service providers will bear great loss. To improve user repurchase behavior, service providers can take measures to directly promote user repurchase on the one hand. On the other hand, they need to curb users' switching behavior. From these two perspectives, this paper examined the effect of trust, satisfaction as "enablers" and switching barriers as "inhibitors" on mobile users repurchase behavior. The results showed that these three factors had significant effect on user repurchase intention. Service quality and perceived value strongly affected trust and satisfaction, while switching cost determined switching barrier.

Summary 1 The pressor action of the α1A-adrenoceptor (α1A-AR) agonist A61603 (N-[5-(4,5-dihydro-1H-imidazol-2-yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl] methanesulfonamide) and the α1-ARs agonist phenylephrine and their blockade by selective α1-ARs antagonists in the isolated mesenteric vascular bed of wild-type (WT) mice and α1D-AR knockout (KO α1D-AR) mice were evaluated. 2 The apparent potency of A61603 to increase the perfusion pressure in the mesenteric vascular bed of WT and KO α1D-AR mice is 86 and 138 times the affinity of phenylephrine, respectively. 3 A61603 also enhanced the perfusion pressure by ≈1.7 fold in the mesenteric vascular bed of WT mice compared with KO α1D-AR mice. 4 Because of its high affinity, low concentrations of the α1A-AR selective antagonist RS100329 (5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl] propyl]-2,4-(1H)-pyrimidinedione) shifted the agonist concentration–response curves to the right in the mesenteric vascular bed of WT and KO α1D-AR mice. 5 The α1D-AR selective antagonist BMY7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5] decane-7,9-dione) did not modify the A61603 or the phenylephrine-induced pressor effect. 6 The α1B/D-ARs alkylating antagonist chloroethylclonidine (CEC) shifted the agonist concentration–response curves to the right and decreased the maximum phenylephrine-induced vascular contraction in KO α1D-AR mice when compared to WT mice; however, CEC only slightly modified the contraction induced by A61603. 7 The results indicate that the isolated mesenteric vascular bed of WT and KO α1D-AR mice expresses α1A-AR, that the pressor action of α1A-AR is up-regulated for α1D-AR in WT mice and suggest an important role of α1B-AR in the vascular pressure evoked by phenylephrine in KO α1D-AR mice.