The Environmental and Economic Effects of European Emissions Trading

In 2005, the EU introduced an emissions trading system in order to pursue its Kyoto obligations. This instrument gives emitters the flexibility to undertake reduction measures in the most cost-efficient way and mobilizes market forces for the protection of the earth's climate. In this paper, we analyse the effects of emissions trading in Europe, with some special reference to the case of Germany. We look at the value of the flexibility gained by trading compared to fixed quotas. The analysis will be undertaken with a modified version of the GTAP-E model using the latest GTAP version 6 data base. It is based on the national allocation plans as submitted to and approved by the EU. We find that, if the NAP is combined with a regional emissions trading scheme, then Germany, Great Britain, and Czech Republic are the main sellers of emissions permits, while Belgium, Denmark, Finland, and Sweden are the main buyers. The welfare gains from regional emissions trading - for the trading sectors only - are largest for Belgium, Denmark, and Great Britain; smaller for Finland, Sweden, and smallest for Germany and other regions. When we take into account the economy-wide and terms of trade effects of emissions trading, however, the (negative) terms of trade effects can offset the (positive) allocative efficiency gains for the cases of the Netherland and Italy, while all other regions ended up with positive net welfare gains. All regions, however, experienced positive increases in real GDP as a result of regional emissions trading.

Phase locking a clock oscillator to a coherent atomic ensemble

The sensitivity of an atomic interferometer increases when the phase evolution of its quantum superposition state is measured over a longer interrogation interval. In practice, a limit is set by the measurement process, which returns not the phase, but its projection in terms of population difference on two energetic levels. The phase interval over which the relation can be inverted is thus limited to the interval $[-\pi/2,\pi/2]$; going beyond it introduces an ambiguity in the read out, hence a sensitivity loss. Here, we extend the unambiguous interval to probe the phase evolution of an atomic ensemble using coherence preserving measurements and phase corrections, and demonstrate the phase lock of the clock oscillator to an atomic superposition state. We propose a protocol based on the phase lock to improve atomic clocks under local oscillator noise, and foresee the application to other atomic interferometers such as inertial sensors.Comment: 9 pages, 7 figure

Feedback control of trapped coherent atomic ensembles

We demonstrate how to use feedback to control the internal states of trapped coherent ensembles of two-level atoms, and to protect a superposition state against the decoherence induced by a collective noise. Our feedback scheme is based on weak optical measurements with negligible back-action and coherent microwave manipulations. The efficiency of the feedback system is studied for a simple binary noise model and characterized in terms of the trade-off between information retrieval and destructivity from the optical probe. We also demonstrate the correction of more general types of collective noise. This technique can be used for the operation of atomic interferometers beyond the standard Ramsey scheme, opening the way towards improved atomic sensors.Comment: 9 pages, 6 figure

Heterodyne non-demolition measurements on cold atomic samples: towards the preparation of non-classical states for atom interferometry

We report on a novel experiment to generate non-classical atomic states via quantum non-demolition (QND) measurements on cold atomic samples prepared in a high finesse ring cavity. The heterodyne technique developed for the QND detection exhibits an optical shot-noise limited behavior for local oscillator optical power of a few hundred \muW, and a detection bandwidth of several GHz. This detection tool is used in single pass to follow non destructively the internal state evolution of an atomic sample when subjected to Rabi oscillations or a spin-echo interferometric sequence.Comment: 23 page

Interatomic exchange coupling of BCC iron

We performed first-principle calculations on the exchange interaction (EI) between atoms in BCC-Fe strained volumetrically. Our results show that the volume-dependence of the EI deviates considerably from the Bethe-Slater curve. This behavior is discussed in terms of the on-site and/or inter-site direct exchange interactions between electrons.Comment: 22 pages, 7 figure

Insulin-stimulated phosphorylation of endothelial nitric oxide synthase at serine-615 contributes to nitric oxide synthesis

Insulin stimulates endothelial NO (nitric oxide) synthesis via PKB (protein kinase B)/Akt-mediated phosphorylation and activation of eNOS (endothelial NO synthase) at Ser-1177. In previous studies, we have demonstrated that stimulation of eNOS phosphorylation at Ser-1177 may be required, yet is not sufficient for insulin-stimulated NO synthesis. We therefore investigated the role of phosphorylation of eNOS at alternative sites to Ser-1177 as candidate parallel mechanisms contributing to insulin-stimulated NO synthesis. Stimulation of human aortic endothelial cells with insulin rapidly stimulated phosphorylation of both Ser-615 and Ser-1177 on eNOS, whereas phosphorylation of Ser-114, Thr-495 and Ser-633 was unaffected. Insulin-stimulated Ser-615 phosphorylation was abrogated by incubation with the PI3K (phosphoinositide 3-kinase) inhibitor wortmannin, infection with adenoviruses expressing a dominant-negative mutant PKB/Akt or pre-incubation with TNFα (tumour necrosis factor α), but was unaffected by high culture glucose concentrations. Mutation of Ser-615 to alanine reduced insulin-stimulated NO synthesis, whereas mutation of Ser-615 to aspartic acid increased NO production by NOS in which Ser-1177 had been mutated to an aspartic acid residue. We propose that the rapid PKB-mediated stimulation of phosphorylation of Ser-615 contributes to insulin-stimulated NO synthesis

Acyl hydrolases from trans-AT polyketide synthases target acetyl units on acyl carrier proteins

Acyl hydrolase (AH) domains are a common feature of trans-AT PKSs. They have been hypothesised to perform a proofreading function by removing acyl chains from stalled sites. This study determines the substrate tolerance of the AH PedC for a range of acyl-ACPs. Clear preference towards short, linear acyl-ACPs is shown, with acetyl-ACP the best substrate. These results imply a more targeted housekeeping role for PedC: namely the removal of unwanted acetyl groups from ACP domains caused by erroneous transfer of acetyl-CoA, or possibly by decarboxylation of malonyl-ACP

Direct Observation of Martensitic Phase-Transformation Dynamics in Iron by 4D Single-Pulse Electron Microscopy

The in situ martensitic phase transformation of iron, a complex solid-state transition involving collective atomic displacement and interface movement, is studied in real time by means of four-dimensional (4D) electron microscopy. The iron nanofilm specimen is heated at a maximum rate of ∼10^(11) K/s by a single heating pulse, and the evolution of the phase transformation from body-centered cubic to face-centered cubic crystal structure is followed by means of single-pulse, selected-area diffraction and real-space imaging. Two distinct components are revealed in the evolution of the crystal structure. The first, on the nanosecond time scale, is a direct martensitic transformation, which proceeds in regions heated into the temperature range of stability of the fcc phase, 1185−1667 K. The second, on the microsecond time scale, represents an indirect process for the hottest central zone of laser heating, where the temperature is initially above 1667 K and cooling is the rate-determining step. The mechanism of the direct transformation involves two steps, that of (barrier-crossing) nucleation on the reported nanosecond time scale, followed by a rapid grain growth typically in ∼100 ps for 10 nm crystallites

Loss of autophagy protein ATG5 impairs cardiac capacity in mice and humans through diminishing mitochondrial abundance and disrupting Ca2+Ca^{\text{2+}} cycling

Aims Autophagy protects against the development of cardiac hypertrophy and failure. While aberrant Ca2+ handling promotes myocardial remodelling and contributes to contractile dysfunction, the role of autophagy in maintaining Ca2+ homeostasis remains elusive. Here, we examined whether Atg5 deficiency-mediated autophagy promotes early changes in subcellular Ca2+ handling in ventricular cardiomyocytes, and whether those alterations associate with compromised cardiac reserve capacity, which commonly precedes the onset of heart failure. Methods and results RT–qPCR and immunoblotting demonstrated reduced Atg5 gene and protein expression and decreased abundancy of autophagy markers in hypertrophied and failing human hearts. The function of ATG5 was examined using cardiomyocyte-specific Atg5-knockout mice (Atg5−/−). Before manifesting cardiac dysfunction, Atg5−/− mice showed compromised cardiac reserve in response to β-adrenergic stimulation. Consequently, effort intolerance and maximal oxygen consumption were reduced during treadmill-based exercise tolerance testing. Mechanistically, cellular imaging revealed that Atg5 deprivation did not alter spatial and functional organization of intracellular Ca2+ stores or affect Ca2+ cycling in response to slow pacing or upon acute isoprenaline administration. However, high-frequency stimulation exposed stunted amplitude of Ca2+ transients, augmented nucleoplasmic Ca2+ load, and increased CaMKII activity, especially in the nuclear region of hypertrophied Atg5−/− cardiomyocytes. These changes in Ca2+ cycling were recapitulated in hypertrophied human cardiomyocytes. Finally, ultrastructural analysis revealed accumulation of mitochondria with reduced volume and size distribution, meanwhile functional measurements showed impaired redox balance in Atg5−/− cardiomyocytes, implying energetic unsustainability due to overcompensation of single mitochondria, particularly under increased workload. Conclusion Loss of cardiac Atg5-dependent autophagy reduces mitochondrial abundance and causes subtle alterations in subcellular Ca2+ cycling upon increased workload in mice. Autophagy-related impairment of Ca2+ handling is progressively worsened by β-adrenergic signalling in ventricular cardiomyocytes, thereby leading to energetic exhaustion and compromised cardiac reserve

AKT activity orchestrates marginal zone B cell development in mice and humans.

The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells or abolish its impact on FoxO transcription factors highlight the AKT-FoxO axis as an on-off switch for MZ B cell formation in mice. In humans, splenic immunoglobulin (Ig) D <sup>+</sup> CD27 <sup>+</sup> B cells, proposed as an MZ B cell equivalent, display higher AKT signaling than naive IgD <sup>+</sup> CD27 <sup>-</sup> and memory IgD <sup>-</sup> CD27 <sup>+</sup> B cells and develop in an AKT-dependent manner from their precursors in vitro, underlining the conservation of this developmental pathway. Consistently, CD148 is identified as a receptor indicative of the level of AKT signaling in B cells, expressed at a higher level in MZ B cells than FO B cells in mice as well as humans