The energetics response to a warmer climate: relative contributions from the transient and stationary eddies

We use the Lorenz Energy Cycle (LEC) to evaluate changes in global energetic activity due to CO<sub>2</sub>-doubling in the coupled atmosphere-ocean ECHAM5/MPI-OM model. Globally, the energetic activity – measured as the total conversion rate of available potential energy into kinetic energy – decreases by about 4 %. This weakening results from a dual response that consists of a strengthening of the LEC in the upper-troposphere and a weakening in the lower and middle troposphere. This is fully consistent with results from a coarser resolution version of the same coupled model. We further use our experiments to investigate the individual contributions of the transient and stationary eddy components to the main energetics response. <br><br> The transient eddy terms have a larger contribution to the total energetic activity than the stationary ones. We find that this is also true in terms of their 2 × CO<sub>2</sub>-response. Changes in the transient eddy components determine the main energetics response, whereas the stationary eddy components have very small contributions. Hence, the dual response – strengthening in the upper troposphere and weakening below – concerns mainly the transient eddy terms. We can relate qualitatively this response to the two main features of the 2 × CO<sub>2</sub> warming pattern: (a) the tropical upper-tropospheric warming increases the pole-to-equator temperature gradient – strengthening the energetic activity above – and enhances static stability – weakening the energetic activity below; and (b) the high-latitude surface warming decreases the pole-to-equator temperature gradient in the lower troposphere – weakening the energetic activity below. Despite the small contribution from the stationary eddies to the main energetics response, changes in stationary eddy available potential energy (<i>P</i><sub>se</sub>) reflect some features of the warming pattern: stronger land-sea contrasts at the subtropics and weaker land-sea contrasts at the high northern latitudes affect <i>P</i><sub>se</sub> regionally, but do not affect the global energetics response

Veganism

Narrowly understood, veganism is the practice of excluding all animal products from one’s diet, with the exception of human milk. More broadly, veganism is not only a food ethics, but it encompasses all other areas of life. As defined by the Vegan Society when it became an established charity in the UK in 1979, veganism is best understood as “a philosophy and way of living which seeks to exclude – as far as is possible and practicable – all forms of exploitation of, and cruelty to, animals for food, clothing or any other purpose; and by extension, promotes the development and use of animal-free alternatives for the benefit of humans, animals and the environment”. There are two main moral justifications for veganism, both of which rely on a common assumption: that sentience, i.e., the capacity to feel pleasure and pain, is the necessary and sufficient trait to be morally considerable. In what follows, I present these two justifications and a third one which, although less popular, captures some core intuitions among vegans. I then present a challenge faced by veganism and two arguments that reject it as discriminatory, and briefly conclude

COA6 facilitates cytochrome c oxidase biogenesis as thiol-reductase for copper metallochaperones in mitochondria.

The mitochondrial cytochrome c oxidase, the terminal enzyme of the respiratory chain, contains heme and copper centers for electron transfer. The conserved COX2 subunit contains the CuA site, a binuclear copper center. The copper chaperones SCO1, SCO2, and COA6 are required for CuA center formation. Loss of function of these chaperones and the concomitant cytochrome c oxidase deficiency cause severe human disorders. Here we analyzed the molecular function of COA6 and the consequences of COA6 deficiency for mitochondria. Our analyses show that loss of COA6 causes combined complex I and complex IV deficiency and impacts membrane potential driven protein transport across the inner membrane. We demonstrate that COA6 acts as a thiol-reductase to reduce disulphide bridges of critical cysteine residues in SCO1 and SCO2. Cysteines within the CX3CXNH domain of SCO2 mediate its interaction with COA6 but are dispensable for SCO2-SCO1 interaction. Our analyses define COA6 as thiol-reductase, which is essential for CuA biogenesis