Quasi-Homogeneous Thermodynamics and Black Holes

We propose a generalized thermodynamics in which quasi-homogeneity of the thermodynamic potentials plays a fundamental role. This thermodynamic formalism arises from a generalization of the approach presented in paper [1], and it is based on the requirement that quasi-homogeneity is a non-trivial symmetry for the Pfaffian form $\delta Q_{rev}$. It is shown that quasi-homogeneous thermodynamics fits the thermodynamic features of at least some self-gravitating systems. We analyze how quasi-homogeneous thermodynamics is suggested by black hole thermodynamics. Then, some existing results involving self-gravitating systems are also shortly discussed in the light of this thermodynamic framework. The consequences of the lack of extensivity are also recalled. We show that generalized Gibbs-Duhem equations arise as a consequence of quasi-homogeneity of the thermodynamic potentials. An heuristic link between this generalized thermodynamic formalism and the thermodynamic limit is also discussed.Comment: 39 pages, uses RevteX. Published version (minor changes w.r.t. the original one

Classical Equations for Quantum Systems

The origin of the phenomenological deterministic laws that approximately govern the quasiclassical domain of familiar experience is considered in the context of the quantum mechanics of closed systems such as the universe as a whole. We investigate the requirements for coarse grainings to yield decoherent sets of histories that are quasiclassical, i.e. such that the individual histories obey, with high probability, effective classical equations of motion interrupted continually by small fluctuations and occasionally by large ones. We discuss these requirements generally but study them specifically for coarse grainings of the type that follows a distinguished subset of a complete set of variables while ignoring the rest. More coarse graining is needed to achieve decoherence than would be suggested by naive arguments based on the uncertainty principle. Even coarser graining is required in the distinguished variables for them to have the necessary inertia to approach classical predictability in the presence of the noise consisting of the fluctuations that typical mechanisms of decoherence produce. We describe the derivation of phenomenological equations of motion explicitly for a particular class of models. Probabilities of the correlations in time that define equations of motion are explicitly considered. Fully non-linear cases are studied. Methods are exhibited for finding the form of the phenomenological equations of motion even when these are only distantly related to those of the fundamental action. The demonstration of the connection between quantum-mechanical causality and causalty in classical phenomenological equations of motion is generalized. The connections among decoherence, noise, dissipation, and the amount of coarse graining necessary to achieve classical predictability are investigated quantitatively.Comment: 100pages, 1 figur

Self-consistent anisotropic oscillator with cranked angular and vortex velocities

The Kelvin circulation is the kinematical Hermitian observable that measures the true character of nuclear rotation. For the anisotropic oscillator, mean field solutions with fixed angular momentum and Kelvin circulation are derived in analytic form. The cranking Lagrange multipliers corresponding to the two constraints are the angular and vortex velocities. Self-consistent solutions are reported with a constraint to constant volume.Comment: 12 pages, LaTex/RevTex, Phys. Rev. C4

Visualization of Spatiotemporal Energy Dynamics of Hippocampal Neurons by Mass Spectrometry during a Kainate-Induced Seizure

We report the use of matrix-assisted laser desorption/ionization (MALDI) imaging mass spectrometry combined with capillary electrophoresis (CE) mass spectrometry to visualize energy metabolism in the mouse hippocampus by imaging energy-related metabolites. We show the distribution patterns of ATP, ADP, and AMP in the hippocampus as well as changes in their amounts and distribution patterns in a murine model of limbic, kainate-induced seizure. As an acute response to kainate administration, we found massive and moderate reductions in ATP and ADP levels, respectively, but no significant changes in AMP levels—especially in cells of the CA3 layer. The results suggest the existence of CA3 neuron-selective energy metabolism at the anhydride bonds of ATP and ADP in the hippocampal neurons during seizure. In addition, metabolome analysis of energy synthesis pathways indicates accelerated glycolysis and possibly TCA cycle activity during seizure, presumably due to the depletion of ATP. Consistent with this result, the observed energy depletion significantly recovered up to 180 min after kainate administration. However, the recovery rate was remarkably low in part of the data-pixel population in the CA3 cell layer region, which likely reflects acute and CA3-selective neural death. Taken together, the present approach successfully revealed the spatiotemporal energy metabolism of the mouse hippocampus at a cellular resolution—both quantitatively and qualitatively. We aim to further elucidate various metabolic processes in the neural system

Oxr1 Is Essential for Protection against Oxidative Stress-Induced Neurodegeneration

Oxidative stress is a common etiological feature of neurological disorders, although the pathways that govern defence against reactive oxygen species (ROS) in neurodegeneration remain unclear. We have identified the role of oxidation resistance 1 (Oxr1) as a vital protein that controls the sensitivity of neuronal cells to oxidative stress; mice lacking Oxr1 display cerebellar neurodegeneration, and neurons are less susceptible to exogenous stress when the gene is over-expressed. A conserved short isoform of Oxr1 is also sufficient to confer this neuroprotective property both in vitro and in vivo. In addition, biochemical assays indicate that Oxr1 itself is susceptible to cysteine-mediated oxidation. Finally we show up-regulation of Oxr1 in both human and pre-symptomatic mouse models of amyotrophic lateral sclerosis, indicating that Oxr1 is potentially a novel neuroprotective factor in neurodegenerative disease

Deletion of the Mitochondrial Superoxide Dismutase sod-2 Extends Lifespan in Caenorhabditis elegans

The oxidative stress theory of aging postulates that aging results from the accumulation of molecular damage caused by reactive oxygen species (ROS) generated during normal metabolism. Superoxide dismutases (SODs) counteract this process by detoxifying superoxide. It has previously been shown that elimination of either cytoplasmic or mitochondrial SOD in yeast, flies, and mice results in decreased lifespan. In this experiment, we examine the effect of eliminating each of the five individual sod genes present in Caenorhabditis elegans. In contrast to what is observed in other model organisms, none of the sod deletion mutants shows decreased lifespan compared to wild-type worms, despite a clear increase in sensitivity to paraquat- and juglone-induced oxidative stress. In fact, even mutants lacking combinations of two or three sod genes survive at least as long as wild-type worms. Examination of gene expression in these mutants reveals mild compensatory up-regulation of other sod genes. Interestingly, we find that sod-2 mutants are long-lived despite a significant increase in oxidatively damaged proteins. Testing the effect of sod-2 deletion on known pathways of lifespan extension reveals a clear interaction with genes that affect mitochondrial function: sod-2 deletion markedly increases lifespan in clk-1 worms while clearly decreasing the lifespan of isp-1 worms. Combined with the mitochondrial localization of SOD-2 and the fact that sod-2 mutant worms exhibit phenotypes that are characteristic of long-lived mitochondrial mutants—including slow development, low brood size, and slow defecation—this suggests that deletion of sod-2 extends lifespan through a similar mechanism. This conclusion is supported by our demonstration of decreased oxygen consumption in sod-2 mutant worms. Overall, we show that increased oxidative stress caused by deletion of sod genes does not result in decreased lifespan in C. elegans and that deletion of sod-2 extends worm lifespan by altering mitochondrial function

Drosophila cbl Is Essential for Control of Cell Death and Cell Differentiation during Eye Development

Activation of cell surface receptors transduces extracellular signals into cellular responses such as proliferation, differentiation and survival. However, as important as the activation of these receptors is their appropriate spatial and temporal down-regulation for normal development and tissue homeostasis. The Cbl family of E3-ubiquitin ligases plays a major role for the ligand-dependent inactivation of receptor tyrosine kinases (RTKs), most notably the Epidermal Growth Factor Receptor (EGFR) through ubiquitin-mediated endocytosis and lysosomal degradation.Here, we report the mutant phenotypes of Drosophila cbl (D-cbl) during eye development. D-cbl mutants display overgrowth, inhibition of apoptosis, differentiation defects and increased ommatidial spacing. Using genetic interaction and molecular markers, we show that most of these phenotypes are caused by increased activity of the Drosophila EGFR. Our genetic data also indicate a critical role of ubiquitination for D-cbl function, consistent with biochemical models.These data may provide a mechanistic model for the understanding of the oncogenic activity of mammalian cbl genes