Riemann's theorem for quantum tilted rotors

The angular momentum, angular velocity, Kelvin circulation, and vortex velocity vectors of a quantum Riemann rotor are proven to be either (1) aligned with a principal axis or (2) lie in a principal plane of the inertia ellipsoid. In the second case, the ratios of the components of the Kelvin circulation to the corresponding components of the angular momentum, and the ratios of the components of the angular velocity to those of the vortex velocity are analytic functions of the axes lengths.Comment: 8 pages, Phys. Rev.

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

Disk Planet Interactions and Early Evolution in Young Planetary Systems

We study and review disk protoplanet interactions using local shearing box simulations. These suffer the disadvantage of having potential artefacts arising from periodic boundary conditions but the advantage, when compared to global simulations, of being able to capture much of the dynamics close to the protoplanet at high resolution for low computational cost. Cases with and without self sustained MHD turbulence are considered. The conditions for gap formation and the transition from type I migration are investigated and found to depend on whether the single parameter M_p R^3/(M_* H^3), with M_p, M_*, R and H being the protoplanet mass, the central mass, the orbital radius and the disk semi-thickness respectively exceeds a number of order unity. We also investigate the coorbital torques experienced by a moving protoplanet in an inviscid disk. This is done by demonstrating the equivalence of the problem for a moving protoplanet to one where the protoplanet is in a fixed orbit which the disk material flows through radially as a result of the action of an appropriate external torque. For sustainable coorbital torques to be realized a quasi steady state must be realized in which the planet migrates through the disk without accreting significant mass. In that case although there is sensitivity to computational parameters, in agreement with earlier work by Masset & Papaloizou (2003) based on global simulations, the coorbital torques are proportional to the migration speed and result in a positive feedback on the migration, enhancing it and potentially leading to a runaway. This could lead to a fast migration for protoplanets in the Saturn mass range in massive disks and may be relevant to the mass period correlation for extrasolar planets which gives a preponderance of sub Jovian masses at short orbital period.Comment: To appear in Celestial Mechanics and Dynamical Astronomy (with higher resolution figures

Enhanced Software for Scheduling Space-Shuttle Processing

The Ground Processing Scheduling System (GPSS) computer program is used to develop streamlined schedules for the inspection, repair, and refurbishment of space shuttles at Kennedy Space Center. A scheduling computer program is needed because space-shuttle processing is complex and it is frequently necessary to modify schedules to accommodate unanticipated events, unavailability of specialized personnel, unexpected delays, and the need to repair newly discovered defects. GPSS implements constraint-based scheduling algorithms and provides an interactive scheduling software environment. In response to inputs, GPSS can respond with schedules that are optimized in the sense that they contain minimal violations of constraints while supporting the most effective and efficient utilization of space-shuttle ground processing resources. The present version of GPSS is a product of re-engineering of a prototype version. While the prototype version proved to be valuable and versatile as a scheduling software tool during the first five years, it was characterized by design and algorithmic deficiencies that affected schedule revisions, query capability, task movement, report capability, and overall interface complexity. In addition, the lack of documentation gave rise to difficulties in maintenance and limited both enhanceability and portability. The goal of the GPSS re-engineering project was to upgrade the prototype into a flexible system that supports multiple- flow, multiple-site scheduling and that retains the strengths of the prototype while incorporating improvements in maintainability, enhanceability, and portability

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

Pten (phosphatase and tensin homologue gene) haploinsufficiency promotes insulin hypersensitivity

AIMS/HYPOTHESIS: Insulin controls glucose metabolism via multiple signalling pathways, including the phosphatidylinositol 3-kinase (PI3K) pathway in muscle and adipose tissue. The protein/lipid phosphatase Pten (phosphatase and tensin homologue deleted on chromosome 10) attenuates PI3K signalling by dephosphorylating the phosphatidylinositol 3,4,5-trisphosphate generated by PI3K. The current study was aimed at investigating the effect of haploinsufficiency for Pten on insulin-stimulated glucose uptake. MATERIALS AND METHODS: Insulin sensitivity in Pten heterozygous (Pten(+/−)) mice was investigated in i.p. insulin challenge and glucose tolerance tests. Glucose uptake was monitored in vitro in primary cultures of myocytes from Pten(+/−) mice, and in vivo by positron emission tomography. The phosphorylation status of protein kinase B (PKB/Akt), a downstream signalling protein in the PI3K pathway, and glycogen synthase kinase 3β (GSK3β), a substrate of PKB/Akt, was determined by western immunoblotting. RESULTS: Following i.p. insulin challenge, blood glucose levels in Pten(+/−) mice remained depressed for up to 120 min, whereas glucose levels in wild-type mice began to recover after approximately 30 min. After glucose challenge, blood glucose returned to normal about twice as rapidly in Pten(+/−) mice. Enhanced glucose uptake was observed both in Pten(+/−) myocytes and in skeletal muscle of Pten(+/−) mice by PET. PKB and GSK3β phosphorylation was enhanced and prolonged in Pten(+/−) myocytes. CONCLUSIONS/INTERPRETATION: Pten is a key negative regulator of insulin-stimulated glucose uptake in vitro and in vivo. The partial reduction of Pten due to Pten haploinsufficiency is enough to elicit enhanced insulin sensitivity and glucose tolerance in Pten(+/−) mice

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

Sub region-specific modulation of synchronous neuronal burst firing after a kainic acid insult in organotypic hippocampal cultures

<p>Abstract</p> <p>Background</p> <p>Excitotoxicity occurs in a number of pathogenic states including stroke and epilepsy. The adaptations of neuronal circuits in response to such insults may be expected to play an underlying role in pathogenesis. Synchronous neuronal firing can be induced in isolated hippocampal slices and involves all regions of this structure, thereby providing a measure of circuit activity. The effect of an excitotoxic insult (kainic acid, KA) on Mg²⁺-free-induced synchronized neuronal firing was tested in organotypic hippocampal culture by measuring extracellular field activity in CA1 and CA3.</p> <p>Results</p> <p>Within 24 hrs of the insult regional specific changes in neuronal firing patterns were evident as: (i) a dramatic <it>reduction </it>in the ability of CA3 to generate firing; and (ii) a contrasting <it>increase </it>in the frequency and duration of synchronized neuronal firing events in CA1. Two distinct processes underlie the increased propensity of CA1 to generate synchronized burst firing; a lack of ability of the CA3 region to 'pace' CA1 resulting in an increased frequency of synchronized events; and a change in the 'intrinsic' properties limited to the CA1 region, which is responsible for increased event duration. Neuronal quantification using NeuN immunoflurescent staining and stereological confocal microscopy revealed no significant cell loss in hippocampal sub regions, suggesting that changes in the properties of neurons within this region were responsible for the KA-mediated excitability changes.</p> <p>Conclusion</p> <p>These results provide novel insight into adaptation of hippocampal circuits following excitotoxic injury. KA-mediated disruption of the interplay between CA3 and CA1 clearly increases the propensity to synchronized firing in CA1.</p