52 research outputs found

    Fibre bundle formulation of nonrelativistic quantum mechanics: I. Introduction. The evolution transport

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    We propose a new systematic fibre bundle formulation of nonrelativistic quantum mechanics. The new form of the theory is equivalent to the usual one but it is in harmony with the modern trends in theoretical physics and potentially admits new generalizations in different directions. In it a pure state of some quantum system is described by a state section (along paths) of a (Hilbert) fibre bundle. Its evolution is determined through the bundle (analogue of the) Schr\"odinger equation. Now the dynamical variables and the density operator are described via bundle morphisms (along paths). The mentioned quantities are connected by a number of relations derived in this work. The present first part of this investigation is devoted to the introduction of basic concepts on which the fibre bundle approach to quantum mechanics rests. We show that the evolution of pure quantum-mechanical states can be described as a suitable linear transport along paths, called evolution transport, of the state sections in the Hilbert fibre bundle of states of a considered quantum system.Comment: 26 standard (11pt, A4) LaTeX 2e pages. The packages AMS-LaTeX and amsfonts are required. Revised: new material, references, and comments are added. Minor style chages. Continuation of quan-ph/9803083. For continuation of the this series see http://www.inrne.bas.bg/mathmod/bozhome

    Use of multi-trait and random regression models to identify genetic variation in tolerance to porcine reproductive and respiratory syndrome virus

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    Background: A host can adopt two response strategies to infection: resistance (reduce pathogen load) and tolerance (minimize impact of infection on performance). Both strategies may be under genetic control and could thus be targeted for genetic improvement. Although there is evidence that supports a genetic basis for resistance to porcine reproductive and respiratory syndrome (PRRS), it is not known whether pigs also differ genetically in tolerance. We determined to what extent pigs that have been shown to vary genetically in resistance to PRRS also exhibit genetic variation in tolerance. Multi-trait linear mixed models and random regression sire models were fitted to PRRS Host Genetics Consortium data from 1320 weaned pigs (offspring of 54 sires) that were experimentally infected with a virulent strain of PRRS virus to obtain genetic parameter estimates for resistance and tolerance. Resistance was defined as the inverse of within-host viral load (VL) from 0 to 21 (VL21) or 0 to 42 (VL42) days post-infection and tolerance as the slope of the reaction-norm of average daily gain (ADG21, ADG42) on VL21 or VL42. Results: Multi-trait analysis of ADG associated with either low or high VL was not indicative of genetic variation in tolerance. Similarly, random regression models for ADG21 and ADG42 with a tolerance slope fitted for each sire did not result in a better fit to the data than a model without genetic variation in tolerance. However, the distribution of data around average VL suggested possible confounding between level and slope estimates of the regression lines. Augmenting the data with simulated growth rates of non-infected half-sibs (ADG0) helped resolve this statistical confounding and indicated that genetic variation in tolerance to PRRS may exist if genetic correlations between ADG0 and ADG21 or ADG42 are low to moderate. Conclusions: Evidence for genetic variation in tolerance of pigs to PRRS was weak when based on data from infected piglets only. However, simulations indicated that genetic variance in tolerance may exist and could be detected if comparable data on uninfected relatives were available. In conclusion, of the two defense strategies, genetics of tolerance is more difficult to elucidate than genetics of resistance.</p

    Mutualism and Adaptive Divergence: Co-Invasion of a Heterogeneous Grassland by an Exotic Legume-Rhizobium Symbiosis

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    Species interactions play a critical role in biological invasions. For example, exotic plant and microbe mutualists can facilitate each other's spread as they co-invade novel ranges. Environmental context may influence the effect of mutualisms on invasions in heterogeneous environments, however these effects are poorly understood. We examined the mutualism between the legume, Medicago polymorpha, and the rhizobium, Ensifer medicae, which have both invaded California grasslands. Many of these invaded grasslands are composed of a patchwork of harsh serpentine and relatively benign non-serpentine soils. We grew legume genotypes collected from serpentine or non-serpentine soil in both types of soil in combination with rhizobium genotypes from serpentine or non-serpentine soils and in the absence of rhizobia. Legumes invested more strongly in the mutualism in the home soil type and trends in fitness suggested that this ecotypic divergence was adaptive. Serpentine legumes had greater allocation to symbiotic root nodules in serpentine soil than did non-serpentine legumes and non-serpentine legumes had greater allocation to nodules in non-serpentine soil than did serpentine legumes. Therefore, this invasive legume has undergone the rapid evolution of divergence for soil-specific investment in the mutualism. Contrary to theoretical expectations, the mutualism was less beneficial for legumes grown on the stressful serpentine soil than on the non-serpentine soil, possibly due to the inhibitory effects of serpentine on the benefits derived from the interaction. The soil-specific ability to allocate to a robust microbial mutualism may be a critical, and previously overlooked, adaptation for plants adapting to heterogeneous environments during invasion

    The Initial-Final Mass Relation among White Dwarfs in Wide Binaries

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    We present the initial-final mass relation derived from 10 white dwarfs in wide binaries that consist of a main sequence star and a white dwarf. The temperature and gravity of each white dwarf was measured by fitting theoretical model atmospheres to the observed spectrum using a χ2\chi^{2} fitting algorithm. The cooling time and mass was obtained using theoretical cooling tracks. The total age of each binary was estimated from the chromospheric activity of its main sequence component to an uncertainty of about 0.17 dex in log \textit{t} The difference between the total age and white dwarf cooling time is taken as the main sequence lifetime of each white dwarf. The initial mass of each white dwarf was then determined using stellar evolution tracks with a corresponding metallicity derived from spectra of their main sequence companions, thus yielding the initial-final mass relation. Most of the initial masses of the white dwarf components are between 1 - 2 M⊙_{\odot}. Our results suggest a correlation between the metallicity of a white dwarf's progenitor and the amount of post-main-sequence mass loss it experiences - at least among progenitors with masses in the range of 1 - 2 M⊙_{\odot}. A comparison of our observations to theoretical models suggests that low mass stars preferentially lose mass on the red giant branch.Comment: 28 pages, 8 figures, accepted for publication in Ap

    Behavioural and educational outcomes following extremely preterm birth : current controversies and future directions

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    As a consequence of improved survival rates for extremely preterm (EP; <28 weeks of gestation) births, there is a growing body of evidence detailing the impact of extreme prematurity on outcomes throughout childhood and adolescence. Historically, attention first focused on documenting rates of sensory impairments and severe neurodevelopmental disabilities. However, over recent years, there has been growing interest in the impact of EP birth on long term mental health and educational outcomes. In this chapter we review literature relating to the impact of EP birth on attention, social and emotional problems, psychiatric disorders and educational outcomes. We also outline current controversies in the field. In particular, we present emergent research exploring developmental trajectories to determine whether the sequelae associated with EP birth represent a developmental delay or persistent deficit, and we consider what approaches to intervention may be most fruitful in improving behavioural and educational outcomes in this population

    Inhibition of protein ubiquitination by paraquat and 1-methyl-4-phenylpyridinium impairs ubiquitin-dependent protein degradation pathways

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    Intracytoplasmic inclusions of protein aggregates in dopaminergic cells (Lewy bodies) are the pathological hallmark of Parkinson’s disease (PD). Ubiquitin (Ub), alpha [α]-synuclein, p62/sequestosome 1 and oxidized proteins are major components of Lewy bodies. However, the mechanisms involved in the impairment of misfolded/oxidized protein degradation pathways in PD are still unclear. PD is linked to mitochondrial dysfunction and environmental pesticide exposure. In this work, we evaluated the effect of the pesticide paraquat (PQ) and the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+) on Ub-dependent protein degradation pathways. No increase in the accumulation of Ub-bound proteins or aggregates was observed in dopaminergic cells (SK-N-SH) treated with PQ or MPP+, or in mice chronically exposed to PQ. PQ decreased Ub protein content, but not its mRNA transcription. Protein synthesis inhibition with cycloheximide depleted Ub levels and potentiated PQ–induced cell death. Inhibition of proteasomal activity by PQ was found to be a late event in cell death progression, and had no effect on either the toxicity of MPP+ or PQ, or the accumulation of oxidized sulfenylated, sulfonylated (DJ-1/PARK7 and peroxiredoxins) and carbonylated proteins induced by PQ. PQ- and MPP+-induced Ub protein depletion prompted the dimerization/inactivation of the Ub-binding protein p62 that regulates the clearance of ubiquitinated proteins by autophagic. We confirmed that PQ and MPP+ impaired autophagy flux, and that the blockage of autophagy by the overexpression of a dominant-negative form of the autophagy protein 5 (dnAtg5) stimulated their toxicity, but there was no additional effect upon inhibition of the proteasome. PQ induced an increase in the accumulation of α-synuclein in dopaminergic cells and membrane associated foci in yeast cells. Our results demonstrate that inhibition of protein ubiquitination by PQ and MPP+ is involved in the dysfunction of Ub-dependent protein degradation pathways
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