255 research outputs found

    Thermobarometric studies on the Levack Gneisses: Footwall rocks to the Sudbury Igneous Complex

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    Granulite and amphibolite facies gneisses and migmatites of the Levack Gneiss Complex occupy a zone up to 8 km wide around the northern part of the Sudbury Igneous Complex (SIC). Orthopyroxene- and garnet-bearing tonalitic and semipelitic assemblages of granulite facies grade occur within 3 km of the SIC together with lenses of mafic and pyroxenitic rock compositions normally represented by an amphibole +/- cpx-rich assemblage; amphibolite facies assemblages dominate elsewhere in this terrain. These 2.711-Ga gneisses were introduced by (1) the Cartier Granite Batholith during late Archaean to early Proterozoic time and (2) the SIC, at 1.85 Ga, which produced a contact aureole 1-1.5 km wide in which pyroxene hornfelses are common within 200-300 m of the contact. A suite of 12 samples including both the opx-gt and amphibole-rich rock compositions have been studied. Garnets in the semipelitic gneisses are variably replaced by a plg-bio assemblage. Thermobarometric calculations using a variety of barometers and thermometers reported in the literature suggest that the granulite facies assemblages formed at depths in the 21-28 km range (6-8 kbar). Textures and mineral chemistry in the garnet-bearing semipelitic rocks indicate that this terrain underwent a second metamorphic event during uplift to depth in the 5-11 km range (2-3 kbar) and at temperatures as low as 500-550 C. This latter event is distinct from thermal recrystallization caused by the emplacement of the SIC; it probably represents metamorphism attributable to intrusion of the Cartier Granite Batholith. These data allow two interpretations for the crustal uplift of the Levack Gneisses: (1) The gneisses were tectonically uplifted prior to the Sudbury Event (due to intrusion of the Cartier Batholith); or (2) the gneisses were raised to epizonal levels as a result of meteorite impact at 1.85 Ga

    Zero-variance principle for Monte Carlo algorithms

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    We present a general approach to greatly increase at little cost the efficiency of Monte Carlo algorithms. To each observable to be computed we associate a renormalized observable (improved estimator) having the same average but a different variance. By writing down the zero-variance condition a fundamental equation determining the optimal choice for the renormalized observable is derived (zero-variance principle for each observable separately). We show, with several examples including classical and quantum Monte Carlo calculations, that the method can be very powerful.Comment: 9 pages, Latex, to appear in Phys. Rev. Let

    Comments on Sweeny and Gliozzi dynamics for simulations of Potts models in the Fortuin-Kasteleyn representation

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    We compare the correlation times of the Sweeny and Gliozzi dynamics for two-dimensional Ising and three-state Potts models, and the three-dimensional Ising model for the simulations in the percolation prepresentation. The results are also compared with Swendsen-Wang and Wolff cluster dynamics. It is found that Sweeny and Gliozzi dynamics have essentially the same dynamical critical behavior. Contrary to Gliozzi's claim (cond-mat/0201285), the Gliozzi dynamics has critical slowing down comparable to that of other cluster methods. For the two-dimensional Ising model, both Sweeny and Gliozzi dynamics give good fits to logarithmic size dependences; for two-dimensional three-state Potts model, their dynamical critical exponent z is 0.49(1); the three-dimensional Ising model has z = 0.37(2).Comment: RevTeX, 4 pages, 5 figure

    Auger Recombination in Semiconductor Quantum Wells

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    The principal mechanisms of Auger recombination of nonequilibrium carriers in semiconductor heterostructures with quantum wells are investigated. It is shown for the first time that there exist three fundamentally different Auger recombination mechanisms of (i) thresholdless, (ii) quasi-threshold, and (iii) threshold types. The rate of the thresholdless Auger process depends on temperature only slightly. The rate of the quasi-threshold Auger process depends on temperature exponentially. However, its threshold energy essentially varies with quantum well width and is close to zero for narrow quantum wells. It is shown that the thresholdless and the quasi-threshold Auger processes dominate in narrow quantum wells, while the threshold and the quasi-threshold processes prevail in wide quantum wells. The limiting case of a three-dimensional (3D)Auger process is reached for infinitely wide quantum wells. The critical quantum well width is found at which the quasi-threshold and threshold Auger processes merge into a single 3D Auger process. Also studied is phonon-assisted Auger recombination in quantum wells. It is shown that for narrow quantum wells the act of phonon emission becomes resonant, which in turn increases substantially the coefficient of phonon-assisted Auger recombination. Conditions are found under which the direct Auger process dominates over the phonon-assisted Auger recombination at various temperatures and quantum well widths.Comment: 38 pages, 7 figure

    Quantum Monte Carlo Loop Algorithm for the t-J Model

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    We propose a generalization of the Quantum Monte Carlo loop algorithm to the t-J model by a mapping to three coupled six-vertex models. The autocorrelation times are reduced by orders of magnitude compared to the conventional local algorithms. The method is completely ergodic and can be formulated directly in continuous time. We introduce improved estimators for simulations with a local sign problem. Some first results of finite temperature simulations are presented for a t-J chain, a frustrated Heisenberg chain, and t-J ladder models.Comment: 22 pages, including 12 figures. RevTex v3.0, uses psf.te

    Hemodynamic Effects of Anthrax Toxins in the Rabbit Model and the Cardiac Pathology Induced by Lethal Toxin

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    Anthrax lethal toxin (LeTx) and edema toxin (EdTx) have been shown to alter hemodynamics in the rodent model, while LeTx primarily is reported to induce extensive tissue pathology. However, the rodent model has limitations when used for comparison to higher organisms such as humans. The rabbit model, on the other hand, has gained recognition as a useful model for studying anthrax infection and its pathophysiological effects. In this study, we assessed the hemodynamic effects of lethal toxin (LeTx) and edema toxin (EdTx) in the rabbit model using physiologically relevant amounts of the toxins. Moreover, we further examine the pathological effects of LeTx on cardiac tissue. We intravenously injected Dutch-belted rabbits with either low-dose and high-dose recombinant LeTx or a single dose of EdTx. The animals’ heart rate and mean arterial pressure were continuously monitored via telemetry until either 48 or 72 h post-challenge. Additional animals challenged with LeTx were used for cardiac troponin I (cTnI) quantitation, cardiac histopathology, and echocardiography. LeTx depressed heart rate at the lower dose and mean arterial pressure (MAP) at the higher dose. EdTx, on the other hand, temporarily intensified heart rate while lowering MAP. Both doses of LeTx caused cardiac pathology with the higher dose having a more profound effect. Lastly, left-ventricular dilation due to LeTx was not apparent at the given time-points. Our study demonstrates the hemodynamic effects of anthrax toxins, as well as the pathological effects of LeTx on the heart in the rabbit model, and it provides further evidence for the toxins’ direct impact on the heart

    Evolutionary consequences of feedbacks between within-host competition and disease control

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    Lay Summary: Competition often occurs among diverse parasites within a single host, but control efforts could change its strength. We examined how the interplay between competition and control could shape the evolution of parasite traits like drug resistance and disease severity

    Spatio-Temporal Patterns of Barmah Forest Virus Disease in Queensland, Australia

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    Background Barmah Forest virus (BFV) disease is a common and wide-spread mosquito-borne disease in Australia. This study investigated the spatio-temporal patterns of BFV disease in Queensland, Australia using geographical information system (GIS) tools and geostatistical analysis. Methods/Principal Findings We calculated the incidence rates and standardised incidence rates of BFV disease. Moran's I statistic was used to assess the spatial autocorrelation of BFV incidences. Spatial dynamics of BFV disease was examined using semi-variogram analysis. Interpolation techniques were applied to visualise and display the spatial distribution of BFV disease in statistical local areas (SLAs) throughout Queensland. Mapping of BFV disease by SLAs reveals the presence of substantial spatio-temporal variation over time. Statistically significant differences in BFV incidence rates were identified among age groups (χ2 = 7587, df = 7327,p<0.01). There was a significant positive spatial autocorrelation of BFV incidence for all four periods, with the Moran's I statistic ranging from 0.1506 to 0.2901 (p<0.01). Semi-variogram analysis and smoothed maps created from interpolation techniques indicate that the pattern of spatial autocorrelation was not homogeneous across the state. Conclusions/Significance This is the first study to examine spatial and temporal variation in the incidence rates of BFV disease across Queensland using GIS and geostatistics. The BFV transmission varied with age and gender, which may be due to exposure rates or behavioural risk factors. There are differences in the spatio-temporal patterns of BFV disease which may be related to local socio-ecological and environmental factors. These research findings may have implications in the BFV disease control and prevention programs in Queensland

    Small Heat Shock Proteins Potentiate Amyloid Dissolution by Protein Disaggregases from Yeast and Humans

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    The authors define how small heat-shock proteins synergize to regulate the assembly and disassembly of a beneficial prion, and then they exploit this knowledge to identify the human amyloid depolymerase
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