47,655 research outputs found

    Stability of Quadratic Projection Methods

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    In this paper we discuss the stability of an alternative pollution-free procedure for computing spectra. The main difference with the Galerkin method lies in the fact that it gives rise to a weak approximate problem which is quadratic in the spectral parameter, instead of linear. Previous accounts on this new procedure can be found in Levitin and Shargorodsky (2002) [math.SP/0212087] and Boulton (2006) [math.SP/0503126].Comment: 19 pages, 4 figures. In this updated version we have made a small number of minor correction

    Modified univibrator compensates for output timing errors

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    One-stage, delay compensation amplifier, added to conventional univibrator circuitry time-synchronizes the trailing edge of the output pulse with the origin of the input pulse. The trailing edge is independent of the amplitude of the input pulse

    Sindbis virus ts103 has a mutation in glycoprotein E2 that leads to defective assembly of virions

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    Sindbis virus mutant ts103 is aberrant in the assembly of virus particles. During virus budding, proper nucleocapsid-glycoprotein interactions fail to occur such that particles containing many nucleocapsids are formed, and the final yield of virus is low. We have determined that a mutation in the external domain of glycoprotein E2, Ala-344-->Val, is the change that leads to this phenotype. Mapping was done by making recombinant viruses between ts103 and a parental strain of the virus, using a full-length cDNA clone of Sindbis virus from which infectious RNA can be transcribed, together with sequence analysis of the region of the genome shown in this way to contain the ts103 lesion. A partial revertant of ts103, called ts103R, was also mapped and sequenced and found to be a second-site revertant in which a change in glycoprotein E1 from lysine to methionine at position 227 partially suppresses the phenotypic effects of the change at E2 position 344. An analysis of revertants from ts103 mutants in which the Ala-->Val change had been transferred into a defined background showed that pseudorevertants were more likely to arise than were true revertants and that the ts103 change itself reverted very infrequently. The assembly defect in ts103 appeared to result from weakened interactions between the virus membrane glycoproteins or between these glycoproteins and the nucleocapsid during budding. Both the E2 mutation leading to the defect in virus assembly and the suppressor mutation in glycoprotein E1 are in the domains external to the lipid bilayer and thus in domains that cannot interact directly with the nucleocapsid. This suggests that in ts103, either the E1-E2 heterodimers or the trimeric spikes (consisting of three E1-E2 heterodimers) are unstable or have an aberrant configuration, and thus do not interact properly with the nucleocapsid, or cannot assembly correctly to form the proper icosahedral array on the surface of the virus

    Versatile analog pulse height computer performs real-time arithmetic operations

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    Multipurpose analog pulse height computer performs real-time arithmetic operations on relatively fast pulses. This computer can be used for identification of charged particles, pulse shape discrimination, division of signals from position sensitive detectors, and other on-line data reduction techniques

    Cubic Polyhedra

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    A cubic polyhedron is a polyhedral surface whose edges are exactly all the edges of the cubic lattice. Every such polyhedron is a discrete minimal surface, and it appears that many (but not all) of them can be relaxed to smooth minimal surfaces (under an appropriate smoothing flow, keeping their symmetries). Here we give a complete classification of the cubic polyhedra. Among these are five new infinite uniform polyhedra and an uncountable collection of new infinite semi-regular polyhedra. We also consider the somewhat larger class of all discrete minimal surfaces in the cubic lattice.Comment: 18 pages, many figure

    Light front field theory of relativistic quark matter

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    Light-front quantization to many-particle systems of finite temperature and density provides a novel approach towards a relativistic description of quark matter and allows us to calculate the perturbative as well as the non-perturbative regime of QCD. Utilizing a Dyson expansion of light-front many-body Green functions we have so far calculated three-quark, quark-quark, and quark-antiquark correlations that lead to the chiral phase transition, the formation of hadrons and color superconductivity in a hot and/or dense environment. Presently, we use an effective zero-range interaction, to compare our results with the more traditional instant form approach where applicable.Comment: contribution to Quark Matter 2005, 18th International Conference on Nucleus Nucleus Colisions, 4 pages, 2 figures, hiph-preprint.sty file neede

    Mutagenesis of the conserved 51-nucleotide region of Sindbis virus

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    We have constructed 25 site-specific mutations in a domain of 51 nucleotides in Sindbis virus that is highly conserved among all alphaviruses sequenced to date. These 51 nucleotides are capable of forming two hairpin structures and are found from nucleotides 155 to 205 in Sindbis virus within the region encoding nsP1. Of the mutations, 21 were silent and did not lead to a change in the amino acid sequence encoded. These silent mutations changed not only the linear sequence but also the stability of the hairpins in most cases. Two double mutants that were constructed led to the replacement of one base pair by another so that the linear sequence was altered but the nature of the hairpins was not. All of the mutants with silent mutations were viable, but 19 of the 21 mutants were severely impaired for growth in both chicken and mosquito cells. Compared with the parental virus, they grew slowly and produced virus at rates of 10(-1) to 10(-4) times the parental rate. Surprisingly, however, the plaques produced by these mutants were indistinguishable from those produced by the parental virus. Two of the silent mutations, found within the first hairpin structure, produced virus at a faster rate than the parental virus. It is clear that the exact sequence of this region is important for some aspect of virus replication. We suggest that one or more proteins, either virus encoded or cellular, bind to the hairpin structures in a sequence-specific fashion in a step that promotes replication of the viral RNA. Of the mutations that resulted in a change of coding, only one of four was viable, suggesting that the amino acid sequence encoded in this domain is essential for virus replication
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