302 research outputs found

    Gaussian quantum operator representation for bosons

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    We introduce a Gaussian quantum operator representation, using the most general possible multimode Gaussian operator basis. The representation unifies and substantially extends existing phase-space representations of density matrices for Bose systems and also includes generalized squeezed-state and thermal bases. It enables first-principles dynamical or equilibrium calculations in quantum many-body systems, with quantum uncertainties appearing as dynamical objects. Any quadratic Liouville equation for the density operator results in a purely deterministic time evolution. Any cubic or quartic master equation can be treated using stochastic methods

    Seaview Survey Photo-quadrat and Image Classification Dataset

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    The primary scientific dataset arising from the XL Catlin Seaview Survey project is the “Seaview Survey Photo-quadrat and Image Classification Dataset”, consisting of: (1) over one million standardised, downward-facing “photo-quadrat” images covering approximately 1m2 of the sea floor; (2) human-classified annotations that can be used to train and validate image classifiers;\ua0(3) benthic cover data arising from the application of machine learning classifiers to the photo-quadrats; and\ua0(4)\ua0the triplets of raw images (covering 360o) from which the photo-quadrats were derived.Photo-quadrats were collected between 2012 and 2018 at 860 transect locations around the world, including: the Caribbean and Bermuda, the Indian Ocean (Maldives, Chagos Archipelago), the Coral Triangle (Indonesia, Philippines, Timor-Leste, Solomon Islands), the Great Barrier Reef, Taiwan and Hawaii.For additional information regarding methodology, data structure, organization and size, please see attached document “Dataset documentation”

    Regulation of phosphorylase kinase by low concentrations of Ca ions upon muscle contraction: the connection between metabolism and muscle contraction and the connection between muscle physiology and Ca-dependent signal transduction

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    It had long been one of the crucial questions in muscle physiology how glycogenolysis is regulated in connection with muscle contraction, when we found the answer to this question in the last half of the 1960s. By that time, the two principal currents of muscle physiology, namely, the metabolic flow starting from glycogen and the mechanisms of muscle contraction, had already been clarified at the molecular level thanks to our senior researchers. Thus, the final question we had to answer was how to connect these two currents. We found that low concentrations of Ca ions (10−7–10−4 M) released from the sarcoplasmic reticulum for the regulation of muscle contraction simultaneously reversibly activate phosphorylase kinase, the enzyme regulating glycogenolysis. Moreover, we found that adenosine 3′,5′-monophosphate (cyclic AMP), which is already known to activate muscle phosphorylase kinase, is not effective in the absence of such concentrations of Ca ions. Thus, cyclic AMP is not effective by itself alone and only modifies the activation process in the presence of Ca ions (at that time, cyclic AMP-dependent protein kinase had not yet been identified). After a while, it turned out that our works have not only provided the solution to the above problem on muscle physiology, but have also been considered as the first report of Ca-dependent protein phosphorylation, which is one of the central problems in current cell biology. Phosphorylase kinase is the first protein kinase to phosphorylate a protein resulting in the change in the function of the phosphorylated protein, as shown by Krebs and Fischer. Our works further showed that this protein kinase is regulated in a Ca-dependent manner. Accordingly, our works introduced the concept of low concentrations of Ca ions, which were first identified as the regulatory substance of muscle contraction, to the vast field of Ca biology including signal transduction

    Clustered mutations in the GRIK2 kainate receptor subunit gene underlie diverse neurodevelopmental disorders

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    Kainate receptors (KARs) are glutamate-gated cation channels with diverse roles in the central nervous system. Bi-allelic loss of function of the KAR-encoding gene GRIK2 causes a nonsyndromic neurodevelopmental disorder (NDD) with intellectual disability and developmental delay as core features. The extent to which mono-allelic variants in GRIK2 also underlie NDDs is less understood because only a single individual has been reported previously. Here, we describe an additional eleven individuals with heterozygous de novo variants in GRIK2 causative for neurodevelopmental deficits that include intellectual disability. Five children harbored recurrent de novo variants (three encoding p.Thr660Lys and two p.Thr660Arg), and four children and one adult were homozygous for a previously reported variant (c.1969G>A [p.Ala657Thr]). Individuals with shared variants had some overlapping behavioral and neurological dysfunction, suggesting that the GRIK2 variants are likely pathogenic. Analogous mutations introduced into recombinant GluK2 KAR subunits at sites within the M3 transmembrane domain (encoding p.Ala657Thr, p.Thr660Lys, and p.Thr660Arg) and the M3-S2 linker domain (encoding p.Ile668Thr) had complex effects on functional properties and membrane localization of homomeric and heteromeric KARs. Both p.Thr660Lys and p.Thr660Arg mutant KARs exhibited markedly slowed gating kinetics, similar to p.Ala657Thr-containing receptors. Moreover, we observed emerging genotype-phenotype correlations, including the presence of severe epilepsy in individuals with the p.Thr660Lys variant and hypomyelination in individuals with either the p.Thr660Lys or p.Thr660Arg variant. Collectively, these results demonstrate that human GRIK2 variants predicted to alter channel function are causative for early childhood development disorders and further emphasize the importance of clarifying the role of KARs in early nervous system development.Genetics of disease, diagnosis and treatmen

    Measurements of differential production cross sections for a Z boson in association with jets in pp collisions at root s=8 TeV

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    Measurements of the t(t)Overbar charge asymmetry using the dilepton decay channel in pp collisions at root s=7 TeV

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    The tt¯ charge asymmetry in proton-proton collisions at s√ = 7 TeV is measured using the dilepton decay channel (ee, e μ , or μμ ). The data correspond to a total integrated luminosity of 5.0 fb −1 , collected by the CMS experiment at the LHC. The tt and lepton charge asymmetries, defined as the differences in absolute values of the rapidities between the reconstructed top quarks and antiquarks and of the pseudorapidities between the positive and negative leptons, respectively, are measured to be A C = −0 . 010 ± 0 . 017 (stat . ) ± 0 . 008 (syst . ) and AlepC = 0 . 009 ± 0 . 010 (stat . ) ± 0 . 006 (syst . ). The lepton charge asymmetry is also measured as a function of the invariant mass, rapidity, and transverse momentum of the tt¯ system. All measurements are consistent with the expectations of the standard model
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