78 research outputs found

    Scaling Of The Coulomb Energy Due To Quantum Fluctuations In The Charge Of A Quantum Dot

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    The charging energy of a quantum dot is measured through the effect of its potential on the conductance of a second dot. This technique allows a measurement of the scaling of the dot's charging energy with the conductance of the tunnel barriers leading to the dot. We find that the charging energy scales quadratically with the reflection probability of the barriers. In a second experiment we study the transition from a single to a double-dot which exhibits a scaling behavior linear in the reflection probability. The observed power-laws agree with a recent theory.Comment: 5 pages, uuencoded and compressed postscript file, with figure

    Giant gravitons in AdS/CFT (I): matrix model and back reaction

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    In this article we study giant gravitons in the framework of AdS/CFT correspondence. First, we show how to describe these configurations in the CFT side using a matrix model. In this picture, giant gravitons are realized as single excitations high above a Fermi sea, or as deep holes into it. Then, we give a prescription to define quasi-classical states and we recover the known classical solution associated to the CFT dual of a giant graviton that grows in AdS. Second, we use the AdS/CFT dictionary to obtain the supergravity boundary stress tensor of a general state and to holographically reconstruct the bulk metric, obtaining the back reaction of space-time. We find that the space-time response to all the supersymmetric giant graviton states is of the same form, producing the singular BPS limit of the three charge Reissner-Nordstr\"om-AdS black holes. While computing the boundary stress tensor, we comment on the finite counterterm recently introduced by Liu and Sabra, and connect it to a scheme-dependent conformal anomaly.Comment: 28 pages, JHEP3 class. v2: typos corrected and references adde

    Recurrent mutations in the U2AF1 splicing factor in myelodysplastic syndromes

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    Myelodysplastic syndromes (MDS) are hematopoietic stem cell disorders that often progress to chemotherapy-resistant secondary acute myeloid leukemia (sAML). We used whole-genome sequencing to perform an unbiased comprehensive screen to discover the somatic mutations in a sample from an individual with sAML and genotyped the loci containing these mutations in the matched MDS sample. Here we show that a missense mutation affecting the serine at codon 34 (Ser34) in U2AF1 was recurrently present in 13 out of 150 (8.7%) subjects with de novo MDS, and we found suggestive evidence of an increased risk of progression to sAML associated with this mutation. U2AF1 is a U2 auxiliary factor protein that recognizes the AG splice acceptor dinucleotide at the 3' end of introns, and the alterations in U2AF1 are located in highly conserved zinc fingers of this protein. Mutant U2AF1 promotes enhanced splicing and exon skipping in reporter assays in vitro. This previously unidentified, recurrent mutation in U2AF1 implicates altered pre-mRNA splicing as a potential mechanism for MDS pathogenesis

    Cluster structure of 13C probed via the 7Li(9Be,13C*->9Be+alpha) reaction

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    A study of the 7Li(9Be,4He9Be)3H reaction at E{beam}=70 MeV has been performed using resonant particle spectroscopy techniques and provides a measurement of alpha-decaying states in 13C. Excited states are observed at 12.0, 13.4, 14.1, 14.6, 15.2, 16.8, 17.9, 18.7, 21.3 and 23.9 MeV. This study provides the first measurement of the three highest energy states. Angular distribution measurements have been performed and have been employed to indicate the transferred angular momentum for the populated states. These data are compared with recent speculations of the presence of chain-like structures in 13C.Comment: accepted for publication in Nuclear Physics

    alpha-decay of excited states in 11C and 11B

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    Studies of the 16O(9Be,alpha7Be)14C and 7Li(9Be,alpha7Li)5He reactions at E{beam}=70 MeV have been performed using resonant particle spectroscopy techniques. The 11C excited states decaying into alpha+7Be(gs) are observed at 8.65, 9.85, 10.7 and 12.1 MeV as well as possible states at 12.6 and 13.4 MeV. This result is the first observation of alpha-decay for excited states above 9 MeV. The alpha+7Li(gs) decay of 11B excited states at 9.2, 10.3, 10.55, 11.2, (11.4), 11.8, 12.5,(13.0), 13.1, (14.0), 14.35, (17.4) and (18.6) MeV is observed. The decay processes are used to indicate the possible three-centre 2alpha+3He(3H) cluster structure of observed states. Two rotational bands corresponding to very deformed structures are suggested for the positive-parity states. Excitations of some observed T=1/2 resonances coincide with the energies of T=3/2 states which are the isobaric analogs of the lowest 11Be states. Some of these states may have mixed isospin.Comment: accepted for publication in Nuclear Physics

    Integrating sequence and array data to create an improved 1000 Genomes Project haplotype reference panel

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    A major use of the 1000 Genomes Project (1000GP) data is genotype imputation in genome-wide association studies (GWAS). Here we develop a method to estimate haplotypes from low-coverage sequencing data that can take advantage of single-nucleotide polymorphism (SNP) microarray genotypes on the same samples. First the SNP array data are phased to build a backbone (or 'scaffold') of haplotypes across each chromosome. We then phase the sequence data 'onto' this haplotype scaffold. This approach can take advantage of relatedness between sequenced and non-sequenced samples to improve accuracy. We use this method to create a new 1000GP haplotype reference set for use by the human genetic community. Using a set of validation genotypes at SNP and bi-allelic indels we show that these haplotypes have lower genotype discordance and improved imputation performance into downstream GWAS samples, especially at low-frequency variants. © 2014 Macmillan Publishers Limited. All rights reserved

    New insights into the genetic etiology of Alzheimer's disease and related dementias

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    Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele
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