36 research outputs found

    Transverse Polarisation of Quarks in Hadrons

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    We review the present state of knowledge regarding the transverse polarisation (or transversity) distributions of quarks. After some generalities on transverse polarisation, we formally define the transversity distributions within the framework of a classification of all leading-twist distribution functions. We describe the QCD evolution of transversity at leading and next-to-leading order. A comprehensive treatment of non-perturbative calculations of transversity distributions (within the framework of quark models, lattice QCD and QCD sum rules) is presented. The phenomenology of transversity (in particular, in Drell-Yan processes and semi-inclusive leptoproduction) is discussed in some detail. Finally, the prospects for future measurements are outlined.Comment: small changes, references added, as finally published in Physics Report

    Quark-hadron duality in electron scattering

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    The duality between partonic and hadronic descriptions of physical phenomena is one of the most remarkable features of strong interaction physics. A classic example of this is in electron-nucleon scattering, in which low-energy cross sections, when averaged over appropriate energy intervals, are found to exhibit the scaling behavior expected from perturbative QCD. We present a comprehensive review of data on structure functions in the resonance region, from which the global and local aspects of duality are quantified, including its flavor, spin and nuclear medium dependence. To interpret the experimental findings, we discuss various theoretical approaches which have been developed to understand the microscopic origins of quark-hadron duality in QCD. Examples from other reactions are used to place duality in a broader context, and future experimental and theoretical challenges are identified.Comment: 198 pages, 80 figures, to appear in Physics Report

    BREAKUP OF HADRON MASSES AND ENERGY-MOMENTUM TENSOR OF QCD

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    Hadron masses are shown to be separable in QCD into contributions of quark and gluon kinetic and potential energies, quark masses, and the trace anomaly. The separation is based on a study of the structure of the QCD energy-momentum tensor and its matrix elements in hadron states. The paper contains two parts. In the first part, a detailed discussion of the renormalization properties of the energy-momentum tensor is given. In the second part, a mass separation formula is derived and then applied to the nucleon, pion, and the QCD vacuum. Implications of the results on hadron structure and non-perturbative QCD dynamics are discussed.Comment: 21 pages, ReVTe

    Disruption of Yarrowia lipolytica TPS1 Gene Encoding Trehalose-6-P Synthase Does Not Affect Growth in Glucose but Impairs Growth at High Temperature

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    We have cloned the Yarrowia lipolytica TPS1 gene encoding trehalose-6-P synthase by complementation of the lack of growth in glucose of a Saccharomyces cerevisiae tps1 mutant. Disruption of YlTPS1 could only be achieved with a cassette placed in the 3′half of its coding region due to the overlap of its sequence with the promoter of the essential gene YlTFC1. The Yltps1 mutant grew in glucose although the Y. lipolytica hexokinase is extremely sensitive to inhibition by trehalose-6-P. The presence of a glucokinase, insensitive to trehalose-6-P, that constitutes about 80% of the glucose phosphorylating capacity during growth in glucose may account for the growth phenotype. Trehalose content was below 1 nmol/mg dry weight in Y. lipolytica, but it increased in strains expressing YlTPS1 under the control of the YlTEF1promoter or with a disruption of YALI0D15598 encoding a putative trehalase. mRNA levels of YlTPS1 were low and did not respond to thermal stresses, but that of YlTPS2 (YALI0D14476) and YlTPS3 (YALI0E31086) increased 4 and 6 times, repectively, by heat treatment. Disruption of YlTPS1 drastically slowed growth at 35°C. Homozygous Yltps1 diploids showed a decreased sporulation frequency that was ascribed to the low level of YALI0D20966 mRNA an homolog of the S. cerevisiae MCK1 which encodes a protein kinase that activates early meiotic gene expression

    Correction to: A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

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    Correction to: A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity.

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    The IPDGC (The International Parkinson Disease Genomics Consortium) and EADB (Alzheimer Disease European DNA biobank) are listed correctly as an author to the article, however, they were incorrectly listed more than once

    A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

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    The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer’s disease risk (AD). The role of PLCG2 in immune system signaling suggests it may also protect against other neurodegenerative diseases and possibly associates with longevity. We studied the effect of the rs72824905-G on seven neurodegenerative diseases and longevity, using 53,627 patients, 3,516 long-lived individuals and 149,290 study-matched controls. We replicated the association of rs72824905-G with reduced AD risk and we found an association with reduced risk of dementia with Lewy bodies (DLB) and frontotemporal dementia (FTD). We did not find evidence for an effect on Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) risks, despite adequate sample sizes. Conversely, the rs72824905-G allele was associated with increased likelihood of longevity. By-proxy analyses in the UK Biobank supported the associations with both dementia and longevity. Concluding, rs72824905-G has a protective effect against multiple neurodegenerative diseases indicating shared aspects of disease etiology. Our findings merit studying the PLCγ2 pathway as drug-target.Pattern Recognition and Bioinformatic
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