354 research outputs found

    Induced Parity Nonconserving Interaction and Enhancement of Two-Nucleon Parity Nonconserving Forces

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    Two-nucleon parity nonconserving (PNC) interaction induced by the single-particle PNC weak potential and the two-nucleon residual strong interaction is considered. An approximate analytical formula for this Induced PNC Interaction (IPNCI) between proton and neutron is derived (Q(rσp×σn)δ(rprn)Q({\bf r} {\bf \sigma}_{p} \times {\bf \sigma}_{n}) \delta({\bf r}_{p}-{\bf r}_{n})), and the interaction constant is estimated. As a result of coherent contributions from the nucleons to the PNC potential, IPNCI is an order of magnitude stronger (A1/3\sim A^{1/3}) than the residual weak two-nucleon interaction and has a different coordinate and isotopic structure (e.g., the strongest part of IPNCI does not contribute to the PNC mean field). IPNCI plays an important role in the formation of PNC effects, e.g., in neutron-nucleus reactions. In that case, it is a technical way to take into account the contribution of the distant (small) components of a compound state which dominates the result. The absence of such enhancement (A1/3\sim A^{1/3}) in the case of T- and P-odd interaction completes the picture.Comment: Phys. Rev. C, to appear; 17 pages, revtex 3, no figure

    History of clinical transplantation

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    How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York

    Meta-analysis of type 2 Diabetes in African Americans Consortium

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    Type 2 diabetes (T2D) is more prevalent in African Americans than in Europeans. However, little is known about the genetic risk in African Americans despite the recent identification of more than 70 T2D loci primarily by genome-wide association studies (GWAS) in individuals of European ancestry. In order to investigate the genetic architecture of T2D in African Americans, the MEta-analysis of type 2 DIabetes in African Americans (MEDIA) Consortium examined 17 GWAS on T2D comprising 8,284 cases and 15,543 controls in African Americans in stage 1 analysis. Single nucleotide polymorphisms (SNPs) association analysis was conducted in each study under the additive model after adjustment for age, sex, study site, and principal components. Meta-analysis of approximately 2.6 million genotyped and imputed SNPs in all studies was conducted using an inverse variance-weighted fixed effect model. Replications were performed to follow up 21 loci in up to 6,061 cases and 5,483 controls in African Americans, and 8,130 cases and 38,987 controls of European ancestry. We identified three known loci (TCF7L2, HMGA2 and KCNQ1) and two novel loci (HLA-B and INS-IGF2) at genome-wide significance (4.15 × 10(-94)<P<5 × 10(-8), odds ratio (OR)  = 1.09 to 1.36). Fine-mapping revealed that 88 of 158 previously identified T2D or glucose homeostasis loci demonstrated nominal to highly significant association (2.2 × 10(-23) < locus-wide P<0.05). These novel and previously identified loci yielded a sibling relative risk of 1.19, explaining 17.5% of the phenotypic variance of T2D on the liability scale in African Americans. Overall, this study identified two novel susceptibility loci for T2D in African Americans. A substantial number of previously reported loci are transferable to African Americans after accounting for linkage disequilibrium, enabling fine mapping of causal variants in trans-ethnic meta-analysis studies.Peer reviewe

    Novel genetic loci associated with hippocampal volume

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    The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

    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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    Peer reviewe

    Search for the associated production of the Higgs boson with a top-quark pair

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    A search for the standard model Higgs boson produced in association with a top-quark pair t t ¯ H (tt¯H) is presented, using data samples corresponding to integrated luminosities of up to 5.1 fb &#8722;1 and 19.7 fb &#8722;1 collected in pp collisions at center-of-mass energies of 7 TeV and 8 TeV respectively. The search is based on the following signatures of the Higgs boson decay: H &#8594; hadrons, H &#8594; photons, and H &#8594; leptons. The results are characterized by an observed t t ¯ H tt¯H signal strength relative to the standard model cross section, &#956; = &#963;/&#963; SM ,under the assumption that the Higgs boson decays as expected in the standard model. The best fit value is &#956; = 2.8 ± 1.0 for a Higgs boson mass of 125.6 GeV

    Identification techniques for highly boosted W bosons that decay into hadrons

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