51 research outputs found
Limits on WWZ and WW\gamma couplings from p\bar{p}\to e\nu jj X events at \sqrt{s} = 1.8 TeV
We present limits on anomalous WWZ and WW-gamma couplings from a search for
WW and WZ production in p-bar p collisions at sqrt(s)=1.8 TeV. We use p-bar p
-> e-nu jjX events recorded with the D0 detector at the Fermilab Tevatron
Collider during the 1992-1995 run. The data sample corresponds to an integrated
luminosity of 96.0+-5.1 pb^(-1). Assuming identical WWZ and WW-gamma coupling
parameters, the 95% CL limits on the CP-conserving couplings are
-0.33<lambda<0.36 (Delta-kappa=0) and -0.43<Delta-kappa<0.59 (lambda=0), for a
form factor scale Lambda = 2.0 TeV. Limits based on other assumptions are also
presented.Comment: 11 pages, 2 figures, 2 table
Zgamma Production in pbarp Collisions at sqrt(s)=1.8 TeV and Limits on Anomalous ZZgamma and Zgammagamma Couplings
We present a study of Z +gamma + X production in p-bar p collisions at
sqrt{S}=1.8 TeV from 97 (87) pb^{-1} of data collected in the eegamma
(mumugamma) decay channel with the D0 detector at Fermilab. The event yield and
kinematic characteristics are consistent with the Standard Model predictions.
We obtain limits on anomalous ZZgamma and Zgammagamma couplings for form factor
scales Lambda = 500 GeV and Lambda = 750 GeV. Combining this analysis with our
previous results yields 95% CL limits |h{Z}_{30}| < 0.36, |h{Z}_{40}| < 0.05,
|h{gamma}_{30}| < 0.37, and |h{gamma}_{40}| < 0.05 for a form factor scale
Lambda=750 GeV.Comment: 17 Pages including 2 Figures. Submitted to PR
A Measurement of the W Boson Mass
We report a measurement of the W boson mass based on an integrated luminosity
of 82 pb from \ppbar collisions at TeV recorded in
1994--1995 by the \Dzero detector at the Fermilab Tevatron. We identify W
bosons by their decays to and extract the mass by fitting the transverse
mass spectrum from 28,323 W boson candidates. A sample of 3,563 dielectron
events, mostly due to Z to ee decays, constrains models of W boson production
and the detector. We measure \mw=80.44\pm0.10(stat)\pm0.07(syst)~GeV. By
combining this measurement with our result from the 1992--1993 data set, we
obtain \mw=80.43\pm0.11 GeV.Comment: 11 pages, 5 figure
On Switch-Reference Phenomena in Kolyma Yukaghir
「環太平洋の言語」成果報告書A2-002ELPR publication series A2-00
MSH2/MSH6 Complex Promotes Error-Free Repair of AID-Induced dU:G Mispairs as well as Error-Prone Hypermutation of A:T Sites
Mismatch repair of AID-generated dU:G mispairs is critical for class switch recombination (CSR) and somatic hypermutation (SHM) in B cells. The generation of a previously unavailable Msh2−/−Msh6−/− mouse has for the first time allowed us to examine the impact of the complete loss of MutSα on lymphomagenesis, CSR and SHM. The onset of T cell lymphomas and the survival of Msh2−/−Msh6−/− and Msh2−/−Msh6−/−Msh3−/− mice are indistinguishable from Msh2−/− mice, suggesting that MSH2 plays the critical role in protecting T cells from malignant transformation, presumably because it is essential for the formation of stable MutSα heterodimers that maintain genomic stability. The similar defects on switching in Msh2−/−, Msh2−/−Msh6−/− and Msh2−/−Msh6−/−Msh3−/− mice confirm that MutSα but not MutSβ plays an important role in CSR. Analysis of SHM in Msh2−/−Msh6−/− mice not only confirmed the error-prone role of MutSα in the generation of strand biased mutations at A:T bases, but also revealed an error-free role of MutSα when repairing some of the dU:G mispairs generated by AID on both DNA strands. We propose a model for the role of MutSα at the immunoglobulin locus where the local balance of error-free and error-prone repair has an impact in the spectrum of mutations introduced during Phase 2 of SHM
Heterozygous Mutation of Opa1 in Drosophila Shortens Lifespan Mediated through Increased Reactive Oxygen Species Production
Optic atrophy 1 (OPA1) is a dynamin-like GTPase located in the inner mitochondrial membrane and mutations in OPA1 are associated with autosomal dominant optic atrophy (DOA). OPA1 plays important roles in mitochondrial fusion, cristae remodeling and apoptosis. Our previous study showed that dOpa1 mutation caused elevated reactive oxygen species (ROS) production and resulted in damage and death of the cone and pigment cells in Drosophila eyes. Since ROS-induced oxidative damage to the cells is one of the primary causes of aging, in this study, we examined the effects of heterozygous dOpa1 mutation on the lifespan. We found that heterozygous dOpa1 mutation caused shortened lifespan, increased susceptibility to oxidative stress and elevated production of ROS in the whole Drosophila. Antioxidant treatment partially restored lifespan in the male dOpa1 mutants, but had no effects in the females. Heterozygous dOpa1 mutation caused an impairment of respiratory chain complex activities, especially complexes II and III, and reversible decreased aconitase activity. Heterozygous dOpa1 mutation is also associated with irregular and dysmorphic mitochondria in the muscle. Our results, for the first time, demonstrate the important role of OPA1 in aging and lifespan, which is most likely mediated through augmented ROS production
Replication Protein A (RPA) Hampers the Processive Action of APOBEC3G Cytosine Deaminase on Single-Stranded DNA
deamination assays and expression of A3G in yeast, we show that replication protein A (RPA), the eukaryotic single-stranded DNA (ssDNA) binding protein, severely inhibits the deamination activity and processivity of A3G. on long ssDNA regions. This resembles the “hit and run” single base substitution events observed in yeast., we propose that RPA plays a role in the protection of the human genome cell from A3G and other deaminases when they are inadvertently diverged from their natural targets. We propose a model where RPA serves as one of the guardians of the genome that protects ssDNA from the destructive processive activity of deaminases by non-specific steric hindrance
Evolutionary Conservation of the Functional Modularity of Primate and Murine LINE-1 Elements
LINE-1 (L1) retroelements emerged in mammalian genomes over 80 million years ago with a few dominant subfamilies amplifying over discrete time periods that led to distinct human and mouse L1 lineages. We evaluated the functional conservation of L1 sequences by comparing retrotransposition rates of chimeric human-rodent L1 constructs to their parental L1 counterparts. Although amino acid conservation varies from ∼35% to 63% for the L1 ORF1p and ORF2p, most human and mouse L1 sequences can be functionally exchanged. Replacing either ORF1 or ORF2 to create chimeric human-mouse L1 elements did not adversely affect retrotransposition. The mouse ORF2p retains retrotransposition-competency to support both Alu and L1 mobilization when any of the domain sequences we evaluated were substituted with human counterparts. However, the substitution of portions of the mouse cys-domain into the human ORF2p reduces both L1 retrotransposition and Alu trans-mobilization by 200–1000 fold. The observed loss of ORF2p function is independent of the endonuclease or reverse transcriptase activities of ORF2p and RNA interaction required for reverse transcription. In addition, the loss of function is physically separate from the cysteine-rich motif sequence previously shown to be required for RNP formation. Our data suggest an additional role of the less characterized carboxy-terminus of the L1 ORF2 protein by demonstrating that this domain, in addition to mediating RNP interaction(s), provides an independent and required function for the retroelement amplification process. Our experiments show a functional modularity of most of the LINE sequences. However, divergent evolution of interactions within L1 has led to non-reciprocal incompatibilities between human and mouse ORF2 cys-domain sequences
Study of the ZZ\gamma and Z\gamma\gamma Couplings in Z(\nu\nu)\gamma Production
We have measured the ZZ-gamma and Z-gamma-gamma couplings by studying p-bar p
-> (missing ET) gamma + X events at sqrt(s)=1.8 TeV with the D0 detector at the
Fermilab Tevatron Collider. This first study of hadronic Z-gamma production in
the neutrino decay channel gives the most stringent limits on anomalous
couplings available. A fit to the transverse energy spectrum of the photon in
the candidate event sample, based on a data set corresponding to an integrated
luminosity of 13.1 pb^(-1), yields 95% CL limits on the anomalous CP-conserving
ZZ-gamma couplings of |h^Z_(30)|<0.9, |h^Z_(40)|<0.21, for a form-factor scale
Lambda = 500 GeV. Combining these results with our previous measurement using Z
-> ee and mu-mu yields the limits:|h^Z_(30)|<0.8, |h^Z_(40)|<0.19 (Lambda = 500
GeV) and |h^Z_(30)|<0.4, |h^Z_(40)|<0.06 (Lambda = 750 GeV).Comment: 10 pages, 2 figures, 2 table
Studies of Gauge Boson Pair Production and Trilinear Couplings
The gauge boson pair production processes Wg, WW, WZ, and Zg were studied
using pbarp collisions corresponding to an integrated luminosity of ~14 pb-1 at
a center-of-mass energy of sqrt(s) = 1.8 TeV. Analysis of Wg prod with
subsequent W boson decay to lv (l=e,mu) is reported, including a fit to the pT
spectrum of the photons which leads to limits on anomalous WWg couplings. A
search for WW prod with subsequent decay to l-lbar-v-vbar (l=e,mu) is presented
leading to an upper limit on the WW prod cross section and limits on anomalous
WWg and WWZ couplings. A search for high pT W bosons in WW and WZ prod is
described, where one W boson decays to an ev and the second W boson or the Z
boson decays to two jets. A maximum likelihood fit to the pT spectrum of W
bosons resulted in limits on anomalous WWg and WWZ couplings. A combined fit to
the three data sets which provided the tightest limits on anomalous WWg and WWZ
couplings is also described. Limits on anomalous ZZg and Zgg couplings are
presented from an analysis of the photon ET spectrum in Zg events in the decay
channels (ee, mu-mu, and v-vbar) of the Z boson.Comment: 77 Pages including 40 Figures. Submitted to PR
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