69 research outputs found
Search for the standard model Higgs boson decaying to a pair in events with no charged leptons and large missing transverse energy using the full CDF data set
We report on a search for the standard model Higgs boson produced in
association with a vector boson in the full data set of proton-antiproton
collisions at TeV recorded by the CDF II detector at the
Tevatron, corresponding to an integrated luminosity of 9.45 fb. We
consider events having no identified charged lepton, a transverse energy
imbalance, and two or three jets, of which at least one is consistent with
originating from the decay of a quark. We place 95% credibility level upper
limits on the production cross section times standard model branching fraction
for several mass hypotheses between 90 and . For a Higgs
boson mass of , the observed (expected) limit is 6.7
(3.6) times the standard model prediction.Comment: Accepted by Phys. Rev. Let
Search for the standard model Higgs boson decaying to a bb pair in events with one charged lepton and large missing transverse energy using the full CDF data set
We present a search for the standard model Higgs boson produced in
association with a W boson in sqrt(s) = 1.96 TeV p-pbar collision data
collected with the CDF II detector at the Tevatron corresponding to an
integrated luminosity of 9.45 fb-1. In events consistent with the decay of the
Higgs boson to a bottom-quark pair and the W boson to an electron or muon and a
neutrino, we set 95% credibility level upper limits on the WH production cross
section times the H->bb branching ratio as a function of Higgs boson mass. At a
Higgs boson mass of 125 GeV/c2 we observe (expect) a limit of 4.9 (2.8) times
the standard model value.Comment: Submitted to Phys. Rev. Lett (v2 contains clarifications suggested by
PRL
Search for the standard model Higgs boson decaying to a bb pair in events with two oppositely-charged leptons using the full CDF data set
We present a search for the standard model Higgs boson produced in
association with a Z boson in data collected with the CDF II detector at the
Tevatron, corresponding to an integrated luminosity of 9.45/fb. In events
consistent with the decay of the Higgs boson to a bottom-quark pair and the Z
boson to electron or muon pairs, we set 95% credibility level upper limits on
the ZH production cross section times the H -> bb branching ratio as a function
of Higgs boson mass. At a Higgs boson mass of 125 GeV/c^2 we observe (expect) a
limit of 7.1 (3.9) times the standard model value.Comment: To be submitted to Phys. Rev. Let
Measurement of the forward-backward asymmetry in Λ0b and Λ¯0b baryon production in pp¯ collisions at s√=1.96 TeV
We measure the forward-backward asymmetry in the production of Λ0b and Λ¯0b baryons as a function of rapidity in pp¯ collisions at s√=1.96 TeV using 10.4 fb−1 of data collected with the D0 detector at the Fermilab Tevatron collider. The asymmetry is determined by the preference of Λ0b or Λ¯0b particles to be produced in the direction of the beam protons or antiprotons, respectively. The measured asymmetry integrated over rapidity y in the range 0.1<|y|<2.0 is A=0.04±0.07(stat)±0.02(syst)
The genetic architecture of the human cerebral cortex
INTRODUCTION
The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure.
RATIONALE
To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations.
RESULTS
We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness).
Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness.
To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity.
We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism.
CONCLUSION
This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function
Measurement of the difference of CP-violating asymmetries in D0 -> K+K- and D0 ->pi+pi- decays at CDF
We report a measurement of the difference (Delta Acp) between time-integrated
CP--violating asymmetries in D0-> K+ K- and D0-> pi+pi- decays reconstructed in
the full data set of proton-antiproton collisions collected by the Collider
Detector at Fermilab, corresponding to 9.7 fb-1 of integrated luminosity. The
strong decay D*+->D0 pi+ is used to identify the charm meson at production as
D0 or anti-D0. We measure Delta Acp = [-0.62 +- 0.21 (stat) +- 0.10 (syst)] %,
which differs from zero by 2.7 Gaussian standard deviations.This result
supports similar evidence for CP violation in charm-quark decays obtained in
proton-proton collisions.Comment: Phys. Rev. Lett. 109, 111801 (2012
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