204 research outputs found

    Studying the Underlying Event in Drell-Yan and High Transverse Momentum Jet Production at the Tevatron

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    We study the underlying event in proton-antiproton collisions by examining the behavior of charged particles (transverse momentum pT > 0.5 GeV/c, pseudorapidity |\eta| < 1) produced in association with large transverse momentum jets (~2.2 fb-1) or with Drell-Yan lepton-pairs (~2.7 fb-1) in the Z-boson mass region (70 < M(pair) < 110 GeV/c2) as measured by CDF at 1.96 TeV center-of-mass energy. We use the direction of the lepton-pair (in Drell-Yan production) or the leading jet (in high-pT jet production) in each event to define three regions of \eta-\phi space; toward, away, and transverse, where \phi is the azimuthal scattering angle. For Drell-Yan production (excluding the leptons) both the toward and transverse regions are very sensitive to the underlying event. In high-pT jet production the transverse region is very sensitive to the underlying event and is separated into a MAX and MIN transverse region, which helps separate the hard component (initial and final-state radiation) from the beam-beam remnant and multiple parton interaction components of the scattering. The data are corrected to the particle level to remove detector effects and are then compared with several QCD Monte-Carlo models. The goal of this analysis is to provide data that can be used to test and improve the QCD Monte-Carlo models of the underlying event that are used to simulate hadron-hadron collisions.Comment: Submitted to Phys.Rev.

    Measurement of the W+WW^+W^- Production Cross Section and Search for Anomalous WWγWW\gamma and WWZWWZ Couplings in ppˉp \bar p Collisions at s=1.96\sqrt{s} = 1.96 TeV

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    This Letter describes the current most precise measurement of the WW boson pair production cross section and most sensitive test of anomalous WWγWW\gamma and WWZWWZ couplings in ppˉp \bar p collisions at a center-of-mass energy of 1.96 TeV. The WWWW candidates are reconstructed from decays containing two charged leptons and two neutrinos, where the charged leptons are either electrons or muons. Using data collected by the CDF II detector from 3.6 fb1^{-1} of integrated luminosity, a total of 654 candidate events are observed with an expected background contribution of 320±47320 \pm 47 events. The measured total cross section is σ(ppˉW+W+X)=12.1±0.9(stat)1.4+1.6(syst)\sigma (p \bar p \to W^+ W^- + X) = 12.1 \pm 0.9 \textrm{(stat)} ^{+1.6}_{-1.4} \textrm{(syst)} pb, which is in good agreement with the standard model prediction. The same data sample is used to place constraints on anomalous WWγWW\gamma and WWZWWZ couplings.Comment: submitted to Phys. Rev. Let

    Study of CP violation in Dalitz-plot analyses of B0 --> K+K-KS, B+ --> K+K-K+, and B+ --> KSKSK+

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    We perform amplitude analyses of the decays B0K+KKS0B^0 \to K^+K^-K^0_S, B+K+KK+B^+ \rightarrow K^+K^-K^+, and B+KS0KS0K+B^+ \to K^0_S K^0_S K^+, and measure CP-violating parameters and partial branching fractions. The results are based on a data sample of approximately 470×106470\times 10^6 BBˉB\bar{B} decays, collected with the BABAR detector at the PEP-II asymmetric-energy BB factory at the SLAC National Accelerator Laboratory. For B+K+KK+B^+ \to K^+K^-K^+, we find a direct CP asymmetry in B+ϕ(1020)K+B^+ \to \phi(1020)K^+ of ACP=(12.8±4.4±1.3)A_{CP}= (12.8\pm 4.4 \pm 1.3)%, which differs from zero by 2.8σ2.8 \sigma. For B0K+KKS0B^0 \to K^+K^-K^0_S, we measure the CP-violating phase βeff(ϕ(1020)KS0)=(21±6±2)\beta_{\rm eff} (\phi(1020)K^0_S) = (21\pm 6 \pm 2)^\circ. For B+KS0KS0K+B^+ \to K^0_S K^0_S K^+, we measure an overall direct CP asymmetry of ACP=(45+4±2)A_{CP} = (4 ^{+4}_{-5} \pm 2)%. We also perform an angular-moment analysis of the three channels, and determine that the fX(1500)f_X(1500) state can be described well by the sum of the resonances f0(1500)f_0(1500), f2(1525)f_2^{\prime}(1525), and f0(1710)f_0(1710).Comment: 35 pages, 68 postscript figures. v3 - minor modifications to agree with published versio

    Impact of cognitive stimulation on ripples within human epileptic and non-epileptic hippocampus

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    Background: Until now there has been no way of distinguishing between physiological and epileptic hippocampal ripples in intracranial recordings. In the present study we addressed this by investigating the effect of cognitive stimulation on interictal high frequency oscillations in the ripple range (80-250 Hz) within epileptic (EH) and non-epileptic hippocampus (NH). Methods: We analyzed depth EEG recordings in 10 patients with intractable epilepsy, in whom hippocampal activity was recorded initially during quiet wakefulness and subsequently during a simple cognitive task. Using automated detection of ripples based on amplitude of the power envelope, we analyzed ripple rate (RR) in the cognitive and resting period, within EH and NH. Results: Compared to quiet wakefulness we observed a significant reduction of RR during cognitive stimulation in EH, while it remained statistically marginal in NH. Further, we investigated the direct impact of cognitive stimuli on ripples (i.e. immediately post-stimulus), which showed a transient statistically significant suppression of ripples in the first second after stimuli onset in NH only. Conclusion: Our results point to a differential reactivity of ripples within EH and NH to cognitive stimulation

    Malaria Parasite Invasion of the Mosquito Salivary Gland Requires Interaction between the Plasmodium TRAP and the Anopheles Saglin Proteins

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    SM1 is a twelve-amino-acid peptide that binds tightly to the Anopheles salivary gland and inhibits its invasion by Plasmodium sporozoites. By use of UV-crosslinking experiments between the peptide and its salivary gland target protein, we have identified the Anopheles salivary protein, saglin, as the receptor for SM1. Furthermore, by use of an anti-SM1 antibody, we have determined that the peptide is a mimotope of the Plasmodium sporozoite Thrombospondin Related Anonymous Protein (TRAP). TRAP binds to saglin with high specificity. Point mutations in TRAP's binding domain A abrogate binding, and binding is competed for by the SM1 peptide. Importantly, in vivo down-regulation of saglin expression results in strong inhibition of salivary gland invasion. Together, the results suggest that saglin/TRAP interaction is crucial for salivary gland invasion by Plasmodium sporozoites

    Virtual Partner Interaction (VPI): Exploring Novel Behaviors via Coordination Dynamics

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    Inspired by the dynamic clamp of cellular neuroscience, this paper introduces VPI—Virtual Partner Interaction—a coupled dynamical system for studying real time interaction between a human and a machine. In this proof of concept study, human subjects coordinate hand movements with a virtual partner, an avatar of a hand whose movements are driven by a computerized version of the Haken-Kelso-Bunz (HKB) equations that have been shown to govern basic forms of human coordination. As a surrogate system for human social coordination, VPI allows one to examine regions of the parameter space not typically explored during live interactions. A number of novel behaviors never previously observed are uncovered and accounted for. Having its basis in an empirically derived theory of human coordination, VPI offers a principled approach to human-machine interaction and opens up new ways to understand how humans interact with human-like machines including identification of underlying neural mechanisms

    A Complete Pathway Model for Lipid A Biosynthesis in Escherichia coli.

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    Lipid A is a highly conserved component of lipopolysaccharide (LPS), itself a major component of the outer membrane of Gram-negative bacteria. Lipid A is essential to cells and elicits a strong immune response from humans and other animals. We developed a quantitative model of the nine enzyme-catalyzed steps of Escherichia coli lipid A biosynthesis, drawing parameters from the experimental literature. This model accounts for biosynthesis regulation, which occurs through regulated degradation of the LpxC and WaaA (also called KdtA) enzymes. The LpxC degradation signal appears to arise from the lipid A disaccharide concentration, which we deduced from prior results, model results, and new LpxK overexpression results. The model agrees reasonably well with many experimental findings, including the lipid A production rate, the behaviors of mutants with defective LpxA enzymes, correlations between LpxC half-lives and cell generation times, and the effects of LpxK overexpression on LpxC concentrations. Its predictions also differ from some experimental results, which suggest modifications to the current understanding of the lipid A pathway, such as the possibility that LpxD can replace LpxA and that there may be metabolic channeling between LpxH and LpxB. The model shows that WaaA regulation may serve to regulate the lipid A production rate when the 3-deoxy-D-manno-oct-2-ulosonic acid (KDO) concentration is low and/or to control the number of KDO residues that get attached to lipid A. Computation of flux control coefficients showed that LpxC is the rate-limiting enzyme if pathway regulation is ignored, but that LpxK is the rate-limiting enzyme if pathway regulation is present, as it is in real cells. Control also shifts to other enzymes if the pathway substrate concentrations are not in excess. Based on these results, we suggest that LpxK may be a much better drug target than LpxC, which has been pursued most often
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