Publications by authors named "Piacentino G"

We present a new measurement of the positive muon magnetic anomaly, a_{μ}≡(g_{μ}-2)/2, from the Fermilab Muon g-2 Experiment using data collected in 2019 and 2020. We have analyzed more than 4 times the number of positrons from muon decay than in our previous result from 2018 data. The systematic error is reduced by more than a factor of 2 due to better running conditions, a more stable beam, and improved knowledge of the magnetic field weighted by the muon distribution, ω[over ˜]_{p}^{'}, and of the anomalous precession frequency corrected for beam dynamics effects, ω_{a}.

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Article Synopsis
  • The Higgs boson, crucial for the standard model of particle physics, helps mediate the weak force between elementary particles, and its mass is closely regulated by the model's symmetries.
  • Researchers measured the mass of the boson using data from proton-antiproton collisions at the Tevatron collider, accumulating about 4 million candidates to achieve a very precise measurement.
  • This new mass measurement shows a significant discrepancy with what is expected from the standard model, suggesting potential gaps in our current understanding of particle physics.
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We present the first results of the Fermilab National Accelerator Laboratory (FNAL) Muon g-2 Experiment for the positive muon magnetic anomaly a_{μ}≡(g_{μ}-2)/2. The anomaly is determined from the precision measurements of two angular frequencies. Intensity variation of high-energy positrons from muon decays directly encodes the difference frequency ω_{a} between the spin-precession and cyclotron frequencies for polarized muons in a magnetic storage ring.

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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline associated with the deposition of amyloid-β (Aβ) plaques, hyperphosphorylation of tau protein, and neuronal loss. Vascular inflammation and leukocyte trafficking may contribute to AD pathogenesis, and a better understanding of these inflammation mechanisms could therefore facilitate the development of new AD therapies. Here we show that T cells extravasate in the proximity of cerebral VCAM-1 vessels in 3xTg-AD transgenic mice, which develop both Aβ and tau pathologies.

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A search for the exotic meson X(5568) decaying into the B_{s}^{0}π^{±} final state is performed using data corresponding to 9.6  fb^{-1} from pp[over ¯] collisions at sqrt[s]=1960  GeV recorded by the Collider Detector at Fermilab. No evidence for this state is found and an upper limit of 6.

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The CDF and D0 experiments at the Fermilab Tevatron have measured the asymmetry between yields of forward- and backward-produced top and antitop quarks based on their rapidity difference and the asymmetry between their decay leptons. These measurements use the full data sets collected in proton-antiproton collisions at a center-of-mass energy of sqrt[s]=1.96  TeV.

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Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by the pathological accumulation of amyloid beta (Aβ) peptides and neurofibrillary tangles containing hyperphosphorylated neuronal tau protein. AD pathology is also characterized by chronic brain inflammation, which promotes disease pathogenesis. In this context, the blood-brain barrier (BBB), a highly specialized endothelial cell membrane that lines cerebral microvessels, represents the interface between neural cells and circulating cells of the immune system.

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Article Synopsis
  • * The measured t-channel cross section is σ_{t}=2.25_{-0.31}^{+0.29} pb, along with a two-dimensional analysis of s- and t-channel cross sections.
  • * The combined s+t channel cross section is σ_{s+t}=3.30_{-0.40}^{+0.52} pb, and the measurement of the top-to-bottom quark coupling yields |V_{tb}|=1.02_{-0.
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We report on a search for charged massive resonances decaying to top (t) and bottom (b) quarks in the full data set of proton-antiproton collisions at a center-of-mass energy of √[s]=1.96  TeV collected by the CDF II detector at the Tevatron, corresponding to an integrated luminosity of 9.5  fb(-1).

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Inflammation is a pathological hallmark of Alzheimer's disease, and innate immune cells have been shown to contribute to disease pathogenesis. In two transgenic models of Alzheimer's disease (5xFAD and 3xTg-AD mice), neutrophils extravasated and were present in areas with amyloid-β (Aβ) deposits, where they released neutrophil extracellular traps (NETs) and IL-17. Aβ42 peptide triggered the LFA-1 integrin high-affinity state and rapid neutrophil adhesion to integrin ligands.

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Combined constraints from the CDF and D0 Collaborations on models of the Higgs boson with exotic spin J and parity P are presented and compared with results obtained assuming the standard model value JP=0+. Both collaborations analyzed approximately 10  fb(-) of proton-antiproton collisions with a center-of-mass energy of 1.96 TeV collected at the Fermilab Tevatron.

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A search for particles with the same mass and couplings as those of the standard model Higgs boson but different spin and parity quantum numbers is presented. We test two specific alternative Higgs boson hypotheses: a pseudoscalar Higgs boson with spin-parity J^{P}=0^{-} and a gravitonlike Higgs boson with J^{P}=2^{+}, assuming for both a mass of 125  GeV/c^{2}. We search for these exotic states produced in association with a vector boson and decaying into a bottom-antibottom quark pair.

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  • The study presents measurements of CP-violating asymmetries in the decay of neutral bottom hadrons at the Fermilab Tevatron using upgraded detector technology and a significant dataset.
  • Two specific decay processes were analyzed: Λ(b)⁰ decaying to pπ⁻ and pK⁻, showing no significant asymmetry in their measurements.
  • In contrast, notable CP-violating asymmetries were identified in the decays of B(s)⁰ to K⁻π⁺ and B⁰ to K⁺π⁻, aligning with existing world averages and confirming significant deviations from zero.
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We measure the inclusive forward-backward asymmetry of the charged-lepton pseudorapidities from top-quark pairs produced in proton-antiproton collisions and decaying to final states that contain two charged leptons (electrons or muons). The data are collected with the Collider Detector at Fermilab and correspond to an integrated luminosity of 9.1 fb(-1).

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  • A search was conducted for the production of single top quarks via an s-channel virtual W boson, analyzing events with imbalanced transverse energy, b-tagged jets, and no leptons.
  • This study measured a cross section of 1.12 pb (with uncertainty) for this process, achieving a significance of 1.9 standard deviations.
  • The results were combined with another method involving imbalanced transverse momentum, b-tagged jets, and one lepton, yielding a higher cross section of 1.36 pb and a significance of 4.2 standard deviations.
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We report evidence for s-channel single-top-quark production in proton-antiproton collisions at center-of-mass energy sqrt[s] = 1.96 TeV using a data set that corresponds to an integrated luminosity of 9.4 fb(-1) collected by the Collider Detector at Fermilab.

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We report the first observation of single-top-quark production in the s channel through the combination of the CDF and D0 measurements of the cross section in proton-antiproton collisions at a center-of-mass energy of 1.96 TeV. The data correspond to total integrated luminosities of up to 9.

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We present a measurement of the ratio of the top-quark branching fractions R=B(t→Wb)/B(t→Wq), where q represents any quark flavor, in events with two charged leptons, imbalance in total transverse energy, and at least two jets. The measurement uses proton-antiproton collision data at center-of-mass energy 1.96 TeV, corresponding to an integrated luminosity of 8.

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Selectins play a central role in leukocyte trafficking by mediating tethering and rolling on vascular surfaces. Here we have reported that T cell immunoglobulin and mucin domain 1 (TIM-1) is a P-selectin ligand. We have shown that human and murine TIM-1 binds to P-selectin, and that TIM-1 mediates tethering and rolling of T helper 1 (Th1) and Th17, but not Th2 and regulatory T cells on P-selectin.

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A search for forbidden and exotic Z boson decays in the diphoton mass spectrum is presented for the first time in hadron collisions, based on data corresponding to 10.0 fb(-1) of integrated luminosity from proton-antiproton collisions at √s = 1.96 TeV collected by the CDF experiment.

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We measure the time dependence of the ratio of decay rates for D0→K(+)π(-) to the Cabibbo-favored decay D(0)→K(-)π(+). The charge conjugate decays are included. A signal of 3.

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We present a measurement of the total decay width of the top quark using events with top-antitop quark pair candidates reconstructed in the final state with one charged lepton and four or more hadronic jets. We use the full Tevatron run II data set of sqrt[s]=1.96  TeV proton-antiproton collisions recorded by the CDF II detector.

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We report a measurement of the differential cross section dσ/d(cosθ(t)) for top-quark pair production as a function of the top-quark production angle in proton-antiproton collisions at sqrt[s] = 1.96 TeV. This measurement is performed using data collected with the CDF II detector at the Tevatron, corresponding to an integrated luminosity of 9.

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Regulatory T cells (Tregs) maintain tolerance toward self-antigens and suppress autoimmune diseases, although the underlying molecular mechanisms are unclear. In this study, we show that mice deficient for P-selectin glycoprotein ligand-1 (PSGL-1) develop a more severe form of experimental autoimmune encephalomyelitis than wild type animals do, suggesting that PSGL-1 has a role in the negative regulation of autoimmunity. We found that Tregs lacking PSGL-1 were unable to suppress experimental autoimmune encephalomyelitis and failed to inhibit T cell proliferation in vivo in the lymph nodes.

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We report on a measurement of the cross section for direct-photon production in association with a heavy quark using the full data set of sqrt[s]=1.96  TeV proton-antiproton collisions corresponding to 9.1  fb-1 of integrated luminosity collected by the CDF II detector at the Fermilab Tevatron.

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