196 research outputs found
Search for Third Generation Vector Leptoquarks in p anti-p Collisions at sqrt(s) = 1.96 TeV
We describe a search for a third generation vector leptoquark (VLQ3) that
decays to a b quark and tau lepton using the CDF II detector and 322 pb^(-1) of
integrated luminosity from the Fermilab Tevatron. Vector leptoquarks have been
proposed in many extensions of the standard model (SM). Observing a number of
events in agreement with SM expectations, assuming Yang-Mills (minimal)
couplings, we obtain the most stringent upper limit on the VLQ3 pair production
cross section of 344 fb (493 fb) and lower limit on the VLQ3 mass of 317
GeV/c^2 (251 GeV/c^2) at 95% C.L.Comment: 7 pages, 2 figures, submitted to PR
Observation of Exclusive Gamma Gamma Production in p pbar Collisions at sqrt{s}=1.96 TeV
We have observed exclusive \gamma\gamma production in proton-antiproton
collisions at \sqrt{s}=1.96 TeV, using data from 1.11 \pm 0.07 fb^{-1}
integrated luminosity taken by the Run II Collider Detector at Fermilab. We
selected events with two electromagnetic showers, each with transverse energy
E_T > 2.5 GeV and pseudorapidity |\eta| < 1.0, with no other particles detected
in -7.4 < \eta < +7.4. The two showers have similar E_T and azimuthal angle
separation \Delta\phi \sim \pi; 34 events have two charged particle tracks,
consistent with the QED process p \bar{p} to p + e^+e^- + \bar{p} by two-photon
exchange, while 43 events have no charged tracks. The number of these events
that are exclusive \pi^0\pi^0 is consistent with zero and is < 15 at 95% C.L.
The cross section for p\bar{p} to p+\gamma\gamma+\bar{p} with |\eta(\gamma)| <
1.0 and E_T(\gamma) > 2.5$ GeV is
2.48^{+0.40}_{-0.35}(stat)^{+0.40}_{-0.51}(syst) pb.Comment: 7 pages, 4 figure
Effect of natalizumab on disease progression in secondary progressive multiple sclerosis (ASCEND). a phase 3, randomised, double-blind, placebo-controlled trial with an open-label extension
Background: Although several disease-modifying treatments are available for relapsing multiple sclerosis, treatment effects have been more modest in progressive multiple sclerosis and have been observed particularly in actively relapsing subgroups or those with lesion activity on imaging. We sought to assess whether natalizumab slows disease progression in secondary progressive multiple sclerosis, independent of relapses. Methods: ASCEND was a phase 3, randomised, double-blind, placebo-controlled trial (part 1) with an optional 2 year open-label extension (part 2). Enrolled patients aged 18–58 years were natalizumab-naive and had secondary progressive multiple sclerosis for 2 years or more, disability progression unrelated to relapses in the previous year, and Expanded Disability Status Scale (EDSS) scores of 3·0–6·5. In part 1, patients from 163 sites in 17 countries were randomly assigned (1:1) to receive 300 mg intravenous natalizumab or placebo every 4 weeks for 2 years. Patients were stratified by site and by EDSS score (3·0–5·5 vs 6·0–6·5). Patients completing part 1 could enrol in part 2, in which all patients received natalizumab every 4 weeks until the end of the study. Throughout both parts, patients and staff were masked to the treatment received in part 1. The primary outcome in part 1 was the proportion of patients with sustained disability progression, assessed by one or more of three measures: the EDSS, Timed 25-Foot Walk (T25FW), and 9-Hole Peg Test (9HPT). The primary outcome in part 2 was the incidence of adverse events and serious adverse events. Efficacy and safety analyses were done in the intention-to-treat population. This trial is registered with ClinicalTrials.gov, number NCT01416181. Findings: Between Sept 13, 2011, and July 16, 2015, 889 patients were randomly assigned (n=440 to the natalizumab group, n=449 to the placebo group). In part 1, 195 (44%) of 439 natalizumab-treated patients and 214 (48%) of 448 placebo-treated patients had confirmed disability progression (odds ratio [OR] 0·86; 95% CI 0·66–1·13; p=0·287). No treatment effect was observed on the EDSS (OR 1·06, 95% CI 0·74–1·53; nominal p=0·753) or the T25FW (0·98, 0·74–1·30; nominal p=0·914) components of the primary outcome. However, natalizumab treatment reduced 9HPT progression (OR 0·56, 95% CI 0·40–0·80; nominal p=0·001). In part 1, 100 (22%) placebo-treated and 90 (20%) natalizumab-treated patients had serious adverse events. In part 2, 291 natalizumab-continuing patients and 274 natalizumab-naive patients received natalizumab (median follow-up 160 weeks [range 108–221]). Serious adverse events occurred in 39 (13%) patients continuing natalizumab and in 24 (9%) patients initiating natalizumab. Two deaths occurred in part 1, neither of which was considered related to study treatment. No progressive multifocal leukoencephalopathy occurred. Interpretation: Natalizumab treatment for secondary progressive multiple sclerosis did not reduce progression on the primary multicomponent disability endpoint in part 1, but it did reduce progression on its upper-limb component. Longer-term trials are needed to assess whether treatment of secondary progressive multiple sclerosis might produce benefits on additional disability components. Funding: Biogen
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.
Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field
Search for exclusive Z boson production and observation of high mass ppbar->gammagamma->p+ll+pbar events in ppbar collisions at sqrt(s) = 1.96 TeV
submitted to Phys. Rev. LettWe present a search for exclusive Z boson production in proton-antiproton collisions at sqrt(s) = 1.96 TeV, using the CDF II detector at Fermilab. We observe no exclusive Z->ll candidates and place the first upper limit on the exclusive Z cross section in hadron collisions, sigma(exclu) gammagamma->p+ll+pbar, and measure the cross section for M(ll) > 40 GeV/c2 and |eta(l)|This Letter presents a search for exclusive Z boson production in proton-antiproton collisions at √s=1.96 TeV, using the CDF II detector. No exclusive Z→l+l- candidates are observed and the first upper limit on the exclusive Z cross section in hadron collisions is found to be σexcl(Z)40 GeV/c2 and |ηl|<4 is found to be σ=0.24-0.10+0.13 pb, which is consistent with the standard model prediction.Peer reviewe
Search for high-mass diphoton states and limits on Randall-Sundrum gravitons at CDF
We have performed a search for new particles which decay to two photons using 1.2 fb(-1) of integrated luminosity from p (p) over bar collisions at root s = 1.96 TeV collected using the CDF II detector at the Fermilab Tevatron. We find the diphoton mass spectrum to be in agreement with the standard model expectation, and set limits on the cross section times branching ratio for the Randall-Sundrum graviton, as a function of diphoton mass. We subsequently derive lower limits for the graviton mass of 230 GeV/c(2) and 850 GeV/c(2), at the 95% confidence level, for coupling parameters (k=(M) over barP(1)) of 0.01 and 0.1, respectively
Observation of B-s(0)-\u3e K+K- and measurements of branching fractions of charmless two-body decays of B-0 and B-s(0) mesons in pp collisions at root s=1.96 TeV
We search for decays of the type B-(s)(0)-\u3e h(+)h(\u27-) (where h,h(\u27)=K or pi) in 180 pb(-1) of (p) over barp collisions collected at the Tevatron by the upgraded Collider Detector at Fermilab. We report the first observation of the new mode B-s(0)-\u3e K+K- with a yield of 236 +/- 32 events, corresponding to (f(s)/f(d))xB(B-s(0)-\u3e K+K-)/B(B-0 -\u3e K+pi(-))=0.46 +/- 0.08(stat)+/- 0.07(syst), where f(s)/f(d) is the ratio of production fractions of B-s(0) and B-0. We find results in agreement with world averages for the B-0 modes, and set the following new limits at 90% C.L.: B(B-s(0)-\u3e K-pi(+))\u3c 5.6x10(-6) and B(B-s(0)-\u3epi(+)pi(-))\u3c 1.7x10(-6)
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