55,160 research outputs found

    Measurement of the ratio of prompt χ c to J / ψ production in pp collisions at √s = 7 TeV

    No full text
    The prompt production of charmonium χ c and J / ψ states is studied in proton-proton collisions at a centre-of-mass energy of √s = 7 TeV at the Large Hadron Collider. The χ c and J / ψ mesons are identified through their decays χ c → J / ψ γ and J / ψ → μ + μ - using 36 pb - 1 of data collected by the LHCb detector in 2010. The ratio of the prompt production cross-sections for χ c and J / ψ, σ (χ c → J / ψ γ) / σ (J / ψ), is determined as a function of the J / ψ transverse momentum in the range 2 < p T J / ψ < 15 GeV / c. The results are in excellent agreement with next-to-leading order non-relativistic expectations and show a significant discrepancy compared with the colour singlet model prediction at leading order, especially in the low p T J / ψ region

    A 2 h periodic variation in the low-mass X-ray binary Ser X-1

    No full text
    Spectroscopy of the low-mass X-ray binary Ser X-1 using the Gran Telescopio Canarias have revealed a ?2 h periodic variability that is present in the three strongest emission lines. We tentatively interpret this variability as due to orbital motion, making it the first indication of the orbital period of Ser X-1. Together with the fact that the emission lines are remarkably narrow, but still resolved, we show that a main-sequence K dwarf together with a canonical 1.4 M? neutron star gives a good description of the system. In this scenario, the most likely place for the emission lines to arise is the accretion disc, instead of a localized region in the binary (such as the irradiated surface or the stream-impact point), and their narrowness is due instead to the low inclination (?10°) of Ser X-1

    Evidence for the decay B0→J/ψω and measurement of the relative branching fractions of meson decays to J/ψη and J/ψη′

    No full text
    First evidence of the B 0 → J / ψ ω decay is found and the B s 0 → J / ψ η and B s 0 → J / ψ η ′ decays are studied using a dataset corresponding to an integrated luminosity of 1.0 fb -1 collected by the LHCb experiment in proton-proton collisions at a centre-of-mass energy of sqrt(s) = 7 TeV. The branching fractions of these decays are measured relative to that of the B 0 → J / ψ ρ 0 decay:frac(B (B 0 → J / ψ ω), B (B 0 → J / ψ ρ 0)) = 0.89 ± 0.19 (stat) - 0.13 + 0.07 (syst),frac(B (B s 0 → J / ψ η), B (B 0 → J / ψ ρ 0)) = 14.0 ± 1.2 (stat) - 1.5 + 1.1 (syst) - 1.0 + 1.1 (frac(f d, f s)),frac(B (B s 0 → J / ψ η ′), B (B 0 → J / ψ ρ 0)) = 12.7 ± 1.1 (stat) - 1.3 + 0.5 (syst) - 0.9 + 1.0 (frac(f d, f s)), where the last uncertainty is due to the knowledge of f d / f s, the ratio of b-quark hadronization factors that accounts for the different production rate of B 0 and B s 0 mesons. The ratio of the branching fractions of B s 0 → J / ψ η ′ and B s 0 → J / ψ η decays is measured to befrac(B (B s 0 → J / ψ η ′), B (B s 0 → J / ψ η)) = 0.90 ± 0.09 (stat) - 0.02 + 0.06 (syst)

    Measurement of the Bs0J/ψKS0B_s^0\to J/\psi K_S^0 branching fraction

    No full text
    The B 0 s → J/ψK 0 S branching fraction is measured in a data sample corresponding to 0.41 fb−1 of integrated luminosity collected with the LHCb detector at the LHC. This channel is sensitive to the penguin contributions affecting the sin 2β measurement from B 0 → J/ψK 0 S . The time-integrated branching fraction is measured to be B(B 0 s → J/ψK 0 S ) = (1.83±0.28)×10−5 . This is the most precise measurement to date

    Measurement of the time-dependent CP asymmetry in B0 -> J/ψ KS0 decays

    No full text
    This Letter reports a measurement of the CP violation observables SJ/ψK0S and CJ/ψK0S in the decay channel B0→J/ψK0S performed with 1.0 fb−1 of pp collisions at s√=7 TeV collected by the LHCb experiment. The fit to the data yields SJ/ψK0S=0.73±0.07(stat)±0.04(syst) and CJ/ψK0S=0.03±0.09(stat)±0.01(syst). Both values are consistent with the current world averages and within expectations from the Standard Model

    Restless legs syndrome: diagnosis, treatment and pathophysiology

    No full text
    This cumulative dissertation presents four articles focussing on diagnosis, treatment and pathophysiology of the restless legs syndrome: 1) Fulda S, Beitinger ME, Reppermund S, Winkelmann J, Wetter TC. Short-term attention and verbal fluency is decreased in restless legs syndrome patients. Movement Disorders 2010; 25: 2641-2648. DOI 10.1002/mds.23353 2) Fulda S, Wetter TC. Where dopamine meets opioids: a meta-analysis of the placebo effect in restless legs syndrome treatment studies. Brain 2008; 131: 902-917. DOI 10.1093/brain/awm244 3) Fulda S, Stalla GK, Wetter TC. Prevalence of the restless legs syndrome in transsexual patients: the hormonal hypothesis revisited. Journal of Neurology 2007; 254: 1748-1749. DOI 10.1007/100415-007-0624-6 4) Winkelmann J, Schormaier B, Lichtner P, Ripke S, Xiong L, Jalilzadeh S, Fulda S, Pütz B, Eckstein G, Hauk S, Trenkwalder C, Zimprich A, Stiasny-Kolster K, Oertel W, Bachmann CG, Paulus W, Peglau I, Eisensehr I, Montplaisir J, Turecki G, Rouleau G, Gieger C, Illig T, Wichmann HE, Holsboer F, Müller-Myhsok B, Meitinger T. Genome-wide association study of restless legs syndrome identifies common variants in three genomic regions. Nat Genet 2007; 39(8): 1000-1006. DOI 10.1038/ng209

    Regulation of cell death in cancer - possible implications for immunotherapy

    No full text
    Since most anticancer therapies including immunotherapy trigger programmed cell death in cancer cells, defective cell death programs can lead to treatment resistance and tumor immune escape. Therefore, evasion of programmed cell death may provide one possible explanation as to why cancer immunotherapy has so far only shown modest clinical benefits for children with cancer. A better understanding of the molecular mechanisms that regulate sensitivity and resistance to programmed cell death is expected to open new perspectives for the development of novel experimental treatment strategies to enhance the efficacy of cancer immunotherapy in the future

    Observation of the Lambda(0)(b) -> J/psi p pi(-) decay

    No full text
    The first observation of the Cabibbo-suppressed decay Λ b → J/ψpπ is reported using a data sample of proton-proton collisions at 7 and 8 TeV, corresponding to an integrated luminosity of 3 fb-1. A prominent signal is observed and the branching fraction relative to the decay mode Λ b → J/ψpK is determined to be B (Λb → J / ψp π-/ B Λ b → J / ψp K- = 0.0824 ± 0.0025 stat ± 0.0042 syst. A search for direct CP violation is performed. The difference in the CP asymmetries between these two decays is found to be A CP (Λb → J / ψp π-) - A CP (Λb → J / ψp K-) = + 5.7 ± 2.4 stat ± 1.2 syst %, which is compatible with CP symmetry at the 2.2σ level. [Figure not available: see fulltext.] © 2014 The Author(s)

    Shifting the balance of mitochondrial apoptosis: therapeutic perspectives

    No full text
    Signaling via the intrinsic (mitochondrial) pathway of apoptosis represents one of the critical signal transduction cascades that control the regulation of cell death. This pathway is typically altered in human cancers, thereby providing a suitable target for therapeutic intervention. Members of the Bcl-2 family of proteins as well as cell survival signaling cascades such as the PI3K/Akt/mTOR pathway are involved in the regulation of mitochondria-mediated apoptosis. Therefore, further insights into the molecular mechanisms that form the basis for the control of mitochondria-mediated apoptosis will likely open new perspectives to bypass evasion of apoptosis and treatment resistance in human cancers

    Author Correction: Establishment and equilibrium levels of deleterious mutations in large populations (Scientific Reports, (2019), 9, 1, (10384), 10.1038/s41598-019-46803-7)

    No full text
    The original version of this Article contained errors. Affiliations 1 and 2 were reversed. Secondly, Affiliation 7 was incorrectly given as ‘Institute for Cellular and Molecular Medicine, Department of Immunology, and SAMRC Extramural Unit for Stem Cell Research and Therapy, Faculty of Health Sciences, University of Pretoria, Pretoria, 0084, South Africa’. Thirdly, an affiliation was omitted for the author Michael S. Pepper, which is now listed as Affiliation 8. Fourthly, Affiliation 1 was omitted for the author Johan W. Viljoen. Finally, Augustinus J. van Zyl was incorrectly affiliated with ‘Institute for Maternal and Child Health, IRCCS ‘Burlo Garofolo’, Trieste, Italy.’ The correct author affiliations are listed below: Affiliation 1: Department of Electrical, Electronic and Computer Engineering, EBIT, University of Pretoria, Pretoria 0028, South Africa Johan W. Viljoen and J. Pieter de Villiers Affiliation 2: Development, Research and Technology Department, Hensoldt Optronics, Centu..
    corecore