Precision measurement of the B0s-B¯0s oscillation frequency with the decay B0s → D−sπ+

A key ingredient to searches for physics beyond the Standard Model in B0s mixing phenomena is the measurement of the B0s– ${{\overline{ {\mathrm {B}}}{}}^0_{\mathrm { s}}}$ oscillation frequency, which is equivalent to the mass difference Δms of the B0s mass eigenstates. Using the world's largest B0s meson sample accumulated in a dataset, corresponding to an integrated luminosity of 1.0 fb−1, collected by the LHCb experiment at the CERN LHC in 2011, a measurement of Δms is presented. A total of about 34 000 B0s → D−sπ+ signal decays are reconstructed, with an average decay time resolution of 44 fs. The oscillation frequency is measured to be Δms = 17.768 ± 0.023 (stat) ± 0.006 (syst) ps−1, which is the most precise measurement to date

Differential branching fraction and angular analysis of the decay B s0 → φμ + μ -

The determination of the differential branching fraction and the first angular analysis of the decay Bs0 → φμ + μ - are presented using data, corresponding to an integrated luminosity of 1.0 fb-1, collected by the LHCb experiment at √s=7 TeV. The differential branching fraction is determined in bins of q 2, the invariant dimuon mass squared. Integration over the full q 2 range yields a total branching fraction of B (Bs0 → φμ + μ -(7.07 -0.59+0.64± 0.71± 0.71) × 10 -7, where the first uncertainty is statistical, the second systematic, and the third originates from the branching fraction of the normalisation channel. An angular analysis is performed to determine the angular observables F L, S 3, A 6, and A 9. The observables are consistent with Standard Model expectations. [Figure not available: see fulltext.] © 2013 CERN for the benefit of the LHCb collaboration

Observation of B_{c}^{+}→J/ψD_{s}^{+} and B_{c}^{+}→J/ψD_{s}^{*+} decays

The decays B+c→J/ψD+s and B+c→J/ψD*+s are observed for the first time using a dataset, corresponding to an integrated luminosity of 3  fb−1, collected by the LHCb experiment in proton-proton collisions at center-of-mass energies of s√=7 and 8 TeV. The statistical significance for both signals is in excess of 9 standard deviations. The following ratios of branching fractions are measured to be B(B+c→J/ψD+s)B(B+c→J/ψπ+)=2.90±0.57±0.24, B(B+c→J/ψD*+s)B(B+c→J/ψD+s)=2.37±0.56±0.10, where the first uncertainties are statistical and the second systematic. The mass of the B+c meson is measured to be mB+c=6276.28±1.44(stat)±0.36(syst)  MeV/c2, using the B+c→J/ψD+s decay mode

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

Measurement of Υ Production in pp Collisions at √s = 2.76 TeV

The production of Υ(1S), Υ(2S) and Υ(3S) mesons decaying into the dimuon final state is studied with the LHCb detector using a data sample corresponding to an integrated luminosity of 3.3 pb^−1 collected in proton–proton collisions at a centre-of-mass energy of √s = 2.76 TeV. The differential production cross-sections times dimuon branching fractions are measured as functions of the Υ transverse momentum and rapidity, over the ranges p_T < 15 GeV/c and 2.0 < y < 4.5. The total cross-sections in this kinematic region, assuming unpolarised production, are measured to be σ(pp → Υ(1S) X) × B(Υ(1S) → μ+ μ−) = 1.111 ± 0.043 ± 0.044 nb, σ(pp → Υ(2S) X) × B(Υ(2S) → μ+ μ−) = 0.264 ± 0.023 ± 0.011 nb, σ(pp → Υ(3S) X) × B(Υ(3S) → μ+ μ−) = 0.159 ± 0.020 ± 0.007 nb, where the first uncertainty is statistical and the second systematic

The drugs don't work-or do they? Pharmacological and transgenic studies of the contribution of NMDA and GluR-A-containing AMPA receptors to hippocampal-dependent memory.

OBJECTIVE: The aim of this article is to provide a review of studies using N-methyl-D-aspartate (NMDA) receptor antagonists to assess the hippocampal long-term potentiation (LTP)/learning hypothesis. DISCUSSION: In particular, we will re-examine the validity of both (1) the original hippocampal LTP/spatial learning hypothesis of Morris and (2) the sensorimotor account put forward by Cain, among others, both from the point of view of the pharmacological studies on which they were based and with regard to recent studies with genetically modified mice. More specifically, we will review the pharmacological studies in the light of recent work on the glutamate receptor A (GluR-A or GluR1) L-alpha-amino-3-hydroxy-5-methyl-4-isoxazelopropionate (AMPA) receptor sub-unit knockout mouse. We will argue that neither the original hippocampal LTP/spatial learning hypothesis nor a sensorimotor account can adequately explain all of the available data. We argue instead that hippocampal synaptic plasticity, which requires NMDA receptors for its induction and GluR-A-containing AMPA receptors for its continued expression, contributes to a process whereby appropriate behavioural responses are selected rapidly on the basis of conditional information provided by the context. These contextual cues could include not only the spatial context (i.e. the 'where') and the temporal context (the 'when'), but also other aspects of context, such as internal state cues (hunger and fear state), and can be used to rapidly and flexibly alter valences of specific response options. RECOMMENDATIONS: We also suggest that there is a separate, distinct, NMDA/GluR-A-independent mechanism through which the context can gradually (incrementally or decrementally) alter the valence of a particular response option