Averages of bb-hadron, cc-hadron, and τ\tau-lepton properties as of summer 2014

This article reports world averages of measurements of $b$-hadron, $c$-hadron, and $\tau$-lepton properties obtained by the Heavy Flavor Averaging Group (HFAG) using results available through summer 2014. For the averaging, common input parameters used in the various analyses are adjusted (rescaled) to common values, and known correlations are taken into account. The averages include branching fractions, lifetimes, neutral meson mixing parameters, $CP$ violation parameters, parameters of semileptonic decays and CKM matrix elements.Comment: 436 pages, many figures and tables. Online updates available at http://www.slac.stanford.edu/xorg/hfag

APOE-ε4 Shapes the Cerebral Organization in Cognitively Intact Individuals as Reflected by Structural Gray Matter Networks

Gray matter networks (GMn) provide essential information on the intrinsic organization of the brain and appear to be disrupted in Alzheimer’s disease (AD). Apolipoprotein E (APOE)-ε4 represents the major genetic risk factor for AD, yet the association between APOE-ε4 and GMn has remained unexplored. Here, we determine the impact of APOE-ε4 on GMn in a large sample of cognitively unimpaired individuals, which was enriched for the genetic risk of AD. We used independent component analysis to retrieve sources of structural covariance and analyzed APOE group differences within and between networks. Analyses were repeated in a subsample of amyloid-negative subjects. Compared with noncarriers and heterozygotes, APOE-ε4 homozygotes showed increased covariance in one network including primarily right-lateralized, parietal, inferior frontal, as well as inferior and middle temporal regions, which mirrored the formerly described AD-signature. This result was confirmed in a subsample of amyloid-negative individuals. APOE-ε4 carriers showed reduced covariance between two networks encompassing frontal and temporal regions, which constitute preferential target of amyloid deposition. Our data indicate that, in asymptomatic individuals, APOE-ε4 shapes the cerebral organization in a way that recapitulates focal morphometric alterations observed in AD patients, even in absence of amyloid pathology. This suggests that structural vulnerability in neuronal networks associated with APOE-ε4 may be an early event in AD pathogenesis, possibly upstream of amyloid deposition

The decay Bs -> mu+ mu-: updated SUSY constraints and prospects

We perform a study of the impact of the recently released limits on BR(Bs -> mu+ mu-) by LHCb and CMS on several SUSY models. We show that the obtained constraints can be superior to those which are derived from direct searches for SUSY particles in some scenarios, and the use of a double ratio of purely leptonic decays involving Bs -> mu+ mu- can further strengthen such constraints. We also discuss the experimental sensitivity and prospects for observation of Bs -> mu+ mu- during the sqrt(s)=7 TeV run of the LHC, and its potential implications.Comment: 30 pages, 21 figures. v2: Improved discussion of constraints from B -> tau nu, references adde

Mechanism of completion of peptidyltransferase centre assembly in eukaryotes.

During their final maturation in the cytoplasm, pre-60S ribosomal particles are converted to translation-competent large ribosomal subunits. Here, we present the mechanism of peptidyltransferase centre (PTC) completion that explains how integration of the last ribosomal proteins is coupled to release of the nuclear export adaptor Nmd3. Single-particle cryo-EM reveals that eL40 recruitment stabilises helix 89 to form the uL16 binding site. The loading of uL16 unhooks helix 38 from Nmd3 to adopt its mature conformation. In turn, partial retraction of the L1 stalk is coupled to a conformational switch in Nmd3 that allows the uL16 P-site loop to fully accommodate into the PTC where it competes with Nmd3 for an overlapping binding site (base A2971). Our data reveal how the central functional site of the ribosome is sculpted and suggest how the formation of translation-competent 60S subunits is disrupted in leukaemia-associated ribosomopathies.Bloodwise, MRC, Wellcome Trus

Observation of Two Resonant Structures in e+e- to pi+ pi- psi(2S) via Initial State Radiation at Belle

The cross section for e+e- to pi+ pi- psi(2S) between threshold and \sqrt{s}=5.5 GeV is measured using 673 fb^{-1} of data on and off the \Upsilon(4S) resonance collected with the Belle detector at KEKB. Two resonant structures are observed in the pi+ pi- psi(2S) invariant mass distribution, one at 4361\pm 9\pm 9 MeV/c2 with a width of 74\pm 15\pm 10 MeV/c2, and another at 4664\pm 11\pm 5 MeV/c2 with a width of 48\pm 15\pm 3 MeV/c2, if the mass spectrum is parameterized with the coherent sum of two Breit-Wigner functions. These values do not match those of any of the known charmonium states.Comment: 10 pages, 5 figures, 2 tables, version to appear in Phys. Rev. Let

Measurements of Charmless Hadronic b->s Penguin Decays in the pi+pi-K+pi- Final State and First Observation of B0 -> rho0K+pi-

We report measurements of charmless hadronic B^0 decays into the pi+pi-K+pi+ final state. The analysis uses a sample of 657x10^6 BBbar pairs collected with the Belle detector at the KEKB asymmetric-energy e+e- collider at the Y(4S) resonance. The decay B^0 -> rho0 Kpi is observed for the first time; the significance is 5.0sigma and the corresponding partial branching fraction for M_Kpi in (0.75,1.20) GeV/c^2 is [2.8 +- 0.5(stat) +-0.5(syst)] x 10^{-6}. We also obtain the first evidence for B^0 -> f0Kpi with 3.5sigma significance and for B^0 -> pi+pi-K*0 with 4.5sigma significance. For the two-body decays B^0 -> rho0K*0 and B^0 -> f0K*0, the significances are 2.7sigma and 2.5sigma, respectively, and the upper limits on the branching fractions are 3.4x10^{-6} and 2.2x10^{-6} at 90% confidence level.Comment: 6 pages, 3 figures. accepted by PRD(RC