The clustering of ultra-high energy cosmic rays and their sources

The sky distribution of cosmic rays with energies above the 'GZK cutoff' holds important clues to their origin. The AGASA data, although consistent with isotropy, shows evidence for small-angle clustering, and it has been argued that such clusters are aligned with BL Lacertae objects, implicating these as sources. It has also been suggested that clusters can arise if the cosmic rays come from the decays of very massive relic particles in the Galactic halo, due to the expected clumping of cold dark matter. We examine these claims and show that both are in fact not justified.Comment: 13 pages, 8 figures, version in press at Phys. Rev.

Search for TeV Scale Physics in Heavy Flavour Decays

The subject of heavy flavour decays as probes for physics beyond the TeV scale is covered from the experimental perspective. Emphasis is placed on the more traditional Beyond the Standard Model topics that have potential for impact in the short term, with the physics explained. We do unabashedly promote our own phemonenology work.Comment: 10 pages, 9 figures (now fixed); Submitted for the SUSY07 proceeding

BB flavour tagging using charm decays at the LHCb experiment

An algorithm is described for tagging the flavour content at production of neutral $B$ mesons in the LHCb experiment. The algorithm exploits the correlation of the flavour of a $B$ meson with the charge of a reconstructed secondary charm hadron from the decay of the other $b$ hadron produced in the proton-proton collision. Charm hadron candidates are identified in a number of fully or partially reconstructed Cabibbo-favoured decay modes. The algorithm is calibrated on the self-tagged decay modes $B^+ \to J/\psi \, K^+$ and $B^0 \to J/\psi \, K^{*0}$ using $3.0\mathrm{\,fb}^{-1}$ of data collected by the LHCb experiment at $pp$ centre-of-mass energies of $7\mathrm{\,TeV}$ and $8\mathrm{\,TeV}$. Its tagging power on these samples of $B \to J/\psi \, X$ decays is $(0.30 \pm 0.01 \pm 0.01) \%$.Comment: All figures and tables, along with any supplementary material and additional information, are available at http://lhcbproject.web.cern.ch/lhcbproject/Publications/LHCbProjectPublic/LHCb-PAPER-2015-027.htm

Comprehensive analysis of epigenetic clocks reveals associations between disproportionate biological ageing and hippocampal volume

The concept of age acceleration, the difference between biological age and chronological age, is of growing interest, particularly with respect to age-related disorders, such as Alzheimer’s Disease (AD). Whilst studies have reported associations with AD risk and related phenotypes, there remains a lack of consensus on these associations. Here we aimed to comprehensively investigate the relationship between five recognised measures of age acceleration, based on DNA methylation patterns (DNAm age), and cross-sectional and longitudinal cognition and AD-related neuroimaging phenotypes (volumetric MRI and Amyloid-β PET) in the Australian Imaging, Biomarkers and Lifestyle (AIBL) and the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Significant associations were observed between age acceleration using the Hannum epigenetic clock and cross-sectional hippocampal volume in AIBL and replicated in ADNI. In AIBL, several other findings were observed cross-sectionally, including a significant association between hippocampal volume and the Hannum and Phenoage epigenetic clocks. Further, significant associations were also observed between hippocampal volume and the Zhang and Phenoage epigenetic clocks within Amyloid-β positive individuals. However, these were not validated within the ADNI cohort. No associations between age acceleration and other Alzheimer’s disease-related phenotypes, including measures of cognition or brain Amyloid-β burden, were observed, and there was no association with longitudinal change in any phenotype. This study presents a link between age acceleration, as determined using DNA methylation, and hippocampal volume that was statistically significant across two highly characterised cohorts. The results presented in this study contribute to a growing literature that supports the role of epigenetic modifications in ageing and AD-related phenotypes

Observation of the B0 → ρ0ρ0 decay from an amplitude analysis of B0 → (π+π−)(π+π−) decays

Proton–proton collision data recorded in 2011 and 2012 by the LHCb experiment, corresponding to an integrated luminosity of 3.0 fb−1, are analysed to search for the charmless B0 → ρ0ρ0 decay. More than 600 B0 → (π+π−)(π+π−) signal decays are selected and used to perform an amplitude analysis, under the assumption of no CP violation in the decay, from which the B0 → ρ0ρ0 decay is observed for the first time with 7.1 standard deviations significance. The fraction of B0 → ρ0ρ0 decays yielding a longitudinally polarised final state is measured to be fL = 0.745+0.048 −0.058(stat) ± 0.034(syst). The B0 → ρ0ρ0 branching fraction, using the B0 → φK∗(892)0 decay as reference, is also reported as B(B0 → ρ0ρ0) = (0.94 ± 0.17(stat) ± 0.09(syst) ± 0.06(BF)) × 10−6

Observation of the decay B0s → ψ(2S)K +π−

The decay B0 s → ψ(2S)K +π− is observed using a data set corresponding to an integrated luminosity of 3.0 fb−1 collected by the LHCb experiment in pp collisions at centre-of-mass energies of 7 and 8 TeV. The branching fraction relative to the B0 → ψ(2S)K +π− decay mode is measured to be B(B0 s → ψ(2S)K +π−) B(B0 → ψ(2S)K +π−) = 5.38 ± 0.36 (stat) ± 0.22 (syst) ± 0.31 (f s/ fd)%, where f s/ fd indicates the uncertainty due to the ratio of probabilities for a b quark to hadronise into a B0 s or B0 meson. Using an amplitude analysis, the fraction of decays proceeding via an intermediate K∗(892)0 meson is measured to be 0.645 ± 0.049 (stat) ± 0.049 (syst) and its longitudinal polarisation fraction is 0.524 ± 0.056 (stat) ± 0.029 (syst). The relative branching fraction for this component is determined to be B(B0 s → ψ(2S)K∗(892)0) B(B0 → ψ(2S)K∗(892)0) = 5.58 ± 0.57 (stat) ± 0.40 (syst) ± 0.32 (f s/ fd)%. In addition, the mass splitting between the B0 s and B0 mesons is measured as M(B0 s ) − M(B0) = 87.45 ± 0.44 (stat) ± 0.09 (syst) MeV/c2

Measurement of the CP-violating phase β in B0 → J/ψπ+π− decays and limits on penguin effects

Time-dependent CP violation is measured in the (—) B 0 → J/ψπ+π− channel for each π+π− resonant final state using data collected with an integrated luminosity of 3.0 fb−1 in pp collisions using the LHCb detector. The final state with the largest rate, J/ψρ0(770), is used to measure the CP-violating angle 2βeff to be (41.7 ± 9.6+2.8 −6.3)◦. This result can be used to limit the size of penguin amplitude contributions to CP violation measurements in, for example, (—) B 0 s → J/ψφ decays. Assuming approximate SU(3) flavour symmetry and neglecting higher order diagrams, the shift in the CP-violating phase φs is limited to be within the interval [−1.05◦,+1.18◦] at 95% confidence level. Changes to the limit due to SU(3) symmetry breaking effects are also discussed

Erratum: first observation of the rare Bþ → DþKþπ− decay [Phys. Rev. D 93, 051101(R) (2016)]

No abstract available

Expanding the clinical phenotype of individuals with a 3-bp in-frame deletion of the NF1 gene (c.2970_2972del): an update of genotype–phenotype correlation

Purpose: Neurofibromatosis type 1 (NF1) is characterized by a highly variable clinical presentation, but almost all NF1-affected adults present with cutaneous and/or subcutaneous neurofibromas. Exceptions are individuals heterozygous for the NF1 in-frame deletion, c.2970_2972del (p.Met992del), associated with a mild phenotype without any externally visible tumors. Methods: A total of 135 individuals from 103 unrelated families, all carrying the constitutional NF1 p.Met992del pathogenic variant and clinically assessed using the same standardized phenotypic checklist form, were included in this study. Results: None of the individuals had externally visible plexiform or histopathologically confirmed cutaneous or subcutaneous neurofibromas. We did not identify any complications, such as symptomatic optic pathway gliomas (OPGs) or symptomatic spinal neurofibromas; however, 4.8% of individuals had nonoptic brain tumors, mostly low-grade and asymptomatic, and 38.8% had cognitive impairment/learning disabilities. In an individual with the NF1 constitutional c.2970_2972del and three astrocytomas, we provided proof that all were NF1-associated tumors given loss of heterozygosity at three intragenic NF1 microsatellite markers and c.2970_297