The LHCb experiment is dedicated to precision measurements of CP violation and rare decays of B hadrons at the Large Hadron Collider (LHC) at CERN (Geneva). The initial configuration and expected performance of the detector and associated systems, as established by test beam measurements and simulation studies, is described.

The calibration and performance of the opposite-side flavour tagging algorithms used for the measurements of time-dependent asymmetries at the LHCb experiment are described. The algorithms have been developed using simulated events and optimized and calibrated with B+→J/ψK+, B0→J/ψK∗0 and B0→D∗−μ+νμ decay modes with 0.37 fb−1 of data collected in pp collisions at during the 2011 physics run. The opposite-side tagging power is determined in the B+→J/ψK+ channel to be (2.10±0.08±0.24) %, where the first uncertainty is statistical and the second is systematic.

The production of J/ψ mesons in proton-proton collisions at √ s = 7 TeV is studied with the LHCb detector at the LHC. The differential cross-section for prompt J/ψ production is measured as a function of the J/ψ transverse momentum p T and rapidity y in the fiducial region p T ∈ [0; 14] GeV/c and y ∈ [2.0; 4 cross-section and fraction of J/ψ from b-hadron decays are also measured in the same p T and y ranges. The analysis is based on a data sample corresponding to an integrated luminosity of 5.2 pb −1 . The measured cross-sections integrated over the fiducial region are 10.52 ± 0.04 ± 1.40−2.20 µb for prompt J/ψ production and 1.14 ± 0.01 ± 0.16 µb for J/ψ from b-hadron decays, where the first uncertainty is statistical and the second systematic. The prompt J/ψ production cross-section is obtained assuming no J/ψ polarisation and the third error indicates the acceptance uncertainty due to this assumption.

Barrett’s Esophagus is an increasingly common disease that is strongly associated with reflux of stomach acid and usually a hiatus hernia. Barrett’s Esophagus strongly predisposes to esophageal adenocarcinoma (EAC), a tumour with a very poor prognosis. We have undertaken the first genome-wide association study on Barrett’s Esophagus, comprising 1,852 UK cases and 5,172 UK controls in discovery and 5,986 cases and 12,825 controls in the replication. Two regions were associated with disease risk: chromosome 6p21, rs9257809 (Pcombined=4.09×10−9, OR(95%CI) =1.21(1.13-1.28)) and chromosome 16q24, rs9936833 (Pcombined=2.74×10−10, OR(95%CI) =1.14(1.10-1.19)). The top SNP on chromosome 6p21 is within the major histocompatibility complex, and the closest protein-coding gene to rs9936833 on chromosome 16q24 is FOXF1, which is implicated in esophageal development and structure. We found evidence that the genetic component of Barrett’s Esophagus is mediated by many common variants of small effect and that SNP alleles predisposing to obesity also increase risk for Barrett’s Esophagus.

No abstract