Observation of B-s(0) -> chi(c1)phi decay and study of B-0 -> chi K-c1,K-2*(0) decays

The first observation of the decay B-s(0) -> chi(c1)phi and a study of B-0 -> chi K-c1,K-2*(0) decays are presented. The analysis is performed using a dataset, corresponding to an integrated luminosity of 1.0 fb(-1), collected by the LHCb experiment in pp collisions at a centre-of-mass energy of 7 TeV. The following ratios of branching fractions are measured: B(B-s(0) -> chi(c1)phi)/B(B-s(0) -> J/psi phi) = (18.9 +/- 1.8 (stat) +/- 1.3 (syst) +/- 0.8(B)) x 10(-2), B(B-0 -> chi K-c1*(0))//B(B-0 -> J/psi K*(0)) = (19.8 +/- 1.1 (stat) +/- 1.2 (syst) +/- 0.9(B)) x 10(-2), B(B-0 -> chi K-c2*(0))//B(B-0 -> chi K-c1*(0)) = (17.1 +/- 5.0 (stat) +/- 1.7 (syst) +/- 1.1(B)) x 10(-2), where the third uncertainty is due to the limited knowledge of the branching fractions of chi(c) -> J/psi gamma modes

First measurement of time-dependent CP violation in Bs0→K+K− B_s^0\to K^+K^- decays

Direct and mixing-induced CP-violating asymmetries in B-s(0) -> K+K- decays are measured for the first time using a data sample of p p collisions, corresponding to an integrated luminosity of 1.0 fb(-1), collected with the LHCb detector at a centre-of-mass energy of 7 TeV. The results are C-KK = 0.14 +/- 0.11 +/- 0.03 and S-KK = 0.30 +/- 0.12 +/- 0.04, where the first uncertainties are statistical and the second systematic. The corresponding quantities are also determined for B-0 -> pi(+)pi(-) decays to be C-pi pi = -0.38 +/- 0.15 +/- 0.02 and S-pi pi = -0.71 +/- 0.13 +/- 0.02, in good agreement with existing measurements

Observation of the decay B-s(0) -> (D)over-bar(0)phi

First observation of the decay B-s(0) -> (D) over bar (0)phi is reported using pp collision data, corresponding to an integrated luminosity of 1.0 fb(-1), collected by the LHCb experiment at a centre-of-mass energy of 7 TeV. The significance of the signal is 6.5 standard deviations. The branching fraction is measured relative to that of the decay B-S(0) -> (D) over bar (0)phi to be beta B-S(0) -> (D) over bar (0)phi/beta B-S(0) -> (D) over bar (0)(K) over bar*(0) = 0.069 +/- 0.013 (stat) +/- 0.007 (syst). The first measurement of the ratio of branching fractions for the decays beta B-S(0) -> (D) over bar (0)(K) over bar*(0) and beta B-S(0) -> (D) over bar (0)(K) over bar*(0) is found to be beta B-S(0) -> (D) over bar (0)(K) over bar*(0/)beta B-S(0) -> (D) over bar (0)(K) over bar*(0=7.8) +/- 0.7(stat) +/- 0.3 (syst) +/- 0.6 (f(s)/f(d)) where the last uncertainty is due to the ratio of the B(s)(0)and B-0 fragmentation fractions

Measurement of the flavour-specific CP-violating asymmetry a(sl)(s) in B-s(0) decays

The CP-violating asymmetry a(sl)(s), is studied using semileptonic decays of B-s(0) and (B) over bar (0)(s) mesons produced in pp collisions at a centre-of-mass energy of 7 TeV at the LHC, exploiting a data sample corresponding to an integrated luminosity of 1.0 fb(-1). The reconstructed final states are D-s(+/-)mu(+/-)(s), with the D-s(+/-) particle decaying in the phi pi(+/-) mode. The D-s(+/-)mu(+/-)(s) yields are summed over B-s(0) and (B) over bar (0)(s) initial states, and integrated with respect to decay time. Data-driven methods are used to measure efficiency ratios. We obtain a(sl)(s) = (-0.06 +/- 0.50 +/- 0.36)%, where the first uncertainty is statistical and the second systematic

Model-independent search for CP violation in D-0 > K-K+pi(-)pi(+) and D-0 -> pi(-)pi(+)pi(+)pi(-) decays

A search for CP violation in the phase-space structures of 130 and 15 decays to the final states K-K+pi(-)pi(+) and pi(-)pi(+)pi(+)pi(-) is presented. The search is carried out with a data set corresponding to an integrated luminosity of 1.0 fb(-1) collected in 2011 by the LHCb experiment in pp collisions at a centre-of-mass energy of 7 TeV. For the K-K+pi(-)pi(+) final state, the four-body phase space is divided into 32 bins, each bin with approximately 1800 decays. The p-value under the hypothesis of no CP violation is 9.1%, and in no bin is a CP asymmetry greater than 6.5% observed. The phase space of the pi(-)pi(+)pi(+)pi(-). final state is partitioned into 128 bins, each bin with approximately 2500 decays. The p-value under the hypothesis of no CP violation is 41%, and in no bin is a CP asymmetry greater than 5.5% observed. All results are consistent with the hypothesis of no CP violation at the current sensitivity

Stroke genetics informs drug discovery and risk prediction across ancestries

: Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries

Second IVIg course in Guillain-Barré syndrome with poor prognosis. The non-randomised ISID study

Objective To compare disease course in patients with Guillain-Barré syndrome (GBS) with a poor prognosis who were treated with one or with two intravenous immunoglobulin (IVIg) courses. Methods From the International GBS Outcome Study, we selected patients whose modified Erasmus GBS Outcome Score at week 1 predicted a poor prognosis. We compared those treated with one IVIg course to those treated with two IVIg courses. The primary endpoint, the GBS disability scale at 4 weeks, was assessed with multivariable ordinal regression. Results Of 237 eligible patients, 199 patients received a single IVIg course. Twenty patients received an α early' second IVIg course (1-2 weeks after start of the first IVIg course) and 18 patients a α late' second IVIg course (2-4 weeks after start of IVIg). At baseline and 1 week, those receiving two IVIg courses were more disabled than those receiving one course. Compared with the one course group, the adjusted OR for a better GBS disability score at 4 weeks was 0.70 (95%CI 0.16 to 3.04) for the early group and 0.66 (95%CI 0.18 to 2.50) for the late group. The secondary endpoints were not in favour of a second IVIg course. Conclusions This observational study did not show better outcomes after a second IVIg course in GBS with poor prognosis. The study was limited by small numbers and baseline imbalances. Lack of improvement was likely an incentive to start a second IVIg course. A prospective randomised trial is needed to evaluate whether a second IVIg course improves outcome in GBS