Search for B⁺_c→π⁺μ⁺μ⁻ decays and measurement of the branching fraction ratio <i>B</i>(B⁺_c→ψ(2<i>S</i>)π⁺)/<i>B</i>(B⁺_c→<i>J</i>/ψπ⁺)

The first search for nonresonant B+c→π+μ+μ− decays is reported. The analysis uses proton-proton collision data collected with the LHCb detector between 2011 and 2018, corresponding to an integrated luminosity of 9 fb−1. No evidence for an excess of signal events over background is observed and an upper limit is set on the branching fraction ratio B(B+c→π+μ+μ−)/B(B+c→J/ψπ+)&lt;2.1×10−4 at 90% confidence level. Additionally, an updated measurement of the ratio of the B+c→ψ(2S)π+ and B+c→J/ψπ+ branching fractions is reported. The ratio B(B+c→ψ(2S)π+)/B(B+c→J/ψπ+) is measured to be 0.254±0.018±0.003±0.005, where the first uncertainty is statistical, the second systematic, and the third is due to the uncertainties on the branching fractions of the leptonic J/ψ and ψ(2S) decays. This measurement is the most precise to date and is consistent with previous LHCb results

Calcium channel blockade blunts the renal effects of acute nitric oxide synthase inhibition in healthy humans

Montanari A, Lazzeroni D, Pelà G, Crocamo A, Lytvyn Y, Musiari L, Cabassi A, Cherney DZ. Calcium channel blockade blunts the renal effects of acute nitric oxide synthase inhibition in healthy humans. Am J Physiol Renal Physiol 312: F870–F878, 2017. First published February 8, 2017; doi:10.1152/ajprenal.00568. 2016.—Our aim was to investigate whether blockade of calcium channels (CCs) or angiotensin II type 1 receptors (AT1R) modulates renal responses to nitric oxide synthesis inhibition (NOSI) in humans. Fourteen sodium-replete, healthy volunteers underwent 90-min infusions of 3.0 g·kg1·min1 NG-nitro-L-arginine methyl ester (L-NAME) on 3 occasions, preceded by 3 days of either placebo (PL), 10 mg of manidipine (MANI), or 50 mg of losartan (LOS). At each phase, mean arterial pressure (MAP), glomerular filtration rate (GFR; inulin), renal blood flow (RBF; p-aminohippurate), urinary sodium (UNaV), and 8-isoprostane (U8-iso-PGF2V; an oxidative stress marker) were measured. With PL L -NAME, the following changes were observed: 6% MAP (P 0.005 vs. baseline), 10% GFR, 20% RBF, 49% UNaV (P 0.001), and 120% U8-iso-PGF2V (P 0.01). In contrast, MAP did not increase during LOS L-NAME or MANI L-NAME (P 0.05 vs. baseline), whereas renal changes were the same during LOS L-NAME vs. PL L-NAME (ANOVA, P 0.05). However, during MANI L-NAME, changes vs. baseline in GFR (6%), RBF (12%), and UNaV (34%) were blunted vs. PL L-NAME and LOS L-NAME (P 0.005), and the rise in U8-iso-PGF2V was almost abolished (37%, P 0.05 vs. baseline; P 0.01 vs. PL L-NAME or LOS L-NAME). We conclude that, since MANI blunted L-NAME-induced renal hemodynamic changes, CCs participate in the renal responses to NOSI in healthy, sodium-replete humans independent of changes in MAP and without the apparent contribution of the AT1R. Because the rise in U8-iso-PGF2V was essentially prevented during MANI L-NAME, CC blockade may oppose the renal effects of NOSI in part by counteracting oxidative stress responses to acutely impaired renal NO bioavailability

Observation of the<i> B</i>⁺_c → <i>J/ψ</i>π⁺π⁰ decay

The frst observation of the B+c → J/ψπ+π0 decay is reported with high significance using proton-proton collision data, corresponding to an integrated luminosity of 9 fb−1, collected with the LHCb detector at centre-of-mass energies of 7, 8, and 13 TeV. The ratio ofits branching fraction relative to the B+c → J/ψπ+ channel is measured to beBB+c →J/ψπ+π0BB+c →J/ψπ+= 2.80 ± 0.15 ± 0.11 ± 0.16 ,where the first uncertainty is statistical, the second systematic and the third related to imprecise knowledge of the branching fractions for B+ → J/ψK∗+ and B+c → J/ψπ+ decays, which are used to determine the π0 detection efficiency. The π+π0 mass spectrum is found to be consistent with the dominance of an intermediate ρ+ contribution in accordance witha model based on QCD factorisation.<br/

The ALICE trigger electronics

The ALICE trigger system (TRG) consists of a Central Trigger Processor (CTP) and up to 24 Local Trigger Units (LTU) for each sub-detector. The CTP receives and processes trigger signals from trigger detectors and the outputs from the CTP are 3 levels of hardware triggers: L0, L1 and L2. The 24 sub-detectors are dynamically partitioned in up to 6 independent clusters. The trigger information is propagated through the LTUs to the Front-end electronics (FEE) of each sub-detector via LVDS cables and optical fibres. The trigger information sent from LTU to FEE can be monitored online for possible errors using the newly developed TTCit board. After testing and commissioning of the trigger system itself on the surface, the ALICE trigger electronics has been installed and tested in the experimental cavern with appropriate ALICE experimental software. Testing the Alice trigger system with detectors on the surface and in the experimental cavern in parallel is progressing very well. Currently one setup is used for testing on the surface; another is installed in experimental cavern. This paper describes the current status of ALICE trigger electronics, online error trigger monitoring and appropriate software for this electronics