Measurement of the ratios of branching fractions R(D*) and R(D0)

The ratios of branching fractions R ( D ∗ ) ≡ B ( ¯ B → D ∗ τ − ¯ ν τ ) / B ( ¯ B → D ∗ μ − ¯ ν μ ) and R ( D 0 ) ≡ B ( B − → D 0 τ − ¯ ν τ ) / B ( B − → D 0 μ − ¯ ν μ ) are measured, assuming isospin symmetry, using a sample of proton-proton collision data corresponding to 3.0     fb − 1 of integrated luminosity recorded by the LHCb experiment during 2011 and 2012. The tau lepton is identified in the decay mode τ − → μ − ν τ ¯ ν μ . The measured values are R ( D ∗ ) = 0.281 ± 0.018 ± 0.024 and R ( D 0 ) = 0.441 ± 0.060 ± 0.066 , where the first uncertainty is statistical and the second is systematic. The correlation between these measurements is ρ = − 0.43 . The results are consistent with the current average of these quantities and are at a combined 1.9 standard deviations from the predictions based on lepton flavor universality in the standard model

Search for rare decays of D0 mesons into two muons

A search for the very rare D 0 → μ + μ − decay is performed using data collected by the LHCb experiment in proton-proton collisions at √ s = 7 , 8, and 13 TeV, corresponding to an integrated luminosity of 9     fb − 1 . The search is optimized for D 0 mesons from D * + → D 0 π + decays but is also sensitive to D 0 mesons from other sources. No evidence for an excess of events over the expected background is observed. An upper limit on the branching fraction of this decay is set at B ( D 0 → μ + μ − ) < 3.1 × 10 − 9 at a 90% C.L. This represents the world’s most stringent limit, constraining models of physics beyond the standard model

First measurement of the Z→μ+μ− angular coefficients in the forward region of pp collisions at √s = 13 TeV

The first study of the angular distribution of μ + μ − pairs produced in the forward rapidity region via the Drell-Yan reaction p p → γ ∗ / Z + X → ℓ + ℓ − + X is presented, using data collected with the LHCb detector at a center-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 5.1     fb − 1 . The coefficients of the five leading terms in the angular distribution are determined as a function of the dimuon transverse momentum and rapidity. The results are compared to various theoretical predictions of the Z -boson production mechanism and can also be used to probe transverse-momentum-dependent parton distributions within the proton

Test of lepton universality in b→sℓ+ℓ− decays

The first simultaneous test of muon-electron universality using B + → K + ℓ + ℓ − and B 0 → K * 0 ℓ + ℓ − decays is performed, in two ranges of the dilepton invariant-mass squared, q 2 . The analysis uses beauty mesons produced in proton-proton collisions collected with the LHCb detector between 2011 and 2018, corresponding to an integrated luminosity of 9     fb − 1 . Each of the four lepton universality measurements reported is either the first in the given q 2 interval or supersedes previous LHCb measurements. The results are compatible with the predictions of the Standard Model

Activation of σ-Receptors Induces Binge-like Drinking in Sardinian Alcohol-Preferring Rats

Sigma (σ) receptors have been implicated in the behavioral and motivational effects of alcohol and psychostimulants. Sigma receptor antagonists reduce the reinforcing effects of alcohol and excessive alcohol intake in both genetic (alcohol-preferring rats) and environmental (chronic alcohol-induced) models of alcoholism. The present study tested the hypothesis that pharmacological activation of σ-receptors facilitates ethanol reinforcement and induces excessive, binge-like ethanol intake. The effects of repeated subcutaneous treatment with the selective σ-receptor agonist 1,3-di-(2-tolyl)guanidine (DTG; 15 mg/kg, twice a day for 7 days) on operant ethanol (10%) self-administration were studied in Sardinian alcohol-preferring (sP) rats. To confirm that the effect of DTG was mediated by σ-receptors, the effects of pretreatment with the selective σ-receptor antagonist BD-1063 (7 mg/kg, subcutaneously) were determined. To assess the specificity of action, the effects of DTG on the self-administration of equally reinforcing solutions of saccharin or sucrose were also determined. Finally, gene expression of opioid receptors in brain areas implicated in ethanol reinforcement was analyzed in ethanol-naive sP rats treated acutely or repeatedly with DTG, because of the well-established role of the opioid system in alcohol reinforcement and addiction. Repeatedly administered DTG progressively and dramatically increased ethanol self-administration in sP rats and increased blood alcohol levels, which reached mean values close to 100 mg% in 1 h drinking sessions. Repeated DTG treatment also increased the rats' motivation to work for alcohol under a progressive-ratio schedule of reinforcement. BD-1063 prevented the effects of DTG, confirming that σ-receptors mediate the effects of DTG. Repeated DTG treatment also increased the self-administration of the non-drug reinforcers saccharin and sucrose. Naive sP rats repeatedly treated with DTG showed increased mRNA expression of μ- and δ-opioid receptors in the ventral tegmental area. These results suggest a key facilitatory role for σ-receptors in the reinforcing effects of alcohol and identify a potential mechanism that contributes to binge-like and excessive drinking

Cocaine Blocks Effects of Hunger Hormone, Ghrelin, Via Interaction with Neuronal Sigma-1 Receptors

Despite ancient knowledge on cocaine appetite-suppressant action, the molecular basis of such fact remains unknown. Addiction/eating disorders (e.g., binge eating, anorexia, bulimia) share a central control involving reward circuits. However, we here show that the sigma-1 receptor (σ R) mediates cocaine anorectic effects by interacting in neurons with growth/hormone/secretagogue (ghrelin) receptors. Cocaine increases colocalization of σ R and GHS-R1a at the cell surface. Moreover, in transfected HEK-293T and neuroblastoma SH-SY5Y cells, and in primary neuronal cultures, pretreatment with cocaine or a σ R agonist inhibited ghrelin-mediated signaling, in a similar manner as the GHS-R1a antagonist YIL-781. Results were similar in G protein-dependent (cAMP accumulation and calcium release) and in partly dependent or independent (ERK1/2 phosphorylation and label-free) assays. We provide solid evidence for direct interaction between receptors and the functional consequences, as well as a reliable structural model of the macromolecular σ R-GHS-R1a complex, which arises as a key piece in the puzzle of the events linking cocaine consumption and appetitive/consummatory behaviors