89,121 research outputs found
Evidence for the decay B0→J/ψω and measurement of the relative branching fractions of meson decays to J/ψη and J/ψη′
No full textFirst evidence of the B 0 → J / ψ ω decay is found and the B s 0 → J / ψ η and B s 0 → J / ψ η ′ decays are studied using a dataset corresponding to an integrated luminosity of 1.0 fb -1 collected by the LHCb experiment in proton-proton collisions at a centre-of-mass energy of sqrt(s) = 7 TeV. The branching fractions of these decays are measured relative to that of the B 0 → J / ψ ρ 0 decay:frac(B (B 0 → J / ψ ω), B (B 0 → J / ψ ρ 0)) = 0.89 ± 0.19 (stat) - 0.13 + 0.07 (syst),frac(B (B s 0 → J / ψ η), B (B 0 → J / ψ ρ 0)) = 14.0 ± 1.2 (stat) - 1.5 + 1.1 (syst) - 1.0 + 1.1 (frac(f d, f s)),frac(B (B s 0 → J / ψ η ′), B (B 0 → J / ψ ρ 0)) = 12.7 ± 1.1 (stat) - 1.3 + 0.5 (syst) - 0.9 + 1.0 (frac(f d, f s)), where the last uncertainty is due to the knowledge of f d / f s, the ratio of b-quark hadronization factors that accounts for the different production rate of B 0 and B s 0 mesons. The ratio of the branching fractions of B s 0 → J / ψ η ′ and B s 0 → J / ψ η decays is measured to befrac(B (B s 0 → J / ψ η ′), B (B s 0 → J / ψ η)) = 0.90 ± 0.09 (stat) - 0.02 + 0.06 (syst)
Measurement of the CP-violating phase \phi s in Bs->J/\psi\pi+\pi- decays
No full textMeasurement of the mixing-induced CP-violating phase phi_s in Bs decays is of prime importance in probing new physics. Here 7421 +/- 105 signal events from the dominantly CP-odd final state J/\psi pi+ pi- are selected in 1/fb of pp collision data collected at sqrt{s} = 7 TeV with the LHCb detector. A time-dependent fit to the data yields a value of phi_s=-0.019^{+0.173+0.004}_{-0.174-0.003} rad, consistent with the Standard Model expectation. No evidence of direct CP violation is found
Observations of Bºs→ψ(2S)η and Bº(s)→ψ(2S)π+π- decays
No full textFirst observations of the B0s
→ψ(2S)η, B0 →ψ(2S)π
+
π
− and B0s
→ψ(2S)π
+
π
− decays are made
using a dataset corresponding to an integrated luminosity of 1.0 fb−1 collected by the LHCb experiment in
proton–proton collisions at a centre-of-mass energy of
√
s = 7 TeV. The ratios of the branching fractions
of each of the ψ(2S) modes with respect to the corresponding J/ψ decays are
B(B0s
→ψ(2S)η)
÷
B(B0s
→J/ψη)
= 0.83± 0.14 (stat)±0.12 (syst) ±0.02 (B),
;
B(B0→ψ(2S)π
+
π
−
)
÷
B(B0→J/ψπ
+
π
−
)
= 0.56± 0.07 (stat)±0.05 (syst)± 0.01 (B),
;
B(B0s
→ψ(2S)π
+
π
−
)
÷
B(B0s
→J/ψπ
+
π
−
)
= 0.34± 0.04 (stat)±0.03 (syst)± 0.01 (B),
where the third uncertainty corresponds to the uncertainties of the dilepton branching fractions of the J/ψ
and ψ(2S) meson decays
Measurement of the ratio of prompt χ c to J / ψ production in pp collisions at √s = 7 TeV
No full textThe prompt production of charmonium χ c and J / ψ states is studied in proton-proton collisions at a centre-of-mass energy of √s = 7 TeV at the Large Hadron Collider. The χ c and J / ψ mesons are identified through their decays χ c → J / ψ γ and J / ψ → μ + μ - using 36 pb - 1 of data collected by the LHCb detector in 2010. The ratio of the prompt production cross-sections for χ c and J / ψ, σ (χ c → J / ψ γ) / σ (J / ψ), is determined as a function of the J / ψ transverse momentum in the range 2 < p T J / ψ < 15 GeV / c. The results are in excellent agreement with next-to-leading order non-relativistic expectations and show a significant discrepancy compared with the colour singlet model prediction at leading order, especially in the low p T J / ψ region
Anti-inflammatory and antiosteo-clastogenesis properties of endogenous melanocortin receptor type 3 in experimental arthritis
No full textThe development of biological therapies has improved management of rheumatoid arthritis. However, costs and unresponsiveness to therapy in a sizeable proportion of patients limit their use, making it imperative to identify new targets for drug development programs. Here we investigated the melanocortin-receptor type 3 (MC3) pathway. Gene-deficient mice were subjected to a model of serum-transfer-induced arthritis and joints analyzed for gene expression (cytokines, MCs) and morphology. Pharmacological analyses were also conducted in this model. Osteoclastogenesis was studied from bone marrow cells. Mc3−/− mice displayed an exacerbated inflammatory arthritis, associated with prominent bone erosion and higher articular expression of Rankl. Osteoclastogenesis studied from Mc3−/− bone marrow cells revealed a higher degree of responsiveness to Rankl, linked to prolonged NF-κB activation compared to wild types. Up-regulation of a discrete set of inflammatory genes, including Il-1β, Il-6, and Nos2, was measured in Mc3−/− mice, and a marked up-regulation of joint Mc3 accompanied arthritis resolution in wild-type mice. Administration of an MC3 agonist, D[Trp8]-γ-MSH, attenuated disease incidence and severity in wild-type but not Mc3−/− mice. Overall, these findings identify MC3-mediated signaling as a beneficial pathway in experimental arthritis; hence this receptor is a novel target for the development of therapeutics for arthritis.—Patel, H. B., Bombardieri, M., Sampaio, A. L. F., D'Acquisto, F., Gray, M., Grieco, P., Getting, S. J., Pitzalis, C., Perretti, M. Anti-inflammatory and antiosteoclastogenesis properties of endogenous melanocortin receptor type 3 in experimental arthritis
Melanocortin type 3 receptor null mice are refractory to the inhibitory actions of a selective receptor agonist in experimental acute inflammation
No full textMeasurement of the branching fraction
No full textThe B
0
s
→ J/ψK
0
S
branching fraction is measured in a data sample corresponding to 0.41 fb−1
of integrated luminosity collected with the LHCb detector at the LHC. This channel is sensitive to
the penguin contributions affecting the sin 2β measurement from B
0
→ J/ψK
0
S
. The time-integrated
branching fraction is measured to be B(B
0
s
→ J/ψK
0
S
) = (1.83±0.28)×10−5
. This is the most precise
measurement to date
Antiallergic cromones inhibit neutrophil recruitment onto vascular endothelium via Annexin-A1 mobilization
No full textObjective—To determine whether a mechanism exists that could operate on application of cromones, antiallertic "mast cell–stabilizing" drugs that release the anti-inflammatory protein annexin-A1 (Anx-A1) from U937 cells and inhibit polymorphonuclear leukocyte (PMN) trafficking, because PMNs can synthesize and release large amounts of Anx-A1.
Methods and Results—Intravital microscopy was used to monitor the actions of cromones in the inflamed microcirculation. Reperfusion injury provoked a dramatic increase in adherent and emigrated leukocytes in the mesenteric vascular bed, associated with augmented tissue levels of myeloperoxidase. Nedocromil, 2 to 20 mg/kg, significantly (P<0.05) inhibited cell adhesion and emigration, as well as myeloperoxidase release, in wild-type but not Anx-A1-/- mice. Short pretreatment of human PMNs with nedocromil, 10 nmol/L, inhibited cell adhesion (P<0.05) in the flow chamber assay, and this effect was reversed by specific anti-AnxA1 or a combination of anti–formyl peptide receptors 1 and 2, but not irrelevant control, antibodies. Western blotting experiments revealed that cromones stimulate protein kinase C–dependent phosphorylation and release Anx-A1 in human PMNs.
Conclusion—We propose a novel mechanism to explain the anti-inflammatory actions of cromones on PMN trafficking, an effect that has long puzzled investigators
Measurement of the time-dependent CP asymmetry in B0 -> J/ψ KS0 decays
No full textThis Letter reports a measurement of the CP violation observables SJ/ψK0S and CJ/ψK0S in the decay channel B0→J/ψK0S performed with 1.0 fb−1 of pp collisions at s√=7 TeV collected by the LHCb experiment. The fit to the data yields SJ/ψK0S=0.73±0.07(stat)±0.04(syst) and CJ/ψK0S=0.03±0.09(stat)±0.01(syst). Both values are consistent with the current world averages and within
expectations from the Standard Model
[D-Trp8]-{gamma}-MSH exhibits anti-inflammatory efficacy in mice bearing a non-functional MC1R (recessive yellow e/e mouse).
No full text- …
