1,411 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)
Effects of Superheat and Solute Additions on the Grain Size in Binary Copper Alloys
No full text© The Author(s) 2019. By utilizing data from the literature, we examine the effects of superheat and solute additions on the grain size (as measured by columnar grain length) in binary copper alloys. Our investigation provides support for an Arrhenius-like behavior of the superheat on the grain size. We also find a correlation between the columnar grain length at a constant degree of superheat and the variation of the reciprocal of the true growth restriction factor (1/Q) with P, Mg, Mn, Pb, and Sn solute additions to be a power of law of 1/3, which gave a better fit than a linear one.EPSRC (UK
Effect of viscosity and density gradients on turbulent channel flows
No full textWe perform Direct Numerical Simulations (DNS) of a turbulent channel flow with temperature dependent density and viscosity. The Navier-Stokes equations are solved using their low Mach number formulation. In the simulations performed, the fluid is internally heated and the temperature at the walls is fixed. The friction Reynolds number based on half channel height and wall friction velocity is Reτ = 395. The modulation of turbulence, which is caused by the density and viscosity gradients, is characterized using the semi-local scaling of Huang et al. [1995, JFM]
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
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
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
Measurement 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
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
Programmed Cell Death Dynamics in Hyperglycemia
No full textClick on the Resource Link to find this item in the ACPHS Library catalog.Necroptosis is a type of inflammatory programmed cell death (PCD) that is dependent on kinases RIP1, RIP3 and MLKL. Necroptosis differs from apoptosis, which is dependent on caspases and is a non-inflammatory PCD. Activation of necroptosis stimulates glycolysis, producing toxic by-products such as reactive oxygen species (ROS) and advanced glycation end products (AGEs) that induce cell damage. Previous work has shown that necroptosis is upregulated in hyperglycemic conditions. These findings suggest that hyperglycemia may induce a shift from apoptosis to necroptosis following extrinsic death receptor:ligand interaction. Here, we show that hyperglycemia does not enhance extrinsic apoptosis but, rather, potentiates a shift to RIP1-dependent necroptosis using specific pharmacologic inhibitors and a RIP1 mutant cell line in cell death assays. This was the result of increased levels and activity of RIP1, RIP3, and MLKL as well as decreased levels and activity of executioner caspases in hyperglycemic conditions following stimulation with apoptotic ligands. The shift to necroptosis was driven by RIP1 as mutation of this gene using CRISPR-Cas9 caused cell death to revert to caspase-dependent apoptosis in hyperglycemic conditions. Effects of hyperglycemia in neonatal hypoxia-ischemia (HI) brain injury, normally driven by apoptosis, was explored by measuring expression of critical proteins. In cerebral tissue from hyperglycemic neonatal mice that had undergone HI brain injury, levels of RIP1 (total and phosphorylated), RIP3, and MLKL increased, while levels of executioner caspases decreased, suggesting that this cell death shift occurs in vivo. The shift from apoptosis to necroptosis also depended on glycolysis, which was shown by using the glycolysis inhibitor, 2-deoxyglucose. Furthermore, the increased production of mitochondrial ROS in high glucose conditions was shown to have relevance with respect to the shift to necroptosis, by affecting expression of executioner caspases as well as inducing the hyperactivation of RIP1 via oligomerization. AGEs, on the other hand, were found to not have a significant role in the shift. This work is significant as it demonstrates a shift from non-inflammatory to inflammatory cell death and determining the mechanisms of the shift to necroptosis is crucial to develop therapeutic strategies that could restrain the direct effects of hyperglycemia in ischemic injuries.MS in Molecular Bioscienceshttps://acphs.on.worldcat.org/oclc/107887709
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