29,782 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 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
A 2 h periodic variation in the low-mass X-ray binary Ser X-1
No full textSpectroscopy of the low-mass X-ray binary Ser X-1 using the Gran Telescopio Canarias have revealed a ?2 h periodic variability that is present in the three strongest emission lines. We tentatively interpret this variability as due to orbital motion, making it the first indication of the orbital period of Ser X-1. Together with the fact that the emission lines are remarkably narrow, but still resolved, we show that a main-sequence K dwarf together with a canonical 1.4 M? neutron star gives a good description of the system. In this scenario, the most likely place for the emission lines to arise is the accretion disc, instead of a localized region in the binary (such as the irradiated surface or the stream-impact point), and their narrowness is due instead to the low inclination (?10°) of Ser X-1
The L-p-to-L-q boundedness of commutators with applications to the Jacobian operator
No full textSupplying the missing necessary conditions, we complete the characterisation of the L-p -> L-q boundedness of commutators [b, T] of pointwise multiplication and Calderon-Zygmund operators, for arbitrary pairs of 1 q, our results are new even for special classical operators with smooth kernels. As an application, we show that every f is an element of L-p(R-d) can be represented as a convergent series of normalised Jacobians J(u) = det del uof u is an element of (over dot(W))(1,dp)(R-d)(d). This extends, from p = 1 to p > 1, a result of Coifman, Lions, Meyer and Semmes about J:. (over dot(W))(1,d)(R-d)(d) -> H-1(R-d), and supports a conjecture of Iwaniec about the solvability of the equation Ju = f is an element of L-p(R-d). (C) 2021 The Author(s). Published by Elsevier Masson SAS.Peer reviewe
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
Precision measurements of B[psi(3686) -> pi(+)pi(-)J/psi] and B[J/psi -> l(+)l(-)]
No full text<p>Based on (106.41 +/- 0.86) x 10(6) psi(3686) events collected with the BESIII detector at the BEPCII collider, the branching fractions of psi(3686) -> pi(+)pi(-)J/psi, J/psi -> e(+)e(-), and J/psi -> mu(+)mu(-) are measured. We obtain B[psi(3686) -> pi(+)pi(-)J/psi] = (34.98 +/- 0.02 +/- 0.45)%, B[J/psi -> e(+)e(-)] = (5.983 +/- 0.007 +/- 0.037)%, and B[J/psi -> mu(+)mu(-)] = (5.973 +/- 0.0007 +/- 0.038)%. The measurement of B[psi(3686) -> pi(+)pi(-)J/psi] confirms the CLEO-c measurement, and is apparently larger than the others. The measured J/psi leptonic decay branching fractions agree with previous experiments within one standard deviation. These results lead to B[J/psi -> l(+)l(-)] = (5.978 +/- 0.005 +/- 0.040)% by averaging over the e(+)e(-) and mu(+)mu(-) channels and a ratio of B[J/psi -> e(+)e(-)]/B[J/psi -> mu(+)mu(-)] = 1.0017 +/- 0.0017 +/- 0.0033, which tests e- mu universality at the four tenths of a percent level. All the measurements presented in this paper are the most precise in the world to date.</p>
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 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
Hundreds of variants clustered in genomic loci and biological pathways affect human height
No full textMost common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits(1), but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait(2,3). The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P<0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways
Autocrine induction of tumor protease production and invasion by a metallothionein-regulated TGF-beta 1 (Ser223, 225).
No full textAn expression vector was constructed in which TGF-beta-1 was placed under the control of the metallothionein promoter. Cys223 and Cys225 in the TGF-beta-1 propeptide were converted to serines, mutations which result in dissociation of the pro-peptide and secretion of bioactive TGF-beta-1 [Brunner,A.M., Marquardt,H., Malacko,A.R., Lioubin,M.N. and Purchio,A.F. (1989) J. Biol. Chem., 264, 13660-13664]. A fibrosarcoma was transfected with this plasmid and a clone (17.18) was selected in which TGF-beta-1 mRNA was able to be induced six-fold following zinc sulphate treatment. These cells increased the secretion of bioactive TGF-beta-1 14-fold and exhibited a coincidental increase in jun-B mRNA expression, suggesting that secreted TGF-beta-1 was acting to induce this early response gene by autocrine activation. Following zinc sulphate induction, the tumor cells became progressively more motile and able to invade collagen gels. In contrast to parental tumor not bearing the TGF-beta-1 expression vector, zinc sulphate stimulation of clone 17.18 enhanced collagenase IV and procathepsin L mRNA levels and enhanced the secretion of many collagenolytic proteases into the medium. Since the action of TGF-beta generally decreases proteolysis by suppression of protease transcription, we compared the response of normal parental fibroblasts to ras-transformed fibrosarcomas and confirmed that TGF-beta could greatly enhance collagenase IV and procathepsin L mRNA levels while having little effect on non-transformed fibroblasts. These experiments indicate that induction of TGF-beta secretion can enhance motility and protease production through autocrine activation, thus increasing the invasion potential of fibrosarcomas.PT: J; CR: ANZANO MA, 1985, MOL CELL BIOL, V5, P242 BARNARD JA, 1990, BIOCHIM BIOPHYS ACTA, V1032, P79 BERNHARD EJ, 1990, CANCER RES, V50, P3872 BRUNNER AM, 1989, J BIOL CHEM, V264, P13660 CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156 COFFEY RJ, 1987, CANCER RES, V47, P4590 DANIELPOUR D, 1989, J CELL PHYSIOL, V138, P79 DERYNCK R, 1987, CANCER RES, V47, P707 EDWARDS DR, 1987, EMBO J, V6, P1889 EGAN SE, 1987, MOL CELL BIOL, V7, P830 FELGNER PL, 1987, P NATL ACAD SCI USA, V84, P7413 GARBISA S, 1987, CANCER RES, V47, P1523 GENTRY LE, 1988, MOL CELL BIOL, V8, P4162 HEUSSEN C, 1980, ANAL BIOCHEM, V102, P196 KIM SJ, 1989, J BIOL CHEM, V264, P402 KIM SJ, 1989, J BIOL CHEM, V264, P7041 LAIHO M, 1986, J CELL BIOL 1, V103, P2403 LAIHO M, 1987, J BIOL CHEM, V262, P17467 LAWRENCE D, 1985, BIOCHEM BIOPH RES CO, V133, P1026 LIOTTA LA, 1988, CANCER SURV, V7, P631 LIOTTA LA, 1990, CANCER METAST REV, V9, P285 LIOTTA LA, 1991, CELL, V64, P327 LYONS RM, 1988, J CELL BIOL, V106, P1659 MASON RW, 1987, BIOCHEM J, V248, P449 MASSAGUE J, 1990, ANNU REV CELL BIOL, V6, P597 MATRISIAN LM, 1986, MOL CELL BIOL, V6, P1679 MATRISIAN LM, 1986, P NATL ACAD SCI USA, V83, P9413 MCDONNELL SE, 1990, MOL CELL BIOL, V10, P4284 NATHAN C, 1991, J CELL BIOL, V113, P981 OSTROWSKI LE, 1988, MOL CARCINOGEN, V1, P13 PERTOVAARA L, 1989, MOL CELL BIOL, V9, P1255 POSTLETHWAITE AE, 1987, J EXP MED, V165, P251 ROBERTS AB, 1988, BRIT J CANCER, V57, P594 ROBERTS AB, 1989, PEPTIDE GROWTH FACTO ROBERTS AB, 1990, PHILOS T ROY SOC B, V327, P145 SATO Y, 1989, J CELL BIOL, V109, P309 SCHOR SL, 1982, INT J CANCER, V29, P57 SCHWARZ LC, 1988, CANCER RES, V48, P6999 SCHWARZ LC, 1990, GROWTH FACTORS, V3, P115 SHIELDS JM, 1984, IMMUNOLOGY, V51, P259 SLOANE BF, 1986, P NATL ACAD SCI USA, V83, P2483 SPORN MB, 1985, NATURE, V313, P745 STETLERSTEVENSO.WG, 1990, CANCER METAST REV, V9, P289 STETLERSTEVENSO.WG, 1990, J BIOL CHEM, V265, P13933 WAHL SM, 1987, P NATL ACAD SCI USA, V84, P5788 WAKEFIELD LM, 1988, J BIOL CHEM, V263, P7646 WEIDNER KM, 1990, J CELL BIOL, V111, P2097 WELCH DR, 1990, P NATL ACAD SCI USA, V87, P7678 WILHELM SM, 1989, J BIOL CHEM, V264, P17213; NR: 49; TC: 113; J9: EMBO J; PG: 7; GA: HM836Source type: Electronic(1
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