50,889 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)
A review of flow-induced noise from finite wall-mounted cylinders
No full textAbstract not availableRic Porteous, Danielle J. Moreau, Con J. Doola
Flow-induced noise of a wall-mounted finite airfoil at low-to-moderate Reynolds number
No full textAbstract not availableDanielle J.Moreau, Zebb Prime, Ric Porteous, Con J. Doolan, Vincent Valea
Measurement of the B0–B0 oscillation frequency Δmd with the decays B0→D−π+ and B0→ J/ψK∗0
No full textThe B
0
–B
0
oscillation frequency Δmd is measured by the LHCb experiment using a dataset corresponding
to an integrated luminosity of 1.0 fb−1
of proton–proton collisions at √
s = 7 TeV, and is found to be
Δmd
=0.5156±0.0051 (stat.)±0.0033 (syst.) ps−1
. The measurement is based on results from analyses
of the decays B
0
→ D
−π
+ (D
−
→ K
+π
−π
−) and B
0
→ J/ψK
∗0
(J/ψ →μ
+μ
−,K
∗0
→ K
+π
−) and
their charge conjugated modes
Search for the rare decays J/y -> D-s(-) rho(+) and J/psi -> <(D)over bar(0)<(K)over bar*(0)
No full textA search for the rare decays of J/psi -> D-S(-) rho(+) + c.c. and J/psi -> D-S(-)rho(+) + c.c.) <1.3 x 10(-5) and beta(J/psi -
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
Modulation of NMDA receptor surface expression by DISC1 and its pathway partners
No full textDisrupted in Schizophrenia 1 (DISC1) is a well supported risk factor for
schizophrenia, bipolar disorder and major recurrent depression. DISC1 is a
multifunctional multicompartmentalised scaffold protein with essential roles in
neuronal proliferation, differentiation, migration and integration. DISC1 also
modulates pathways of vital importance for neuronal signalling and plasticity. One of
the major hypotheses for the cause of psychiatric illness is N-methyl-D-aspartate
(NMDA) receptor hypofunction. It was observed that NMDA receptor antagonists
can induce symptoms of schizophrenia in unaffected individuals, and exacerbate
symptoms in patients with schizophrenia. Recent work in our laboratory showed that
DISC1 complexes with NMDA receptors within the cell body and at synapse of
neurons. Here I studied whether DISC1, or DISC1 missense variants, affect the
trafficking of NMDA receptors. This was done by quantifying surface NMDA
receptor expression in the presence of DISC1 or variant DISC1. I found that one
common variant, 607F, causes a significant reduction in surface expressed NMDA
receptors. I went on to show that DISC1 reduces the number of internalised receptors
associating with early RAB5-containing endosomes. This indicates that DISC1 may
be involved in the trafficking and recycling of NMDA receptors, a process that may
be affected by the missense DISC1 variant 607F. Further to this I studied the effects
on NMDA receptor trafficking of DISC1 pathway partners Nuclear Distribution
Element 1 (NDE1) and Trafficking-protein kinesin binding 1 (TRAK1), both
regulators of neuronal intracellular trafficking. Phosphorylation of NDE1 at T131 has
been shown to be modulated by DISC1. Using phospho-mimic and phospho-dead
NDE1 expression constructs I observed a significant reduction in the surface-expressed
NMDA receptors in cells expressing the phospho-mimic form of NDE1.
NDE1 may therefore be involved in the trafficking of NMDA receptors, and this role
may be modulated by phosphorylation of NDE1. Finally, TRAK1 was shown to
associate robustly with the GluN2B subunit, and to decrease the surface expression
of NMDA receptors, most likely by sequestering them. The TRAK1-induced
GluN2B sequestration may be an artefact, but the association of the trafficking
molecule TRAK1 with this subunit may point towards a role in NMDA receptor
trafficking. These proteins have been shown to associate with each other and may
form a complex in order to traffic NMDA receptors. Disruption of this complex by
defective DISC1 expression may affect NMDA receptor trafficking. In the brain this
could conceivably contribute to NMDA receptor hypofunction and the development
of psychiatric illness
Early alterations in airway mucociliary clearance and inflammation of the lamina propria in CF mice
No full text In cystic fibrosis (CF), whether cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction leads to decreased mucociliary clearance and mucus hypersecretion, before bacterial infection, remains an open question. To answer this question, we quantified in a blind trial the mucociliary transport velocity, the histological state, and the degree of inflammation of the tracheal mucosa in 23 cftr(m1HGU/cftr(m1HGU) transgenic mice (Dorin, J. R., P. Dickinson, E. W. F. W. Alton, S. N. Smith, D. M. Geddes, B. J. Stevenson, W. L. Kimber, S. Fleming, A. R. Clark, M. L. Hooper, L. Anderson, R. S. P. Beddington, and D. J. Porteous. Nature Lond. 359: 211-215, 1992) and in 30 control littermates housed in pathogen-free conditions. The nasal and tracheal transepithelial potential difference (PD) measured in basal conditions was significantly more negative in the cftr(m1HGU) mutant mice as compared with the control mice (nasal PD: -7.1 +/- 0.6 and -4.6 +/- 0.5 mV, respectively, P < 0.01; tracheal PD: -30.8 +/- 2.1 and -21.4 +/- 1.8 mV, respectively, P < 0.04). In the cftr(m1HGU)/cftr(m1HGU) mice, the mucociliary transport velocity was significantly lower (14.2 +/- 4.4 microm/mm, P < 0.04) compared with the control mice (30.6 +/- 5.9 microm/mm). The number of inflammatory cells in the lamina propria was significantly higher in the cftr(m1HGU)/cftr(m1HGU) mice (1048.7 +/- 124.7 cells/mm2, P < 0.03) compared with the control mice (640.5 +/- 58.2 cells/mm2). These results suggest that in CF, decreased airway mucociliary clearance and airway submucosal inflammation represent early alterations, before any airway infection. </jats:p
Search for the weak decays J/psi -> D-s(()*()-) e(+)nu(e) + c.c.
No full textUsing a sample of 2.25 x 10(8) J/psi events collected with the BESIII detector at the BEPCII collider, we search for the J/psi semileptonic weak decay J/psi -> D-s(-) e(+)nu(e) +c.c. with a much higher sensitivity than previous searches. We also perform the first search for J/psi -> D-s(*-) e(+) nu(e) + c.c. No significant excess of a signal above background is observed in either channel. At the 90% confidence level, the upper limits are determined to be B(J/psi -> D-s(-) e(+) nu(e) + c.c.) D-s*(-) e(+) nu(e) + c.c.) <1.8 x 10(-6), respectively. Both are consistent with Standard Model predictions
The R&D Tax Incentives
No full textThis article sets out some background information and reflections of the author on the R&D tax incentive schemes included in the Common Corporate Tax Base (CCTB) Proposal. In particular the author analyzes the stimulus to private R&D through ad hoc tax incentives included in the CCTB Proposal and dives into the actual provisions included in the Proposal highlighting the most relevant issues connected with their design and interpretation. Moreover, the author explores the interaction between the CCTB Proposal and the granting by Member States of domestic R&D tax incentives
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