41 research outputs found
Ultrahigh sensitivity of slow-light gyroscope
Slow light generated by Electromagnetically Induced Transparency is extremely
susceptible with respect to Doppler detuning. Consequently, slow-light
gyroscopes should have ultrahigh sensitivity
Measurement of prompt hadron production ratios in collisions at 0.9 and 7 TeV
The charged-particle production ratios , , ,
, and are measured with the LHCb detector using of collisions delivered by the LHC at TeV and
at TeV. The measurements are performed as a
function of transverse momentum and pseudorapidity . The
production ratios are compared to the predictions of several Monte Carlo
generator settings, none of which are able to describe adequately all
observables. The ratio is also considered as a function of rapidity
loss, , and is used to constrain models of
baryon transport.Comment: Incorrect entries in Table 2 corrected. No consequences for rest of
pape
Study of the lineshape of the chi(c1) (3872) state
A study of the lineshape of the chi(c1) (3872) state is made using a data sample corresponding to an integrated luminosity of 3 fb(-1) collected in pp collisions at center-of-mass energies of 7 and 8 TeV with the LHCb detector. Candidate chi(c1)(3872) and psi(2S) mesons from b-hadron decays are selected in the J/psi pi(+)pi(-) decay mode. Describing the lineshape with a Breit-Wigner function, the mass splitting between the chi(c1 )(3872) and psi(2S) states, Delta m, and the width of the chi(c1 )(3872) state, Gamma(Bw), are determined to be (Delta m=185.598 +/- 0.067 +/- 0.068 Mev,)(Gamma BW=1.39 +/- 0.24 +/- 0.10 Mev,) where the first uncertainty is statistical and the second systematic. Using a Flatte-inspired model, the mode and full width at half maximum of the lineshape are determined to be (mode=3871.69+0.00+0.05 MeV.)(FWHM=0.22-0.04+0.13+0.07+0.11-0.06-0.13 MeV, ) An investigation of the analytic structure of the Flatte amplitude reveals a pole structure, which is compatible with a quasibound D-0(D) over bar*(0) state but a quasivirtual state is still allowed at the level of 2 standard deviations
Measurement of the CKM angle in and decays with
A measurement of -violating observables is performed using the decays
and , where the meson is
reconstructed in one of the self-conjugate three-body final states and (commonly denoted ). The decays are analysed in bins of the -decay phase space, leading
to a measurement that is independent of the modelling of the -decay
amplitude. The observables are interpreted in terms of the CKM angle .
Using a data sample corresponding to an integrated luminosity of
collected in proton-proton collisions at centre-of-mass
energies of , , and with the LHCb experiment,
is measured to be . The hadronic
parameters , , , and ,
which are the ratios and strong-phase differences of the suppressed and
favoured decays, are also reported
Bi-allelic TTI1 variants cause an autosomal-recessive neurodevelopmental disorder with microcephaly.
Telomere maintenance 2 (TELO2), Tel2 interacting protein 2 (TTI2), and Tel2 interacting protein 1 (TTI1) are the three components of the conserved Triple T (TTT) complex that modulates activity of phosphatidylinositol 3-kinase-related protein kinases (PIKKs), including mTOR, ATM, and ATR, by regulating the assembly of mTOR complex 1 (mTORC1). The TTT complex is essential for the expression, maturation, and stability of ATM and ATR in response to DNA damage. TELO2- and TTI2-related bi-allelic autosomal-recessive (AR) encephalopathies have been described in individuals with moderate to severe intellectual disability (ID), short stature, postnatal microcephaly, and a movement disorder (in the case of variants within TELO2). We present clinical, genomic, and functional data from 11 individuals in 9 unrelated families with bi-allelic variants in TTI1. All present with ID, and most with microcephaly, short stature, and a movement disorder. Functional studies performed in HEK293T cell lines and fibroblasts and lymphoblastoid cells derived from 4 unrelated individuals showed impairment of the TTT complex and of mTOR pathway activity which is improved by treatment with Rapamycin. Our data delineate a TTI1-related neurodevelopmental disorder and expand the group of disorders related to the TTT complex