The in vitro bioactivity of two novel hydrophilic, partially degradable bone cements

Composite bone cements were prepared with bioactive glasses (MgO–SiO2–3CaO Æ P2O5) of different reactivities. The matrix of these so-called hydrophilic, partially degradable and bioactive cements was composed of a starch/cellulose acetate blend and poly(2-hydroxyethyl methacrylate). The addition of 30 wt.% of glasses to this system made them bioactive in acellular medium: a dense apatite layer formed on the surface after 7 days of immersion in simulated body fluid. This was demonstrated both by microscopic and infrared spectroscopic techniques. The composition of the glass and, consequently, its structure was found to have important effects on the rate of the apatite formation. The combination of reactivity obtained by one formulation with the hydrophilic and degradable character of these cements makes them a very promising alternative to conventional acrylic bone cements, by allowing a better stabilization of the implant and a stronger adhesion to the bone

Search for the doubly heavy baryon Ξbc+\it{\Xi}_{bc}^{+} decaying to J/ψΞc+J/\it{\psi} \it{\Xi}_{c}^{+}

A first search for the $\it{\Xi}_{bc}^{+}\to J/\it{\psi}\it{\Xi}_{c}^{+}$ decay is performed by the LHCb experiment with a data sample of proton-proton collisions, corresponding to an integrated luminosity of $9\,\mathrm{fb}^{-1}$ recorded at centre-of-mass energies of 7, 8, and $13\mathrm{\,Te\kern -0.1em V}$. Two peaking structures are seen with a local (global) significance of $4.3\,(2.8)$ and $4.1\,(2.4)$ standard deviations at masses of $6571\,\mathrm{Me\kern -0.1em V\!/}c^2$ and $6694\,\mathrm{Me\kern -0.1em V\!/}c^2$, respectively. Upper limits are set on the $\it{\Xi}_{bc}^{+}$ baryon production cross-section times the branching fraction relative to that of the $B_{c}^{+}\to J/\it{\psi} D_{s}^{+}$ decay at centre-of-mass energies of 8 and $13\mathrm{\,Te\kern -0.1em V}$, in the $\it{\Xi}_{bc}^{+}$ and in the $B_{c}^{+}$ rapidity and transverse-momentum ranges from 2.0 to 4.5 and 0 to $20\,\mathrm{Ge\kern -0.1em V\!/}c$, respectively. Upper limits are presented as a function of the $\it{\Xi}_{bc}^{+}$ mass and lifetime.Comment: All figures and tables, along with machine-readable versions and any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-005.html (LHCb public pages

Measurement of CP asymmetries and branching fraction ratios of B− decays to two charm mesons

The $CP$ asymmetries of seven $B^-$ decays to two charm mesons are measured using data corresponding to an integrated luminosity of $9\text{fb}^{-1}$ of proton-proton collisions collected by the LHCb experiment. Decays involving a $D^{*0}$ or $D^{*-}_s$ meson are analysed by reconstructing only the $D^0$ or $D^-_s$ decay products. This paper presents the first measurement of $\mathcal{A}^{CP}(B^- \rightarrow D^{*-}_s D^0)$ and $\mathcal{A}^{CP}(B^- \rightarrow D^{-}_s D^{*0})$, and the most precise measurement of the other five $CP$ asymmetries. There is no evidence of $CP$ violation in any of the analysed decays. Additionally, two ratios between branching fractions of selected decays are measured.The CP asymmetries of seven B$^{−}$ decays to two charm mesons are measured using data corresponding to an integrated luminosity of 9 fb$^{−1}$ of proton-proton collisions collected by the LHCb experiment. Decays involving a D$^{*0}$ or ${D}_s^{\ast -}$ meson are analysed by reconstructing only the D$^{0}$ or ${D}_s^{-}$ decay products. This paper presents the first measurement of $\mathcal{A} ^{CP}$(B$^{−}$→${D}_s^{\ast -}$D$^{0}$) and $\mathcal{A} ^{CP}$(B$^{−}$→${D}_s^{-}$D$^{∗0}$), and the most precise measurement of the other five CP asymmetries. There is no evidence of CP violation in any of the analysed decays. Additionally, two ratios between branching fractions of selected decays are measured.[graphic not available: see fulltext]The $CP$ asymmetries of seven $B^-$ decays to two charm mesons are measured using data corresponding to an integrated luminosity of $9\text{ fb}^{-1}$ of proton-proton collisions collected by the LHCb experiment. Decays involving a $D^{*0}$ or $D^{*-}_s$ meson are analysed by reconstructing only the $D^0$ or $D^-_s$ decay products. This paper presents the first measurement of $\mathcal{A}^{CP}(B^- \rightarrow D^{*-}_s D^0)$ and $\mathcal{A}^{CP}(B^- \rightarrow D^{-}_s D^{*0})$, and the most precise measurement of the other five $CP$ asymmetries. There is no evidence of $CP$ violation in any of the analysed decays. Additionally, two ratios between branching fractions of selected decays are measured

Helium identification with LHCb

The identification of helium nuclei at LHCb is achieved using a method based on measurements of ionisation losses in the silicon sensors and timing measurements in the Outer Tracker drift tubes. The background from photon conversions is reduced using the RICH detectors and an isolation requirement. The method is developed using pp collision data at √(s) = 13 TeV recorded by the LHCb experiment in the years 2016 to 2018, corresponding to an integrated luminosity of 5.5 fb-1. A total of around 105 helium and antihelium candidates are identified with negligible background contamination. The helium identification efficiency is estimated to be approximately 50% with a corresponding background rejection rate of up to O(10^12). These results demonstrate the feasibility of a rich programme of measurements of QCD and astrophysics interest involving light nuclei

Momentum scale calibration of the LHCb spectrometer

For accurate determination of particle masses accurate knowledge of the momentum scale of the detectors is crucial. The procedure used to calibrate the momentum scale of the LHCb spectrometer is described and illustrated using the performance obtained with an integrated luminosity of 1.6 fb-1 collected during 2016 in pp running. The procedure uses large samples of J/ψ → μ + μ - and B+ → J/ψ K + decays and leads to a relative accuracy of 3 × 10-4 on the momentum scale

Curvature-bias corrections using a pseudomass method

Momentum measurements for very high momentum charged particles, such as muons from electroweak vector boson decays, are particularly susceptible to charge-dependent curvature biases that arise from misalignments of tracking detectors. Low momentum charged particles used in alignment procedures have limited sensitivity to coherent displacements of such detectors, and therefore are unable to fully constrain these misalignments to the precision necessary for studies of electroweak physics. Additional approaches are therefore required to understand and correct for these effects. In this paper the curvature biases present at the LHCb detector are studied using the pseudomass method in proton-proton collision data recorded at centre of mass energy √(s)=13 TeV during 2016, 2017 and 2018. The biases are determined using Z→μ + μ - decays in intervals defined by the data-taking period, magnet polarity and muon direction. Correcting for these biases, which are typically at the 10-4 GeV-1 level, improves the Z→μ + μ - mass resolution by roughly 18% and eliminates several pathological trends in the kinematic-dependence of the mean dimuon invariant mass

Muscarinic receptor-mediated activation of p70 S6 kinase 1 (S6K1) in 1321N1 astrocytoma cells: permissive role of phosphoinositide 3-kinase

In 1321N1 astrocytoma cells, carbachol stimulation of M3 muscarinic cholinergic receptors, coupled to phospholipase C, evoked a persistent 10–20-fold activation of p70 S6 kinase (S6K1). This response was abolished by chelation of cytosolic Ca2+ and reproduced by the Ca2+ ionophore ionomycin, but was not prevented by down-regulation or inhibition of protein kinase C. Carbachol-stimulated activation and phosphorylation of S6K1 at Thr389 were prevented by rapamycin, an inhibitor of mTOR (mammalian target of rapamycin), or by wortmannin, a phosphoinositide 3-kinase (PI3K) inhibitor. Carbachol also stimulated the phosphorylation of eukaryotic initiation factor 4E-binding protein-1 (4E-BP1), a second mTOR-dependent event, with similar potency to its effect on S6K1. This response was blocked by rapamycin, but was not markedly affected by 100 nM wortmannin, implying separate roles for mTOR and PI3K in S6K1 activation. Wortmannin abolished the carbachol-stimulated rise in PtdIns(3,4,5)P3 and greatly reduced unstimulated levels of this lipid. By contrast, an inhibitor of epidermal growth factor receptor kinase, AG1478, which prevents carbachol-stimulated ErbB3 transactivation, PI3K recruitment and protein kinase B activation in 1321N1 cells, reduced activation of S6K1 by no more than 30%. This effect was overcome by 10 nM insulin, which on its own did not stimulate S6K1, but increased cellular PtdIns(3,4,5)P3 concentrations comparably with carbachol alone. These observations distinguish obligatory roles for mTOR and PI3K in regulating S6K1, but imply that minimal PI3K activity is sufficient to permit stimulation of S6K1 by other activating factors such as increased cytosolic Ca2+ concentrations, which are essential to the muscarinic receptor-mediated response. Moreover, 4E-BP1 and hence, presumably, mTOR can be regulated independently of PI3K activation through these mechanisms

Differential coupling of G-protein-linked receptors to Ca2+mobilization through inositol(1,4,5)trisphosphate or ryanodine receptors in cerebellar granule cells in primary culture

Rat cerebellar granule cells in primary culture possess muscarinic, metabotropic glutamatergic, histaminergic and α‐adrenergic receptors which couple to phosphoinositide‐specific phospholipase C. We have determined the ability of these receptors to elevate inositol(1,4,5)trisphosphate and to release intracellular calcium, in order to establish the correlation between these two responses. In resting cerebellar granule cells, only the muscarinic agonist carbachol evoked significant increases in both inositol(1,4,5)trisphosphate and cytoplasmic free Ca2+. Mild depolarization (20 mm KCl) enhanced inositol(1,4,5)trisphosphate elevation by carbachol and histamine, but not by noradrenaline or the metabotropic glutamate agonist 1S,3R ACPD. In contrast, Ca2+‐release responses were modified differently by 20 mm KCl‐depolarization: the responses to carbachol, histamine and 1S,3R ACPD, but not the responses to noradrenaline, were markedly enhanced. The contribution of ryanodine‐sensitive Ca2+‐release channels (ryanodine receptors) to the calcium release signal in depolarized cells was determined. Ryanodine (10 μm) inhibited most effectively the cytoplasmic Ca2+ elevation evoked by 1S,3R ACPD (> 90%), while Ca2+ release upon stimulation by carbachol and histamine was only inhibited by ≈ 60% and remained larger than in the absence of KCl. Our data are consistent with a specific coupling between metabotropic glutamate receptors and ryanodine‐sensitive Ca2+‐release channels which may not require generation of inositol(1,4,5)trisphosphate

The stereoselective recognition of substrates by phosphoinositide kinases.

Soluble phosphatidylinositol (PtdIns) 4- and 3-kinase activities were partially purified and characterized from human placental extracts. The placental PtdIns 4-kinase (type 3) has a K(m) for ATP of 460 M and is kinetically different to a partially purified human erythrocyte, membrane- bound, PtdIns 4-kinase (type 2). These three inositol lipid kinases were then used to compare their substrate specificities against the four synthetic stereoisomers of dipalmitoyl PtdIns. Only the placental 4-kinase was influenced by the chirality of the glycerol moiety of PtdIns. However, neither of the 4-kinases was able to phosphorylate. L-PtdIns and, therefore, these kinases have an absolute requirement for the inositol ring to be linked to the glyceryl backbone of the lipid through the D-1 position. Phosphoinositide 3-kinase, on the other hand, was found to phosphorylate both D- and L-PtdIns. While the 3-kinase phosphorylated exclusively the D-3 position of D-PtdIns, further analyses demonstrated that the same enzyme phosphorylated two sites on L-PtdIns, namely the D-6 and D-5 positions of the inositol ring. Some implications of these findings are discussed