Υ and Υ′ leptonic widths, abμ, and mb from full lattice QCD

We determine the decay rate to leptons of the ground-state ϒ meson and its first radial excitation in lattice QCD for the first time. We use radiatively improved nonrelativistic QCD for the b quarks and include u, d, s and c quarks in the sea with u=d masses down to their physical values. We find Γðϒ → eþe−Þ ¼ 1.19ð11Þ keV and Γðϒ0 → eþe−Þ ¼ 0.69ð9Þ keV, both in good agreement with experimental results. The decay constants we obtain are included in a summary plot of meson decay constants from lattice QCD given in the Conclusions. We also test time moments of the vector current-current correlator against values determined from the b-quark contribution to σðeþe− → hadronsÞ and calculate the b-quark piece of the hadronic vacuum polarization contribution to the anomalous magnetic moment of the muon, ab μ ¼ 0.271ð37Þ × 10−10. Finally we determine the b-quark mass, obtaining in the MS scheme, ¯ m¯ bðm¯ b; nf ¼ 5Þ ¼ 4.196ð23Þ GeV, the most accurate result from lattice QCD to date

B-meson decay constants: a more complete picture from full lattice QCD

We extend the picture of $B$-meson decay constants obtained in lattice QCD beyond those of the $B$, $B_s$ and $B_c$ to give the first full lattice QCD results for the $B^*$, $B^*_s$ and $B^*_c$. We use improved NonRelativistic QCD for the valence $b$ quark and the Highly Improved Staggered Quark (HISQ) action for the lighter quarks on gluon field configurations that include the effect of $u/d$, $s$ and $c$ quarks in the sea with $u/d$ quark masses going down to physical values. For the ratio of vector to pseudoscalar decay constants, we find $f_{B^*}/f_B$ = 0.941(26), $f_{B^*_s}/f_{B_s}$ = 0.953(23) (both $2\sigma$ less than 1.0) and $f_{B^*_c}/f_{B_c}$ = 0.988(27). Taking correlated uncertainties into account we see clear indications that the ratio increases as the mass of the lighter quark increases. We compare our results to those using the HISQ formalism for all quarks and find good agreement both on decay constant values when the heaviest quark is a $b$ and on the dependence on the mass of the heaviest quark in the region of the $b$. Finally, we give an overview plot of decay constants for gold-plated mesons, the most complete picture of these hadronic parameters to date.Comment: 20 pages, 9 figures. Minor updates to the discussion in several places and some additional reference

A lattice investigation of exotic tetraquark channels

We perform an $n_f=2+1$ lattice study of a number of channels where past claims exist in the literature for the existence of strong-interaction-stable light-heavy tetraquarks. We find no evidence for any such deeply-bound states, beyond the $J^P=1^+$, $I=0$ $ud\bar{b}\bar{b}$ and $I=1/2$ $ls\bar{b}\bar{b}$ states already identified in earlier lattice studies. We also describe a number of systematic improvements to our previous lattice studies, including working with larger $m_\pi L$ to better suppress possible finite volume effects, employing extended sinks to better control excited-state contamination, and expanding the number of operators used in the GEVP analyses. Our results also allow us to rule out several phenomenological models which predict significant tetraquark binding in channels where no such binding is found.Comment: 41 pages, 12 figure

Entropy Production of Brownian Macromolecules with Inertia

We investigate the nonequilibrium steady-state thermodynamics of single Brownian macromolecules with inertia under feedback control in isothermal ambient fluid. With the control being represented by a velocity-dependent external force, we find such open systems can have a negative entropy production rate and we develop a mesoscopic theory consistent with the second law. We propose an equilibrium condition and define a class of external forces, which includes a transverse Lorentz force, leading to equilibrium.Comment: 10 pages, 1 figur

The response of the tandem pore potassium channel TASK-3 (K2P9.1) to voltage : gating at the cytoplasmic mouth

Although the tandem pore potassium channel TASK-3 is thought to open and shut at its selectivity filter in response to changes of extracellular pH, it is currently unknown whether the channel also shows gating at its inner, cytoplasmic mouth through movements of membrane helices M2 and M4.We used two electrode voltage clamp and single channel recording to show that TASK-3 responds to voltage in a way that reveals such gating. In wild-type channels, Popen was very low at negative voltages, but increased with depolarisation. The effect of voltage was relatively weak and the gating charge small, ∼0.17.Mutants A237T (in M4) and N133A (in M2) increased Popen at a given voltage, increasing mean open time and the number of openings per burst. In addition, the relationship between Popen andvoltagewas shifted to lesspositive voltages. Mutation of putative hinge glycines (G117A, G231A), residues that are conserved throughout the tandem pore channel family, reduced Popen at a given voltage, shifting the relationship with voltage to a more positive potential range. None of these mutants substantially affected the response of the channel to extracellular acidification. We have used the results from single channel recording to develop a simple kinetic model to show how gating occurs through two classes of conformation change, with two routes out of the open state, as expected if gating occurs both at the selectivity filter and at its cytoplasmic mouth

Mechanical behaviour of degradable phosphate glass fibres and composites-a review

Biodegradable materials are potentially an advantageous alternative to the traditional metallic fracture fixation devices used in the reconstruction of bone tissue defects. This is due to the occurrence of stress shielding in the surrounding bone tissue that arises from the absence of mechanical stimulus to the regenerating bone due to the mismatch between the elastic modulus of bone and the metal implant. However although degradable polymers may alleviate such issues, these inert materials possess insufficient mechanical properties to be considered as a suitable alternative to current metallic devices at sites of sufficient mechanical loading. Phosphate based glasses are an advantageous group of materials for tissue regenerative applications due to their ability to completely degrade in vivo at highly controllable rates based on the specific glass composition. Furthermore the release of the glass's constituent ions can evoke a therapeutic stimulus in vivo (i.e. osteoinduction) whilst also generating a bioactive response. The processing of these materials into fibres subsequently allows them to act as reinforcing agents in degradable polymers to simultaneously increase its mechanical properties and enhance its in vivo response. However despite the various review articles relating to the compositional influences of different phosphate glass systems, there has been limited work summarising the mechanical properties of different phosphate based glass fibres and their subsequent incorporation as a reinforcing agent in degradable composite materials. As a result, this review article examines the compositional influences behind the development of different phosphate based glass fibre compositions intended as composite reinforcing agents along with an analysis of different potential composite configurations. This includes variations in the fibre content, matrix material and fibre architecture as well as other novel composites designs

Identification of amino acid residues of the NR2A subunit that control glutamate potency in recombinant NR1/NR2A NMDA receptors

The NMDA type of ligand-gated glutamate receptor requires the presence of both glutamate and glycine for gating. These receptors are hetero-oligomers of NR1 and NR2 subunits. Previously it was thought that the binding sites for glycine and glutamate were formed by residues on the NR1 subunit. Indeed, it has been shown that the effects of glycine are controlled by residues on the NR1 subunit, and a “Venus flytrap” model for the glycine binding site has been suggested by analogy with bacterial periplasmic amino acid binding proteins. By analysis of 10 mutant NMDA receptors, we now show that residues on the NR2A subunit control glutamate potency in recombinant NR1/NR2A receptors, without affecting glycine potency. Furthermore, we provide evidence that, at least for some mutated residues, the reduced potency of glutamate cannot be explained by alteration of gating but has to be caused primarily by impairing the binding of the agonist to the resting state of the receptor. One NR2A mutant, NR2A(T671A), had anEC50for glutamate 1000-fold greater than wild type and a 255-fold reduced affinity for APV, yet it had single-channel openings very similar to those of wild type. Therefore we propose that the glutamate binding site is located on NR2 subunits and (taking our data together with previous work) is not on the NR1 subunit. Our data further imply that each NMDA receptor subunit possesses a binding site for an agonist (glutamate or glycine).</jats:p