We present updated results for the nucleon axial charge and electromagnetic (EM) form factors, which include a significant increase in statistics for all ensembles (up to 4000 measurements), as well ...as the addition of ensembles with pion masses down to \(m_\pi\sim195\) MeV. We also present results for the average quark momentum fraction. The new data allows us to perform a thorough study of the systematic effects encountered in the lattice extraction. We concentrate on systematic effects due to excited-state contaminations for each of the quantities, which we check using several different time separations between the operators at the source and sink through a comparison of plateau fits and the summed operator insertion method (which provides a mechanism to suppress the excited-state contamination). We confirm our earlier finding that a reliable extraction of the axial charge must be based on a method which eliminates excited-state contaminations. Similar conclusions apply to our EM form factor calculations . The measurements are calculated using the CLS ensembles with non-perturbatively O(a) improved Wilson fermions in \(N_f=2\) QCD.
We present results for the isospin-0 \(\pi\pi\) s-wave scattering length calculated in twisted mass lattice QCD. We use three \(N_f = 2\) ensembles with unitary pion mass at its physical value, ...240~MeV and 330~MeV respectively. We also use a large set of \(N_f = 2 + 1 +1\) ensembles with unitary pion masses varying in the range of 230~MeV - 510~MeV at three different values of the lattice spacing. A mixed action approach with the Osterwalder-Seiler action in the valence sector is adopted to circumvent the complications arising from isospin symmetry breaking of the twisted mass quark action. Due to the relatively large lattice artefacts in the \(N_f = 2 + 1 +1\) ensembles, we do not present the scattering lengths for these ensembles. Instead, taking the advantage of the many different pion masses of these ensembles, we qualitatively discuss the pion mass dependence of the scattering properties of this channel based on the results from the \(N_f = 2 + 1 +1\) ensembles. The scattering length is computed for the \(N_f = 2\) ensembles and the chiral extrapolation is performed. At the physical pion mass, our result \(M_\pi a^\mathrm{I=0}_0 = 0.198(9)(6)\) agrees reasonably well with various experimental measurements and theoretical predictions.
We report on our calculation of the nucleon axial charge gA in QCD with two flavours of dynamical quarks. A detailed investigation of systematic errors is performed, with a particular focus on ...contributions from excited states to three-point correlation functions. The use of summed operator insertions allows for a much better control over such contamination. After performing a chiral extrapolation to the physical pion mass, we find gA=1.223 +/- 0.063 (stat) +0.035 -0.060 (syst), in good agreement with the experimental value.
We present results for the \(I=2\) \(\pi\pi\) scattering length using \(N_f=2+1+1\) twisted mass lattice QCD for three values of the lattice spacing and a range of pion mass values. Due to the use of ...Laplacian Heaviside smearing our statistical errors are reduced compared to previous lattice studies. A detailed investigation of systematic effects such as discretisation effects, volume effects, and pollution of excited and thermal states is performed. After extrapolation to the physical point using chiral perturbation theory at NLO we obtain \(M_\pi a_0=-0.0442(2)_\mathrm{stat}(^{+4}_{-0})_\mathrm{sys}\).
We present physics results from simulations of QCD using \(N_f = 2\) dynamical Wilson twisted mass fermions at the physical value of the pion mass. These simulations were enabled by the addition of ...the clover term to the twisted mass quark action. We show evidence that compared to previous simulations without this term, the pion mass splitting due to isospin breaking is almost completely eliminated. Using this new action, we compute the masses and decay constants of pseudoscalar mesons involving the dynamical up and down as well as valence strange and charm quarks at one value of the lattice spacing, \(a \approx 0.09\) fm. Further, we determine renormalized quark masses as well as their scale-independent ratios, in excellent agreement with other lattice determinations in the continuum limit. In the baryon sector, we show that the nucleon mass is compatible with its physical value and that the masses of the \(\Delta\) baryons do not show any sign of isospin breaking. Finally, we compute the electron, muon and tau lepton anomalous magnetic moments and show the results to be consistent with extrapolations of older ETMC data to the continuum and physical pion mass limits. We mostly find remarkably good agreement with phenomenology, even though we cannot take the continuum and thermodynamic limits.
Form factors in lattice QCD Brandt, B B; Capitani, S; M Della Morte ...
arXiv.org,
06/2011
Paper, Journal Article
Odprti dostop
Lattice simulations of QCD have produced precise estimates for the masses of the lowest-lying hadrons which show excellent agreement with experiment. By contrast, lattice results for the vector and ...axial vector form factors of the nucleon show significant deviations from their experimental determination. We present results from our ongoing project to compute a variety of form factors with control over all systematic uncertainties. In the case of the pion electromagnetic form factor we employ partially twisted boundary conditions to extract the pion charge radius directly from the linear slope of the form factor near vanishing momentum transfer. In the nucleon sector we focus specifically on the possible contamination from contributions of higher excited states. We argue that summed correlation functions offer the possibility of eliminating this source of systematic error. As an illustration of the method we discuss our results for the axial charge, gA, of the nucleon.
We report on our on-going project to compute mesonic and baryonic two- and three-point correlation functions in simulations using Nf=2 flavours of O(a) improved Wilson quarks and the Wilson plaquette ...action. We present performance figures for the DD-HMC algorithm on commodity cluster hardware and discuss the issue of critical slowing down, which is particularly pronounced for the topological charge. The effectiveness of stochastic noise sources and Jacobi smearing are investigated. Our preliminary results obtained at three quark masses on 96x48^3 at beta=5.5 imply that the lattice spacing is about 0.06 fm, while the smallest pion mass in the current runs is around 360 MeV, which corresponds to m_pi*L=5.3.
We present an update on our on-going project to compute hadronic observables for Nf=2 flavours of O(a) improved Wilson fermions at small lattice spacings. The procedure to determine the lattice scale ...via the mass of the Omega baryon is described. Furthermore we present preliminary results for the pion form factor computed using twisted boundary conditions, and report on the implementation of a novel approach to determine the contribution of the hadronic vacuum polarisation to the anomalous magnetic moment of the muon.
Pancreatic ductal adenocarcinomas (PDACs) are highly resistant to treatment due to changes in various signalling pathways. CK1 isoforms play important regulatory roles in these pathways.
We analysed ...the expression levels of CK1 delta and epsilon (CK1delta/in) in pancreatic tumour cells in order to validate the effects of CK1 inhibition by 3-2,4,6-(trimethoxyphenyl)methylidenyl-indolin-2-one (IC261) on their proliferation and sensitivity to anti-CD95 and gemcitabine.
CK1delta/in expression levels were investigated by using western blotting and immunohistochemistry. Cell death was analysed by FACS analysis. Gene expression was assessed by real-time PCR and western blotting. The putative anti-tumoral effects of IC261 were tested in vivo in a subcutaneous mouse xenotransplantation model for pancreatic cancer.
We found that CK1delta/in are highly expressed in pancreatic tumour cell lines and in higher graded PDACs. Inhibition of CK1delta/in by IC261 reduced pancreatic tumour cell growth in vitro and in vivo. Moreover, IC261 decreased the expression levels of several anti-apoptotic proteins and sensitised cells to CD95-mediated apoptosis. However, IC261 did not enhance gemcitabine-mediated cell death either in vitro or in vivo.
Targeting CK1 isoforms by IC261 influences both pancreatic tumour cell growth and apoptosis sensitivity in vitro and the growth of induced tumours in vivo, thus providing a promising new strategy for the treatment of pancreatic tumours.
Circulating branched-chain amino acid (BCAA) levels are elevated in obesity/diabetes and are a sensitive predictor for type 2 diabetes. Here we show in rats that insulin dose-dependently lowers ...plasma BCAA levels through induction of hepatic protein expression and activity of branched-chain α-keto acid dehydrogenase (BCKDH), the rate-limiting enzyme in the BCAA degradation pathway. Selective induction of hypothalamic insulin signaling in rats and genetic modulation of brain insulin receptors in mice demonstrate that brain insulin signaling is a major regulator of BCAA metabolism by inducing hepatic BCKDH. Short-term overfeeding impairs the ability of brain insulin to lower BCAAs in rats. High-fat feeding in nonhuman primates and obesity and/or diabetes in humans is associated with reduced BCKDH protein in liver. These findings support the concept that decreased hepatic BCKDH is a major cause of increased plasma BCAAs and that hypothalamic insulin resistance may account for impaired BCAA metabolism in obesity and diabetes.
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•Insulin, but not glucose, is a major regulator of circulating BCAAs•Hypothalamic insulin lowers plasma BCAAs and induces hepatic BCAA catabolism•Acute overfeeding impairs the ability of brain insulin to lower circulating BCAAs•High-fat feeding in primates or obese/diabetic humans decreases hepatic BCKDH
Circulating branched-chain amino acid (BCAA) levels are elevated in obesity and diabetes. Shin et al. describe a brain insulin pathway that decreases BCAA levels by enhancing its degradation in the liver. High-fat-fed rodents and nonhuman primates, as well as diabetics, have reduced amounts of the enzyme responsible for degradation.
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