156 research outputs found

    The pion vector form factor from lattice QCD and NNLO chiral perturbation theory

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    We present a comprehensive study of the electromagnetic form factor, the decay constant and the mass of the pion computed in lattice QCD with two degenerate O(a)-improved Wilson quarks at three different lattice spacings in the range 0.05-0.08fm and pion masses between 280 and 630MeV at mπ L ≥ 4. Using partially twisted boundary conditions and stochastic estimators, we obtain a dense set of precise data points for the form factor at very small momentum transfers, allowing for a model-independent extraction of the charge radius. Chiral Perturbation Theory (ChPT) augmented by terms which model lattice artefacts is then compared to the data. At next-to-leading order the effective theory fails to produce a consistent description of the full set of pion observables but describes the data well when only the decay constant and mass are considered. By contrast, using the next-to-next-to-leading order expressions to perform global fits result in a consistent description of all data. We obtain ⟨r2π⟩ = 0.481(33)(13)fm2 as our final result for the charge radius at the physical point. Our calculation also yields estimates for the pion decay constant in the chiral limit, Fπ/F = 1.080(16)(6), the quark condensate, Σ1/3MSbar (2GeV) = 261(13)(1)MeV and several low-energy constants of SU(2) ChPT

    Stringing Spins and Spinning Strings

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    We apply recently developed integrable spin chain and dilatation operator techniques in order to compute the planar one-loop anomalous dimensions for certain operators containing a large number of scalar fields in N =4 Super Yang-Mills. The first set of operators, belonging to the SO(6) representations [J,L-2J,J], interpolate smoothly between the BMN case of two impurities (J=2) and the extreme case where the number of impurities equals half the total number of fields (J=L/2). The result for this particular [J,0,J] operator is smaller than the anomalous dimension derived by Frolov and Tseytlin [hep-th/0304255] for a semiclassical string configuration which is the dual of a gauge invariant operator in the same representation. We then identify a second set of operators which also belong to [J,L-2J,J] representations, but which do not have a BMN limit. In this case the anomalous dimension of the [J,0,J] operator does match the Frolov-Tseytlin prediction. We also show that the fluctuation spectra for this [J,0,J] operator is consistent with the string prediction.Comment: 27 pages, 4 figures, LaTex; v2 reference added, typos fixe

    Association between the Perioperative Antioxidative Ability of Platelets and Early Post-Transplant Function of Kidney Allografts: A Pilot Study

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    BACKGROUND: Recent studies have demonstrated that the actions of platelets may unfavorably influence post-transplant function of organ allografts. In this study, the association between post-transplant graft function and the perioperative activity of platelet antioxidants was examined among kidney recipients divided into early (EGF), slow (SGF), and delayed graft function (DGF) groups. METHODOLOGY/PRINCIPAL FINDINGS: Activities of superoxide dismutase, catalase, glutathione transferase (GST), glutathione peroxidase, and glucose-6-phosphate dehydrogenase (G6P) were determined and levels of glutathione, oxidized glutathione, and isoprostane were measured in blood samples collected immediately before and during the first and fifth minutes of renal allograft reperfusion. Our results demonstrated a significant increase in isoprostane levels in all groups. Interestingly, in DGF patients, significantly lower levels of perioperative activity of catalase (p<0.02) and GST (p<0.02) were observed. Moreover, in our study, the activity of platelet antioxidants was associated with intensity of perioperative oxidative stress. For discriminating SGF/DGF from EGF, sensitivity, specificity, and positive and negative predictive values of platelet antioxidants were 81-91%, 50-58%, 32-37%, and 90-90.5%, respectively. CONCLUSIONS: During renal transplantation, significant changes occur in the activity of platelet antioxidants. These changes seem to be associated with post-transplant graft function and can be potentially used to differentiate between EGF and SGF/DGF. To the best of our knowledge, this is the first study to reveal the potential protective role of platelets in the human transplantation setting

    Loss of the coxsackie and adenovirus receptor contributes to gastric cancer progression

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    Loss of the coxsackie and adenovirus receptor (CAR) has previously been observed in gastric cancer. The role of CAR in gastric cancer pathobiology, however, is unclear. We therefore analysed CAR in 196 R0-resected gastric adenocarcinomas and non-cancerous gastric mucosa samples using immunohistochemistry and immunofluorescence. Coxsackie and adenovirus receptor was found at the surface and foveolar epithelium of all non-neoplastic gastric mucosa samples (n=175), whereas only 56% of gastric cancer specimens showed CAR positivity (P<0.0001). Loss of CAR correlated significantly with decreased differentiation, increased infiltrative depths, presence of distant metastases, and was also associated with reduced carcinoma-specific survival. To clarify whether CAR impacts the tumorbiologic properties of gastric cancer, we subsequently determined the role of CAR in proliferation, migration, and invasion of gastric cancer cell lines by application of specific CAR siRNA or ectopic expression of a human full-length CAR cDNA. These experiments showed that RNAi-mediated CAR knock down resulted in increased proliferation, migration, and invasion of gastric cancer cell lines, whereas enforced ectopic CAR expression led to opposite effects. We conclude that the association of reduced presence of CAR in more severe disease states, together with our findings in gastric cancer cell lines, suggests that CAR functionally contributes to gastric cancer pathogenesis, showing features of a tumour suppressor

    Targeting lymphangiogenesis to prevent tumour metastasis

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    Recent studies involving animal models of cancer and clinicopathological analyses of human tumours suggest that the growth of lymphatic vessels (lymphangiogenesis) in or nearby tumours is associated with the metastatic spread of cancer. The best validated molecular signalling system for tumour lymphangiogenesis involves the secreted proteins vascular endothelial growth factor-C (VEGF-C) and VEGF-D that induce growth of lymphatic vessels via activation of VEGF receptor-3 (VEGFR-3) localised on the surface of lymphatic endothelial cells. In this review, we discuss the evidence supporting a role for this signalling system in the spread of cancer and potential approaches for blocking this system to prevent tumour metastasis
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