894 research outputs found

    Instanton Contribution to the Proton and Neutron Electric Form Factors

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    We study the instanton contribution to the proton and neutron electric form factors. Using the single instanton approximation, we perform the calculations in a mixed time-momentum representation in order to obtain the form factors directly in momentum space. We find good agreement with the experimentally measured electric form factor of the proton. For the neutron, our result falls short of the experimental data. We argue that this discrepancy is due to the fact that we neglect the contribution of the sea quarks. We compare to lattice calculations and a relativistic version of the quark-diquark model.Comment: 8 pages, 5 figures, updated references, to appear in Phys. Lett.

    What doesn't kill you makes you stranger: Dipeptidyl peptidase-4 (CD26) proteolysis differentially modulates the activity of many peptide hormones and cytokines generating novel cryptic bioactive ligands

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    Dipeptidyl peptidase 4 (DPP4) is an exopeptidase found either on cell surfaces where it is highly regulated in terms of its expression and surface availability (CD26) or in a free/circulating soluble constitutively available and intrinsically active form. It is responsible for proteolytic cleavage of many peptide substrates. In this review we discuss the idea that DPP4-cleaved peptides are not necessarily inactivated, but rather can possess either a modified receptor selectivity, modified bioactivity, new antagonistic activity, or even a novel activity relative to the intact parent ligand. We examine in detail five different major DPP4 substrates: glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), peptide tyrosine-tyrosine (PYY), and neuropeptide Y (NPY), and stromal derived factor 1 (SDF-1 aka CXCL12). We note that discussion of the cleaved forms of these five peptides are underrepresented in the research literature, and are both poorly investigated and poorly understood, representing a serious research literature gap. We believe they are understudied and misinterpreted as inactive due to several factors. This includes lack of accurate and specific quantification methods, sample collection techniques that are inherently inaccurate and inappropriate, and a general perception that DPP4 cleavage inactivates its ligand substrates. Increasing evidence points towards many DPP4-cleaved ligands having their own bioactivity. For example, GLP-1 can work through a different receptor than GLP-1R, DPP4-cleaved GIP can function as a GIP receptor antagonist at high doses, and DPP4-cleaved PYY, NPY, and CXCL12 can have different receptor selectivity, or can bind novel, previously unrecognized receptors to their intact ligands, resulting in altered signaling and functionality. We believe that more rigorous research in this area could lead to a better understanding of DPP4’s role and the biological importance of the generation of novel cryptic ligands. This will also significantly impact our understanding of the clinical effects and side effects of DPP4-inhibitors as a class of anti-diabetic drugs that potentially have an expanding clinical relevance. This will be specifically relevant in targeting DPP4 substrate ligands involved in a variety of other major clinical acute and chronic injury/disease areas including inflammation, immunology, cardiology, stroke, musculoskeletal disease and injury, as well as cancer biology and tissue maintenance in aging

    Gad65 is recognized by t-cells, but not by antibodies from nod-mice

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    Since the 64kDa-protein glutamic acid decarboxylase (GAD) is one of the major autoantigens in T-cell mediated Type 1 diabetes, its relevance as a T-cell antigen needs to be clarified. After isolation of splenic T-cells from non-obese diabetic (NOD) mice, a useful model for human Type 1 diabetes, we found that these T-cells proliferate spontaneously when incubated with human GAD65, but only marginally after incubation with GAD67, both recombinated in the baculovirus system. No effect was observed with non-diabetic NOD mice or with T-cells from H-2 identical NON-NOD-H-2g7 control mice. It has been published previously that NOD mice develop autoantibodies against a 64kDa protein detected with mouse beta cells. In immunoprecipitation experiments with sera from the same NOD mice and 33S-methionine-labelled GAD, no autoantibody binding could be detected. We conclude firstly that GAD65 is an important T-cell antigen which is relevant early in the development of Type 1 diabetes and secondly that there is an antigenic epitope in the human GAD65 molecule recognized by NOD T-cells, but not by NOD autoantibodies precipitating conformational epitopes. Our results therefore provide further evidence that GAD65 is a T-cell antigen in NOD mice, being possibly also involved in very early processes leading to the development of human Type 1 diabetes

    Щодо утворення сімейств атомарних радіальних базисних функцій

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    Наведено схему побудови сімейств атомарних радіальних базисних функцій, які є нескінченно диференційовними фінітними розв'язками функціонально-диференціальних рівнянь, породжених операторами Лапласа та Гельмгольца.The scheme of building a family of atomic radial basis functions which are infinitely differentiable finite solutions of the functional-differential equations containing the Laplace and Helmholtz operators is introduced

    Extended Gari-Krumpelmann model fits to nucleon electromagnetic form factors

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    Nucleon electromagnetic form factor data (including recent data) is fitted with models that respect the confinement and asymptotic freedom properties of QCD. Gari-Krumpelmann (GK) type models, which include the major vector meson pole contributions and at high momentum transfer conform to the predictions of perturbative QCD, are combined with Hohler-Pietarinen (HP) models, which also include the width of the rho meson and the addition of higher mass vector meson exchanges, but do not evolve into the explicit form of PQCD at high momentum transfer. Different parameterizations of the GK model's hadronic form factors, the effect of including the width of the rho meson and the addition of the next (in mass) isospin 1 vector meson are considered. The quality of fit and the consistency of the parameters select three of the combined HP/GK type models. Projections are made to the higher momentum transfers which are relevant to electron-deuteron experiments. The projections vary little for the preferred models, removing much of the ambiguity in electron-nucleus scattering predictions.Comment: 18pp, 7 figures, using RevTeX with BoxedEPS macros; 1 new figure, minor textual changes; email correspondence to [email protected]

    Effect of recent R_p and R_n measurements on extended Gari-Krumpelmann model fits to nucleon electromagnetic form factors

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    The Gari-Krumpelmann (GK) models of nucleon electromagnetic form factors, in which the rho, omega, and phi vector meson pole contributions evolve at high momentum transfer to conform to the predictions of perturbative QCD (pQCD), was recently extended to include the width of the rho meson by substituting the result of dispersion relations for the pole and the addition of rho' (1450) isovector vector meson pole. This extended model was shown to produce a good overall fit to all the available nucleon electromagnetic form factor (emff) data. Since then new polarization data shows that the electric to magnetic ratios R_p and R_n obtained are not consistent with the older G_{Ep} and G_{En} data in their range of momentum transfer. The model is further extended to include the omega' (1419) isoscalar vector meson pole. It is found that while this GKex cannot simultaneously fit the new R_p and the old G_{En} data, it can fit the new R_p and R_n well simultaneously. An excellent fit to all the remaining data is obtained when the inconsistent G_{Ep} and G_{En} is omitted. The model predictions are shown up to momentum transfer squared, Q^2, of 8 GeV^2/c^2.Comment: 14 pages, 8 figures, using RevTeX4; email correspondence to [email protected] ; minor typos corrected, figures added, conclusions extende

    Neutron charge form factor at large q2q^2

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    The neutron charge form factor GEn(q)G_{En}(q) is determined from an analysis of the deuteron quadrupole form factor FC2F_{C2} data. Recent calculations, based on a variety of different model interactions and currents, indicate that the contributions associated with the uncertain two-body operators of shorter range are relatively small for FC2F_{C2}, even at large momentum transfer qq. Hence, GEn(q)G_{En}(q) can be extracted from FC2F_{C2} at large q2q^2 without undue systematic uncertainties from theory.Comment: 8 pages, 3 figure
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