Renormalization-Scale-Invariant PQCD Predictions for R_e+e- and the Bjorken Sum Rule at Next-to-Leading Order

We discuss application of the physical QCD effective charge $\alpha_V$, defined via the heavy-quark potential, in perturbative calculations at next-to-leading order. When coupled with the Brodsky-Lepage-Mackenzie prescription for fixing the renormalization scales, the resulting series are automatically and naturally scale and scheme independent, and represent unambiguous predictions of perturbative QCD. We consider in detail such commensurate scale relations for the $e^+e^-$ annihilation ratio $R_{e^+e^-}$ and the Bjorken sum rule. In both cases the improved predictions are in excellent agreement with experiment.Comment: 13 Latex pages with 5 figures; to be published in Physical Review

Pseudoscalar Meson Mixing in Effective Field Theory

We show that for any effective field theory of colorless meson fields, the mixing schemes of particle states and decay constants are not only related but also determined exclusively by the kinetic and mass Lagrangian densities. In the general case, these are bilinear in terms of the intrinsic fields and involve non-diagonal kinetic and mass matrices. By applying three consecutive steps this Lagrangian can be reduced into the standard quadratic form in terms of the physical fields. These steps are : (i) the diagonalization of the kinetic matrix, (ii) rescaling of the fields, and (iii) the diagonalization of the mass matrix. In case, where the dimensions of the non-diagonal kinetic and mass sub-matrices are respectively, $k\times k$ and $n\times n$, this procedure leads to mixing schemes which involve $[k(k-1)/2] + [n(n-1)/2]$ angles and $k$ field rescaling parameters. This observation holds true irrespective with the type of particle interactions presumed. The commonly used mixing schemes, correspond to a proper choice of the kinetic and mass matrices, and are derived as special cases. In particular, $\eta$-$\eta '$ mixing, requires one angle, if and only if, the kinetic term with the intrinsic fields has a quadratic form.Comment: REVTeX, 6 page

How large could the R-parity violating couplings be?

We investigate in detail the predictions coming from the d=4 operators for proton decay. We find the most general constraints for the R-parity violating couplings coming from proton decay, taking into account all fermion mixing and in different supersymmetric scenarios.Comment: 8 pages, several corrections, to appear in J.Phys.G (2005

Can we distinguish between h^{SM} and h^0 in split supersymmetry?

We investigate the possibility to distinguish between the Standard Model Higgs boson and the lightest Higgs boson in Split Supersymmetry. We point out that the best way to distinguish between these two Higgs bosons is through the decay into two photons. It is shown that there are large differences of several percent between the predictions for \Gamma(h\to\gamma\gamma) in the two models, making possible the discrimination at future photon-photon colliders. Once the charginos are discovered at the next generation of collider experiments, the well defined predictions for the Higgs decay into two photons will become a cross check to identify the light Higgs boson in Split Supersymmetry.Comment: 8 pages, 3 Figures, typos fixed, version published in J.Phys. G31 (2005) 563-56

Electroweak pinch technique to all orders

The generalization of the pinch technique to all orders in the electroweak sector of the Standard Model within the class of the renormalizable 't Hooft gauges, is presented. In particular, both the all-order PT gauge-boson-- and scalar--fermions vertices, as well as the diagonal and mixed gauge-boson and scalar self-energies are explicitly constructed. This is achieved through the generalization to the Standard Model of the procedure recently applied to the QCD case, which consist of two steps: (i) the identification of special Green's functions, which serve as a common kernel to all self-energy and vertex diagrams, and (ii) the study of the (on-shell) Slavnov-Taylor identities they satisfy. It is then shown that the ghost, scalar and scalar--gauge-boson Green's functions appearing in these identities capture precisely the result of the pinching action at arbitrary order. It turns out that the aforementioned Green's functions play a crucial role, their net effect being the non-trivial modification of the ghost, scalar and scalar--gauge-boson diagrams of the gauge-boson-- or scalar--fermions vertex we have started from, in such a way as to dynamically generate the characteristic ghost and scalar sector of the background field method. The pinch technique gauge-boson and scalar self-energies are also explicitly constructed by resorting to the method of the background-quantum identities.Comment: 48 pages, 8 figures; v2: typos correcte

Mesenchymal stromal cells inhibit NLRP3 inflammasome activation in a model of Coxsackievirus B3-induced inflammatory cardiomyopathy

Inflammation in myocarditis induces cardiac injury and triggers disease progression to heart failure. NLRP3 inflammasome activation is a newly identified amplifying step in the pathogenesis of myocarditis. We previously have demonstrated that mesenchymal stromal cells (MSC) are cardioprotective in Coxsackievirus B3 (CVB3)-induced myocarditis. In this study, MSC markedly inhibited left ventricular (LV) NOD2, NLRP3, ASC, caspase-1, IL-1β, and IL-18 mRNA expression in CVB3-infected mice. ASC protein expression, essential for NLRP3 inflammasome assembly, increased upon CVB3 infection and was abrogated in MSC-treated mice. Concomitantly, CVB3 infection in vitro induced NOD2 expression, NLRP3 inflammasome activation and IL-1β secretion in HL-1 cells, which was abolished after MSC supplementation. The inhibitory effect of MSC on NLRP3 inflammasome activity in HL-1 cells was partly mediated via secretion of the anti-oxidative protein stanniocalcin-1. Furthermore, MSC application in CVB3-infected mice reduced the percentage of NOD2-, ASC-, p10- and/or IL-1β- positive splenic macrophages, natural killer cells, and dendritic cells. The suppressive effect of MSC on inflammasome activation was associated with normalized expression of prominent regulators of myocardial contractility and fibrosis to levels comparable to control mice. In conclusion, MSC treatment in myocarditis could be a promising strategy limiting the adverse consequences of cardiac and systemic NLRP3 inflammasome activation

Higgs Boson Mass in Low Scale Gauge Mediation Models

We consider low scale gauge mediation models with a very light gravitino m_{3/2}~16 eV, in the light of recent experimental hints on the Higgs boson mass. The light gravitino is very interesting since there is no gravitino over-production problem, but it seems difficult to explain the Higgs boson mass of ~125 GeV. This is because of the conflict between the light gravitino mass and heavy SUSY particle masses needed for producing the relatively heavy Higgs boson mass. We consider two possible extensions in this paper: a singlet extension of the Higgs sector, and strongly coupled gauge mediation. We show that there is a large parameter space, in both scenarios, where the Higgs boson mass of ~125 GeV is explained without any conflict with such a very light gravitino.Comment: 23 pages, 5 figure

Salt transiently inhibits mitochondrial energetics in mononuclear phagocytes

BACKGROUND: Dietary high salt (HS) is a leading risk factor for mortality and morbidity. Serum sodium transiently increases postprandially, but can also accumulate at sites of inflammation affecting differentiation and function of innate and adaptive immune cells. Here, we focus on how changes in extracellular sodium, mimicking alterations in the circulation and tissues, affect the early metabolic, transcriptional and functional adaption of human and murine mononuclear phagocytes (MNP). METHODS: Using Seahorse technology, pulsed stable isotope-resolved metabolomics and enzyme activity assays we characterize the central carbon metabolism and mitochondrial function of human and murine MNP under HS in vitro. HS as well as pharmacologic uncoupling of the electron transport chain (ETC) under normal salt (NS) is used to analyze mitochondrial function on immune cell activation and function (as determined by E.coli killing and CD4(+) T cell migration capacity). In two independent clinical studies we analyze the impact of a HS diet over two weeks (NCT02509962) and short-term salt challenge by a single meal (NCT04175249) on mitochondrial function of human monocytes in vivo. RESULTS: Extracellular sodium was taken up into the intracellular compartment followed by the inhibition of mitochondrial respiration in murine and human macrophages (MΦ). Mechanistically, HS reduces mitochondrial membrane potential, ETC complex II activity, oxygen consumption, and ATP production independently of the polarization status of MΦ. Subsequently, cell activation is altered with improved bactericidal function in HS-treated M1-like MΦ and diminished CD4(+) T cell migration in HS-treated M2-like MΦ. Pharmacologic uncoupling of the ETC under NS phenocopies HS-induced transcriptional changes and bactericidal function of human and murine MNP. Clinically, also in vivo rise in plasma sodium concentration within the physiological range reversibly reduces mitochondrial function in human monocytes. In both, a 14-day and single meal HS challenge, healthy volunteers displayed a plasma sodium increase of ̃x = 2mM and ̃x = 2.3mM, respectively, that correlated with decreased monocytic mitochondrial oxygen consumption. CONCLUSIONS: Our data identify the disturbance of mitochondrial respiration as the initial step by which HS mechanistically influences immune cell function. While these functional changes might help to resolve bacterial infections, a shift towards pro-inflammation could accelerate inflammatory CVD

Candesartan Attenuates Diabetic Retinal Vascular Pathology by Restoring Glyoxalase-I Function

This is an uncopyedited electronic version of an article accepted for publication in Diabetes. The American Diabetes Association, publisher of Diabetes, is not responsible for any errors or omissions in this version of the manuscript or any version derived from it by third parties. The definitive publisher-authenticated version will be available in a future issue of Diabetes in print and online a