Impact of NNLO QED corrections on lepton-proton scattering at MUSE

We present the complete next-to-next-to-leading order (NNLO) pure pointlike QED corrections to lepton-proton scattering, including three-photon-exchange contributions, and investigate their impact in the case of the MUSE experiment. These corrections are computed with no approximation regarding the energy of the emitted photons and taking into account lepton-mass effects. We contrast the NNLO QED corrections to known next-to-leading order corrections, where we include the elastic two-photon exchange (TPE) through a simple hadronic model calculation with a dipole ansatz for the proton electromagnetic form factors. We show that, in the low-momentum-transfer region accessed by the MUSE experiment, the improvement due to more sophisticated treatments of the TPE, including inelastic TPE, is of similar if not smaller size than some of the NNLO QED corrections. Hence, the latter have to be included in a precision determination of the low-energy proton structure from scattering data, in particular for electron-proton scattering. For muon-proton scattering, the NNLO QED corrections are considerably smaller

Impact of NNLO QED corrections on lepton-proton scattering at MUSE

We present the complete next-to-next-to-leading order (NNLO) pure pointlike QED corrections to lepton-proton scattering, including three-photon-exchange contributions, and investigate their impact in the case of the MUSE experiment. These corrections are computed with no approximation regarding the energy of the emitted photons and taking into account lepton-mass effects. We contrast the NNLO QED corrections to known next-to-leading order corrections, where we include the elastic two-photon exchange (TPE) through a simple hadronic model calculation with a dipole ansatz for the proton electromagnetic form factors. We show that, in the low-momentum-transfer region accessed by the MUSE experiment, the improvement due to more sophisticated treatments of the TPE, including inelastic TPE, is of similar if not smaller size than some of the NNLO QED corrections. Hence, the latter have to be included in a precision determination of the low-energy proton structure from scattering data, in particular for electron-proton scattering. For muon-proton scattering, the NNLO QED corrections are considerably smaller

Impact of NNLO QED corrections on lepton-proton scattering at MUSE

We present the complete next-to-next-to-leading order (NNLO) pure pointlike QED corrections to lepton-proton scattering, including three-photon-exchange contributions, and investigate their impact in the case of the MUSE experiment. These corrections are computed with no approximation regarding the energy of the emitted photons and taking into account lepton-mass effects. We contrast the NNLO QED corrections to known next-to-leading order corrections, where we include the elastic two-photon exchange (TPE) through a simple hadronic model calculation with a dipole ansatz for the proton electromagnetic form factors. We show that, in the low-momentum-transfer region accessed by the MUSE experiment, the improvement due to more sophisticated treatments of the TPE, including inelastic TPE, is of similar if not smaller size than some of the NNLO QED corrections. Hence, the latter have to be included in a precision determination of the low-energy proton structure from scattering data, in particular for electron-proton scattering. For muon-proton scattering, the NNLO QED corrections are considerably smaller.Comment: Article to be submitted to the EPJ A Topical Collection: Radiative Corrections: From Medium to High Energy Experiments. 23 pages, 9 figure

Soluble Guanylate Cyclase Stimulation Prevents Fibrotic Tissue Remodeling and Improves Survival in Salt-Sensitive Dahl Rats

A direct pharmacological stimulation of soluble guanylate cyclase (sGC) is an emerging therapeutic approach to the management of various cardiovascular disorders associated with endothelial dysfunction. Novel sGC stimulators, including riociguat (BAY 63-2521), have a dual mode of action: They sensitize sGC to endogenously produced nitric oxide (NO) and also directly stimulate sGC independently of NO. Little is known about their effects on tissue remodeling and degeneration and survival in experimental malignant hypertension.Mortality, hemodynamics and biomarkers of tissue remodeling and degeneration were assessed in Dahl salt-sensitive rats maintained on a high salt diet and treated with riociguat (3 or 10 mg/kg/d) for 14 weeks. Riociguat markedly attenuated systemic hypertension, improved systolic heart function and increased survival from 33% to 85%. Histological examination of the heart and kidneys revealed that riociguat significantly ameliorated fibrotic tissue remodeling and degeneration. Correspondingly, mRNA expression of the pro-fibrotic biomarkers osteopontin (OPN), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and plasminogen activator inhibitor-1 (PAI-1) in the myocardium and the renal cortex was attenuated by riociguat. In addition, riociguat reduced plasma and urinary levels of OPN, TIMP-1, and PAI-1.Stimulation of sGC by riociguat markedly improves survival and attenuates systemic hypertension and systolic dysfunction, as well as fibrotic tissue remodeling in the myocardium and the renal cortex in a rodent model of pressure and volume overload. These findings suggest a therapeutic potential of sGC stimulators in diseases associated with impaired cardiovascular and renal functions

Reduction of cortical parvalbumin expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

The inhibitory GABAergic system in the brain is involved in the etiology of various psychiatric problems, including autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and others. These disorders are influenced not only by genetic but also by environmental factors, such as preterm birth, although the mechanisms underlying are not known. In a translational hyperoxia model, exposing mice pups at age P5 to 80% oxygen for 48 hours to mimic a steep rise of oxygen exposure caused by preterm birth from in utero into room air, we documented a persistent reduction of cortical mature parvalbumin expressing interneurons until adulthood. Developmental delay of cortical myelin was observed together with decreased expression of oligodendroglial glial cell-derived neurotrophic factor (GDNF), a factor being involved in interneuronal development. Electrophysiological and morphological properties of remaining interneurons were unaffected. Behavioral deficits were observed for social interaction, learning, and attention. These results elucidate that neonatal oxidative stress can lead to decreased interneuron density and to psychiatric symptoms. The obtained cortical myelin deficit and decreased oligodendroglial GDNF expression indicate an impaired oligodendroglial-interneuronal interplay contributes to interneuronal damage

Plasma biochemical measurements in the vehicle- and riociguat-treated Dahl/ss rats maintained on a high-salt diet.

<p>AST = aspartate amino transferase, ALT = alanine amino transferase, GLDH = glutamate dehydrogenase, LDH = lactate dehydrogenase, CK = creatinine kinase, PRA = plasma renin activity, ANP = atrial natriuretic peptide, BNP = B-type natriuretic peptide. Data are mean±SEM;</p><p>*p<0.05,</p><p>**p<0.01,</p><p>***p<0.001 vs. the vehicle-treated animals.</p

Histopathological evaluation of the hearts and kidneys from the vehicle- and riociguat-treated Dahl/ss rats maintained on a high-salt diet.

<p>Data are mean±SEM;</p><p>*p<0.05,</p><p>**p<0.01,</p><p>***p<0.001 vs. the vehicle-treated animals.</p