Resolving Charged Hadrons in QED -- Gauge Invariant Interpolating Operators

Standard interpolating operators for charged mesons, e.g. $J_{B} = \bar b i \gamma_5 u$ for $B^-$, are not gauge invariant in QED and therefore problematic for perturbative methods. We propose a gauge invariant interpolating operator by adding an auxiliary charged scalar $\Phi_B$, ${\cal J}_{B}^{(0)} = J_B \, \Phi_B$, which reproduces all the universal soft and collinear logs. The modified LSZ-factor is shown to be infrared finite which is a necessary condition for validating the approach. At ${\cal O}(\alpha)$, this is equivalent to a specific Dirac dressing of charged operators. A generalisation thereof, using iterated integrals, establishes the equivalence to all orders and provides a transparent alternative viewpoint. The method is discussed by the example of the leptonic decay $B^- \to \ell^- \bar \nu$ for which a numerical study is to follow. The formalism itself is valid for any spin, flavour and set of final states (e.g. $B^- \to \pi^0 \ell^- \bar \nu$).Comment: 4 Fig, 17 pp + ref

On the RK R_{K} Theory Error

To quantify the theory error on $R_K$, essentially means to quantify the uncertainty due to QED corrections since the latter breaks lepton flavour universality through the lepton masses. Since experiment uses photon shower programs, e.g. \texttt{PHOTOS}, to capture QED effects, assessing the uncertainty involves investigating effects not captured by the specific use of these tools. This includes structure-dependent corrections, potentially large non-logarithmic terms and charmonium resonances entering the lower bin by migration of radiation. We are able to close in on these loopholes. For example, using gauge invariance, we show that structure-dependent QED corrections do not lead to additional (sizeable) hard-collinear logs of the form ${\cal O}(\alpha) \ln m_\ell/m_B$. Hence, from the theory point of view $R_K$ is a safe observable.Comment: CKM21 proceedings 8p

QED Corrections in B¯→K¯ℓ+ℓ− at the Double-Differential Level

We present a detailed analysis of QED corrections to $\bar{B} \to \bar{K} \ell^+ \ell^-$ decays at the double-differential level. Cancellations of soft and collinear divergences are demonstrated analytically using the phase space slicing method. Whereas soft divergences are found to cancel at the differential level, the cancellation of the hard-collinear logs $\ln m_\ell$ require, besides photon-inclusiveness, a specific choice of kinematic variables. In particular, hard-collinear logs in the lepton-pair invariant mass distribution ($q^2$), are sizeable and need to be treated with care when comparing with experiment. Virtual and real amplitudes are evaluated using an effective mesonic Lagrangian. Crucially, we show that going beyond this approximation does not introduce any further infrared sensitive terms. All analytic computations are performed for generic charges and are therefore adaptable to semileptonic decays such as $B \to D \ell \bar \nu$.Comment: 47 pages, 9 figures, v2 quasi identical to JHEP versio

Breakdown of collinear factorization in the exclusive photoproduction of a π0γ \pi ^{0}\gamma pair with large invariant mass

We study the exclusive photoproduction of a $\pi ^{0}\gamma$ pair with large invariant mass $M_{\gamma \pi}^2$, which is sensitive to the exchange of either two quarks or two gluons in the $t$-channel. In this letter, we show that the process involving two-gluon exchanges does not factorize in the Bjorken limit at the leading twist. This can be explicitly demonstrated by the fact that there exist diagrams, which contribute at the leading twist, for which Glauber gluons remain trapped, due to the pinching of the contour integrations of both the plus and minus component of the Glauber gluon momentum. For the same reason, $\pi^0$-nucleon scattering to two photons also suffers from the same issue. On the other hand, we stress that there are no issues with respect to collinear factorization for the quark channels. By considering an analysis of all potential reduced diagrams of leading pinch surfaces, we argue that the quark channel is safe from Glauber pinches, and therefore, a collinear factorization in that case follows through without any problems. This means that processes where gluon exchanges are forbidden, such as the exclusive photoproduction of $\pi ^{\pm}\gamma$ and $\rho^{0,\,\pm} \gamma$, are unaffected by the factorization breaking effects we point out in this letter.Comment: 11 pages, 4 figure

B meson decays, conformal anomalies and gauge invariance

In this thesis, we discuss the calculation of conformal anomalies using curved spacetime and heat-kernel techniques, and QED corrections to semi-leptonic decays of the pseudoscalar B meson at the full differential level. In the first chapter, the basic ideas of conformal field theory are reviewed, including the importance of the trace of the energy-momentum tensor as a measure of conformal symmetry breaking, and the use of curved spacetime in calculations. In the second chapter, we perform computations of the conformal anomalies for the spin-0, spin- 1/2 and spin-1 fields in curved spacetime using the De-Witt-Schwinger point splitting method and heat-kernel techniques. Particular focus is given to the spin-1 gauge field, where it is explicitly shown how gauge invariance is obtained, a result that has been overlooked in the literature, and which is also a source of ambiguities in different regularisation schemes. We then proceed to discuss the application of these results on positivity theorems in Chapter 3. It is shown that they could potentially provide tighter bounds on the conformal window in QCD. In chapter 4, a calculation of the QED corrections to the B¯ → K` ¯ +`− decay process at the double differential rate is introduced, using an effective mesonic Lagrangian. Particular focus is given to the cancellation of infrared soft and collinear divergences between the real and virtual contributions using the phase-space slicing method, which is discussed in Chapter 5. Hard-collinear divergences, appearing in the form of logs of the lepton mass, are shown to cancel depending on the differential variables used and the experimental photon energy cut. Plots and results are given in chapter 6, and some comments on the value of RK and lepton flavour universality are made

QED in B→Kℓ+ℓ− LFU ratios: theory versus experiment, a Monte Carlo study

Using analytic results obtained in a meson effective theory, that includes all infrared sensitive logs, we build a dedicated Monte Carlo framework to describe QED corrections in $\bar B \to \bar K \ell^+\ell^-$ for a generic form factor. For the neutral mode $\bar B^0 \to \bar K^0 \ell^+\ell^-$, we perform a detailed numerical comparison versus those obtained with the general-purpose photon-shower tool PHOTOS. The comparison indicates a good agreement, at the few per-mil level, when focusing on the rare mode only. In addition, our framework allows us to investigate the impact of the charmonium resonances. Interference effects, not described by PHOTOS in the experimental analysis, are found to be small in the dilepton invariant mass region $q^2 < 6 \textrm{GeV}^2$, which is used to determine $R_{K^{(*)}}$. Using a semi-analytic framework we assess the full, rare and resonant, mode. Based thereupon, we discuss strategies to check the subtraction of the resonant mode, which has a sizeable impact at $q^2 \approx 6 \textrm{GeV}^2$ in the electron mode.Comment: 23pp+refs, 9 Figs, version to appear in JHEP, using same number of subtractions in dispersion relation everywher

The regulation of cardiac intermediary metabolism by NADPH oxidases

NADPH oxidases (NOXs), enzymes whose primary function is to generate reactive oxygen species, are important regulators of the heart’s physiological function and response to pathological insults. The role of NOX-driven redox signalling in pathophysiological myocardial remodelling, including processes such as interstitial fibrosis, contractile dysfunction, cellular hypertrophy, and cell survival, is well recognized. While the NOX2 isoform promotes many detrimental effects, the NOX4 isoform has attracted considerable attention as a driver of adaptive stress responses both during pathology and under physiological states such as exercise. Recent studies have begun to define some of the NOX4-modulated mechanisms that may underlie these adaptive responses. In particular, novel functions of NOX4 in driving cellular metabolic changes have emerged. Alterations in cellular metabolism are a recognized hallmark of the heart’s response to physiological and pathological stresses. In this review, we highlight the emerging roles of NOX enzymes as important modulators of cellular intermediary metabolism in the heart, linking stress responses not only to myocardial energetics but also other functions. The novel interplay of NOX-modulated redox signalling pathways and intermediary metabolism in the heart is unravelling a new aspect of the fascinating biology of these enzymes which will inform a better understanding of how they drive adaptive responses. We also discuss the implications of these new findings for therapeutic approaches that target metabolism in cardiac disease

Nox4 reprograms cardiac substrate metabolism via protein O-GlcNAcylation to enhance stress adaptation.

Cardiac hypertrophic remodeling during chronic hemodynamic stress is associated with a switch in preferred energy substrate from fatty acids to glucose, usually considered to be energetically favorable. The mechanistic interrelationship between altered energy metabolism, remodeling, and function remains unclear. The ROS-generating NADPH oxidase-4 (Nox4) is upregulated in the overloaded heart, where it ameliorates adverse remodeling. Here, we show that Nox4 redirects glucose metabolism away from oxidation but increases fatty acid oxidation, thereby maintaining cardiac energetics during acute or chronic stresses. The changes in glucose and fatty acid metabolism are interlinked via a Nox4-ATF4-dependent increase in the hexosamine biosynthetic pathway, which mediates the attachment of O-linked N-acetylglucosamine (O-GlcNAcylation) to the fatty acid transporter CD36 and enhances fatty acid utilization. These data uncover a potentially novel redox pathway that regulates protein O-GlcNAcylation and reprograms cardiac substrate metabolism to favorably modify adaptation to chronic stress. Our results also suggest that increased fatty acid oxidation in the chronically stressed heart may be beneficial

Myocardial NADPH oxidase-4 regulates the physiological response to acute exercise.

Regular exercise has widespread health benefits. Fundamental to these beneficial effects is the ability of the heart to intermittently and substantially increase its performance without incurring damage, but the underlying homeostatic mechanisms are unclear. We identify the ROS-generating NADPH oxidase-4 (Nox4) as an essential regulator of exercise performance in mice. Myocardial Nox4 levels increase during acute exercise and trigger activation of the transcription factor Nrf2, with the induction of multiple endogenous antioxidants. Cardiomyocyte-specific Nox4-deficient (csNox4KO) mice display a loss of exercise-induced Nrf2 activation, cardiac oxidative stress and reduced exercise performance. Cardiomyocyte-specific Nrf2-deficient (csNrf2KO) mice exhibit similar compromised exercise capacity, with mitochondrial and cardiac dysfunction. Supplementation with an Nrf2 activator or a mitochondria-targeted antioxidant effectively restores cardiac performance and exercise capacity in csNox4KO and csNrf2KO mice respectively. The Nox4/Nrf2 axis therefore drives a hormetic response that is required for optimal cardiac mitochondrial and contractile function during physiological exercise