QCD Corrections to QED Vacuum Polarization

We compute QCD corrections to QED calculations for vacuum polarization in background magnetic fields. Formally, the diagram for virtual $e\bar{e}$ loops is identical to the one for virtual $q\bar{q}$ loops. However due to confinement, or to the growth of $\alpha_s$ as $p^2$ decreases, a direct calculation of the diagram is not allowed. At large $p^2$ we consider the virtual $q\bar{q}$ diagram, in the intermediate region we discuss the role of the contribution of quark condensates \left and at the low-energy limit we consider the $\pi^0$, as well as charged pion $\pi^+\pi^-$ loops. Although these effects seem to be out of the measurement accuracy of photon-photon laboratory experiments they may be relevant for $\gamma$-ray burst propagation. In particular, for emissions from the center of the galaxy (8.5 kpc), we show that the mixing between the neutral pseudo-scalar pion $\pi_0$ and photons renders a deviation from the power-law spectrum in the $TeV$ range. As for scalar quark condensates \left and virtual $q\bar{q}$ loops are relevant only for very high radiation density $\sim 300 MeV/fm^3$ and very strong magnetic fields of order $\sim 10^{14} T$.Comment: 15 pages, 4 figures; Final versio

Quantum Vacuum Experiments Using High Intensity Lasers

The quantum vacuum constitutes a fascinating medium of study, in particular since near-future laser facilities will be able to probe the nonlinear nature of this vacuum. There has been a large number of proposed tests of the low-energy, high intensity regime of quantum electrodynamics (QED) where the nonlinear aspects of the electromagnetic vacuum comes into play, and we will here give a short description of some of these. Such studies can shed light, not only on the validity of QED, but also on certain aspects of nonperturbative effects, and thus also give insights for quantum field theories in general.Comment: 9 pages, 8 figur

Extracellular superoxide dismutase is a major determinant of nitric oxide bioavailability: in vivo and ex vivo evidence from ecSOD-deficient mice.

The bioavailability of nitric oxide (NO) within the vascular wall is limited by superoxide anions (O2.-). The relevance of extracellular superoxide dismutase (ecSOD) for the detoxification of vascular O2.- is unknown. We determined the involvement of ecSOD in the control of blood pressure and endothelium-dependent responses in angiotensin II-induced hypertension and renovascular hypertension induced by the two-kidney, one-clip model in wild-type mice and mice lacking the ecSOD gene. Blood pressure was identical in sham-operated ecSOD+/+ and ecSOD-/- mice. After 6 days of angiotensin II-treatment and 2 and 4 weeks after renal artery clipping, blood pressure was significantly higher in ecSOD-/- than ecSOD+/+ mice. Recombinant ecSOD selectively decreased blood pressure in hypertensive ecSOD-/- mice, whereas ecSOD had no effect in normotensive and hypertensive ecSOD+/+ mice. Compared with sham-operated ecSOD+/+ mice, sham-operated ecSOD-/- mice exhibited attenuated acetylcholine-induced relaxations. These responses were further depressed in vessels from clipped animals. Vascular O2.-, as measured by lucigenin chemiluminescence, was higher in ecSOD-/- compared with ecSOD+/+ mice and was increased by clipping. The antioxidant tiron normalized relaxations in vessels from sham-operated and clipped ecSOD-/-, as well as from clipped ecSOD+/+ mice. In contrast, in vivo application of ecSOD selectively enhanced endothelium-dependent relaxation in vessels from ecSOD-/- mice. These data reveal that endogenous ecSOD is a major antagonistic principle to vascular O2.-, controlling blood pressure and vascular function in angiotensin II-dependent models of hypertension. ecSOD is expressed in such an abundance that even in situations of high oxidative stress no relative lack of enzyme activity occurs