Axion Protection from Flavor

The QCD axion fails to solve the strong CP problem unless all explicit PQ violating, Planck-suppressed, dimension n<10 operators are forbidden or have exponentially small coefficients. We show that all theories with a QCD axion contain an irreducible source of explicit PQ violation which is proportional to the determinant of the Yukawa interaction matrix of colored fermions. Generically, this contribution is of low operator dimension and will drastically destabilize the axion potential, so its suppression is a necessary condition for solving the strong CP problem. We propose a mechanism whereby the PQ symmetry is kept exact up to n=12 with the help of the very same flavor symmetries which generate the hierarchical quark masses and mixings of the SM. This "axion flavor protection" is straightforwardly realized in theories which employ radiative fermion mass generation and grand unification. A universal feature of this construction is that the heavy quark Yukawa couplings are generated at the PQ breaking scale.Comment: 16 pages, 2 figure

Debris disks as signposts of terrestrial planet formation. II Dependence of exoplanet architectures on giant planet and disk properties

We present models for the formation of terrestrial planets, and the collisional evolution of debris disks, in planetary systems that contain multiple unstable gas giants. We previously showed that the dynamics of the giant planets introduces a correlation between the presence of terrestrial planets and debris disks. Here we present new simulations that show that this connection is qualitatively robust to changes in: the mass distribution of the giant planets, the width and mass distribution of the outer planetesimal disk, and the presence of gas in the disk. We discuss how variations in these parameters affect the evolution. Systems with equal-mass giant planets undergo the most violent instabilities, and these destroy both terrestrial planets and the outer planetesimal disks that produce debris disks. In contrast, systems with low-mass giant planets efficiently produce both terrestrial planets and debris disks. A large fraction of systems with low-mass outermost giant planets have stable gaps between these planets that are frequently populated by planetesimals. Planetesimal belts between outer giant planets may affect debris disk SEDs. If Earth-mass seeds are present in outer planetesimal disks, the disks radially spread to colder temperatures. We argue that this may explain the very low frequency of > 1 Gyr-old solar-type stars with observed 24 micron excesses. Among the (limited) set of configurations explored, the best candidates for hosting terrestrial planets at ~1 AU are stars older than 0.1-1 Gyr with bright debris disks at 70 micron but with no currently-known giant planets. These systems combine evidence for rocky building blocks, with giant planet properties least likely to undergo destructive dynamical evolution. We predict an anti-correlation between debris disks and eccentric giant planets, and a positive correlation between debris disks and terrestrial planets.Comment: Astronomy and Astrophysics, in press. Movies from simulations are at http://www.obs.u-bordeaux1.fr/e3arths/raymond/movies_debris.htm

Genome-Wide Analyses Reveal a Role for Peptide Hormones in Planarian Germline Development

Genomic/peptidomic analyses of the planarian Schmidtea mediterranea identifies >200 neuropeptides and uncovers a conserved neuropeptide required for proper maturation and maintenance of the reproductive system

Hypofibrinolysis in diabetes: a therapeutic target for the reduction of cardiovascular risk

An enhanced thrombotic environment and premature atherosclerosis are key factors for the increased cardiovascular risk in diabetes. The occlusive vascular thrombus, formed secondary to interactions between platelets and coagulation proteins, is composed of a skeleton of fibrin fibres with cellular elements embedded in this network. Diabetes is characterised by quantitative and qualitative changes in coagulation proteins, which collectively increase resistance to fibrinolysis, consequently augmenting thrombosis risk. Current long-term therapies to prevent arterial occlusion in diabetes are focussed on anti-platelet agents, a strategy that fails to address the contribution of coagulation proteins to the enhanced thrombotic milieu. Moreover, antiplatelet treatment is associated with bleeding complications, particularly with newer agents and more aggressive combination therapies, questioning the safety of this approach. Therefore, to safely control thrombosis risk in diabetes, an alternative approach is required with the fibrin network representing a credible therapeutic target. In the current review, we address diabetes-specific mechanistic pathways responsible for hypofibrinolysis including the role of clot structure, defects in the fibrinolytic system and increased incorporation of anti-fibrinolytic proteins into the clot. Future anti-thrombotic therapeutic options are discussed with special emphasis on the potential advantages of modulating incorporation of the anti-fibrinolytic proteins into fibrin networks. This latter approach carries theoretical advantages, including specificity for diabetes, ability to target a particular protein with a possible favourable risk of bleeding. The development of alternative treatment strategies to better control residual thrombosis risk in diabetes will help to reduce vascular events, which remain the main cause of mortality in this condition