Identification of non-ordinary mesons from the dispersive connection between their poles and their Regge trajectories: the f0(500) resonance

We show how the Regge trajectory of a resonance can be obtained from its pole in a scattering process and analytic constraints in the complex angular momentum plane. The method is suited for resonances that dominate an elastic scattering amplitude. In particular, from the rho(770) resonance pole in pion-pion scattering, we obtain its linear Regge trajectory, characteristic of ordinary quark-antiquark states. In contrast, the f0(500) pole -the sigma meson- which dominates scalar isoscalar pion-pion scattering, yields a non-linear trajectory with a much smaller slope at the f0(500) mass. Conversely, imposing a linear Regge trajectory for the f0(500), with a slope of typical size, yields an elastic amplitude at odds with the data. This provides strong support for the non-ordinary nature of the sigma meson.Comment: 8 pages, 4 figure

Regge trajectory of the f_0(500) resonance from a dispersive connection to its pole

We report here our results on how to obtain the Regge trajectory of a resonance from its pole in a scattering process by imposing analytic constraints in the complex angular momentum plane. The method, suited for resonances that dominate an elastic scattering amplitude, has been applied to the {\rho}(770) and the f_0(500) resonances. Whereas for the former we obtain a linear Regge trajectory, characteristic of ordinary quark-antiquark states, for the latter we find a non-linear trajectory with a much smaller slope at the resonance mass. This provides a strong indication of the non-ordinary nature of the sigma meson.Comment: 4 pages, 2 figures, to appear in the proceedings of the "Seventh International Symposium on Chiral Symmetry in Hadrons and Nuclei

Enhanced non-quark-antiquark and non-glueball Nc behavior of light scalar mesons

We show that the latest and very precise dispersive data analyses require a large and very unnat- ural fine-tuning of the 1/Nc expansion at Nc = 3 if the f_0(600) and K(800) light scalar mesons are to be considered predominantly quark-antiquark states, which is not needed for light vector mesons. For this, we use scattering observables whose 1/Nc corrections are suppressed further than one power of 1/Nc for quark-antiquark or glueball states, thus enhancing contributions of other nature. This is achieved without using unitarized ChPT, but if it is used we can also show that it is not just that the coefficients of the 1/Nc expansion are unnatural, but that the expansion itself does not even follow the expected 1/Nc scaling of a glueball or a quark-antiquark meson.Comment: Discussion disfavoring a glueball interpretation added. Version published in Phys. Rev.

Determination of SU(2) Chiral Perturbation Theory low energy constants from a precise description of pion-pion scattering threshold parameters

We determine the values of the one- and two-loop low energy constants appearing in the SU(2) Chiral Perturbation Theory calculation of pion-pion scattering. For this we use a recent and precise sum rule determination of some scattering lengths and slopes that appear in the effective range expansion. In addition we provide sum rules for these coefficients up to third order in the expansion. Our results when using only the scattering lengths and slopes of the S, P, D and F waves are consistent with previous determinations, but seem to require higher order contributions if they are to accommodate the third order coefficients of the effective range expansion.Comment: 16 pages. Version published in Phys. Rev. D. Enlarged discussions in several sections, appendices and many references added. Results and conclusions unchange

Essential role of the Cdk2 activator RingoA in meiotic telomere tethering to the nuclear envelope

Cyclin-dependent kinases (CDKs) play key roles in cell cycle regulation. Genetic analysis in mice has revealed an essential role for Cdk2 in meiosis, which renders Cdk2 knockout (KO) mice sterile. Here we show that mice deficient in RingoA, an atypical activator of Cdk1 and Cdk2 that has no amino acid sequence homology to cyclins, are sterile and display meiotic defects virtually identical to those observed in Cdk2 KO mice including non-homologous chromosome pairing, unrepaired double-strand breaks, undetectable sex-body and pachytene arrest. Interestingly, RingoA is required for Cdk2 targeting to telomeres and RingoA KO spermatocytes display severely affected telomere tethering as well as impaired distribution of Sun1, a protein essential for the attachment of telomeres to the nuclear envelope. Our results identify RingoA as an important activator of Cdk2 at meiotic telomeres, and provide genetic evidence for a physiological function of mammalian Cdk2 that is not dependent on cyclins

Microheater Actuators as a Versatile Platform for Strain Engineering in 2D Materials

We present microfabricated thermal actuators to engineer the biaxial strain in two-dimensional (2D) materials. These actuators are based on microheater circuits patterned onto the surface of a polymer with a high thermal expansion coefficient. By running current through the microheater one can vary the temperature of the polymer and induce a controlled biaxial expansion of its surface. This controlled biaxial expansion can be transduced to biaxial strain to 2D materials, placed onto the polymer surface, which in turn induces a shift of the optical spectrum. Our thermal strain actuators can reach a maximum biaxial strain of 0.64%, and they can be modulated at frequencies up to 8 Hz. The compact geometry of these actuators results in a negligible spatial drift of 0.03 μm/°C, which facilitates their integration in optical spectroscopy measurements. We illustrate the potential of this strain engineering platform to fabricate a strain-actuated optical modulator with single-layer MoS2

Neuronal p38α mediates synaptic and cognitive dysfunction in an Alzheimer’s mouse model by controlling β-amyloid production.

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a severe and progressive neuronal loss leading to cognitive dysfunctions. Previous reports, based on the use of chemical inhibitors, have connected the stress kinase p38α to neuroinflammation, neuronal death and synaptic dysfunction. To explore the specific role of neuronal p38α signalling in the appearance of pathological symptoms, we have generated mice that combine expression of the 5XFAD transgenes to induce AD symptoms with the downregulation of p38α only in neurons (5XFAD/p38α∆-N). We found that the neuronal-specific deletion of p38α improves the memory loss and long-term potentiation impairment induced by 5XFAD transgenes. Furthermore, 5XFAD/p38α∆-N mice display reduced amyloid-β accumulation, improved neurogenesis, and important changes in brain cytokine expression compared with 5XFAD mice. Our results implicate neuronal p38α signalling in the synaptic plasticity dysfunction and memory impairment observed in 5XFAD mice, by regulating both amyloid-β deposition in the brain and the relay of this accumulation to mount an inflammatory response, which leads to the cognitive deficits.post-print1848 K