Implications of a new light gauge boson for neutrino physics

We study the impact of light gauge bosons on neutrino physics. We show that they can explain the NuTeV anomaly and also escape the constraints from neutrino experiments if they are very weakly coupled and have a mass of a few GeV. Lighter gauge bosons with stronger couplings could explain both the NuTeV anomaly and the positive anomalous magnetic moment of the muon. However, in the simple model we consider in this paper (say a purely vectorial extra U(1) current), they appear to be in conflict with the precise measurements of \nu-e elastic scattering cross sections. The surprising agreement that we obtain between our naive model and the NuTeV anomaly for a Z' mass of a few GeV may be a coincidence. However, we think it is interesting enough to deserve attention and perhaps a more careful analysis, especially since a new light gauge boson is a very important ingredient for the Light Dark Matter scenario.Comment: 9 page

On universality of the coupling of neutrinos to Z

We employ an effective Lagrangian approach and use LEP data to place severe bounds on universality violations of the couplings of $\nu_e$, $\nu_\mu$, and $\nu_\tau$ to the $Z$ boson. Our results justify the assumption of universality in these couplings that is usually made, as for example in the analysis of solar neutrinos detected at SNO.Comment: 8 pages, no figures. A few comments added. It matches version to be published in PR

Le concept de maladies virales émergentes : quel risque de zoonose pour La Réunion ?

A La Réunion, le risque d'émergence de maladies virales est constitué par plusieurs zoonoses virales qu'il convient de surveiller: infections à virus Sindbis, virus de l'encéphalite japonaise, virus Wesselsbron, virus Nipah, virus Zika, virus West Nile, virus de la fièvre de la vallée du Rift. La lutte contre ces maladies virales émergentes (MVE) passe par une détection précoce des cas et donc un système de surveillance doté d'un véritable réseau d'information, d'alerte et de prévention international. (Résumé d'auteur

Eustachian tube lumen opening into an abnormally pneumatized sphenoid bone.

Morphological abnormalities of left temporal and sphenoid bone were discovered in a 17-year-old boy during a post-traumatic cranial CT scan examination. The patient had not suffered from audiological disorders previously. He did not complain of hearing loss, vertigo or autophony. Further clinical investigations were normal including micro-otoscopy and nasopharyngeal endoscopy. The Valsalva maneuver was correctly performed. Audiometry and tympanometry were without any particularity

Differential roles of p39Mos–Xp42Mpk1 cascade proteins on Raf1 phosphorylation and spindle morphogenesis in Xenopus oocytes

AbstractFully-grown G2-arrested Xenopus oocytes resume meiosis upon hormonal stimulation. Resumption of meiosis is characterized by germinal vesicle breakdown, chromosome condensation, and organization of a bipolar spindle. These cytological events are accompanied by activation of MPF and the p39Mos–MEK1–Xp42Mpk1–p90Rsk pathways. The latter cascade is activated upon p39Mos accumulation. Using U0126, a MEK1 inhibitor, and p39Mos antisense morpholino and phosphorothioate oligonucleotides, we have investigated the role of the members of the p39Mos–MEK1–Xp42Mpk1–p90Rsk in spindle morphogenesis. First, we have observed at a molecular level that prevention of p39Mos accumulation always led to MEK1 phosphorylation defects, even when meiosis was stimulated through the insulin Ras-dependent pathway. Moreover, we have observed that Raf1 phosphorylation that occurs during meiosis resumption was dependent upon the activity of MEK1 or Xp42Mpk1 but not p90Rsk. Second, inhibition of either p39Mos accumulation or MEK1 inhibition led to the formation of a cytoplasmic aster-like structure that was associated with condensed chromosomes. Spindle morphogenesis rescue experiments using constitutively active Rsk and purified murine Mos protein suggested that p39Mos or p90Rsk alone failed to promote meiotic spindle organization. Our results indicate that activation of the p39Mos–MEK1–Xp42Mpk1–p90Rsk pathway is required for bipolar organization of the meiotic spindle at the cortex