Next-to-leading order QCD corrections to Z boson pair production via vector-boson fusion

Vector-boson fusion processes are an important tool for the study of electroweak symmetry breaking at hadron colliders, since they allow to distinguish a light Higgs boson scenario from strong weak boson scattering. We here consider the channels WW->ZZ and ZZ->ZZ as part of electroweak Z boson pair production in association with two tagging jets. We present the calculation of the NLO QCD corrections to the cross sections for p p -> e+ e- mu+ mu- + 2 jets and p p -> e+ e- nu_mu nubar_mu + 2 jets via vector-boson fusion at order alpha_s alpha^6, which is performed in the form a NLO parton-level Monte Carlo program. The corrections to the integrated cross sections are found to be modest, while the shapes of some kinematical distributions change appreciably at NLO. Residual scale uncertainties typically are at the few percent level.Comment: 12 pages, 4 figure

Next-to-leading order QCD corrections to W+W- production via vector-boson fusion

Vector-boson fusion processes constitute an important class of reactions at hadron colliders, both for signals and backgrounds of new physics in the electroweak interactions. We consider what is commonly referred to as W+W- production via vector-boson fusion (with subsequent leptonic decay of the Ws), or, more precisely, e+ nu_e mu- nubar_mu + 2 jets production in proton-proton scattering, with all resonant and non-resonant Feynman diagrams and spin correlations of the final-state leptons included, in the phase-space regions which are dominated by t-channel electroweak-boson exchange. We compute the next-to-leading order QCD corrections to this process, at order alpha^6 alpha_s. The QCD corrections are modest, changing total cross sections by less than 10%. Remaining scale uncertainties are below 2%. A fully-flexible next-to-leading order partonic Monte Carlo program allows to demonstrate these features for cross sections within typical vector-boson-fusion acceptance cuts. Modest corrections are also found for distributions.Comment: 29 pages, 14 figure

Direct Photons at RHIC

The PHENIX experiment has measured direct photons in $\sqrt{s_{NN}} = 200$ GeV Au+Au collisions and p+p collisions. The fraction of photons due to direct production in Au+Au collisions is shown as a function of $p_T$ and centrality. This measurement is compared with expectation from pQCD calculations. Other possible sources of direct photons are discussed.Comment: 7 pages, 5 figures, presented at Hot Quarks 2004, Taos, N

A motivational approach to support healthy habits in long-term child–robot interaction

We examine the use of role-switching as an intrinsic motivational mechanism to increase engagement in long-term child–robot interaction. The present study describes a learning framework where children between 9 and 11-years-old interact with a robot to improve their knowledge and habits with regards to healthy life-styles. Experiments were carried out in Italy where 41 children were divided in three groups interacting with: (i) a robot with a role-switching mechanism, (ii) a robot without a role-switching mechanism and (iii) an interactive video. Additionally, a control group composed of 43 more children, who were not exposed to any interactive approach, was used as a baseline of the study. During the intervention period, the three groups were exposed to three interactive sessions once a week. The aim of the study was to find any difference in healthy-habits acquisition based on alternative interactive systems, and to evaluate the effectiveness of the role-switch approach as a trigger for engagement and motivation while interacting with a robot. The results provide evidence that the rate of children adopting healthy habits during the intervention period was higher for those interacting with a robot. Moreover, alignment with the robot behaviour and achievement of higher engagement levels were also observed for those children interacting with the robot that used the role-switching mechanism. This supports the notion that role-switching facilitates sustained long-interactions between a child and a robot

PLXNA1 and PLXNA3 cooperate to pattern the nasal axons that guide gonadotropin-releasing hormone neurons

Gonadotropin-releasing hormone (GnRH) neurons regulate puberty onset and sexual reproduction by secreting GnRH to activate and maintain the hypothalamic-pituitary-gonadal axis. During embryonic development, GnRH neurons migrate along olfactory and vomeronasal axons through the nose into the brain, where they project to the median eminence to release GnRH. The secreted glycoprotein SEMA3A binds its receptors neuropilin (NRP) 1 or NRP2 to position these axons for correct GnRH neuron migration, with an additional role for the NRP co-receptor PLXNA1. Accordingly, mutations in SEMA3A, NRP1, NRP2 and PLXNA1 have been linked to defective GnRH neuron development in mice and inherited GnRH deficiency in humans. Here, we show that only the combined loss of PLXNA1 and PLXNA3 phenocopied the full spectrum of nasal axon and GnRH neuron defects of SEMA3A knockout mice. Together with Plxna1, the human orthologue of Plxna3 should therefore be investigated as a candidate gene for inherited GnRH deficiency

Plxna1 and Plxna3 cooperate to pattern the nasal axons that guide gonadotropin-releasing hormone neurons

The gonadotropin releasing hormone (GnRH) neurons regulate puberty onset and sexual reproduction by secreting GnRH to activate and maintain the hypothalamic-pituitary gonadal axis. During embryonic development, GnRH neurons migrate along olfactory and vomeronasal axons through the nose into the brain, where they project to the median eminence to release GnRH. The secreted glycoprotein SEMA3A binds its receptors neuropilin (NRP) 1 or NRP2 to position these axons for correct GnRH neuron migration, with an additional role for the NRP co-receptor PLXNA1. Accordingly, mutations in SEMA3A, NRP1, NRP2 and PLXNA1 have been linked to defective GnRH neuron development in mice and inherited GnRH deficiency in humans. Here, we show that only the combined loss of PLXNA1 and PLXNA3 phenocopied the full spectrum of nasal axon and GnRH neuron defects of SEMA3A knockout mice. Together with Plxna1, the human ortholog of Plxna3 should therefore be investigated as a candidate gene for inherited GnRH deficiency

In vitro, ex vivo and in vivo techniques to study neuronal migration in the developing cerebral cortex

Neuronal migration is a fundamental biological process that underlies proper brain development and neuronal circuit formation. In the developing cerebral cortex, distinct neuronal populations, producing excitatory, inhibitory and modulatory neurotransmitters, are generated in different germinative areas and migrate along various routes to reach their final positions within the cortex. Different technical approaches and experimental models have been adopted to study the mechanisms regulating neuronal migration in the cortex. In this review, we will discuss the most common in vitro, ex vivo and in vivo techniques to visualize and study cortical neuronal migration