Radio and Far-Infrared Emission as Tracers of Star Formation and AGN in Nearby Cluster Galaxies

We have studied the radio and far-infrared (FIR) emission from 114 galaxies in the 7 nearest clusters (<100 Mpc) with prominent X-ray emission to investigate the impact of the cluster environment on the star formation and AGN activity in the member galaxies. The X-ray selection criterion is adopted to focus on the most massive and dynamically relaxed clusters. A large majority of cluster galaxies show an excess in radio emission over that predicted from the radio-FIR correlation, the fraction of sources with radio excess increases toward cluster cores, and the radial gradient in the FIR/radio flux ratio is a result of radio enhancement. Of the radio-excess sources, 70% are early-type galaxies and the same fraction host an AGN. The galaxy density drops by a factor of 10 from the composite cluster center out to 1.5 Mpc, yet galaxies show no change in FIR properties over this region, and show no indication of mass segregation. We have examined in detail the physical mechanisms that might impact the FIR and radio emission of cluster galaxies. While collisional heating of dust may be important for galaxies in cluster centers, it appears to have a negligible effect on the observed FIR emission for our sample galaxies. The correlations between radio and FIR luminosity and radius could be explained by magnetic compression from thermal ICM pressure. We also find that simple delayed harassment cannot fully account for the observed radio, FIR, and mid-IR properties of cluster galaxies.Comment: 21 pages, 15 figures, Accepted by Ap

The effects of enhanced Z penguins on lepton polarizations in B→Xsℓ+ℓ−B \to X_s \ell^+ \ell^-

The sensitivity of the $B \to \pi K$ mode to electroweak penguins and the recent experimental data for the $B \to \pi \pi$, $\pi K$ modes has given rise to what is known as the ``$B \to \pi K$ puzzle''. Recently it has been observed that this {\sl puzzle} can be resolved by considering the new physics which can enter via $Z^0$ penguins. In this note we analyze the effect of this enhanced $Z^0$ penguins on the lepton polarization asymmetries of $b \to s \ell^+ \ell^-$.Comment: Published versio

Little Higgs model effects at γγ collider

Though the predictions of the standard model (SM) are in excellent agreement with experiments there are still several theoretical problems, such as fine-tuning and the hierarchy problem. These problems are associated with the Higgs sector of the SM, where it is widely believed that some "new physics" will take over at the TeV scale. One beyond the SM theory which resolves these problems is the little Higgs model. In this work we shall investigate the effects of the little Higgs model on γγ→γγ scattering, where the process γγ→γγ at high energies occurs in the SM through diagrams involving W, charged quark, and lepton loops (and is, therefore, particularly sensitive to any new physics)

Lepton flavour violation in The Little Higgs model

Little Higgs models with T-parity have a new source of lepton flavour violation. In this paper we consider the anomalous magnetic moment of the muon \gmtwo and the lepton flavour violating decays \mutoeg and \tautomug in Little Higgs model with T-parity \cite{Goyal:2006vq}. Our results shows that present experimental constraints of \mutoeg is much more useful to constrain the new sources of flavour violation which are present in T-parity models.Comment: LaTeX file with 13 eps figures (included

Optogenetic Interrogation of Functional Synapse Formation by Corticospinal Tract Axons in the Injured Spinal Cord

To restore function after injury to the CNS, axons must be stimulated to extend into denervated territory and, critically, must form functional synapses with appropriate targets. We showed previously that forced overexpression of the transcription factor Sox11 increases axon growth by corticospinal tract (CST) neurons after spinal injury. However, behavioral outcomes were not improved, raising the question of whether the newly sprouted axons are able to form functional synapses. Here we developed an optogenetic strategy, paired with single-unit extracellular recordings, to assess the ability of Sox11-stimulated CST axons to functionally integrate in the circuitry of the cervical spinal cord. Initial time course experiments established the expression and function of virally expressed Channelrhodopsin (ChR2) in CST cell bodies and in axon terminals in cervical spinal cord. Pyramidotomies were performed in adult mice to deprive the left side of the spinal cord of CST input, and the right CST was treated with adeno-associated virus (AAV)–Sox11 or AAV–EBFP control, along with AAV–ChR2. As expected, Sox11 treatment caused robust midline crossing of CST axons into previously denervated left spinal cord. Clear postsynaptic responses resulted from optogenetic activation of CST terminals, demonstrating the ability of Sox11-stimulated axons to form functional synapses. Mapping of the distribution of CST-evoked spinal activity revealed overall similarity between intact and newly innervated spinal tissue. These data demonstrate the formation of functional synapses by Sox11-stimulated CST axons without significant behavioral benefit, suggesting that new synapses may be mistargeted or otherwise impaired in the ability to coordinate functional output. SIGNIFICANCE STATEMENT As continued progress is made in promoting the regeneration of CNS axons, questions of synaptic integration are increasingly prominent. Demonstrating direct synaptic integration by regenerated axons and distinguishing its function from indirect relay circuits and target field plasticity have presented technical challenges. Here we force the overexpression of Sox11 to stimulate the growth of corticospinal tract axons in the cervical spinal cord and then use specific optogenetic activation to assess their ability to directly drive postsynaptic activity in spinal cord neurons. By confirming successful synaptic integration, these data illustrate a novel optogenetic-based strategy to monitor and optimize functional reconnection by newly sprouted axons in the injured CNS