Determination of the position angle of stellar spin axes

Measuring the stellar position angle provides valuable information on binary stellar formation or stellar spin axis evolution. We aim to develop a method for determining the absolute stellar position angle using spectro-astrometric analysis of high resolution long-slit spectra. The method has been designed in particular for slowly rotating stars. We investigate its applicability to existing dispersive long-slit spectrographs, identified here by their plate scale, and the size of the resulting stellar sample. The stellar rotation induces a tilt in the stellar lines whose angle depends on the stellar position angle and the orientation of the slit. We developed a rotation model to calculate and reproduce the effects of stellar rotation on unreduced high resolution stellar spectra. Then we retrieved the tilt amplitude using a spectro-astrometric extraction of the position of the photocentre of the spectrum. Finally we present two methods for analysing the position spectrum using either direct measurement of the tilt or a cross-correlation analysis. For stars with large apparent diameter and using a spectrograph with a small plate scale, we show that it is possible to determine the stellar position angle directly within 10deg with a signal-to-noise ratio of the order of 6. Under less favourable conditions, i.e. larger plate scale or smaller stellar diameter, the cross-correlation method yields comparable results. We show that with the currently existing instruments, it is possible to determine the stellar position angle of at least 50 stars precisely, mostly K-type giants with apparent diameter down to 5 milliarcseconds. If we consider errors of around 10deg still acceptable, we may include stars with apparent diameter down to 2 mas in the sample that then comprises also some main sequence stars.Comment: 10 pages, 9 figures, A&A (in press

Portraying the hosts: Stellar science from planet searches

Information on the full session can be found on this website: https://sites.google.com/site/portrayingthehostscs18/We present a compendium of the splinter session on stellar science from planet searches that was organized as part of the Cool Stars 18 conference. Seven speakers discussed techniques to infer stellar information from radial velocity, transit and microlensing data, as well as new instrumentation and missions designed for planet searches that will provide useful for the study of the cool stars

Selective mGluR1 Antagonist EMQMCM Inhibits the Kainate-Induced Excitotoxicity in Primary Neuronal Cultures and in the Rat Hippocampus

Abundant evidence suggests that indirect inhibitory modulation of glutamatergic transmission, via metabotropic glutamatergic receptors (mGluR), may induce neuroprotection. The present study was designed to determine whether the selective antagonist of mGluR1 (3-ethyl-2-methyl-quinolin-6-yl)-(4-methoxy-cyclohexyl)-methanone methanesulfonate (EMQMCM), showed neuroprotection against the kainate (KA)-induced excitotoxicity in vitro and in vivo. In in vitro studies on mouse primary cortical and hippocampal neuronal cultures, incubation with KA (150 μM) induced strong degeneration [measured as lactate dehydrogenase (LDH) efflux] and apoptosis (measured as caspase-3 activity). EMQMCM (0.1–100 μM) added 30 min to 6 h after KA, significantly attenuated the KA-induced LDH release and prevented the increase in caspase-3 activity in the cultures. Those effects were dose- and time-dependent. In in vivo studies KA (2.5 nmol/1 μl) was unilaterally injected into the rat dorsal CA1 hippocampal region. Degeneration was calculated by counting surviving neurons in the CA pyramidal layer using stereological methods. It was found that EMQMCM (5–10 nmol/1 μl) injected into the dorsal hippocampus 30 min, 1 h, or 3 h (the higher dose only) after KA significantly prevented the KA-induced neuronal degeneration. In vivo microdialysis studies in rat hippocampus showed that EMQMCM (100 μM) significantly increased γ-aminobutyric acid (GABA) and decreased glutamate release. When perfused simultaneously with KA, EMQMCM substantially increased GABA release and prevented the KA-induced glutamate release. The obtained results indicate that the mGluR1 antagonist, EMQMCM, may exert neuroprotection against excitotoxicity after delayed treatment (30 min to 6 h). The role of enhanced GABAergic transmission in the neuroprotection is postulated