Search

We report the results of a volume-limited survey using the Australia Telescope Compact Array to search for transient and quiescent radio emission from 15 southern hemisphere ultracool dwarfs. We detect radio emission from 2MASSW J0004348-404405 increasing the number of radio loud ultracool dwarfs to 22. We also observe radio emission from 2MASS J10481463-3956062 and 2MASSI J0339352-352544, two sources with previous radio detections. The radio emission from the three detected sources shows no variability or flare emission. Modelling this quiescent emission we find that it is consistent with optically thin gyrosynchrotron emission from a magnetosphere with an emitting region radius of (1 - 2)$R_*$, magnetic field inclination 20$^{\circ}$ - 80$^{\circ}$, field strength $\sim$10 - 200 G, and power-law electron density $\sim$10$^4$ - 10$^8$ cm$^{-3}$. Additionally, we place upper limits on four ultracool dwarfs with no previous radio observations. This increases the number of ultracool dwarfs studied at radio frequencies to 222. Analysing general trends of the radio emission for this sample of 15 sources, we find that the radio activity increases for later spectral types and more rapidly rotating objects. Furthermore, comparing the ratio of the radio to X-ray luminosities for these sources, we find 2MASS J10481463-3956062 and 2MASSI J0339352-352544 violate the Guedel-Benz relation by more than two orders of magnitude., 10 pages, 7 figures

We present 13 cm and 20 cm radio observations of the magnetic chemically peculiar star CU Virginis taken with the Australia Telescope Compact Array. We detect two circularly polarised radio pulses every rotation period which confirm previous detections. In the first pulse, the lower frequency emission arrives before the higher frequency emission and the ordering reverses in the second pulse. In order to explain the frequency dependence of the time between the two pulses, we construct a geometric model of the magnetosphere of CU Virginis, and consider various emission angles relative to the magnetic field lines. A simple electron cyclotron maser emission model, in which the emission is perpendicular to the magnetic field lines, is not consistent with our data. A model in which the emission is refracted through cold plasma in the magnetosphere is shown to have the correct pulse arrival time frequency dependence.

Innate immune activation beyond the central nervous system is emerging as a vital component of the pathogenesis of neurodegeneration. Huntington’s disease (HD) is a fatal neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. The systemic innate immune system is thought to act as a modifier of disease progression; however, the molecular mechanisms remain only partially understood. Here we use RNA-sequencing to perform whole transcriptome analysis of primary monocytes from thirty manifest HD patients and thirty-three control subjects, cultured with and without a proinflammatory stimulus. In contrast with previous studies that have required stimulation to elicit phenotypic abnormalities, we demonstrate significant transcriptional differences in HD monocytes in their basal, unstimulated state. This includes previously undetected increased resting expression of genes encoding numerous proinflammatory cytokines, such as IL6. Further pathway analysis revealed widespread resting enrichment of proinflammatory functional gene sets, while upstream regulator analysis coupled with Western blotting suggests that abnormal basal activation of the NFOEB pathway plays a key role in mediating these transcriptional changes. That HD myeloid cells have a proinflammatory phenotype in the absence of stimulation is consistent with a priming effect of mutant huntingtin, whereby basal dysfunction leads to an exaggerated inflammatory response once a stimulus is encountered. These data advance our understanding of mutant huntingtin pathogenesis, establish resting myeloid cells as a key source of HD immune dysfunction, and further demonstrate the importance of systemic immunity in the potential treatment of HD and the wider study of neurodegeneration.