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We examine the fate of a dead radio source in which jet injection from the central engine has stopped at an early stage of its evolution (). To this aim, we theoretically evaluate the evolution of the emission from both the lobe and the shell, which are composed of shocked jet matter and a shocked ambient medium (i.e., shell), respectively. Based on a simple dynamical model of expanding lobe and shell, we clarify how the broadband spectrum of each component evolves before and after the cessation of the jet activity. It is shown that the spectrum is strongly dominated by the lobe emission while the jet is active (). On the other hand, once the jet activity has ceased (), the lobe emission fades out rapidly, since fresh electrons are no longer supplied from the jet. Meanwhile, shell emission only shows a gradual decrease, since fresh electrons are continuously supplied from the bow shock that is propagating into the ambient medium. As a result, overall emission from the shell overwhelms that from the lobe at a wide range of frequencies from radio up to gamma-ray soon after the jet activity has ceased. Our result predicts a new class of dead radio sources that are dominated by shell emission. We suggest that the emission from the shell can be probed in particular at radio wavelengths with the Square Kilometer Array phase 1. [ABSTRACT FROM AUTHOR]

We calculate the electron acceleration in random superluminal strong waves (SLSWs) and radiation from them using numerical methods in the context of the termination shocks of pulsar wind nebulae. We pursue the orbit of electrons by solving the equation of motion in the analytically expressed electromagnetic turbulences. These consist of a primary SLS and isotropically distributed secondary electromagnetic waves. Under the dominance of the secondary waves, all electrons gain nearly equal energy. On the other hand, when the primary wave is dominant, selective acceleration occurs. The phase of the primary wave for electrons moving nearly along the wavevector changes very slowly compared with the oscillation of the wave, which is “phase-locked,” and such electrons are continuously accelerated. This acceleration by SLSWs may play a crucial role in pre-shock acceleration. In general, the radiation from the phase-locked population is different from the synchro-Compton radiation. However, when the amplitude of the secondary waves is not extremely weaker than that of the primary wave, the typical frequency can be estimated from synchro-Compton theory using the secondary waves. The primary wave does not contribute to the radiation because the SLSW accelerates electrons almost linearly. This radiation can be observed as a radio knot at the upstream of the termination shocks of the pulsar wind nebulae without counterparts in higher frequency ranges. [ABSTRACT FROM AUTHOR]

Cytomegalovirus (CMV) has been implicated in glioblastoma (GBM); however, a mechanistic connection in vivo has not been established. The purpose of this study is to characterize the effects of murine CMV (MCMV) on GBM growth in murine models. Syngeneic GBM models were established in mice perinatally infected with MCMV. We found that tumor growth was markedly enhanced in MCMV+ mice, with a significant reduction in overall survival compared with that of controls (P < 0.001). We observed increased angiogenesis and tumor blood flow in MCMV+ mice. MCMV reactivation was observed in intratumoral perivascular pericytes and tumor cells in mouse and human GBM specimens, and pericyte coverage of tumor vasculature was strikingly augmented in MCMV+ mice. We identified PDGF-D as a CMV-induced factor essential for pericyte recruitment, angiogenesis, and tumor growth. The antiviral drug cidofovir improved survival in MCMV+ mice, inhibiting MCMV reactivation, PDGF-D expression, pericyte recruitment, and tumor angiogenesis. These data show that MCMV potentiates GBM growth in vivo by increased pericyte recruitment and angiogenesis due to alterations in the secretome of CMV-infected cells. Our model provides evidence for a role of CMV in GBM growth and supports the application of antiviral approaches for GBM therapy. [ABSTRACT FROM AUTHOR]

Pigs are considered a mixing vessel for the generation of novel pandemic influenza A viruses through reassortment because of their susceptibility to both avian and human influenza viruses. However, experiments to understand reassortment in pigs in detail have been limited because experiments with regular-sized pigs are difficult to perform. Miniature pigs have been used as an experimental animal model, but they are still large and require relatively large cages for housing. The microminipig is one of the smallest miniature pigs used for experiments. Introduced in 2010, microminipigs weigh around 10 kg at an early stage of maturity (6 to 7 months old) and are easy to handle. To evaluate the microminipig as an animal model for influenza A virus infection, we compared the receptor distribution of 10-week-old male pigs (Yorkshire Large White) and microminipigs. We found that both animals have SAα2,3Gal and SAα2,6Gal in their respiratory tracts, with similar distributions of both receptor types. We further found that the sensitivity of microminipigs to influenza A viruses was the same as that of larger miniature pigs. Our findings indicate that the microminipig could serve as a novel model animal for influenza A virus infection. [ABSTRACT FROM AUTHOR]