Coase’s Paradox and the Inefficiency of Permanent Strike Replacements

The affinity between the Coase Theorem and the NLRA appears obvious. Both the theorem and the Act acknowledge bargaining as a potentially efficient problem-solving strategy. Both the theorem and the Act set efficiency as a goal. This Article examines this apparent affinity and challenges the idea that the Coase Theorem and the NLRA are compatible

Decreased directed functional connectivity in the psychedelic state

Neuroimaging studies of the psychedelic state offer a unique window onto the neural basis of conscious perception and selfhood. Despite well understood pharmacological mechanisms of action, the large-scale changes in neural dynamics induced by psychedelic compounds remain poorly understood. Using source-localised, steady-state MEG recordings, we describe changes in functional connectivity following the controlled administration of LSD, psilocybin and low-dose ketamine, as well as, for comparison, the (non-psychedelic) anticonvulsant drug tiagabine. We compare both undirected and directed measures of functional connectivity between placebo and drug conditions. We observe a general decrease in directed functional connectivity for all three psychedelics, as measured by Granger causality, throughout the brain. These data support the view that the psychedelic state involves a breakdown in patterns of functional organisation or information flow in the brain. In the case of LSD, the decrease in directed functional connectivity is coupled with an increase in undirected functional connectivity, which we measure using correlation and coherence. This surprising opposite movement of directed and undirected measures is of more general interest for functional connectivity analyses, which we interpret using analytical modelling. Overall, our results uncover the neural dynamics of information flow in the psychedelic state, and highlight the importance of comparing multiple measures of functional connectivity when analysing time-resolved neuroimaging data

Bootes II ReBooted: An MMT/MegaCam Study of An Ultra-Faint Milky Way Satellite

[abridged] We present MMT/Megacam imaging in Sloan $g$ and $r$ of the extremely low luminosity Bo\"otes II Milky Way companion. We use a bootstrap approach to perform robust measurements of, and uncertainties on, Bo\"otes II's distance, luminosity, size, and morphology. We show that Bo\"otes II's stellar population is old and metal-poor ([Fe/H] \lta -2). Assuming a stellar population like that of M92, Bo\"otes II is at a distance of 42 $\pm$ 2 kpc, closer than the initial published estimate of 60 $\pm$ 10 kpc. This distance revision, combined with a more robust measurement of Bo\"otes II's structure with a Plummer model (exponential model) results in a more compact half-light size of $r_h\simeq 36 (33) \pm 9 (10)$ pc and lower luminosity of $M_V\simeq-2.4 (-2.2) \pm 0.7 (0.7)$ mag. This revised size and luminosity move Bo\"otes II into a region of size-luminosity space not previously known to be occupied by old stellar populations, but also occupied by the recently discovered Milky Way satellites Willman 1 and SEGUE 1. We show that the apparently distorted morphology of Bo\"otes II is not statistically significant given the present data. We use a tidal argument to support a scenario where Bo\"otes II is a dwarf galaxy (dark matter dominated) rather than a globular cluster (not dark matter dominated). However, we can not rule out that Bo\"otes II is a star cluster on the verge of disruption, such as Palomar 5.Comment: 10 pages, 8 figures. ApJ accepted. Conclusions are unchanged, but content and figures have changed substantively in this accepted versio

Host-genetic-based outcome of co-infection by PCV2b and PRRSV in pigs

Replication of porcine circovirus type 2 (PCV2), an important worldwide swine pathogen, has been demonstrated to be influenced by host genotype. Specifically, a missense DNA polymorphism (SYNGR2 p.Arg63Cys) within the SYNGR2 gene was demonstrated to contribute to variation in PCV2b viral load and subsequent immune response following infection. PCV2 is known to induce immunosuppression leading to an increase in susceptibility to subsequent infections with other viral pathogens such as porcine reproductive and respiratory syndrome virus (PRRSV). In order to assess the role of SYNGR2 p.Arg63Cys in co-infections, pigs homozygous for the favorable SYNGR2 p.63Cys (N = 30) and unfavorable SYNGR2 p.63Arg (N = 29) alleles were infected with PCV2b followed a week later by a challenge with PRRSV. A lower PCV2b viremia (P \u3c 0.001) and PCV2-specific IgM antibodies (P \u3c 0.005) were observed in SYNGR2 p.63Cys compared to SYNGR2 p.63Arg genotypes. No significant differences in PRRSV viremia and specific IgG antibodies were observed between SYNGR2 genotypes. Lung histology score, an indicator of disease severity, was lower in the pigs with SYNGR2 p.63Cys genotypes (P \u3c 0.05). Variation in the lung histology scores within SYNGR2 genotypes suggests that additional factors, environmental and/or genetic, could be involved in disease severity. Lay Summary: Porcine circovirus type 2 (PCV2) is an important virus involved in the onset of a group of severe disease symptoms commonly known as porcine circovirus associated diseases (PCVAD). Vaccination options exist for PCV2, though the severity of PCVAD can be influenced by the presence of additional co-infecting pathogens, such as porcine reproductive and respiratory syndrome virus (PRRSV), for which vaccination is still a challenge. Host genetic resistance is a potential avenue for solving this problem. Previously, a genetic polymorphism in the SYNGR2 gene was found to be associated with PCV2b viremia and immune response. The aim of this study was to determine the impact of this polymorphism in pigs experimentally co-infected with PCV2b and PRRSV. Pigs were weighed, and blood was collected at various days following infection to measure viremia and antibodies. Histological analysis was performed at the experiment completion to assess disease severity in lungs and lymph nodes. The results showed that variation within the SYNGR2 gene is involved in PCV2b disease progression including lung histology scores, but no evidence was seen in response to PRRSV infection