Measurements of the Cosmological Evolution of Magnetic Fields with the Square Kilometre Array

We investigate the potential of the Square Kilometre Array (SKA) for measuring the magnetic fields in clusters of galaxies via Faraday rotation of background polarised sources. [...] We find that about 10 per cent of the sky is covered by a significant extragalactic Faraday screen. Most of it has rotation measures between 10 and 100 rad/m/m. We argue that the cluster centres should have up to about 5000 rad/m/m. We show that the proposed mid frequency aperture array of the SKA as well as the lowest band of the SKA dish array are well suited to make measurements for most of these rotation measure values, typically requiring a signal-to-noise of ten. We calculate the spacing of sources forming a grid for the purpose of measuring foreground rotation measures: it reaches a spacing of 36 arcsec for a 100 hour SKA observation per field. We also calculate the statistics for background RM measurements in clusters of galaxies. We find that a first phase of the SKA would allow us to take stacking experiments out to high redshifts (>1), and provide improved magnetic field structure measurements for individual nearby clusters. The full SKA aperture array would be able to make very detailed magnetic field structure measurements of clusters with more than 100 background sources per cluster up to a redshift of 0.5 and more than 1000 background sources per cluster for nearby clusters, and could for reasonable assumptions about future measurements of electron densities in high redshift clusters constrain the power law index for the magnetic field evolution to better than dm=0.4, if the magnetic field in clusters should follow B ~ (1+z)^m.Comment: 12 pages, 10 figures, 3 tables, accepted by MNRAS, minor correction to eq (5

The economic value of guaranteed water supply for irrigation under scarcity conditions

Resource /Energy Economics and Policy,

Migration as an adjustment mechanism in the crisis? A comparison of Europe and the United States

The question of whether migration can be an equilibrating force in the labour market is an important criterion for an optimal currency area. It is of particular interest currently in the context of high and rising levels of labour market disparities, in particular within the Eurozone where there is no exchange-rate mechanism available to play this role. We shed some new light on this question by comparing pre- and post-crisis migration movements at the regional level in both Europe and the United States, and their association with asymmetric labour market shocks. We find that recent migration flows have reacted quite significantly to the EU enlargements in 2004 and 2007 and to changes in labour market conditions, particularly in Europe. Indeed, in contrast to the pre-crisis situation and the findings of previous empirical studies, there is tentative evidence that the migration response to the crisis has been considerable in Europe, in contrast to the United States where the crisis and subsequent sluggish recovery were not accompanied by greater interregional labour mobility in reaction to labour market shocks. Our estimates suggest that, if all measured population changes in Europe were due to migration for employment purposes - i.e. an upper-bound estimate - up to about a quarter of the asymmetric labour market shock would be absorbed by migration within a year. However, in the Eurozone the reaction mainly stems from migration of third-country nationals. Even within the group of Eurozone nationals, a significant part of the free mobility stems from immigrants from third countries who have taken on the nationality of their Eurozone host country

Migration as an Adjustment Mechanism in the Crisis? A Comparison of Europe and the United States

The question of whether migration can be an equilibrating force in the labour market is an important criterion for an optimal currency area. It is of particular interest currently in the context of high and rising levels of labour market disparities, in particular within the Eurozone where there is no exchange-rate mechanism available to play this role. We shed some new light on this question by comparing pre- and post-crisis migration movements at the regional level in both Europe and the United States, and their association with asymmetric labour market shocks. We find that recent migration flows have reacted quite significantly to the EU enlargements in 2004 and 2007 and to changes in labour market conditions, particularly in Europe. Indeed, in contrast to the pre-crisis situation and the findings of previous empirical studies, there is tentative evidence that the migration response to the crisis has been considerable in Europe, in contrast to the United States where the crisis and subsequent sluggish recovery were not accompanied by greater interregional labour mobility in reaction to labour market shocks. Our estimates suggest that, if all measured population changes in Europe were due to migration for employment purposes i.e. an upper-bound estimate up to about a quarter of the asymmetric labour market shock would be absorbed by migration within a year. However, in the Eurozone the reaction mainly stems from migration of third-country nationals. Even within the group of Eurozone nationals, a significant part of the free mobility stems from immigrants from third countries who have taken on the nationality of their Eurozone host country

Early social environment influences the behaviour of a family-living lizard

Financial support for this research was provided by the Australian Research Council (DP130102998; grant to M.J.W. and R.B.W.), Natural Sciences and Engineering Research Council of Canada (scholarship to J.L.R.), the Australasian Society for the Study of Animal Behaviour, and Macquarie University. D.W.A.N. was supported by an ARC Discovery Early Career Research Award (DE150101774) and UNSW Vice Chancellors Fellowship.Early social environment can play a significant role in shaping behavioural development. For instance, in many social mammals and birds, isolation rearing results in individuals that are less exploratory, shyer, less social and more aggressive than individuals raised in groups. Moreover, dynamic aspects of social environments, such as the nature of relationships between individuals, can also impact the trajectory of development. We tested if being raised alone or socially affects behavioural development in the family-living tree skink, Egernia striolata. Juveniles were raised in two treatments: alone or in a pair. We assayed exploration, boldness, sociability and aggression repeatedly throughout each juvenile's first year of life, and also assessed social interactions between pairs to determine if juveniles formed dominant–subordinate relationships. We found that male and/or the larger skinks within social pairs were dominant. Developing within this social environment reduced skink growth, and subordinate skinks were more prone to tail loss. Thus, living with a conspecific was costly for E. striolata. The predicted negative effects of isolation failed to materialize. Nevertheless, there were significant differences in behavioural traits depending on the social environment (isolated, dominant or subordinate member of a pair). Isolated skinks were more social than subordinate skinks. Subordinate skinks also became more aggressive over time, whereas isolated and dominant skinks showed invariable aggression. Dominant skinks became bolder over time, whereas isolated and subordinate skinks were relatively stable in their boldness. In summary, our study is evidence that isolation rearing does not consistently affect behaviour across all social taxa. Our study also demonstrates that the social environment plays an important role in behavioural development of a family-living lizard.Publisher PDFPeer reviewe

Automatic Mapping of Atrial Fiber Orientations for Patient-Specific Modeling of Cardiac Electromechanics using Image-Registration

Knowledge of appropriate local fiber architecture is necessary to simulate patient-specific electromechanics in the human heart. However, it is not yet possible to reliably measure in-vivo fiber directions, especially in human atria. Thus, we present a method which defines the fiber architecture in arbitrarily shaped atria using image registration and reorientation methods based on atlas atria with fibers predefined from detailed histological observations. Thereby, it is possible to generate detailed fiber families in every new patient-specific geometry in an automated, time-efficient process. We demonstrate the good performance of the image registration and fiber definition on ten differently shaped human atria. Additionally, we show that characteristics of the electrophysiological activation pattern which appear in the atlas atria also appear in the patients' atria. We arrive at analogous conclusions for coupled electro-mechano-hemodynamical computations

Suppression of RhoG activity is mediated by a syndecan 4–synectin–RhoGDI1 complex and is reversed by PKCα in a Rac1 activation pathway

Fibroblast growth factor 2 (FGF2) is a major regulator of developmental, pathological, and therapeutic angiogenesis. Its activity is partially mediated by binding to syndecan 4 (S4), a proteoglycan receptor. Angiogenesis requires polarized activation of the small guanosine triphosphatase Rac1, which involves localized dissociation from RhoGDI1 and association with the plasma membrane. Previous work has shown that genetic deletion of S4 or its adapter, synectin, leads to depolarized Rac activation, decreased endothelial migration, and other physiological defects. In this study, we show that Rac1 activation downstream of S4 is mediated by the RhoG activation pathway. RhoG is maintained in an inactive state by RhoGDI1, which is found in a ternary complex with synectin and S4. Binding of S4 to synectin increases the latter's binding to RhoGDI1, which in turn enhances RhoGDI1's affinity for RhoG. S4 clustering activates PKCα, which phosphorylates RhoGDI1 at Ser96. This phosphorylation triggers release of RhoG, leading to polarized activation of Rac1. Thus, FGF2-induced Rac1 activation depends on the suppression of RhoG by a previously uncharacterized ternary S4–synectin–RhoGDI1 protein complex and activation via PKCα