Star Formation in the First Galaxies I: Collapse Delayed by Lyman-Werner Radiation

We investigate the process of metal-free star formation in the first galaxies with a high-resolution cosmological simulation. We consider the cosmologically motivated scenario in which a strong molecule-destroying Lyman-Werner (LW) background inhibits effective cooling in low-mass haloes, delaying star formation until the collapse or more massive haloes. Only when molecular hydrogen (H2) can self-shield from LW radiation, which requires a halo capable of cooling by atomic line emission, will star formation be possible. To follow the formation of multiple gravitationally bound objects, at high gas densities we introduce sink particles which accrete gas directly from the computational grid. We find that in a 1 Mpc^3 (comoving) box, runaway collapse first occurs in a 3x10^7 M_sun dark matter halo at z~12 assuming a background intensity of J21=100. Due to a runaway increase in the H2 abundance and cooling rate, a self-shielding, supersonically turbulent core develops abruptly with ~10^4 M_sun in cold gas available for star formation. We analyze the formation of this self-shielding core, the character of turbulence, and the prospects for star formation. Due to a lack of fragmentation on scales we resolve, we argue that LW-delayed metal-free star formation in atomic cooling haloes is very similar to star formation in primordial minihaloes, although in making this conclusion we ignore internal stellar feedback. Finally, we briefly discuss the detectability of metal-free stellar clusters with the James Webb Space Telescope.Comment: 22 pages, 1 new figure, accepted for publication in MNRA

A pilot feasibility study of a randomized controlled trial of goal setting using the Values in Action Inventory of Strengths following brain injury

In a single-blind feasibility pilot randomized controlled trial design, brain injury (BI) participants were recruited from a community rehabilitation centre and randomized into goal-setting using the Values in Action Inventory of Strengths (VIA-IS), and goal-setting as usual. Outcomes included the feasibility and acceptability of the VIA-IS, and its use in setting goals in a BI rehabilitation context, and whether it affected types of goals set (International Classification of Functioning (ICF)). Memory for goals two weeks later was measured, and a sample size calculated for a full-scale trial. Twenty-six BI participants were recruited, and randomized to the VIA-IS (n = 13) and control group (n = 13). Two dropped out of the VIA-IS condition, leaving a total n = 24. The majority (92%) of participants rated the VIA-IS as acceptable; both groups described the goal-setting process as “easy”. VIA-IS feedback varied; over two thirds (73%) of VIA-IS participants used their VIA-IS results to set goals and described it as “helpful”. There were no major differences in ICF categories between groups. A sample size of 66 would be required for a full-scale trial. A full-scale trial with multi-centre design appears warranted though might be more clinically beneficial for difficult to engage BI clients

Biodiversity and environmental stressors along urban walking routes

There is increasing focus on designing liveable cities that promote walking. However, urban walking routes can expose people to adverse environmental conditions that reduce health, well-being and biodiversity. Our primary objective is to assess how urban form is associated with environmental quality, including biodiversity, for people moving through urban spaces. We assess a range of environmental conditions that influence human health and biodiversity (temperature, noise and particulate pollution) and biodiversity of three taxa (trees, butterflies and birds) along 700 m public walking routes embedded in 500 m x 500 m grid cells across three UK towns. Cells are selected using random stratification across an urbanisation intensity gradient. Walking routes in more built-up areas were noisier and hotter; noise levels further increased in areas with more industrial land-use and large roads. There was no evidence of vegetation mitigating noise or temperature, but there was some evidence that increased vegetation cover mitigated small particulate pollution. Walking routes in more built-up environments had lower butterfly, bird and native tree species richness, and reduced butterfly abundance. Large roads were associated with reduced bird species richness and increased noise was associated with reduced bird abundance. Most specific measures of vegetation in the surrounding matrix (median patch size, structural complexity at 1.5 m resolution) were not detectably associated with biodiversity along walking routes, indicating minimal beneficial spill-over. Increased garden cover in the surrounding matrix was associated with less abundant and less species-rich butterfly communities. Our results highlight considerable heterogeneity in the environmental quality of urban walking routes and pedestrians’ potential to experience biodiversity along these routes, driven by reduced quality in areas with more built cover. A greater focus is needed on mitigating adverse effects of specific features of the built environment (roads, industrial areas, noise) surrounding walking routes to enhance the co-benefits of more biodiversity and healthier conditions for pedestrians.

Antiviral immune responses: triggers of or triggered by autoimmunity?

The predisposition of individuals to several common autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, is genetically linked to certain human MHC class II molecules and other immune modulators. However, genetic predisposition is only one risk factor for the development of these diseases, and low concordance rates in monozygotic twins, as well as the geographical distribution of disease risk, suggest the involvement of environmental factors in the development of these diseases. Among these environmental factors, infections have been implicated in the onset and/or promotion of autoimmunity. In this Review, we outline the mechanisms by which viral infection can trigger autoimmune disease and describe the pathways by which infection and immune control of infectious disease might be dysregulated during autoimmunity