The cosmic abundance of cold gas in the local Universe

We determine the cosmic abundance of molecular hydrogen (H2) in the local universe from the xCOLD GASS survey. To constrain the H2 mass function at low masses and correct for the effect of the lower stellar mass limit of 10^9 Msun in the xCOLD GASS survey, we use an empirical approach based on an observed scaling relation between star formation rate and gas mass. We also constrain the HI and HI+H2 mass functions using the xGASS survey, and compare it to the HI mass function from the ALFALFA survey. We find the cosmic abundance of molecular gas in the local Universe to be Omega_H2=(5.34+/-0.47)x10^-5 h^-1. Molecular gas accounts for 19.6 +/- 3.9% of the total abundance of cold gas, Omega_HI+H2=(4.66+/-0.70)x10^-4 h^-1. Galaxies with stellar masses in excess of 10^9 Msun account for 89% of the molecular gas in the local Universe, while in comparison such galaxies only contain 73% of the cold atomic gas as traced by the HI 21cm line. The xCOLD GASS CO, molecular gas and cold gas mass functions and Omega_H2 measurements provide constraints for models of galaxy evolution and help to anchor blind ALMA and NOEMA surveys attempting to determine the abundance of molecular gas at high redshifts

What explains the socioeconomic status gap in activity? : Educational differences in determinants of physical activity and screentime

Designing evidence-based interventions to address socioeconomic disparities in health and health behaviours requires a better understanding of the specific explanatory mechanisms. We aimed to investigate a comprehensive range of potential theoretical mediators of physical activity (PA) and screen time in different socioeconomic status (SES) groups: a high SES group of high school students, and a low SES group of vocational school students. The COM-B system, including the Theoretical Domains Framework (TDF), was used as a heuristic framework to synthesise different theoretical determinants in this exploratory study.Peer reviewe

The impact of interventions to promote healthier ready-to-eat meals (to eat in, to take away or to be delivered) sold by specific food outlets open to the general public: a systematic review.

INTRODUCTION: Ready-to-eat meals sold by food outlets that are accessible to the general public are an important target for public health intervention. We conducted a systematic review to assess the impact of such interventions. METHODS: Studies of any design and duration that included any consumer-level or food-outlet-level before-and-after data were included. RESULTS: Thirty studies describing 34 interventions were categorized by type and coded against the Nuffield intervention ladder: restrict choice = trans fat law (n = 1), changing pre-packed children's meal content (n = 1) and food outlet award schemes (n = 2); guide choice = price increases for unhealthier choices (n = 1), incentive (contingent reward) (n = 1) and price decreases for healthier choices (n = 2); enable choice = signposting (highlighting healthier/unhealthier options) (n = 10) and telemarketing (offering support for the provision of healthier options to businesses via telephone) (n = 2); and provide information = calorie labelling law (n = 12), voluntary nutrient labelling (n = 1) and personalized receipts (n = 1). Most interventions were aimed at adults in US fast food chains and assessed customer-level outcomes. More 'intrusive' interventions that restricted or guided choice generally showed a positive impact on food-outlet-level and customer-level outcomes. However, interventions that simply provided information or enabled choice had a negligible impact. CONCLUSION: Interventions to promote healthier ready-to-eat meals sold by food outlets should restrict choice or guide choice through incentives/disincentives. Public health policies and practice that simply involve providing information are unlikely to be effective

The Generation of Successive Unmarked Mutations and Chromosomal Insertion of Heterologous Genes in Actinobacillus pleuropneumoniae Using Natural Transformation

We have developed a simple method of generating scarless, unmarked mutations in Actinobacillus pleuropneumoniae by exploiting the ability of this bacterium to undergo natural transformation, and with no need to introduce plasmids encoding recombinases or resolvases. This method involves two successive rounds of natural transformation using linear DNA: the first introduces a cassette carrying cat (which allows selection by chloramphenicol) and sacB (which allows counter-selection using sucrose) flanked by sequences to either side of the target gene; the second transformation utilises the flanking sequences ligated directly to each other in order to remove the cat-sacB cassette. In order to ensure efficient uptake of the target DNA during transformation, A. pleuropneumoniae uptake sequences are added into the constructs used in both rounds of transformation. This method can be used to generate multiple successive deletions and can also be used to introduce targeted point mutations or insertions of heterologous genes into the A. pleuropneumoniae chromosome for development of live attenuated vaccine strains. So far, we have applied this method to highly transformable isolates of serovars 8 (MIDG2331), which is the most prevalent in the UK, and 15 (HS143). By screening clinical isolates of other serovars, it should be possible to identify other amenable strains

Factors associated with quality of services for marginalized groups with mental health problems in 14 European countries

This research was financially supported by DG-Sanco (contract: 800197; 2007-2010). The authors would like to thank all of the professionals and services who participated in the PROMO assessment of services. A PhD grant from Fundação para a Ciência e Tecnologia–Portugal (SFRH/BD/66388/2009) to the first author is acknowledged

ERBB4 confers metastatic capacity in Ewing sarcoma.

Metastatic spread is the single-most powerful predictor of poor outcome in Ewing sarcoma (ES). Therefore targeting pathways that drive metastasis has tremendous potential to reduce the burden of disease in ES. We previously showed that activation of the ERBB4 tyrosine kinase suppresses anoikis, or detachment-induced cell death, and induces chemoresistance in ES cell lines in vitro. We now show that ERBB4 is transcriptionally overexpressed in ES cell lines derived from chemoresistant or metastatic ES tumours. ERBB4 activates the PI3K-Akt cascade and focal adhesion kinase (FAK), and both pathways contribute to ERBB4-mediated activation of the Rac1 GTPase in vitro and in vivo. ERBB4 augments tumour invasion and metastasis in vivo, and these effects are blocked by ERBB4 knockdown. ERBB4 expression correlates significantly with reduced disease-free survival, and increased expression is observed in metastatic compared to primary patient-matched ES biopsies. Our findings identify a novel ERBB4-PI3K-Akt-FAK-Rac1 pathway associated with aggressive disease in ES. These results predict that therapeutic targeting of ERBB4, alone or in combination with cytotoxic agents, may suppress the metastatic phenotype in ES