Computer supported argument maps as a policy memory

This paper investigates to what extent Computer Supported Argument Visualisation can be designed to encourage debate and deliberation by citizens on public issues. Such argument maps use icons and arrows to represent the structure of a series of related viewpoints, reducing the amount of text necessary to convey the ideas, thereby clarifying the issue under consideration. Argument maps have the potential to provide a readily accessible medium by which citizens can follow and join in public debates on policy issues. In this paper we describe our approach, type of maps we have chosen to use and then demonstrate the potential of a collection of maps to form a ‘policy memory’ to support policy development. Our case study is the development of the ‘Smoking in Public Places’ policy in the Scottish Parliament. Our overall aim is to engage citizens in democratic decision-making leading to better policy-making and a more engaged citizenry

Pharmacogenetics 4 3 166 170 ENGLAND

Eighteen healthy Caucasians were evaluated for the systemic acetylation of a caffeine metabolite using the urinary caffeine metabolite ratio 5-acetylamino-6-formylamino-3-methyluracil (AFMU) to 1-methylaxanthine (1X) and for N-acetyltransferase activity in peripheral blood mononuclear leukocytes (MNL) using p-aminobenzoic acid (PABA). These are markers for systemic NAT2 and NAT1 N-acetyltransferase activities, respectively. Fourteen slow acetylators and four fast acetylators (the NAT2 polymorphism) were identified by the caffeine metabolite ratio. In slow acetylators who have decreased levels of hepatic NAT2, the AFMU/1X ratio was significantly correlated with PABA acetylation in MNL (r = 0.8; p = 0.0002). These results suggest that significant variation in the acetylation of arylamine substrates susceptible to the classical acetylator polymorphism is attributable to variation in NAT1 activity in the slow acetylator phenotype

Shared polygenic risk and causal inferences in amyotrophic lateral sclerosis

International audienceTo identify shared polygenic risk and causal associations in amyotrophic lateral sclerosis (ALS).Methods: Linkage disequilibrium score regression and Mendelian randomization were applied in a large-scale, data-driven manner to explore genetic correlations and causal relationships between >700 phenotypic traits and ALS. Exposures consisted of publicly available genome-wide association studies (GWASes) summary statistics from MR Base and LD-hub. The outcome data came from the recently published ALS GWAS involving 20,806 cases and 59,804 controls. Multivariate analyses, genetic risk profiling, and Bayesian colocalization analyses were also performed.Results: We have shown, by linkage disequilibrium score regression, that ALS shares polygenic risk genetic factors with a number of traits and conditions, including positive correlations with smoking status and moderate levels of physical activity, and negative correlations with higher cognitive performance, higher educational attainment, and light levels of physical activity. Using Mendelian randomization, we found evidence that hyperlipidemia is a causal risk factor for ALS and localized putative functional signals within loci of interest.Interpretation: Here, we have developed a public resource (https://lng-nia.shinyapps.io/mrshiny) which we hope will become a valuable tool for the ALS community, and that will be expanded and updated as new data become available. Shared polygenic risk exists between ALS and educational attainment, physical activity, smoking, and tenseness/restlessness. We also found evidence that elevated low-desnity lipoprotein cholesterol is a causal risk factor for ALS. Future randomized controlled trials should be considered as a proof of causality. Ann Neurol 2019;85:470-481