Remaking responsibility: complexity and scattered causes in human agency

Contrary to intuitions that human beings are free to think and act with “buck-stopping” freedom, philosophers since Holbach and Hume have argued that universal causation makes free will nonsensical. Contemporary neuroscience has strengthened their case and begun to reveal subtle and counterintuitive mechanisms in the processes of conscious agency. Although some fear that determinism undermines moral responsibility, the opposite is true: free will, if it existed, would undermine coherent systems of justice. Moreover, deterministic views of human choice clarify the conditions in which we ought to protect people from themselves, for example when they cannot give informed consent to medical procedures. Some of the most unresolved questions in this domain are just now emerging; they include robot ethics and the responsibilities of groups. We propose a philosophical and scientific research program to apply complex systems science to these problems

Onset of effect and impact on health-related quality of life, exacerbation rate, lung function, and nasal polyposis symptoms for patients with severe eosinophilic asthma treated with benralizumab (ANDHI): a randomised, controlled, phase 3b trial

International audienc

Defining the role of common variation in the genomic and biological architecture of adult human height

Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated ∼2,000, ∼3,700 and ∼9,500 SNPs explained ∼21%, ∼24% and ∼29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/β-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants