Automated Discovery of Internet Censorship by Web Crawling

Censorship of the Internet is widespread around the world. As access to the web becomes increasingly ubiquitous, filtering of this resource becomes more pervasive. Transparency about specific content that citizens are denied access to is atypical. To counter this, numerous techniques for maintaining URL filter lists have been proposed by various individuals and organisations that aim to empirical data on censorship for benefit of the public and wider censorship research community. We present a new approach for discovering filtered domains in different countries. This method is fully automated and requires no human interaction. The system uses web crawling techniques to traverse between filtered sites and implements a robust method for determining if a domain is filtered. We demonstrate the effectiveness of the approach by running experiments to search for filtered content in four different censorship regimes. Our results show that we perform better than the current state of the art and have built domain filter lists an order of magnitude larger than the most widely available public lists as of Jan 2018. Further, we build a dataset mapping the interlinking nature of blocked content between domains and exhibit the tightly networked nature of censored web resources

Identifying potential emerging human rights implications in Chinese smart cities via machine-learning aided patent analysis

In this work, we investigate smart city technologies primarily through an examination of trends in patent filing. We apply machine learning methods both to explore the increasing rates of patent filing globally for smart city technologies, and also to identify the emerging topics on which companies are choosing to focus their efforts. We focus particularly on deployed and emerging urban systems-of-systems in China, which represent a high proportion of patents filed for smart city technologies, with a view to their potential global impacts. As a leading source of innovation in the development of smart cities, Chinese patent filing exerts significant influence on similar technologies adopted globally. Our global patent analysis highlights emerging trends in smart city innovations, and the increased adoption of technologies and processes that present significant human rights concerns, especially concerns to privacy, freedom of expression, and assembly

Strategic advertising of online news articles as an intervention to influence wildlife product consumers

Changing human behavior is essential for biodiversity conservation, but robust approaches for large scale change are needed. Concepts like repeat message exposure and social reinforcement, as well as mechanisms like online news coverage and targeted advertisements, are currently used by private and public sectors, and could prove powerful for conservation. Thus, to explore their potential in influencing wildlife consumption, we used online advertisements through Facebook, Google, and Outbrain, to promote news articles discussing the use of a Critically Endangered antelope (the Saiga tatarica) as a traditional Chinese medicine in Singapore. Our message, tailored to middle-aged Chinese Singaporean women, framed saiga horn products as being no longer socially endorsed. Through advert performance and in-depth analyses of Facebook user engagement, we assessed audience response. Our message pervaded Singapore's online media (e.g., our adverts were shown almost five million times; and the story ran on seven news outlets), and resulted in widespread desirable audience responses (e.g., 63% of Facebook users' engagements included identifiably positive features like calls for public action to reduce saiga horn consumption, anger at having unknowingly used a Critically Endangered species, and self-pledges to no longer use it; only 13% of engagements included identifiably negative features). This work shows that targeted dissemination of online news articles can have promising results, and may have wide applicability to conservation

Identifying the routes by which children view pornography online: implications for future policy-makers seeking to limit viewing

Report of Expert Panel for DCM

Integrating population variation and protein structural analysis to improve clinical interpretation of missense variation: application to the WD40 domain

We present a generic, multidisciplinary approach for improving our understanding of novel missense variants in recently discovered disease genes exhibiting genetic heterogeneity, by combining clinical and population genetics with protein structural analysis. Using six new de novo missense diagnoses in TBL1XR1 from the Deciphering Developmental Disorders study, together with population variation data, we show that the β-propeller structure of the ubiquitous WD40 domain provides a convincing way to discriminate between pathogenic and benign variation. Children with likely pathogenic mutations in this gene have severely delayed language development, often accompanied by intellectual disability, autism, dysmorphology and gastrointestinal problems. Amino acids affected by likely pathogenic missense mutations are either crucial for the stability of the fold, forming part of a highly conserved symmetrically repeating hydrogen-bonded tetrad, or located at the top face of the β-propeller, where ‘hotspot’ residues affect the binding of β-catenin to the TBLR1 protein. In contrast, those altered by population variation are significantly less likely to be spatially clustered towards the top face or to be at buried or highly conserved residues. This result is useful not only for interpreting benign and pathogenic missense variants in this gene, but also in other WD40 domains, many of which are associated with disease

Protein structure and phenotypic analysis of pathogenic and population missense variants in STXBP1

Background: Syntaxin-binding protein 1, encoded by STXBP1, is highly expressed in the brain and involved in fusing synaptic vesicles with the plasma membrane. Studies have shown that pathogenic loss-of-function variants in this gene result in various types of epilepsies, mostly beginning early in life. We were interested to model pathogenic missense variants on the protein structure to investigate the mechanism of pathogenicity and genotype–phenotype correlations. Methods: We report 11 patients with pathogenic de novo mutations in STXBP1 identified in the first 4293 trios of the Deciphering Developmental Disorder (DDD) study, including six missense variants. We analyzed the structural locations of the pathogenic missense variants from this study and the literature, as well as population missense variants extracted from Exome Aggregation Consortium (ExAC). Results: Pathogenic variants are significantly more likely to occur at highly conserved locations than population variants, and be buried inside the protein domain. Pathogenic mutations are also more likely to destabilize the domain structure compared with population variants, increasing the proportion of (partially) unfolded domains that are prone to aggregation or degradation. We were unable to detect any genotype–phenotype correlation, but unlike previously reported cases, most of the DDD patients with STXBP1 pathogenic variants did not present with very early-onset or severe epilepsy and encephalopathy, though all have developmental delay with intellectual disability and most display behavioral problems and suffered seizures in later childhood. Conclusion: Variants across STXBP1 that cause loss of function can result in severe intellectual disability with or without seizures, consistent with a haploinsufficiency mechanism. Pathogenic missense mutations act through destabilization of the protein domain, making it prone to aggregation or degradation. The presence or absence of early seizures may reflect ascertainment bias in the literature as well as the broad recruitment strategy of the DDD study.The DDD study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051)