Representation of Africa online: sourcing practice and frames of reference

The dominant perspective on the representation of Africa in the western media claims that western media coverage is bias and crisis orientated and the liberal perspective claims that the coverage of Africa is not as negative as is often assumed. However, there is a paucity of literature on the representation of Africa online. This research enquiry is relevant because literature claims that the Internet has the potential to resolve the journalistic predicament of representing other culture through political participation and deliberation. But this requires a re-orientation of the sourcing practice of news organization to embrace sensitivity to and knowledge of African cultures. Moreover, the journalistic predicament can be resolved or not depending on the news gathering approach adopted by the news organization. Literature has identified two approaches, that is, ‘gatekeeping’ used mainly by dominant traditional media and ‘gatewatching’ used by alternative media in their quest to counter mainstream ideology. This study examines the impacts of the ‘gatewatching’ approach adopted by Africa Have Your Say (AHYS) website on its representation and frames of reference of Africa. It uses on-site observation, in-depth interviews and textual analysis to gather data. The study found that although the sourcing practice at the AHYS is elaborate and complex, the ‘gatewatching’ approach makes its susceptible to second level agenda setting. Hence, its frame repeats the attributes and tone used by the mainstream traditional media. However, a minority of users did not use repeat this frame in their comments

“Making voices heard…”: Index on Censorship as Advocacy Journalism

The magazine Index on Censorship has sought, since its launch in 1972, to provide a space where censorship and abuses against freedom of expression have been identified, highlighted and challenged. Originally set up by a collection of writers and intellectuals who were concerned at the levels of state censorship and repression of artists in and under the influence of the Soviet Union and elsewhere, ‘Index’ has provided those championing the values of freedom of expression with a platform for highlighting human rights abuses, curtailment of civil liberties and formal and informal censorship globally. Charting its inception and development between 1971 and 1974, the paper is the first to situate the journal within the specific academic literature on activist media (Janowitz, 1975; Waisbord, 2009; Fisher, 2016). In doing so the paper advances an argument which draws on the drivers and motivations behind the publication’s launch to signal the development of a particular justification or ‘advocacy’ of a left-libertarian civic model of freedom of speech

EPHB4 kinase-inactivating mutations cause autosomal dominant lymphatic-related hydrops fetalis.

Hydrops fetalis describes fluid accumulation in at least 2 fetal compartments, including abdominal cavities, pleura, and pericardium, or in body tissue. The majority of hydrops fetalis cases are nonimmune conditions that present with generalized edema of the fetus, and approximately 15% of these nonimmune cases result from a lymphatic abnormality. Here, we have identified an autosomal dominant, inherited form of lymphatic-related (nonimmune) hydrops fetalis (LRHF). Independent exome sequencing projects on 2 families with a history of in utero and neonatal deaths associated with nonimmune hydrops fetalis uncovered 2 heterozygous missense variants in the gene encoding Eph receptor B4 (EPHB4). Biochemical analysis determined that the mutant EPHB4 proteins are devoid of tyrosine kinase activity, indicating that loss of EPHB4 signaling contributes to LRHF pathogenesis. Further, inactivation of Ephb4 in lymphatic endothelial cells of developing mouse embryos led to defective lymphovenous valve formation and consequent subcutaneous edema. Together, these findings identify EPHB4 as a critical regulator of early lymphatic vascular development and demonstrate that mutations in the gene can cause an autosomal dominant form of LRHF that is associated with a high mortality rate

Restricting digital sites of dissent: commercial social media and free expression

The widespread use of commercial social media platforms by protesters and activists has enhanced protest mobilisation and reporting but it has placed social media providers in the intermediary role as facilitators of dissent and has thereby created new challenges. Companies like Google and Facebook are increasingly restricting content that is published on or distributed through their platforms; they have been subject to obstruction by governments; and their services have been at the core of large-scale data collection and surveillance. This article analyses and categorises forms of infrastructure-based restrictions on free expression and dissent. It shows how private intermediaries have been incorporated into state-led content policies; how they set their own standards for legitimate online communication and intervene accordingly; and how state-based actions and commercial self-regulation intersect in the specific area of online surveillance. Based on a broad review of cases, it situates the role of social media in the wider trend of the privatisation of communications policy and the complex interplay between state-based regulation and commercial rule-making

Pioneers of World Wide Web Fascism: The British Extreme Right and Web 1.0

This chapter explores the ways that, around the turn of the millennium, British fascist organisations, such as the British National Party, and leading ideologues, such as David Irving, developed websites as part of their activism. It uses the Internet Archive’s Wayback Machine to engage in a ‘web history’ of this early online activism by British fascists. It argues that websites could sometimes be used to help present British fascist politics as more respectable, as in the case of the BNP, or alternatively as a way to allow activists access to the fringe cultic milieu of British fascism, steeped in conspiracy theories, overt neo-Nazism and other ideas deeply oppositional to mainstream perspectives. It concludes that, although often amateurish and poorly resourced, British fascist groups were often eager early adopters of Web 1.0, and argues that a deeper understating of this early ‘web history’ offers important context for those studying contemporary forms of extreme right online activism

Janus-faced EPHB4-associated disorders: novel pathogenic variants and unreported intrafamilial overlapping phenotypes.

PURPOSE: Several clinical phenotypes including fetal hydrops, central conducting lymphatic anomaly or capillary malformations with arteriovenous malformations 2 (CM-AVM2) have been associated with EPHB4 (Ephrin type B receptor 4) variants, demanding new approaches for deciphering pathogenesis of novel variants of uncertain significance (VUS) identified in EPHB4, and for the identification of differentiated disease mechanisms at the molecular level. METHODS: Ten index cases with various phenotypes, either fetal hydrops, CM-AVM2, or peripheral lower limb lymphedema, whose distinct clinical phenotypes are described in detail in this study, presented with a variant in EPHB4. In vitro functional studies were performed to confirm pathogenicity. RESULTS: Pathogenicity was demonstrated for six of the seven novel EPHB4 VUS investigated. A heterogeneity of molecular disease mechanisms was identified, from loss of protein production or aberrant subcellular localization to total reduction of the phosphorylation capability of the receptor. There was some phenotype-genotype correlation; however, previously unreported intrafamilial overlapping phenotypes such as lymphatic-related fetal hydrops (LRFH) and CM-AVM2 in the same family were observed. CONCLUSION: This study highlights the usefulness of protein expression and subcellular localization studies to predict EPHB4 variant pathogenesis. Our accurate clinical phenotyping expands our interpretation of the Janus-faced spectrum of EPHB4-related disorders, introducing the discovery of cases with overlapping phenotypes

Increasing female participation in municipal elections via the use of local radio in conflict-affected settings: The case of the West Bank municipal elections 2017

The 2017 West Bank Municipal elections were framed by locally-based non-governmental organisations (NGOs) and the Palestinian Authorities – albeit to a lesser extent – in terms of the desirability of increasing female participation in them in two particular ways: participation as representatives and participation as voters. Both aspects of participation were supported by extensive radio campaigns conducted by locally-based NGOs. The effectiveness of these campaigns and the approaches used form the basis of this article. Using a mixed methods approach consisting of both quantitative and qualitative data, it concludes that radio has endemic socio-technical advantages for reaching women, particularly in conflict-affected areas, and that broadcasting content aimed at women by women is essential in terms of increasing their representation and voting

Novel mutations in PIEZO1 cause an autosomal recessive generalized lymphatic dysplasia with non-immune hydrops fetalis.

Generalized lymphatic dysplasia (GLD) is a rare form of primary lymphoedema characterized by a uniform, widespread lymphoedema affecting all segments of the body, with systemic involvement such as intestinal and/or pulmonary lymphangiectasia, pleural effusions, chylothoraces and/or pericardial effusions. This may present prenatally as non-immune hydrops. Here we report homozygous and compound heterozygous mutations in PIEZO1, resulting in an autosomal recessive form of GLD with a high incidence of non-immune hydrops fetalis and childhood onset of facial and four limb lymphoedema. Mutations in PIEZO1, which encodes a mechanically activated ion channel, have been reported with autosomal dominant dehydrated hereditary stomatocytosis and non-immune hydrops of unknown aetiology. Besides its role in red blood cells, our findings indicate that PIEZO1 is also involved in the development of lymphatic structures

Author Correction: Novel mutations in PIEZO1 cause an autosomal recessive generalized lymphatic dysplasia with non-immune hydrops fetalis.

This Article contains an error in the last sentence of the 'Variant analysis suggests they are pathogenic' section of the Results, which incorrectly reads 'No truncated PIEZO1 protein products were identified in western blot analysis in GLD1:II.3 and GLD2:II.2 (Fig. 2, Supplementary Fig. 6), suggesting that the truncated protein is not stable and therefore degraded.' This should read 'No full-size PIEZO1 protein products were identified in western blot analysis in GLD1:II.3 and GLD2:II.2 (Fig. 2, Supplementary Fig. 6); the three nonsense mutations are predicted to lead to premature termination of the protein, hence it is possible that those truncated proteins will be non-functional or even unstable and degraded.' The error has not been fixed in the PDF or HTML versions of the Article

Mutations in the small nuclear RNA gene <i>RNU2</i>-<i>2</i> cause a severe neurodevelopmental disorder with prominent epilepsy

The major spliceosome includes five small nuclear RNA (snRNAs), U1, U2, U4, U5 and U6, each of which is encoded by multiple genes. We recently showed that mutations in RNU4-2, the gene that encodes the U4-2 snRNA, cause one of the most prevalent monogenic neurodevelopmental disorders. Here, we report that recurrent germline mutations in RNU2-2 (previously known as pseudogene RNU2-2P), a 191-bp gene that encodes the U2-2 snRNA, are responsible for a related disorder. By genetic association, we identified recurrent de novo single-nucleotide mutations at nucleotide positions 4 and 35 of RNU2-2 in nine cases. We replicated this finding in 16 additional cases, bringing the total to 25. We estimate that RNU2-2 syndrome has a prevalence of ~20% that of RNU4-2 syndrome. The disorder is characterized by intellectual disability, autistic behavior, microcephaly, hypotonia, epilepsy and hyperventilation. All cases display a severe and complex seizure phenotype. We found that U2-2 and canonical U2-1 were similarly expressed in blood. Despite mutant U2-2 being expressed in patient blood samples, we found no evidence of missplicing. Our findings cement the role of major spliceosomal snRNAs in the etiologies of neurodevelopmental disorders.</p