135 research outputs found

    Public Media and Political Independence: Lessons for the Future of Journalism From Around the World

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    Profiles how fourteen nations fund and protect the autonomy of public media via multiyear funding, public-linked funding structures, charters, laws, and agencies or boards designed to limit political influence and ensure spending in the public interest

    “Public Service” and the Journalism Crisis: Is the BBC the Answer?

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    Professional journalism is under extraordinary pressure: not only are its traditional business models under enormous strain but it is also regularly accused by the Right of peddling ‘fake news’ and criticized by the Left for failing to play a robust monitorial role. In this situation, there is a temptation to see public service media, and the BBC in particular, as beacons of light in an otherwise gloomy picture. This article attempts to provide a note of caution to those who see the public service model as the most effective means of holding power to account and as the most desirable alternative to the flawed news cultures of both commercial and authoritarian landscapes. It considers some of the structural and institutional factors that constrain the BBC’s journalism and suggests that its intimate relationship with elite power has long undermined its ability to act as a reliable and independent check on power

    Evidence for a Causal Role for \u3ci\u3eEscherichia coli\u3c/i\u3e Strains Identified as Adherent-Invasive (AIEC) in Intestinal Inflammation

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    Enrichment of adherent-invasive Escherichia coli (AIEC) has been consistently detected in subsets of inflammatory bowel disease (IBD) patients. Although some AIEC strains cause colitis in animal models, these studies did not systematically compare AIEC with non-AIEC strains, and causal links between AIEC and disease are still disputed. Specifically, it remains unclear whether AIEC shows enhanced pathogenicity compared to that of commensal E. coli found in the same ecological microhabitat and if the in vitro phenotypes used to classify strains as AIEC are pathologically relevant. Here, we utilized in vitro phenotyping and a murine model of intestinal inflammation to systematically compare strains identified as AIEC with those identified as non-AIEC and relate AIEC phenotypes to pathogenicity. Strains identified as AIEC caused, on average, more severe intestinal inflammation. Intracellular survival/replication phenotypes routinely used to classify AIEC positively correlated with disease, while adherence to epithelial cells and tumor necrosis factor alpha production by macrophages did not. This knowledge was then applied to design and test a strategy to prevent inflammation by selecting E. coli strains that adhered to epithelial cells but poorly survived/replicated intracellularly. Two E. coli strains that ameliorated AIEC-mediated disease were subsequently identified. In summary, our results show a relationship between intracellular survival/replication in E. coli and pathology in murine colitis, suggesting that strains possessing these phenotypes might not only become enriched in human IBD but also contribute to disease. We provide new evidence that specific AIEC phenotypes are pathologically relevant and proof of principle that such mechanistic information can be therapeutically exploited to alleviate intestinal inflammation

    The Role of DNA Double-Strand Breaks in Spontaneous Homologous Recombination in S. cerevisiae

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    Homologous recombination (HR) is a source of genomic instability and the loss of heterozygosity in mitotic cells. Since these events pose a severe health risk, it is important to understand the molecular events that cause spontaneous HR. In eukaryotes, high levels of HR are a normal feature of meiosis and result from the induction of a large number of DNA double-strand breaks (DSBs). By analogy, it is generally believed that the rare spontaneous mitotic HR events are due to repair of DNA DSBs that accidentally occur during mitotic growth. Here we provide the first direct evidence that most spontaneous mitotic HR in Saccharomyces cerevisiae is initiated by DNA lesions other than DSBs. Specifically, we describe a class of rad52 mutants that are fully proficient in inter- and intra-chromosomal mitotic HR, yet at the same time fail to repair DNA DSBs. The conclusions are drawn from genetic analyses, evaluation of the consequences of DSB repair failure at the DNA level, and examination of the cellular re-localization of Rad51 and mutant Rad52 proteins after introduction of specific DSBs. In further support of our conclusions, we show that, as in wild-type strains, UV-irradiation induces HR in these rad52 mutants, supporting the view that DNA nicks and single-stranded gaps, rather than DSBs, are major sources of spontaneous HR in mitotic yeast cells
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