Prophets and loss: how "soft facts" on social media influenced the Brexit campaign and social reactions to the murder of Jo Cox MP

This article examines “soft facts” about security issues in the 2016 Brexit referendum campaign. Soft facts arise when information provenance is uncertain, and are forms of malleable and contingent knowledge, such as rumors, conspiracy theories, and propaganda. There is a growing appreciation that digital communications environments are especially conducive to the dissemination of these kinds of information. Informed by empirical data comprising forty‐five thousand nine hundred and fifty‐seven data points collected by monitoring social media before and after the UK Brexit referendum campaign (June 16–October 12, 2016), the analysis examines how and why a series of soft facts concerning Brexit were mobilized. By developing the concept of “digital prophecy,” the article explores how influence is exerted by online prophets who were connecting current events to past grievances, to advance negative predictions about the future. This starts to capture the tradecraft of digital influencing, in ways that move beyond the structural topologies of communication networks. In policy terms, the analysis reminds us of the need to attend not just to how influence is achieved through fake news (e.g., using social media bots to amplify a message), but also why influence is sought in the first place

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

T-cell- and macrophage-mediated axon damage in the absence of a CNS-specific immune response: involvement of metalloproteinases

Recent evidence has highlighted the fact that axon injury is an important component of multiple sclerosis pathology. The issue of whether a CNS antigen-specific immune response is required to produce axon injury remains unresolved. We investigated the extent and time course of axon injury in a rodent model of a delayed-type hypersensitivity (DTH) reaction directed against the mycobacterium bacille Calmette-Guerin (BCG). Using MRI, we determined whether the ongoing axon injury is restricted to the period during which the blood-brain barrier is compromised. DTH lesions were initiated in adult rats by intracerebral injection of heat-killed BCG followed by a peripheral challenge with BCG. Our findings demonstrate that a DTH reaction to a non-CNS antigen within a CNS white matter tract leads to axon injury. Ongoing axon injury persisted throughout the 3-month period studied and was not restricted to the period of blood-brain barrier breakdown, as detected by MRI enhancing lesions. We have previously demonstrated that matrix metalloproteinases (MMPs) are upregulated in multiple sclerosis plaques and DTH lesions. In this study we demonstrated that microinjection of activated MMPs into the cortical white matter results in axon injury. Our results show that axon injury, possibly mediated by MMPs, is immunologically non-specific and may continue behind an intact blood-brain barrier

Community architecture An evaluation of the case for user participation in architectural design

SIGLEAvailable from British Library Lending Division - LD:D57651/85 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

A revision of the Plateremaeidae (Acari: Oribatei)

The family Plateremaeidae is revised, and includes the following taxa: Plateremaeus Berlese, with the only species P. ornatissimus (Berlese), from Brazil; Allodamaeus Banks, with the species ewingi (Banks), from the USA, coralgablensis, sp. n. (type-locality: USA, Flórida, Coral Gables), and ornatos Balogh & Csiszár, from Argentina; Lophoremaeus, gen. n., with two species: mirabilis Csiszár, from Bulgaria, the type-species, and laminipes (Berlese), n. comb., from Italy; Paralopheremaeus, gen. n., with the species legendrei (Balogh), n. comb., from Madagascar; Calipteremaeus, gen. n., with the species yaginumai (Aoki), n. comb., from Japan; the following species are considered incertae sedis: Plateremaeus carinulatus (Berlese), from Brasil, P. complanatus (Berlese), from Chile, P. rotundatus Berlese, from Japan, and P. tunicatus ( Balogh, from Zaire.<br>A família Plateremaeidae é revista, e inclui os seguintes táxons: Plateremaeus Berlese, com a única espécie P. ornatissimus (Berlese), do Brazil; Allodamaeus Banks, com as espécies ewingi (Banks), dos Estados Unidos, coralgablensis, sp. n. (localidade-tipo: Estados Unidos, Flórida, Coral Gables) e ornatos Balogh & Csziszár, da Argentina; Lophoremaeus, gen. n., com duas espécies: mirabilis Csiszár, da Bulgária, espécie-tipo, e laminipes (Berlese), n. comb., da Itália; Paralopheremaeus, gen. n., com a espécie legendrei (Balogh), n. comb., de Madagascar; Calipteremaeus. gen. n., com a espécie yaginumai (Aoki), n. comb., do Japão; as seguintes espécies são consideradas incertae sedis: Plateremaeus carinulatus (Berlese), do Brasil, P. complanatus (Berlese), do Chile, P. rotundatus Berlese, do Japão, e P. tunicatus (Balogh), do Zaire