Using Social Media Categorical Reactions as a Gateway to Identify Hate Speech in COVID-19 News.

The spread of COVID-19 news on social media provided a particularly prolific ground for emotional commotion, disinformation and hate speech, as uncertainty and fear grew by the day. In this paper, we examine the media coverage of the COVID-19 outburst in Portugal (March-May 2020), the subsequent emotional engagement of audiences and the entropy-based emotional controversy generated as a gateway to detect the presence of hate speech, using computer-assisted qualitative data analysis (CAQDAS) embedded in a cross-sectional descriptive methodology. Our results reveal that negative and volatile categorical emotions ("Angry", "Haha" and "Wow") serve as main engines for controversy, and that controversial news have the highest sharing ratio. Moreover, using a small sample of the most controversial news with the highest overall emotional engagement, we establish a relation between the entropy-based emotional controversy obtained from Facebook's click-based reactions and the presence of cultural and ethnic hate speech, plausibly confirming the click-based categorical emotions as a gateway to hatred comment pools. In doing so, we also reveal that negative emotions alone do not always indicate the presence of hate speech, which may sprout in seemingly humorous social media posts where irony proliferates, and negativity is not apparent. This work adds to the literature on social media categorical emotion detection and its implications for the detection of hate speech.

Using Social Media Categorical Reactions as a Gateway to Identify Hate Speech in COVID-19 News

The spread of COVID-19 news on social media provided a particularly prolific ground for emotional commotion, disinformation and hate speech, as uncertainty and fear grew by the day. In this paper, we examine the media coverage of the COVID-19 outburst in Portugal (March–May 2020), the subsequent emotional engagement of audiences and the entropy-based emotional controversy generated as a gateway to detect the presence of hate speech, using computer-assisted qualitative data analysis (CAQDAS) embedded in a cross-sectional descriptive methodology. Our results reveal that negative and volatile categorical emotions (“Angry”, “Haha” and “Wow”) serve as main engines for controversy, and that controversial news have the highest sharing ratio. Moreover, using a small sample of the most controversial news with the highest overall emotional engagement, we establish a relation between the entropy-based emotional controversy obtained from Facebook’s click-based reactions and the presence of cultural and ethnic hate speech, plausibly confirming the click-based categorical emotions as a gateway to hatred comment pools. In doing so, we also reveal that negative emotions alone do not always indicate the presence of hate speech, which may sprout in seemingly humorous social media posts where irony proliferates, and negativity is not apparent. This work adds to the literature on social media categorical emotion detection and its implications for the detection of hate speech.

Depletion of Arg/Abl2 improves endothelial cell adhesion and prevents vascular leak during inflammation.

Endothelial barrier disruption and vascular leak importantly contribute to organ dysfunction and mortality during inflammatory conditions like sepsis and acute respiratory distress syndrome. We identified the kinase Arg/Abl2 as a mediator of endothelial barrier disruption, but the role of Arg in endothelial monolayer regulation and its relevance in vivo remain poorly understood. Here we show that depletion of Arg in endothelial cells results in the activation of both RhoA and Rac1, increased cell spreading and elongation, redistribution of integrin-dependent cell-matrix adhesions to the cell periphery, and improved adhesion to the extracellular matrix. We further show that Arg is activated in the endothelium during inflammation, both in murine lungs exposed to barrier-disruptive agents, and in pulmonary microvessels of septic patients. Importantly, Arg-depleted endothelial cells were less sensitive to barrier-disruptive agents. Despite the formation of F-actin stress fibers and myosin light chain phosphorylation, Arg depletion diminished adherens junction disruption and intercellular gap formation, by reducing the disassembly of cell-matrix adhesions and cell retraction. In vivo, genetic deletion of Arg diminished vascular leak in the skin and lungs, in the presence of a normal immune response. Together, our data indicate that Arg is a central and non-redundant regulator of endothelial barrier integrity, which contributes to cell retraction and gap formation by increasing the dynamics of adherens junctions and cell-matrix adhesions in a Rho GTPase-dependent fashion. Therapeutic inhibition of Arg may provide a suitable strategy for the treatment of a variety of clinical conditions characterized by vascular leak.