RESUMO
Abusive language in online social media is a pervasive and harmful phenomenon which calls for automatic computational approaches to be successfully contained. Previous studies have introduced corpora and natural language processing approaches for specific kinds of online abuse, mainly focusing on misogyny and racism. A current underexplored area in this context is religious hate, for which efforts in data and methods to date have been rather scattered. This is exacerbated by different annotation schemes that available datasets use, which inevitably lead to poor repurposing of data in wider contexts. Furthermore, religious hate is very much dependent on country-specific factors, including the presence and visibility of religious minorities, societal issues, historical background, and current political decisions. Motivated by the lack of annotated data specifically tailoring religion and the poor interoperability of current datasets, in this article we propose a fine-grained labeling scheme for religious hate speech detection. Such scheme lies on a wider and highly-interoperable taxonomy of abusive language, and covers the three main monotheistic religions: Judaism, Christianity and Islam. Moreover, we introduce a Twitter dataset in two languages-English and Italian-that has been annotated following the proposed annotation scheme. We experiment with several classification algorithms on the annotated dataset, from traditional machine learning classifiers to recent transformer-based language models, assessing the difficulty of two tasks: abusive language detection and religious hate speech detection. Finally, we investigate the cross-lingual transferability of multilingual models on the tasks, shedding light on the viability of repurposing our dataset for religious hate speech detection on low-resource languages. We release the annotated data and publicly distribute the code for our classification experiments at https://github.com/dhfbk/religious-hate-speech.
RESUMO
Lysosomal storage diseases (LSDs) are characterized by the abnormal accumulation of substrates in tissues due to the deficiency of lysosomal proteins. Among the numerous clinical manifestations, chronic inflammation has been consistently reported for several LSDs. However, the molecular mechanisms involved in the inflammatory response are still not completely understood. In this study, we performed text-mining and systems biology analyses to investigate the inflammatory signals in three LSDs characterized by sphingolipid accumulation: Gaucher disease, Acid Sphingomyelinase Deficiency (ASMD), and Fabry Disease. We first identified the cytokines linked to the LSDs, and then built on the extracted knowledge to investigate the inflammatory signals. We found numerous transcription factors that are putative regulators of cytokine expression in a cell-specific context, such as the signaling axes controlled by STAT2, JUN, and NR4A2 as candidate regulators of the monocyte Gaucher disease cytokine network. Overall, our results suggest the presence of a complex inflammatory signaling in LSDs involving many cellular and molecular players that could be further investigated as putative targets of anti-inflammatory therapies.