Detection of abusive language in user generated online content has become an issue of increasing importance in recent years. Most current commercial methods make use of blacklists and regular expressions, however these measures fall short when contending with more subtle, less ham-fisted examples of hate speech. In this work, we develop a machine learning based method to detect hate speech on online user comments from two domains which outperforms a state-ofthe-art deep learning approach. We also develop a corpus of user comments annotated for abusive language, the first of its kind. Finally, we use our detection tool to analyze abusive language over time and in different settings to further enhance our knowledge of this behavior.

The anti-apoptotic molecule Bcl-2 is located in the mitochondrial and endoplasmic reticulum membranes as well as the nuclear envelope. Although its location has not been as rigorously de®ned, the pro-apoptotic molecule Bax appears to be mainly a cytosolic protein which translocates to the mitochondria upon induction of apoptosis. Here we identify a protease activity in mitochondria-enriched membrane fractions from HL-60 cells capable of cleaving Bax which is absent from the cytosolic fraction. Bax protease activity is blocked in vitro by cysteine protease inhibitors including E-64 which distinguishes it from all known caspases and granzyme B, both of which are involved in apoptosis. Protease activity is also blocked by inhibitors against the calciumactivated neutral cysteine endopeptidase calpain. Partial puri®cation of the Bax protease activity from HL-60 cell membrane fractions by column chromatography revealed that a calpain-like activity was the protease responsible for Bax cleavage. In addition, puri®ed calpain enzymes cleaved Bax in a calcium-dependent manner. Pretreatment of HL-60 cells with the speci®c calpain inhibitor calpeptin eectively blocked both drug-induced Bax cleavage and calpain activation, but not PARP cleavage or cell death. These results suggest that calpains and caspases are activated during drug-induced apoptosis and that calpains, along with caspases, may be involved in modulating cell death by acting selectively on cellular substrates.