Judy A. Lawson

TL;DR: The data indicate that activation of the caspase 3 subfamily of cysteine proteases is critical for the development of parenchymal cell apoptosis and excessive hepatocellular apoptosis can be an important signal for transmigration of primed neutrophils sequestered in sinusoids.

TL;DR: The inflammation observed after acetaminophen overdose may be characteristic for a response sufficient to recruit neutrophils for the purpose of removing necrotic cells but is not severe enough to cause additional damage.

TL;DR: In this article, the authors used the Galactosamine/endotoxin (Gal/ET) model of acute liver failure, which involves a neutrophil-mediated parenchymal cell injury.

TL;DR: Excessive parenchymal cell apoptosis represents an important signal for transmigration of primed neutrophils sequestered in sinusoids during endotoxemia in vivo, however, apoptosis per se does not cause neutrophil sequestration in the liver vasculature.

TL;DR: It is concluded that AAP-induced DNA fragmentation does not involve caspases, suggesting a direct activation of endonucleases through elevated Ca2+ levels, and electrophilic metabolites of AAP may inactivate caspase or their activation pathway, indicating that AAP metabolism has the potential to inhibit signal transduction mechanisms of receptor-mediated apoptosis.