Thrombolysis by PLAT/tPA increases serum free IGF1 leading to a decrease of deleterious autophagy following brain ischemia.

Cerebral ischemia is a pathology involving a cascade of cellular mechanisms, leading to the deregulation of proteostasis, including macroautophagy/autophagy, and finally to neuronal death. If it is now accepted that cerebral ischemia induces autophagy, the effect of thrombolysis/energy recovery on proteostasis remains unknown. Here, we investigated the effect of thrombolysis by PLAT/tPA (plasminogen activator, tissue) on autophagy and neuronal death.

[Release of hepatitis A virus into the culture medium, during its replication in PLC/PRF/5 cells].

Hepatitis A virus (HAV), obtained from human feces collected 3 days after the onset of jaundice, was propagated in human hepatocarcinoma cells (PLC/PRF/5). In the course of 5 passages, it was released into the supernatant without cytopathic effect. Released HAV was propagated after inoculation into PLC/PRF/5 cells.