Riccardo Autelli

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.

TL;DR: It is shown that oxidative stress (OS) stimulates BACE1 expression by a mechanism requiring γ‐secretase activity involving the c‐jun N‐terminal kinase (JNK)/c‐jun pathway, thereby promoting production of pathological levels of amyloid β in AD.

TL;DR: This study significantly extends findings both in vitro, in differentiated SK‐N‐BE neuroblastoma cells, and in vivo, in rats subjected to cerebral ischemia, showing that hypoxia up‐regulates BACE1 expression through a biphasic mechanism, and strengthens the hypothesis that oxidative stress is a basic common mechanism of amyloid‐β accumulation.

TL;DR: It is reported that fully activated human HSC/MFs did not undergo spontaneous apoptosis and survived to prolonged serum deprivation, Fas activation, or exposure to nerve growth factor, tumour necrosis factor α, oxidative stress mediators, doxorubicin, and etoposide.