c 14-3-3 promotes cell survival via dynamic interactions with a vast network of binding partners, many of which are involved in stress regulation. We show here that hypoxia (low glucose and oxygen) triggers a rearrangement of the 14-3-3 interactome to favor an interaction with the core autophagy regulator Atg9A. Our data suggest that the localization of mammalian Atg9A to autophagosomes requires phosphorylation on the C terminus of Atg9A at S761, which creates a 14-3-3 docking site. Under basal conditions, this phosphorylation is maintained at a low level and is dependent on both ULK1 and AMPK. However, upon induction of hypoxic stress, activated AMPK bypasses the requirement for ULK1 and mediates S761 phosphorylation directly, resulting in an increase in 14-3-3 interactions, recruitment of Atg9A to LC3-positive autophagosomes, and enhanced autophagosome production. These data suggest a novel mechanism whereby the level of autophagy induction can be modulated by AMPK/ULK1-mediated phosphorylation of mammalian Atg9A.

The novel coronavirus disease 2019 has had a profound impact on healthcare systems around the world. The emergency department (ED) in particular has become the frontline for the identification and care of these patients. While its effects on respiratory symptoms are well recognized, neurologic manifestations have been rarer. We report the case of a patient who presented in cardiac arrest with the return of spontaneous circulation (ROSC). The patient was found to have subarachnoid hemorrhage and later tested positive for COVID-19.

No abstract

The novel coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that originated in China in late 2019, has caused significant morbidity and mortality worldwide. Although fever, cough, and shortness of breath have been recognized as hallmark symptoms, other lesser known complications continue to be described. We report a series of three patients who presented to the emergency department, who tested positive for COVID-19, and were found to have or subsequently developed thromboembolic complications.