Many factors contribute to nervous system dysfunction and failure to regenerate after injury or disease. Here, we describe a previously unrecognized mechanism for nervous system injury. We show that neuronal injury causes rapid, irreversible, and preferential proteolysis of the axon initial segment (AIS) cytoskeleton independently of cell death or axon degeneration, leading to loss of both ion channel clusters and neuronal polarity. Furthermore, we show this is caused by proteolysis of the AIS cytoskeletal proteins ankyrinG and ␤IV spectrin by the calcium-dependent cysteine protease calpain. Importantly, calpain inhibition is sufficient to preserve the molecular organization of the AIS both in vitro and in vivo. We conclude that loss of AIS ion channel clusters and neuronal polarity are important contributors to neuronal dysfunction after injury, and that strategies to facilitate recovery must preserve or repair the AIS cytoskeleton.

Intravenous sedation during colonoscopy has become the standard practice in the United States given its higher patient satisfaction and procedural quality. This practice is not free of side effects as a significant proportion of patients undergoing this procedure tend to have respiratory depression and desaturation events. Obesity, as it relates to higher levels of body mass index (BMI) has a positive correlation with the incidence of hypoxemia. During colonoscopy High flow nasal cannula (HFNC) may potentially improve oxygen performance in patients receiving colonoscopy under intravenous sedation. Here we present 3 cases of patients undergoing adjunctive oxygen therapy with HFNC during colonoscopy with intravenous sedation. We found patients to have lower number of desaturation events and were satisfied with their experience.

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