Impact and Implications of the COVID-19 Pandemic on Urological Training.

INTRODUCTION: COVID-19 has forever impacted health care in the U.S. Changes to health and hospital policies led to disruptions to both patient care and medical training. There is limited understanding of the impact on urology resident training across the U.S. Our aim was to examine trends in urological procedures, as captured by the Accreditation Council for Graduate Medical Education resident case logs, throughout the COVID-19 pandemic. METHODS: Retrospective review of publicly available urology resident case logs between July 2015 and June 2021 was performed. Average case numbers were analyzed via linear regression with different models specifying different assumptions regarding the impact of COVID-19 on procedure in 2020 and onward. Statistical calculations utilized R (version 4.0.2). RESULTS: Analysis favored models which assumed the impact of COVID-related disruptions were specific to 2019-2020. Analysis of procedures performed indicate an average upward trend of urology cases nationally. An average annual increase of 26 procedures between 2016 and 2021 was noted, except for 2020 which saw an average drop of approximately 67 cases. However, in 2021 case volume dramatically increased to the same rate as projected had there not been a disruption in 2020. Stratifying by category of urology procedure revealed evidence for variability between categories in the magnitude of the 2020 decrease. CONCLUSIONS: Despite widespread pandemic-related disruptions in surgical care, urological volume has rebounded and increased, likely having minimal detriment to urological training over time. Urological care is essential and in high demand as evidenced by the uptick in volume across the U.S.

Dyshomeostatic modulation of Ca2+-activated K+ channels in a human neuronal model of KCNQ2 encephalopathy.

Mutations in KCNQ2, which encodes a pore-forming K+ channel subunit responsible for neuronal M-current, cause neonatal epileptic encephalopathy, a complex disorder presenting with severe early-onset seizures and impaired neurodevelopment. The condition is exceptionally difficult to treat, partially because the effects of KCNQ2 mutations on the development and function of human neurons are unknown. Here, we used induced pluripotent stem cells (iPSCs) and gene editing to establish a disease model and measured the functional properties of differentiated excitatory neurons. We find that patient iPSC-derived neurons exhibit faster action potential repolarization, larger post-burst afterhyperpolarization and a functional enhancement of Ca2+-activated K+ channels. These properties, which can be recapitulated by chronic inhibition of M-current in control neurons, facilitate a burst-suppression firing pattern that is reminiscent of the interictal electroencephalography pattern in patients. Our findings suggest that dyshomeostatic mechanisms compound KCNQ2 loss-of-function leading to alterations in the neurodevelopmental trajectory of patient iPSC-derived neurons.