In-Person Clinic Visits After Laparoscopic Cholecystectomy: Lessons Learned From COVID-19 Pandemic.

Introduction: The utility of routine in-person clinic appointments after laparoscopic cholecystectomy (LC) is uncertain, especially after the increase of telehealth visits during the COVID-19 pandemic. The purpose of this study was to evaluate the utility of routine in-person follow-up for patients undergoing LC prior to changes implemented during the pandemic and to determine whether a return to routine in-person follow-up is warranted.

Methods: We retrospectively reviewed follow-up encounters for all patients undergoing LC from April 2018 to February 2020.

Fast-Track Nonelective Laparoscopic Cholecystectomy is Safe and Feasible.

Introduction: Ample evidence exists to support the safety of fast-track discharge after elective laparoscopic cholecystectomy (LC), but there is currently no data available to support the safety of fast-tracking patients undergoing nonelective LC. We sought to determine whether fast-tracking patients undergoing nonelective LC is safe and feasible.

Methods: We performed a retrospective cohort review of 661 consecutive patients undergoing LC at a single teaching institution from April 2018 to January 2020.

A retrospective view of 2020: A unique year for Immunology.

2020 was a year unlike any other for Immunology. Through the SARS-CoV-2 pandemic, with fantastic support from the global immunology community, we worked together to reach new heights. Here, we look back at some of the highlights for Immunology in a challenging and memorable year.

Nitric oxide-dependent activation of CaMKII increases diastolic sarcoplasmic reticulum calcium release in cardiac myocytes in response to adrenergic stimulation.

Spontaneous calcium waves in cardiac myocytes are caused by diastolic sarcoplasmic reticulum release (SR Ca(2+) leak) through ryanodine receptors. Beta-adrenergic (β-AR) tone is known to increase this leak through the activation of Ca-calmodulin-dependent protein kinase (CaMKII) and the subsequent phosphorylation of the ryanodine receptor. When β-AR drive is chronic, as observed in heart failure, this CaMKII-dependent effect is exaggerated and becomes potentially arrhythmogenic.

Sarcoplasmic reticulum K(+) (TRIC) channel does not carry essential countercurrent during Ca(2+) release.

The charge translocation associated with sarcoplasmic reticulum (SR) Ca(2+) efflux is compensated for by a simultaneous SR K(+) influx. This influx is essential because, with no countercurrent, the SR membrane potential (Vm) would quickly (<1 ms) reach the Ca(2+) equilibrium potential and SR Ca(2+) release would cease. The SR K(+) trimeric intracellular cation (TRIC) channel has been proposed to carry the essential countercurrent.