Leadership in Times of Crisis.

SUMMARY: In the wake of the death toll resulting from coronavirus disease of 2019 (COVID-19), in addition to the economic turmoil and strain on our health care systems, plastic surgeons are taking a hard look at their role in crisis preparedness and how they can contribute to crisis response policies in their own health care teams. Leaders in the specialty are charged with developing new clinical policies, identifying weaknesses in crisis preparation, and ensuring survival of private practices that face untenable financial challenges. It is critical that plastic surgery builds on the lessons learned over the past tumultuous year to emerge stronger and more prepared for subsequent waves of COVID-19. In addition, this global health crisis presents a timely opportunity to reexamine how plastic surgeons can display effective leadership during times of uncertainty and stress. Some may choose to emulate the traits and policies of leaders who are navigating the COVID-19 crisis effectively. Specifically, the national leaders who offer empathy, transparent communication, and decisive action have maintained high public approval throughout the COVID-19 crisis, while aggressively controlling viral spread. Crises are an inevitable aspect of modern society and medicine. Plastic surgeons can learn from this pandemic to better prepare for future turmoil.

Lack of current observed in HEK293 cells expressing NALCN channels.

The sodium leak channel NALCN is poorly understood, but is reported as a Na+-permeable, nonselective cation leak channel which regulates resting membrane potential and electrical excitability. Previous work has indicated that NALCN currents can be stimulated by activation of several G protein coupled receptors, including the M3 muscarinic receptor. We undertook a study using voltage clamp electrophysiology to investigate NALCN currents. We compared currents elicited from untransfected control HEK239 cells in response to M3R agonists muscarine or Oxotremorine M to currents elicited from cells transfected with M3R only or the M3R plus NALCN and cDNA encoding accessory proteins UNC-80 and Src. Currents with similar properties were observed in all three groups of cells in response to muscarine agonists, in similar proportions of cells tested, from all three groups of cells. Our findings do not support previous electrophysiological studies suggesting that heterologously expressed NALCN functions as a Na+ leak channel in HEK293 cells. More research will be required to determine the molecular requirements for successful expression of the NALCN channel.

Feeding blueberry diets inhibits angiotensin II-converting enzyme (ACE) activity in spontaneously hypertensive stroke-prone rats.

Feeding flavonoid-rich blueberries to spontaneously hypertensive stroke-prone rats (SHRSP) lowers blood pressure. To determine whether this is due to inhibition of angiotensin-converting enzyme (ACE) activity, as seen with other flavanoid-rich foods, we fed blueberries to SHRSP and normotensive rats and analyzed ACE activity in blood and tissues. After 2 weeks on a control diet, the hypertensive rats showed 56% higher levels of ACE activity in blood as compared with the normotensive rats (p < 0.05). Feeding a 3% blueberry diet for 2 weeks lowered ACE activity in the SHRSP (p < 0.05) but not the normotensive rats. ACE activity in plasma of SHRSP was no longer elevated at weeks 4 and 6, but blueberry feeding inhibited ACE in SHRSP after 6 weeks. Blueberry diets had no effect on ACE activity in lung, testis, kidney, or aorta. Our results suggest that dietary blueberries may be effective in managing early stages of hypertension, partially due to an inhibition of soluble ACE activity.