Effects of COVID-19 hospitalization rates on the incidence of hospital-acquired Candida central line-associated bloodstream infection.

Background: An increase in central line-associated bloodstream infections (CLABSIs) has been reported during the Coronavirus (COVID-19) pandemic; however, few studies have documented causative pathogens, particularly Candida species associated with candidemia.

Methods: This was a retrospective study based on the National Health Care Safety Network surveillance definitions of CLABSI caused by Candida species during pre-COVID-19 (October 2017 to February 2020) and COVID-19 (March 2020 to December 2021) periods within a local community hospital. Candida CLABSI incidence per 1,000 central line days was compared between periods using the χ test and correlated with COVID-19 inpatient hospitalization rates using Pearson correlation.

Activation of protein kinase Cα increases phosphorylation of the UT-A1 urea transporter at serine 494 in the inner medullary collecting duct.

Hypertonicity increases urea transport, as well as the phosphorylation and membrane accumulation of UT-A1, the transporter responsible for urea permeability in the inner medullary collect duct (IMCD). Hypertonicity stimulates urea transport through PKC-mediated phosphorylation. To determine whether PKC phosphorylates UT-A1, eight potential PKC phosphorylation sites were individually replaced with alanine and subsequently transfected into LLC-PK1 cells.

Vasopressin regulation of multisite phosphorylation of UT-A1 in the inner medullary collecting duct.

Vasopressin signaling is critical for the regulation of urea transport in the inner medullary collecting duct (IMCD). Increased urea permeability is driven by a vasopressin-mediated elevation of cAMP that results in the direct phosphorylation of urea transporter (UT)-A1. The identification of cAMP-sensitive phosphorylation sites, Ser(486) and Ser(499), in the rat UT-A1 sequence was the first step in understanding the mechanism of vasopressin action on the phosphorylation-dependent modulation of urea transport.