Background: Sepsis-induced acute kidney injury (AKI) is difficult to prevent because most patients are diagnosed after they develop it. Standard serum and urine creatinine levels are insensitive and nonspecific for detecting kidney injury in its early stages. Glutathione S-transferase (GST) has received little attention as a biomarker in AKI.
View Article and Find Full Text PDFIntroduction: Access to and engagement with primary healthcare can be difficult for marginalized low-income populations residing in inner cities in high-income countries. We designed a study to examine retention in primary care among clients of a novel interdisciplinary primary care clinic in the Downtown Eastside of Vancouver, Canada who did not previously have access to care.
Methods: Beginning in June 2021, clients of the Hope to Health clinic were offered enrolment in a cohort study which involved a baseline and follow-up surveys every six months, and linking their data to information from the clinic's electronic medical records.
Here, we report that the RTN3L-SEC24C endoplasmic reticulum autophagy (ER-phagy) receptor complex, the CUL3KLHL12 E3 ligase that ubiquitinates RTN3L, and the FIP200 autophagy initiating protein, target mutant proinsulin (Akita) condensates for lysosomal delivery at ER tubule junctions. When delivery was blocked, Akita condensates accumulated in the ER. In exploring the role of tubulation in these events, we unexpectedly found that loss of the Parkinson's disease protein, PINK1, reduced peripheral tubule junctions and blocked ER-phagy.
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