We have previously demonstrated that the intracellular, non-GPI anchored CD59 isoforms IRIS-1 and IRIS-2 (Isoforms Rescuing Insulin Secretion 1 and 2) are necessary for insulin secretion from pancreatic β-cells. While investigating their expression across human tissues, we identified IRIS-1 and IRIS-2 mRNA in the human brain, though their protein expression and function remained unclear. This study shows the presence of both IRIS-1 and 2 proteins in the human brain, specifically in neurons and astrocytes.
View Article and Find Full Text PDFBackground And Purpose: We aimed to determine sex differences for periprosthetic joint infections after primary arthroplasty of the hip, knee, ankle, and shoulder in osteoarthritis patients in an international perspective.
Methods: This is a multinational combined arthroplasty registry study. Each arthroplasty registry performed Cox-regression analysis of their data and reported the crude and adjusted hazard ratios (HR) with an a priori designed data form.
Background: Patients with symptomatic knee osteoarthritis may undergo non-surgical interventions such as intra-articular steroid injections and knee arthroscopy. This study aimed to investigate their association with the timing and outcomes of subsequent primary knee replacement.
Methods And Findings: Observational retrospective analysis of linked Clinical Practice Research Datalink, Hospital Episode Statistics, Patient Reported Outcome Measures (CPRD GOLD-HES-PROMS) data of 38,494 patients undergoing primary knee replacements in England.
CD59 is a cell-surface inhibitor of the terminal step in the complement cascade. However, in addition to its complement inhibitory function, a non-canonical role of CD59 in pancreatic beta cells has been identified. Two recently discovered intracellular alternative splice forms of CD59, IRIS-1 and IRIS-2, are involved in insulin exocytosis through interactions with SNARE-complex components.
View Article and Find Full Text PDFIntroduction: The role of the complement inhibitory proteins CD46 and CD59 in the immune response to an acute coronary syndrome (ACS) is unknown. We investigated the relationships between the shedding of CD46 and CD59 into the circulation, reflected by plasma levels of soluble CD46 and CD59, and the risk for post-ACS complications.
Methods: We measured plasma sCD46 and sCD59 in a cohort of 546 ACS patients within 24 h after hospital admission, and after 6-weeks in a subgroup of 114 patients.