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Background: Aboriginal and Torres Strait Islander peoples are disproportionately impacted by type 2 diabetes. Continuous glucose monitoring (CGM) technology (such as Abbott Freestyle Libre 2, previously referred to as Flash Glucose Monitoring) offers real-time glucose monitoring that is convenient and easy to use compared to self-monitoring of blood glucose (SMBG). However, this technology's use is neither widespread nor subsidised for Aboriginal and Torres Strait Islander peoples with type 2 diabetes. Building on existing collaborations with a national network of Aboriginal and Torres Strait Islander communities, this randomised controlled trial aims to assess the effect of CGM compared to SMBG on (i) haemoglobin A1c (HbA1c), (ii) achieving blood glucose targets, (iii) reducing hypoglycaemic episodes and (iv) cost-effective healthcare in an Aboriginal and Torres Strait Islander people health setting. Methods: This is a non-masked, parallel-group, two-arm, individually randomised, controlled trial (ACTRN12621000753853). Aboriginal and Torres Strait Islander adults with type 2 diabetes on injectable therapy and HbA1c ≥ 7.5% (n = 350) will be randomised (1:1) to CGM or SMBG for 6 months. The primary outcome is change in HbA1c level from baseline to 6 months. Secondary outcomes include (i) CGM-derived metrics, (ii) frequency of hypoglycaemic episodes, (iii) health-related quality of life and (iv) incremental cost per quality-adjusted life year gained associated with the CGM compared to SMBG. Clinical trial sites include Aboriginal Community Controlled Organisations, Aboriginal Medical Services, primary care centres and tertiary hospitals across urban, rural, regional and remote Australia. Discussion: The trial will assess the effect of CGM compared to SMBG on HbA1c for Aboriginal and Torres Strait Islander people with type 2 diabetes in Australia. This trial could have long-term benefits in improving diabetes management and providing evidence for funding of CGM in this population. Trial registration: Australian and New Zealand Clinical Trials Registry ACTRN12621000753853. Registered on 15th June 2021. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Can flash glucose monitoring improve glucose management for Aboriginal and Torres Strait Islander peoples with type 2 diabetes? A protocol for a randomised controlled trial." The correction involves the name of the 17th author, which was originally published without a hyphen. The corrected name is An Tran-Duy. The original article has been updated to reflect this correction. The article was authored by Mariam Hachem, Tracey Hearn, Ray Kelly, Audrey Eer, Belinda Moore, Christine Sommerville, Sharon Atkinson-Briggs, Stephen Twigg, Meagan Freund, David O'Neal, David Story, Alex Brown, Anna McLean, Ashim Sinha, John Furler, Richard O'Brien, An Tran-Duy, Philip Clarke, Sabine Braat, Digsu N. Koye, Sandra Eades, Luke Burchill, and Elif Ekinci. [Extracted from the article]

This document is a correction notice for an article titled "Moderate aerobic exercise, but not anticipation of exercise, improves cognitive control." The correction states that the authors' names were listed out of order in the original publication. The correct author order, affiliations, and citation are provided in the correction notice. The article was authored by Maximilian Bergelt, Vanessa Fung Yuan, Richard O'Brien, Wellington Martins dos Santos, and Laura E. Middleton. The study focuses on the effects of moderate aerobic exercise on cognitive control. [Extracted from the article]

G6PC2 encodes a glucose-6-phosphatase catalytic subunit that opposes the action of glucokinase in pancreatic islets, thereby modulating the sensitivity of insulin and glucagon secretion to glucose. In mice, G6pc2 is expressed at ~20-fold higher levels in ß-cells than in a-cells, whereas in humans G6PC2 is expressed at only ~5-fold higher levels in ß-cells. We therefore hypothesize that G6PC2 likely influences glucagon secretion to a greater degree in humans. With a view to generating a humanized mouse that recapitulates augmented G6PC2 expression levels in a-cells, we sought to identify the genomic regions that confer differential mouse G6pc2 expression in a-cells versus ß-cells as well as the evolutionary changes that have altered this ratio in humans. Studies in islet-derived cell lines suggest that the elevated G6pc2 expression in mouse ß-cells versus a-cells is mainly due to a difference in the relative activity of the proximal G6pc2 promoter in these cell types. Similarly, the smaller difference in G6PC2 expression between a-cells and ß-cells in humans is potentially explained by a change in relative proximal G6PC2 promoter activity. However, we show that both glucocorticoid levels and multiple differences in the relative activity of eight transcriptional enhancers between mice and humans likely contribute to differential G6PC2 expression. Finally, we show that a mouse-specific non-coding RNA, Gm13613, whose expression is controlled by G6pc2 enhancer I, does not regulate G6pc2 expression, indicating that altered expression of Gm13613 in a humanized mouse that contains both the human promoter and enhancers should not affect G6PC2 function. [ABSTRACT FROM AUTHOR]