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We suggest that all services take a universal approach to offering support to those who have to fill in forms and paperwork. Ask all staff to operate in this way across your service to ensure that sup...

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YouTube video by BCHFT Knowledge and Library Services

YouTube video by BCHFT Knowledge and Library Services

https://vimeo.com/361806328 Spoken and written word is often misheard or misread and also misunderstood, pictures and visuals may be effective in improving understanding when communicating new or comp...

Chunk and check can be used alongside tools such as teach back to assist in promoting understanding. When we speak to patients and clients there is often a lot of information to be discussed and we ma...

The teach back method is a useful way to confirm that the information you provide is being understood by getting people to 'teach back' what has been discussed and what instruction has been given. Thi...

To mark Black History Month, four nursing staff members pay tribute to those who’ve inspired them in their training and careers

Aims/hypothesis This study aimed to assess the impact of adding dapagliflozin to insulin therapy on key hormonal determinants of glucose regulation and ketogenesis. We hypothesise that dapagliflozin increases glucagon-like peptide 1 (GLP-1), glucagon and ketone body concentrations, based on the results of a pilot study. Methods The study was designed as a randomised, placebo-controlled, open-label, crossover intervention study with two periods (dapagliflozin and placebo intake), including patients of the Department of Diabetes, Endocrinology, Clinical Nutrition & Metabolism, Inselspital, Bern University Hospital, University of Bern. Individuals with type 1 diabetes (C-peptide concentrations <0.1 nmol/l) with a duration >5 years and a BMI of 20–29 kg/m2 were included. They received 10 mg of dapagliflozin or placebo daily for 7 days throughout two independent treatment periods, separated by a 14 day washout period. Allocation was done by a computed randomisation tool (REDCap), without blinding of the participants or the investigators. On day 7 of each treatment period, hyperinsulinaemic–euglycaemic clamps (HECs) and OGTT clamps (OGTTCs) were performed to assess changes in the secretion of GLP-1, glucagon, somatostatin and total ketone bodies. The objective was to evaluate the effects of adding the sodium–glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin to insulin therapy on GLP-1 during OGTTC (primary endpoint), GLP-1 secretion during HEC, and glucagon, somatostatin and ketogenesis during OGTTC and HEC (secondary endpoints). The primary endpoint was concentrations of GLP-1 during OGTTC. Secondary endpoints included GLP-1 during HEC and glucagon, somatostatin and ketone body concentrations during OGTTC and HEC. Results A total of 13 individuals with type 1 diabetes were included and randomised. All of them received dapagliflozin and placebo, finished the sequences per protocol and were analysed per protocol. GLP-1 concentrations did not differ significantly between treatments in the OGTTC (median [IQR] dapagliflozin 192.8 [129.8–257.2] pmol/l vs placebo 176.3 [138.4–227.4] pmol/l; p=0.7) or HEC (median [IQR] dapagliflozin 208.6 [133.6–294.0] pmol/l vs placebo 203.1 [150.2–291.8] pmol/l; p=0.7). Glucagon concentrations did not significantly differ between treatments in the OGTTC (median [IQR] dapagliflozin 1.54 [0.84–3.68] ng/l vs placebo 1.54 [0.82–4.64] ng/l; p=0.8) or HEC (median [IQR] dapagliflozin 1.59 [0.87–3.54] ng/l vs placebo 1.63 [0.91–3.96] ng/l; p=0.3). Somatostatin concentrations remained comparable between treatments during the HEC (median [IQR] dapagliflozin 41.1 [26.8–73.8] pmol/l vs placebo 47.0 [23.0–77.6] pmol/l; p=0.2) and OGTTC (median [IQR] dapagliflozin 51.1 [31.1–77.0] pmol/l vs placebo 45.3 [30.0–70.5] pmol/l; p=0.2). Plasma ketone bodies were higher with dapagliflozin during the HEC (median [IQR] dapagliflozin 0.15 [0.04–0.47] mmol/l vs placebo 0.03 [0.01–0.12] mmol/l; p<0.001) and OGTTC (median [IQR] dapagliflozin 0.10 [0.03–0.22] mmol/l vs placebo 0.03 [0.01–0.12] mmol/l; p<0.001). Conclusions/interpretation Short-term dapagliflozin treatment in type 1 diabetes increases plasma ketone concentrations without affecting the secretion of GLP-1, glucagon or somatostatin. Higher ketone body concentrations highlight the elevated risk of diabetic ketoacidosis associated with the adjunct intake of dapagliflozin. Trial registration ClinicalTrials.gov NCT04035031. Funding Swiss National Science Foundation, project number 32003B_185019. Graphical Abstract

WHO fact sheet on health literacy, including key facts, overview, existing inequalities, the importance and social benefits of health literacy, and WHO's response.

Discover how gender bias impacts women’s pain care and learn strategies to improve assessment, diagnosis and treatment plans.

Recent advances in genome-wide approaches, the availability of isolated human islets for research and the evaluation of novel incretin mimetics in large clinical trials have brought about remarkable progress in our understanding of the role of the pancreatic beta cell in type 2 diabetes. Here, we review key developments in type 2 diabetes initiation, progression and remission, focusing mostly on human studies published in the last 5 years. Progress in multi-omics technologies has enabled researchers to identify links between type 2 diabetes risk variants and gene regulatory networks in islet endocrine cells that control beta cell development, function and stress resilience. These studies support the notion that early abnormalities in insulin secretion, rather than a reduction in beta cell mass, play a fundamental and primary role in early type 2 diabetes pathogenesis. Contributing to these intrinsic beta cell defects are various pathogenic signals from other (endocrine and non-endocrine) islet cells, the exocrine pancreas, the gut and insulin-sensitive tissues. It has also become apparent that beta cells comprise a heterogeneous population that responds differently to stress situations and that sex-related differences in beta cell responses should not be underestimated. Finally, human clinical trials have clearly demonstrated that diabetes remission can be achieved using glucose-lowering therapies and particularly strategies focused on weight loss, including bariatric surgery and, more recently, the use of highly efficient new drugs targeting the incretin system. While progress in the last 5 years has been significant, much remains to be uncovered to bring these advances to the clinic and thereby alleviate the dramatic consequences of type 2 diabetes complications for the hundreds of millions of people who live with this disease. Graphical Abstract

Be a realistic optimist. See life as it is, but focus on what's good

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