591 research outputs found
Hypoglycaemia in clinical diabetes
If you regularly see patients with diabetes who experience hypoglycaemia and need expert guidance, then this is the book for you.Hypoglycaemia in Clinical Diabetes, 3rd Edition once again provides health professionals involved in the management of people with diabetes with an expertly written, comprehensive guide to hypoglycaemia, the most common and feared side effect of insulin treatment for diabetes. With reference to ADA and EASD guidelines throughout, topics covered include the physiology of hypoglycaemia and the body's response to a low blood glucose, its presentation and clinical features, potential morbidity and optimal clinical management in order to achieve and maintain good glycaemic control. Particular attention is paid to the way hypoglycaemia is managed in different groups of patients, such as the elderly, in children, or during pregnancy.New chapters in this edition include: Psychological effects of hypoglycaemia Technology for hypoglycaemia: CSII and CGM Exercise management and hypoglycaemia in type 1 diabetes Neurological sequelae of hypoglycaemiaValuable for diabetologists, endocrinologists, non-specialist physicians and general practitioners, Hypoglycaemia in Clinical Diabetes, 3rd Edition provides expert clinical guidance to this extremely common and potentially serious complication associated with diabetic management
Correction to:Disrupted hypothalamic transcriptomics and proteomics in a mouse model of type 2 diabetes exposed to recurrent hypoglycaemia
The affiliations for Mark Evans, Alison McNeilly and Rory J. McCrimmon have been corrected. The original article has been corrected.</p
Rory O\u27More
Courtship of Rory O\u27More and Kathleen Bawnhttps://egrove.olemiss.edu/kgbsides_uk/1961/thumbnail.jp
HIT4HYPOS Continuous Glucose Monitoring Data Analysis:The Effects of High-Intensity Interval Training on Hypoglycemia in People With Type 1 Diabetes and Impaired Awareness of Hypoglycemia
Aims:To assess the impact of high-intensity interval training (HIIT) on hypoglycemia frequency and duration in people with type 1 diabetes (T1D) with impaired awareness of hypoglycemia (IAH).Methods:Post hoc analysis of four weeks of continuous glucose monitoring (CGM) data from HIT4HYPOS; a parallel-group study comparing HIIT + CGM versus no exercise + CGM in 18 participants with T1D and IAH.Results:When compared with those participating individuals not exercising, HIIT did not increase total hypoglycemia frequency, THypo(L1) 1.44 [1.00-2.77]% versus 2.53 [1.46-4.23]%; P = .335, THypo(L2) 0.25 [0.09-0.37]% versus 0.45 [0.20-0.78]%; P = .146, HIIT + CGM versus CGM, respectively, rate (EventPerWeekHypo 5.30 [3.35-8.27] #/week vs 7.45 [3.54-10.81] #/week, P = .340) or duration (DurationHypo 33.33 [27.60-39.10] minutes vs 39.56 [31.00-48.38] minutes; P = .219, HIIT + CGM vs CGM, respectively). There was a reduction in nocturnal hypoglycemia in those who carried out HIIT, THypo(L1) 0.50 [0.13-0.97]% versus 2.45 [0.77-4.74]%; P = .076; THypo(L2) 0.00 [0.00-0.03]% versus 0.49 [0.13-0.74]%; P = .006, HIIT + CGM versus CGM, respectively.Conclusions/interpretation:Based on CGM data collected from a real-world study of four weeks of HIIT versus no exercise in individuals with T1D and IAH, we conclude that HIIT does not increase hypoglycemia, and in fact reduces exposure to nocturnal hypoglycemia
Stephen Partridge & Erik Kwakkel (eds.). Author, Reader, Book: Medieval Authorship in Theory and Practice
Remembrance of things past:The consequences of recurrent hypoglycaemia in diabetes
Aims: People with type 1 and type 2 diabetes still frequently experience hypoglycaemia, which can be severe, leading to loss of consciousness. This review will examine the cellular consequences of recurrent hypoglycaemia. Methods: This review, based on the Dorothy Hodgkin Lecture given at the Diabetes UK 2022 annual symposium by the author, will discuss our current understanding of the mechanisms by which hypoglycaemia is detected and the consequences of recurrent exposure to hypoglycaemia. Results: Glucose-responsive cells found in the periphery as well as multiple areas of the brain are organised in a classical sensori-motor integrative network encompassing peripheral, hindbrain and hypothalamic components. The mechanism used by glucose-responsive neurons to detect hypoglycaemia parallel those of the classical glucose sensor the pancreatic ß-cell, namely in their use of glucokinase, K ATP channels and AMP-activated protein kinase. Recurrent exposure to hypoglycaemia results in a series of cellular adaptations that may be designed to increase the resilience of cells to future hypoglycaemia. This review also highlights how hypoglycaemia, as an oxidative stressor, may also exacerbate chronic hyperglycaemia-induced increases in oxidative stress and inflammation, leading to damage to vulnerable brain regions. Conclusions: Impaired awareness of hypoglycaemia follows the adaptation of central glucose-responsive neurons to repeated hypoglycaemia and may represent a form of memory called habituation. In diabetes, recurrent hypoglycaemia may have tissue consequences as a result of a profound disruption in the cellular response to a hypoglycaemic challenge that increases vulnerability to oxidative damage.</p
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Open Educational Resources
The production, licensing, use and re-use of learning objects accessible through open access distribution will be the focus of this presentation. Noted author and scholar Dr. Rory McGreal will share his knowledge of the increasing opportunities and challenges associated with the open access publication of learning materials
Early Shakespeare, 1588-1594
Early Shakespeare, 1588–1594 draws together leading scholars of text, performance, and theatre history to offer a rigorous re-appraisal of Shakespeare's early career. The contributors offer rich new critical insights into the theatrical and poetic context in which Shakespeare first wrote and his emergence as an author of note, while challenging traditional readings of his beginnings in the burgeoning theatre industry. Shakespeare's earliest works are treated on their own merit and in their own time without looking forward to Shakespeare's later achievements; contributors situate Shakespeare, in his twenties, in a very specific time, place, and cultural moment. The volume features essays about Shakespeare's early style, characterisation, and dramaturgy, together with analysis of his early co-authors, rivals, and influences (including Lyly, Spenser and Marlowe). This collection provides essential entry points to, and original readings of, the poet-dramatist's earliest extant writings and shines new light on his first activities as a professional author
The physiology and pathophysiology of the neural control of the counterregulatory response
Beall C, Ashford ML, McCrimmon RJ. The physiology and pathophysiology of the neural control of the counterregulatory response. Am J Physiol Regul Integr Comp Physiol 302: R215-R223, 2012. First published November 9, 2011; doi:10.1152/ajpregu.00531.2011.-Despite significant technological and pharmacological advancements, insulin replacement therapy fails to adequately replicate beta-cell function, and so glucose control in type 1 diabetes mellitus (T1D) is frequently erratic, leading to periods of hypoglycemia. Moreover, the counterregulatory response (CRR) to falling blood glucose is impaired in diabetes, leading to an increased risk of severe hypoglycemia. It is now clear that the brain plays a significant role in the development of defective glucose counterregulation and impaired hypoglycemia awareness in diabetes. In this review, the basic intracellular glucose-sensing mechanisms are discussed, as well as the neural networks that respond to and coordinate the body's response to a hypoglycemic challenge. Subsequently, we discuss how the body responds to repeated hypoglycemia and how these adaptations may explain, at least in part, the development of impaired glucose counterregulation in diabetes.</p
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