Background: Glucose variability (GV) remains a key limiting factor in the success of diabetes management. While new technologies, for example, accurate continuous glucose monitoring (CGM) and connected insulin delivery devices, are now available, current treatment standards fail to leverage the wealth of information generated. Expert systems, from automated insulin delivery to advisory systems, are a key missing element to richer, more personalized, glucose management in diabetes.
View Article and Find Full Text PDFObjective: Artificial pancreas (AP) systems are best positioned for optimal treatment of type 1 diabetes (T1D) and are currently being tested in outpatient clinical trials. Our consortium developed and tested a novel adaptive AP in an outpatient, single-arm, uncontrolled multicenter clinical trial lasting 12 weeks.
Research Design And Methods: Thirty adults with T1D completed a continuous glucose monitor (CGM)-augmented 1-week sensor-augmented pump (SAP) period.
Background: Young children 5-8 years old with type 1 diabetes (T1D) exhibit clear needs for improved glycemic control but may be limited in their ability to safely interact with an artificial pancreas system. Our goal was to evaluate the safety and performance of an artificial pancreas (AP) system among young children with T1D.
Research Design And Methods: In a randomized, crossover trial, children with T1D age 5-8 years were enrolled to receive on separate study periods (in random order) either the UVa AP using the DiAs Control Platform software with child-resistant lock-out screens (followed as an out-patient admission) or their usual insulin pump+continuous glucose monitor (CGM) care at home.
Idiopathic primary hyperaldosteronism (IHA) and low-renin essential hypertension (LREH) are common forms of hypertension, characterized by an elevated aldosterone-renin ratio and hypersensitivity to angiotensin II. They are suggested to be 2 states within a disease spectrum that progresses from LREH to IHA as the control of aldosterone production by the renin-angiotensin system is weakened. The mechanism(s) that drives this progression remains unknown.
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