National survey of educational impact on pharmacy learners by volunteering at camps for children with diabetes.

INTRODUCTION: Current literature on pharmacy students' and residents' experience attending camps for children with diabetes focuses on the experience at an individual campsite. The objective of this study was to examine the demographics and gains in understanding that pharmacy learners achieve when volunteering as medical staff at camps for children with type 1 diabetes (T1D). METHODS: National listservs were used to identify pharmacists who precept pharmacy students and residents at diabetes camps. These self-identified pharmacists shared pre- and post-camp electronic surveys with their respective pharmacy learners. Statistical analysis was completed using SPSS Version 25 (IBM, Corp.). RESULTS: Eighty-six pharmacy learners completed the pre-camp survey and 69 completed the post-camp survey. Most were Caucasian, in their fourth professional year, and participated in residential camps that lasted six and one-half days on average. Learners consistently engaged in patient care activities including: carbohydrate counting (87%), bolus insulin dose calculations (86%), treatment of hypo/hyperglycemic episodes (86%), blood glucose testing (83%), blood sugar trend evaluation (78%), basal insulin dosing calculations (74%), and insulin pump site changes (72%). Learners demonstrated statistically significant gains in every index measured with the exception of glucometer use. Eighty-seven percent indicated they learned how to appropriately manage T1D, 37% gained empathy for those living with T1D, and 13% learned how to work in a medical team. CONCLUSIONS: Pharmacy learners who volunteered at diabetes camps experienced large gains in their understanding of concepts and devices, comfort with performing patient care tasks, and compassion for children and their families living with T1D.

Early presynaptic and postsynaptic calcium signaling abnormalities mask underlying synaptic depression in presymptomatic Alzheimer's disease mice.

Alzheimer's disease (AD)-linked presenilin (PS) mutations result in pronounced endoplasmic reticulum calcium disruptions that occur before detectable histopathology and cognitive deficits. More subtly, these early AD-linked calcium alterations also reset neurophysiological homeostasis, such that calcium-dependent presynaptic and postsynaptic signaling appear functionally normal yet are actually operating under aberrant calcium signaling systems. In these 3xTg-AD mouse brains, upregulated ryanodine receptor (RyR) activity is associated with a shift toward synaptic depression, likely through a reduction in presynaptic vesicle stores and increased postsynaptic outward currents through small-conductance calcium-activated potassium SK2 channels. The deviant RyR-calcium involvement in the 3xTg-AD mice also compensates for an intrinsic predisposition for hippocampal long-term depression (LTD) and reduced long-term potentiation (LTP). In this study, we detail the impact of disrupted RyR-mediated calcium stores on synaptic transmission properties, LTD, and calcium-activated membrane channels of hippocampal CA1 pyramidal neurons in presymptomatic 3xTg-AD mice. Using electrophysiological recordings in young 3xTg-AD and nontransgenic (NonTg) hippocampal slices, we show that increased RyR-evoked calcium release in 3xTg-AD mice "normalizes" an altered synaptic transmission system operating under a shifted homeostatic state that is not present in NonTg mice. In the process, we uncover compensatory signaling mechanisms recruited early in the disease process that counterbalance the disrupted RyR-calcium dynamics, namely increases in presynaptic spontaneous vesicle release, altered probability of vesicle release, and upregulated postsynaptic SK channel activity. Because AD is increasingly recognized as a "synaptic disease," calcium-mediated signaling alterations may serve as a proximal trigger for the synaptic degradation driving the cognitive loss in AD.