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1.
Acad Med ; 93(12): 1791-1794, 2018 12.
Article in English | MEDLINE | ID: mdl-29901658

ABSTRACT

Health professions educators face multiple challenges, among them the need to adapt educational methods to new technologies. In the last decades, multiple new digital platforms have appeared in the learning arena, including massive open online courses and social-media-based education. The major critique of these novel methods is the lack of the ability to ascertain the origin, validity, and accountability of the knowledge that is created, shared, and acquired. Recently, a novel technology based on secured data storage and transmission, called blockchain, has emerged as a way to generate networks where validity, trust, and accountability can be created. Conceptually, blockchain is an open, public, distributed, and secure digital registry where information transactions are secured and have a clear origin, explicit pathways, and concrete value. Health professions education based on blockchain will potentially allow improved tracking of content and the individuals who create it, quantify educational impact on multiple generations of learners, and build a relative value of educational interventions. Furthermore, institutions adopting blockchain technology would be able to provide certification and credentialing of health care professionals with no intermediaries. There is potential for blockchain to significantly change the future of health professions education and radically transform how patients, professionals, educators, and learners interact around safe, valid, and accountable information.


Subject(s)
Educational Technology/methods , Health Occupations/education , Information Management/methods , Social Responsibility , Trust , Educational Technology/standards , Humans , Information Management/standards
2.
Am J Emerg Med ; 35(5): 769-772, 2017 May.
Article in English | MEDLINE | ID: mdl-28258839

ABSTRACT

OBJECTIVE: A wide variety of spinal needles are used in clinical practice. Little is currently known regarding the impact of needle length, gauge, and tip type on the needle's ability to measure spinal canal opening pressure. This study aimed to investigate the relationship between these factors and the opening-pressure measurement or time to obtain an opening pressure. METHODS: Thirteen distinct spinal needles, chosen to isolate the effects of length, gauge, and needle-point type, were prospectively tested on a lumbar puncture simulator. The key outcomes were the opening-pressure measurement and the time required to obtain that measure. Pressures were recorded at 10-s intervals until 3 consecutive, identical readings were observed. RESULTS: Time to measure opening pressure increased with increasing spinal needle length, increasing gauge, and the Quincke-type (cutting) point (P<0.001 for all). The time to measurement ranged from 30s to 530s, yet all needle types were able to obtain a consistent opening pressure measure. CONCLUSION: Although opening pressure estimates are unlikely to vary markedly by needle type, the time required to obtain the measurement increased with increasing needle length and gauge and with Quincke-type needles.


Subject(s)
Cerebrospinal Fluid Pressure , Spinal Puncture/instrumentation , Humans , Manikins
3.
J Bioenerg Biomembr ; 47(1-2): 1-11, 2015 Apr.
Article in English | MEDLINE | ID: mdl-25104046

ABSTRACT

Diet composition may affect energy metabolism in a tissue-specific manner. Using C57Bl/6J mice, we tested the effect of ketosis-inducing and non-inducing high fat diets on genes relevant to brain bioenergetic infrastructures, and on proteins that constitute and regulate that infrastructure. At the end of a one-month study period the two high fat diets appeared to differentially affect peripheral insulin signaling, but brain insulin signaling was not obviously altered. Some bioenergetic infrastructure parameters were similarly impacted by both high fat diets, while other parameters were only impacted by the ketogenic diet. For both diets, mRNA levels for CREB, PGC1α, and NRF2 increased while NRF1, TFAM, and COX4I1 mRNA levels decreased. PGC1ß mRNA increased and TNFα mRNA decreased only with the ketogenic diet. Brain mtDNA levels fell in both the ketogenic and non-ketogenic high fat diet groups, although TOMM20 and COX4I1 protein levels were maintained, and mRNA and protein levels of the mtDNA-encoded COX2 subunit were also preserved. Overall, the pattern of changes observed in mice fed ketogenic and non-ketogenic high fat diets over a one month time period suggests these interventions enhance some aspects of the brain's aerobic infrastructure, and may enhance mtDNA transcription efficiency. Further studies to determine which diet effects are due to changes in brain ketone body levels, fatty acid levels, glucose levels, altered brain insulin signaling, or other factors such as adipose tissue-associated hormones are indicated.


Subject(s)
Brain/metabolism , Diet, Ketogenic/adverse effects , Dietary Fats/adverse effects , Energy Metabolism/drug effects , Nerve Tissue Proteins/metabolism , Animals , Brain/pathology , DNA, Mitochondrial/metabolism , Mice , Time Factors
4.
J Alzheimers Dis ; 33(4): 1135-46, 2013.
Article in English | MEDLINE | ID: mdl-23099815

ABSTRACT

Alzheimer's disease (AD) patients have reduced brain acetylcholine and reversing this deficit yields clinical benefits. In this study we explored how increased cholinergic tone impacts cell bioenergetics, which are also perturbed in AD. We treated SH-SY5Y neuroblastoma cells with carbachol, a cholinergic agonist, and tested for bioenergetic flux and bioenergetic infrastructure changes. Carbachol rapidly increased both oxidative phosphorylation and glycolysis fluxes. ATP levels rose slightly, as did cell energy demand, and AMPK phosphorylation occurred. At least some of these effects depended on muscarinic receptor activation, ER calcium release, and ER calcium re-uptake. Our data show that increasing cholinergic signaling enhances cell bioenergetics, and reveal mechanisms that mediate this effect. Phenomena we observed could potentially explain why cholinesterase inhibitor therapy increases AD brain glucose utilization and N-acetyl aspartate levels. The question of whether cholinesterase inhibitors have a disease modifying effect in AD has long been debated; our data suggest a theoretical mechanism through which such an effect could potentially arise.


Subject(s)
Cholinergic Agonists/pharmacology , Energy Metabolism/physiology , Neurons/metabolism , Signal Transduction/physiology , Acetylcholine/metabolism , Carbachol/pharmacology , Cell Line, Tumor , Energy Metabolism/drug effects , Glycolysis/drug effects , Glycolysis/physiology , Humans , Neuroblastoma/metabolism , Neuroblastoma/pathology , Neurons/drug effects , Neurons/pathology , Signal Transduction/drug effects
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