RESUMEN
Purpose: To characterize listenership and perceived educational impact of the ophthalmic podcast "Eyes for Ears". Methods: A cross-sectional, internet-distributed, 9-question Qualtrics survey was made available to podcast listeners. Listenership metrics were analyzed from the podcast host platform. Results: From January 10, 2019 to September 2, 2021, the podcast was downloaded over 422,000 times, averaging about 4442 downloads per episode. 209 Qualtrics survey responses were analyzed from podcast listeners with backgrounds in eye care including medical students, residents, fellows, clinicians and technicians. The majority were residents (60.3%), representative of the target audience of the podcast. Listeners reported using the podcast while commuting (81.3%), felt it increased the time they could spend on self-care (63.2%), and thought it improved their fund of knowledge (99.0%). Respondents recalled feeling better prepared for the OKAP or written boards after using this podcast (before median = 50/100 on Likert Scale, IQR 30-65 vs median = 70/100, IQR 56-81, p <0.001). Respondents identified question banks as the most helpful for OKAP studying, followed by podcasts. Podcasts were preferred over articles and lectures in terms of helpfulness (p < 0.001). Conclusion: The Eyes for Ears podcast has achieved a robust international audience. The surveyed audience felt the podcast was useful for their education and well-being.
RESUMEN
Huntington's disease is a genetic disease caused by a single mutation. It is characterized by progressive movement, emotional and cognitive deficits. R6/2 mice transgenic for exon 1 of the HD gene with 150+ CAG repeats have a progressive neurological phenotype, including deterioration in cognitive function. The mechanism underlying the cognitive deficits in R6/2 mice is unknown, but dysregulated gene expression, reduced neurotransmitter levels and abnormal synaptic function are present before the cognitive decline becomes pronounced. Our goal here was to ameliorate the cognitive phenotype in R6/2 mice using a combination drug therapy (tacrine, moclobemide and creatine) aimed at boosting neurotransmitter levels in the brain. Treatment from 5 weeks of age prevented deterioration in two different cognitive tasks until at least 12 weeks. However, motor deterioration continued unabated. Microarray analysis of global gene expression revealed that many genes significantly up- or down-regulated in untreated R6/2 mice had returned towards normal levels after treatment, though a minority were further dysregulated. Thus dysregulated gene expression was reversed by the combination treatment in the R6/2 mice and probably underlies the observed improvements in cognitive function. Our study shows that cognitive decline caused by a genetic mutation can be slowed by a combination drug treatment, and gives hope that cognitive symptoms in HD can be treated.
