Eyes for Ears: Usage and Efficacy of a Podcast for Ophthalmic Education.

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.

Eyes for Ears-A Medical Education Podcast Feasibility Study.

BACKGROUND: Downloadable audio files called podcasts have become popular within many areas of medical education. They can be a valuable supplement to traditional teaching methods. Medical educators may wish to incorporate podcasts into their curriculum and disseminate their work to a larger audience, but may not know how. PURPOSE: We aim to describe the implementation of a novel medical education podcast series for ophthalmology medical student and resident education, and demonstrate feasibility, sustainability, and acceptance of this learning platform. METHODS: The Basic and Clinical Science Course (BCSC) textbooks and supplementary texts, were used to create a weekly series of ophthalmology review podcasts. Feasibility markers include time and cost of production. Sustainability measures included download markers over time. Acceptance was measured by reviews on Apple iTunes and Twitter followers. RESULTS: Forty-eight episodes were released from January 10, 2019 to March 31, 2020. Costs included $212.18 startup, and $29 monthly. The podcast has had 122,709 downloads to date (466/month January 2019, increased to 17,500/month February 2020). It obtained 331 Twitter followers, and 114 ratings on iTunes, with an average of 5.0 stars. CONCLUSIONS: Medical education podcasts are a feasible way of disseminating educational materials to learners. We demonstrate sustainability and acceptance of this learning platform.

Cross-species evidence from human and rat brain transcriptome for growth factor signaling pathway dysregulation in major depression.

An enhanced understanding of the pathophysiology of depression would facilitate the discovery of new efficacious medications. To this end, we examined hippocampal transcriptional changes in rat models of disease and in humans to identify common disease signatures by using a new algorithm for signature-based clustering of expression profiles. The tool identified a transcriptomic signature comprising 70 probesets able to discriminate depression models from controls in both Flinders Sensitive Line and Learned Helplessness animals. To identify disease-relevant pathways, we constructed an expanded protein network based on signature gene products and performed functional annotation analysis. We applied the same workflow to transcriptomic profiles of depressed patients. Remarkably, a 171-probesets transcriptional signature which discriminated depressed from healthy subjects was identified. Rat and human signatures shared the SCARA5 gene, while the respective networks derived from protein-based significant interactions with signature genes contained 25 overlapping genes. The comparison between the most enriched pathways in the rat and human signature networks identified a highly significant overlap (p-value: 3.85 × 10-6) of 67 terms including ErbB, neurotrophin, FGF, IGF, and VEGF signaling, immune responses and insulin and leptin signaling. In conclusion, this study allowed the identification of a hippocampal transcriptional signature of resilient or susceptible responses in rat MDD models which overlapped with gene expression alterations observed in depressed patients. These findings are consistent with a loss of hippocampal neural plasticity mediated by altered levels of growth factors and increased inflammatory responses causing metabolic impairments as crucial factors in the pathophysiology of MDD.

Early transcriptional changes linked to naturally occurring Huntington's disease mutations in neural derivatives of human embryonic stem cells.

Huntington's disease (HD) is characterized by a late clinical onset despite ubiquitous expression of the mutant gene at all developmental stages. How mutant huntingtin impacts on signalling pathways in the pre-symptomatic period has remained essentially unexplored in humans due to a lack of appropriate models. Using multiple human embryonic stem cell lines derived from blastocysts diagnosed as carrying the mutant huntingtin gene by pre-implantation genetic diagnosis, we explored early developmental changes in gene expression using differential transcriptomics, combined with gain and loss of function strategies. We demonstrated a down-regulation of the HTT gene itself in HD neural cells and identified three genes, the expression of which differs significantly in HD cells when compared with wild-type controls, namely CHCHD2, TRIM4 and PKIB. Similar dysregulation had been observed previously for CHCDH2 and TRIM4 in blood cells from patients. CHCHD2 is involved in mitochondrial function and PKIB in protein kinase A-dependent pathway regulation, which suggests that these functions may be precociously impacted in HD.

A combination drug therapy improves cognition and reverses gene expression changes in a mouse model of Huntington's disease.

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.