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Introduction: Acupuncture is commonly used to treat chronic pain. Patients often access public social media platforms for healthcare information when querying acupuncture. Our study aims to appraise the utility, accuracy, and quality of information available on YouTube, a popular social media platform, on acupuncture for chronic pain treatment. Methods: Using search terms such as "acupuncture for chronic pain" and "acupuncture pain relief", the top 54 videos by view count were selected. Included videos were >1 minute duration, contained audio in English, had >7000 views, and was related to acupuncture. One primary outcome of interest was categorizing each video's usefulness as useful, misleading, or neither. Another primary outcome of interest was the quality and reliability of each video using validated instruments, including the modified DISCERN (mDISCERN) tool and the Global Quality Scale (GQS). The means were calculated for the video production characteristics, production sources, and mDISCERN and GQS scores. Continuous and categorical outcomes were compared using Student's t-test and chi-square test, respectively. Results: Of the 54 videos, 57.4% were categorized as useful, 14.8% were misleading, and 27.8% were neither. Useful videos had a mean GQS and mDISCERN score of 3.77±0.67 and 3.48±0.63, respectively, while misleading videos had mean GQS and mDISCERN score of 2.50±0.53 and 2.38±0.52, respectively. 41.8% of the useful videos were produced by a healthcare institution while none of the misleading videos were produced by a healthcare institution. However, 87.5% of the misleading videos were produced by health media compared to only 25.8% of useful videos from health media. Discussion: As patients increasingly depend on platforms like YouTube for trustworthy information on complementary health practices such as acupuncture, our study emphasizes the critical need for more higher-quality videos from unbiased healthcare institutions and physicians to ensure patients are receiving reliable information regarding this topic.
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Epiretinal membranes (ERMs) are the result of fibro-cellular proliferation that cause distortion and impairment of central vision. We hypothesized that select microRNAs (miRs) regulate retinal fibro-proliferation and ERM formation. Following IRB approval, a pilot study was performed in patients presenting for retina surgery with and without clinical ERMs. Total RNA was isolated from ERM tissue and controls from non-ERM vitreous and subjected to miR profiling via microarray analysis. MiR-494 was identified as the only miR selectively expressed at significantly greater levels, and in silico analysis identified p27 as a putative fibroproliferative gene target of miR-494. In vitro testing of miR-494 and p27 in fibrotic transformation was assessed in spontaneously immortalized human retinal pigment epithelial (RPE) and human Müller cell lines, stimulated to transform into a fibroproliferative state via transforming growth factor beta (TGFß). Fibroproliferative transformation was characterized by de novo cellular expression of alpha smooth muscle actin (αSMA). In both RPE and Müller cells, both TGFß and miR-494 mimic decreased p27 expression. In parallel experiments, transfection with p27 siRNA augmented TGFß-induced αSMA expression, while only in RPE cells did co-transfection with miR-494 inhibitor decrease αSMA levels. These results demonstrate that miR-494 augments fibrotic transformation in both Müller cells and RPEs, however only in RPEs does miR-494 mediate fibrotic transformation via p27. As p27 is known to regulate cellular proliferation and differentiation, future studies should extend clinical testing of miR-494 and/or p27 as a potential novel non-surgical therapy for ERMs, as well as identify relevant miR-494 targets in Müller cells.
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Memory impairment remains a leading disability in survivors of global cerebral ischemia, occurring secondary to delayed neurodegeneration of hippocampal cornu ammonis-1 (CA1) neurons. MicroRNA-200c (miR-200c) is induced following ischemic stress and we have previously demonstrated that pre-treatment with anti-miR-200c is protective against embolic stroke in mice. In the present study we assessed the role of miR-200c on CA1 neurodegeneration, sirtuin-1 (SIRT1), and mitochondrial dynamic protein expression in a mouse model of transient global cerebral ischemia and in vitro in primary mouse astrocyte cultures after simulated ischemia. Mice were subjected to 10 min bilateral common carotid artery occlusion plus hypotension with 5% isoflurane. After 2 h recovery mice were treated with intravenous injection of either anti-miR-200c or mismatch control. Memory function was assessed by Barnes maze at post-injury days 3 and 7. Mice were sacrificed at post-injury day 7 for assessment of brain cell-type specific expression of miR-200c, SIRT1, and the mitochondrial fusion proteins mitofusin-2 (MFN2) and OPA1 via complexed fluorescent in situ hybridization and fluorescent immunohistochemistry. Global cerebral ischemia induced significant loss of CA1 neurons, impaired memory performance and decreased expression of CA1 SIRT1, MFN2, and OPA1. Post-injury treatment with anti-miR-200c significantly improved survival, prevented CA1 neuronal loss, improved post-injury performance in Barnes maze, and was associated with increased post-injury expression of CA1 SIRT1 and MFN2 in astrocytes. In vitro, primary mouse astrocyte cultures pre-treated with miR-200c inhibitor prior to oxygen/glucose deprivation preserved expression of SIRT1 and MFN2, and decreased reactive oxygen species generation, whereas pre-treatment with miR-200c mimic had opposite effects that could be reversed by co-treatment with SIRT1 activator. These results suggest that miR-200c regulates astrocyte mitochondrial homeostasis via targeting SIRT1, and that CA1 astrocyte mitochondria and SIRT1 represent potential post-injury therapeutic targets to preserve cognitive function in survivors of global cerebral ischemia.
