#lowbackpain on TikTok: A New Frontier for Orthopaedic Medical Education.

INTRODUCTION: Low back pain has become a substantial health problem in all developed countries. Many healthcare professionals and content creators have begun sharing their treatment methods and opinions through social media, especially the video-based platform TikTok. TikTok has been downloaded more than 2.6 billion times with over a billion daily users. Its influence on public health makes it imperative that information be accurate and safe. This study aims to analyze TikTok's most popular content on lower back pain and how orthopaedic surgeons contribute on this growing platform. OBJECTIVES: To analyze TikTok's most popular content on lower back pain and how orthopaedic surgeons are and can contribute on this growing platform. METHODS: A TikTok search conducted on April 22, 2023, using the terms '#lowerbackpain'and '#lowbackpainrelief,' resulted in numerous videos, 100 of which met inclusion criteria. Videos were included if they were related to the content, had more than 1000 views, were in English, and were not duplicates. Video characteristics were recorded and evaluated for quality by two reviewers using DISCERN. A two-sample t-test was used to assess differences. RESULTS: Overall, the top videos on lower back pain had an average of 2,061,396 views, with a mean DISCERN score of 34. The mean total DISCERN score was 36 and 34 for physicians and nonphysicians, respectively, while the video by the orthopaedic surgeon (n = 1) scored 31. The most recommended treatments included at-home exercises (n = 75) and visiting a chiropractor (n = 4). CONCLUSION: We find that the information presented by nonphysicians offered quick, at-home fixes to medical problems without offering any research or proven data to support their claims. We cannot overlook Tiktok's immense influence in the realm of orthopaedic health as it has become a sphere of information dissemination and education. Thus, we suggest that there is not necessarily a need for a greater number of surgeons and/or resident physicians to involve themselves on the platform, but rather the involvement of governing bodies and spine societies to put out position statements for our patients.

Dysregulation of TrkB phosphorylation and proBDNF protein in adenylyl cyclase 1 and 8 knockout mice in a model of fetal alcohol spectrum disorder.

Brain-derived neurotrophic factor (BDNF) mediates neuron growth and is regulated by adenylyl cyclases (ACs). Mice lacking AC1/8 (DKO) have a basal reduction in the dendritic complexity of medium spiny neurons in the caudate putamen and demonstrate increased neurotoxicity in the striatum following acute neonatal ethanol exposure compared to wild type (WT) controls, suggesting a compromise in BDNF regulation under varying conditions. Although neonatal ethanol exposure can negatively impact BDNF expression, little is known about the effect on BDNF receptor activation and its downstream signaling, including Akt activation, an established neuroprotective pathway. Therefore, here we determined the effects of AC1/8 deletion and neonatal ethanol administration on BDNF and proBDNF protein expression, and activation of tropomyosin-related kinase B (TrkB), Akt, ERK1/2, and PLCγ. WT and DKO mice were treated with a single dose of 2.5 g/kg ethanol or saline at postnatal days 5-7 to model late-gestational alcohol exposure. Striatal and cortical tissues were analyzed using a BDNF enzyme-linked immunosorbent assay or immunoblotting for proBDNF, phosphorylated and total TrkB, Akt, ERK1/2, and PLCÉ£1. Neither postnatal ethanol exposure nor AC1/8 deletion affected total BDNF protein expression at any time point in either region examined. Neonatal ethanol increased the expression of proBDNF protein in the striatum of WT mice 6, 24, and 48 h after exposure, with DKO mice demonstrating a reduction in proBDNF expression 6 h after exposure. Six and 24 h after ethanol administration, phosphorylation of full-length TrkB in the striatum was significantly reduced in WT mice, but was significantly increased in DKO mice only at 24 h. Interestingly, 48 h after ethanol, both WT and DKO mice demonstrated a reduction in phosphorylated full-length TrkB. In addition, Akt and PLCÉ£1 phosphorylation was also decreased in ethanol-treated DKO mice 48 h after injection. These data demonstrate dysregulation of a potential survival pathway in the AC1/8 knockout mice following early-life ethanol exposure.

Adenylyl cylases 1 and 8 mediate select striatal-dependent behaviors and sensitivity to ethanol stimulation in the adolescent period following acute neonatal ethanol exposure.

Neonatal alcohol exposure in rodents causes dramatic neurodegenerative effects throughout the developing nervous system, particularly in the striatum, acutely after exposure. These acute neurodegenerative effects are augmented in mice lacking adenylyl cyclases 1 and 8 (AC1/8) as neonatal mice with a genetic deletion of both AC isoforms (DKO) have increased vulnerability to ethanol-induced striatal neurotoxicity compared to wild type (WT) controls. While neonatal ethanol exposure is known to negatively impact cognitive behaviors, such as executive functioning and working memory in adolescent and adult animals, the threshold of ethanol exposure required to impinge upon developmental behaviors in mice has not been extensively examined. Therefore, the purpose of this study was to determine the behavioral effects of neonatal ethanol exposure using various striatal-dependent developmental benchmarks and to assess the impact of AC1/8 deletion on this developmental progression. WT and DKO mice were treated with 2.5 g/kg ethanol or saline on postnatal day (P)6 and later subjected to the wire suspension, negative geotaxis, postural reflex, grid hang, tail suspension and accelerating rotarod tests at various time points. At P30, mice were evaluated for their hypnotic responses to 4.0 g/kg ethanol by using the loss of righting reflex assay and ethanol-induced stimulation of locomotor activity after 2.0 g/kg ethanol. Ethanol exposure significantly impaired DKO performance in the negative geotaxis test while genetic deletion of AC1/8 alone increased grid hang time and decreased immobility time in the tail suspension test with a concomitant increase in hindlimb clasping behavior. Locomotor stimulation was significantly increased in animals that received ethanol as neonates, peaking significantly in ethanol-treated DKO mice compared to ethanol-treated WT controls, while sedation duration following high-dose ethanol challenge was unaffected. These data indicate that the maturational parameters examined in the current study may not be sensitive enough to detect effects of a single ethanol exposure during the brain growth spurt period. Genetic deletion of AC1/8 reveals a role for these cylases in attenuating ethanol-induced behavioral effects in the neonatally-exposed adolescent.