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Secondary lung injury after SCI is a major cause of patient mortality, with apoptosis playing a key role. This study aimed to explore the impact of treadmill training and miR145-5p on the MAPK/Erk signaling pathway and apoptosis in rats with complete SCI. SD rats were used to establish T10 segmental complete SCI models and underwent treadmill training 3, 7, or 14 days postinjury. Various techniques including arterial blood gas analysis, lung wet/dry weight ratio, HE staining, immunofluorescence staining, immunohistochemical staining, qRT-PCR, and Western blotting were employed to assess alterations in lung function and the expression levels of crucial apoptosis-related factors. In order to elucidate the specific mechanism, the impact of miR145-5p on the MAPK/Erk pathway and its role in apoptosis in lung cells were confirmed through miR145-5p overexpression and knockdown experiments. Following spinal cord injury (SCI), an increase in apoptosis, activation of the MAPK/Erk pathway, and impairment of lung function were observed in SCI rats. Conversely, treadmill training resulted in a reduction in alveolar cell apoptosis, suppression of the MAPK/Erk pathway, and enhancement of lung function. The gene MAP3K3 was identified as a target of miR145-5p. The influence of miR145-5p on the MAPK/Erk pathway and its impact on apoptosis in alveolar cells were confirmed through the manipulation of miR145-5p expression levels. The upregulation of miR145-5p in spinal cord injury (SCI) rats led to a reduction in MAP3K3 protein expression within lung tissues, thereby inhibiting the MAPK/Erk signaling pathway and decreasing apoptosis. Contrarily, rats with miR145-5p knockdown undergoing treadmill training exhibited an increase in miR145-5p expression levels, resulting in the inhibition of MAP3K3 protein expression in lung tissues, suppression of the MAPK/Erk pathway, and mitigation of lung cell apoptosis. Ultimately, the findings suggest that treadmill training may attenuate apoptosis in lung cells post-spinal cord injury by modulating the MAP3K3 protein through miR145-5p to regulate the MAPK/Erk signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Osteoporotic vertebral compression fractures (OVCF) may necessitate percutaneous vertebral augmentation (PVA), a procedure not without its risks. One notable complication is cement leakage (CL), which can cause significant distress in patients. Despite its clinical importance, there remains a paucity of meta-analyses investigating these complications and their management in the existing literature., Material and Methods: We systematically reviewed PubMed, Cochrane Library, Embase, and Web of Science databases up to February 2024 to identify studies examining CL following PVA treatment in OVCF. We assessed the quality of eligible cohort studies using the Newcastle-Ottawa Scale (NOS), extracted data on incidence, identified risk factors for CL, and conducting meta-analysis with Revman 5.2 software. We calculated odd ratios (OR) and Mean Differences (MD) with 95% confidence interval (CI) applying random effects models., Results: We identified twelve cohort studies that matched our strict inclusion criteria. These studies included a total of 2388 patients and 3392 vertebrae. CL was identified in 1132 vertebrae. Notable risk factors for CL included compromised cortical bone integrity (OR 5.00, 95% CI 3.01~8.29, P<0.00001), presence of intravertebral vacuum clefts (OR 1.68, 95% CI 1.07~2.65, P=0.03), basivertebral foramen sign (OR 1.77, 95% CI 1.09~2.89, P=0.02), and volume of cement used (MD 0.75, 95% CI 0.41~1.10, P<0.0001)., Conclusion: Our findings underscore the significance of cortical bone integrity, intravertebral vacuum cleft, basivertebral foramen sign, and cement volume as principal determinants of CL risk in PVA for OVCF. These insights advocate for tailored surgical strategies to mitigate the risk of CL in this patient population., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)