Objective This study aimed to determine the incidence of spinal infection after vertebral augmentation (SIAVA) and identify its independent risk factors.
Methods This multicenter, retrospective case-control study included patients who underwent percutaneous vertebral augmentation (PVA) for osteoporotic vertebral compression fractures at 4 centers between January 2015 and December 2021. Each SIAVA case was matched with 3 controls using propensity score matching based on demographic and clinical variables. LASSO (least absolute shrinkage and selection operator) regression was used for variable selection, followed by multivariable conditional logistic regression to identify risk factors for SIAVA.
Results Among 7,797 PVA procedures, 42 SIAVA cases were identified, yielding an incidence of 0.54%. The median time from PVA to SIAVA diagnosis was 4.3 (interquartile range, 2.8–11.7) weeks. After 1:3 matching (42 cases vs. 126 controls), multivariable analysis identified 4 independent risk factors: preoperative pulmonary infection (odds ratio [OR], 3.64; 95% confidence interval [CI], 1.21–11.0; p=0.022), intravertebral fluid sign on magnetic resonance imaging (MRI) (OR, 6.17; 95% CI, 1.92–19.9; p=0.002), type D (intradiscal) cement leakage (OR, 2.93; 95% CI, 1.10–7.85; p=0.032), and serum albumin ≤35 g/L (OR, 3.29; 95% CI, 1.15–9.45; p=0.027). Within the infection cohort, 25 patients (59.5%) underwent revision surgery, and 2 deaths (4.8%) occurred during follow-up.
Conclusion The incidence of SIAVA was 0.54%. Preoperative pulmonary infection, intravertebral fluid sign on MRI, type D cement leakage, and serum albumin ≤35 g/L were identified as independent risk factors. These findings may help clinicians implement preoperative risk-reduction strategies.
Objective Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms.
Methods By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway.
Results In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway.
Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.
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Results In different models, we found that the expression of METTL3 and the overall m6A modification level were significantly increased in neurons. After inducing OGD, inhibition of METTL3 activity or expression increased the mRNA and protein levels of Bcl-2, inhibited neuronal apoptosis, and improved neuronal viability in the spinal cord.
Conclusion Inhibition of METTL3 activity or expression can inhibit the apoptosis of spinal cord neurons after SCI through the m6A/Bcl-2 signaling pathway.
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