Purpose. To investigate the relationship between serum cotinine and lumbar bone mineral density (BMD) among 7905 participants aged 30 years and over. Method. A total of 3945 men and 3960 women from the National Health and Nutrition Examination Survey 2011–2018 were included in this cross-sectional analysis. Independent variable was serum cotinine, which is a biomarker of cigarette exposure. The outcome variable was lumbar BMD. We investigated the associations of serum cotinine levels and lumbar BMD using multivariable linear regression models. Results. Serum cotinine concentration was negatively associated with lumbar BMD after adjustment of relevant covariables (β = −0.039, 95% CI: −0.078 to −0.014, P = 0.005 ). However, in the subgroup analysis stratified by gender, this negative association remained only in women (β = −0.072, 95% CI: −0.132 to −0.012, P = 0.019 ). Conclusion. Our study suggested that elevated serum cotinine level correlated with decreased lumbar BMD, especially in women. This finding indicated that reducing cigarette exposure and maintaining serum cotinine at a low level may be beneficial to bone health for adults.

Background Neurofilament light chain (NEFL) has been identified as a biomarker for spinal cord injury (SCI), but its effect and underlying mechanism in SCI remain unclear. Methods SCI rat models were established for in vivo studies. Lipopolysaccharide (LPS)‐induced cell models were used for in vitro studies. The protein and mRNA expression levels of genes were evaluated by western blotting and reverse transcription‐quantitative polymerase chain reaction (RT‒qPCR). The pathological changes in rats after SCI were subjected to histological examinations. The interaction of NEFL and upstream miRNAs was explored using dual‐luciferase reporter gene assays. Results NEFL was highly expressed in SCI rat spinal cord tissues and LPS‐stimulated PC12 cells. NEFL silencing showed an inhibitory effect on the morphological changes of SCI rats and the secretion of inflammatory factors and facilitated functional recovery of SCI rats. MiR‐30b‐5p was demonstrated to target NEFL and negatively regulate NEFL mRNA and protein levels. Downregulation of miR‐30b‐5p in SCI cell and rat models was demonstrated. MiR‐30b‐5p alleviated the inflammatory response in SCI rat models and LPS‐stimulated PC12 cells and promoted functional recovery in rats by targeting NEFL. NEFL activated mTOR signaling. MiR‐30b‐5p inactivated mTOR signaling by negatively regulating NEFL. Conclusion MiR‐30b‐5p alleviated the inflammatory response and facilitated the functional recovery of SCI rats by targeting NEFL to inactivate the mTOR pathway.