Association between blood lead levels and parathyroid hormone among United States adolescents aged 12-19: a cross-sectional study.

Aims: Studies on the association between serum lead levels and parathyroid function in adolescents are lacking. Therefore, in this study, we elucidated the possible association between blood lead levels (BLLs) and the parathyroid hormone (PTH) in adolescents aged 12-19 years in the United States. Methods: In this study, information from the database of the National Health and Nutrition Examination Survey was utilized. The study included 3919 participants from survey cycles between 2003-2004 and 2005-2006. Multivariable linear regression analysis was performed to determine the correlation between BLLs and PTH. Furthermore, smooth curve fitting was utilized to analyze the dose-response relationship between BLLs and PTH. Results: Multivariable linear regression analysis revealed that every 1 µg/dL increase in BLLs was associated with 0.67 pg/mL increase in PTH (ß = 0.67, 95% CI: 0.16-1.18, p < 0.01). However, sex-stratified subgroup analysis revealed that this positive association was only observed in males (ß = 1.16, 95% CI: 0.50-1.83 p < 0.01). Smooth curve fitting revealed a positive correlation between BLLs and PTH. Conclusions: In adolescents in the United States, BLLs are positively correlated with PTH, particularly in males.

Downregulation of miR-210 Promoted Apoptosis of Hippocampal Neurons by Negatively Regulating the TLR4/NF-кB1 Signaling Pathway in a Rat Model of Status Epilepticus.

Purpose: Status epilepticus (SE) is a life-threatening condition causing brain damage, hippocampal necrosis and apoptosis. This study aimed to determine whether microRNA-210 regulates seizure and apoptosis by targeting the TLR4 /NF-κB1 associated signaling pathway. Methods: In a pilocarpine-induced epileptic rat model, the expressions of microRNA-210 (miR-210), TLR4, NF-κB1 and caspase-3 were assessed by a quantitative polymerase chain reaction and Western blotting. Tunel detects hippocampal neuron apoptosis. Results: We found that miR-210, TLR4, NF-κB1 and caspase-3 were upregulated in the hippocampus of the rat model compared with that of control. The knockdown of miR-210 significantly restored the expression levels of TLR4, NF-κB1 and caspase-3 and increased hippocampal apoptosis. Conclusion: These findings showed that the downregulation of miR-210 promoted apoptosis of hippocampal neurons by negatively regulating the TLR4/NF-кB1 signaling pathway.

MicroRNA 322-5p reduced neuronal inflammation via the TLR4/TRAF6/NF-κB axis in a rat epilepsy model.

This study aimed to determine whether microRNA-322-5p regulates seizure and seizure damage by targeting the TLR4/TRAF6/NF-κB-associated inflammatory signaling pathway. In a pilocarpine-induced epileptic rat model, the expressions of miR-322-5p, TLR4, NF-κB, TRAF6, IRF5, IL-1ß, and GABA were assessed by a quantitative polymerase chain reaction and western blotting. Tunel detects hippocampal neuron apoptosis. The results showed that the expression of miR-322-5p significantly decreased in status epilepticus (SE) rats. The reduction of miR-322-5p was accompanied by increased levels of pro-inflammatory cytokines, an increased NF-κB expression, and reduced γ-aminobutyric acid (GABA) levels. Exogenous miR-322-5p reduced the expression of inflammatory molecules and increased the GABA levels in SE rats, and also reduced hippocampal neuronal cell apoptosis caused by epilepsy. In conclusion, the miR-322-5p significantly inhibited the TLR4/TRAF6/NF-κB-associated inflammation and reduced neuronal apoptosis, suggesting that its induction may be of potential interest for novel antiseizure medications.