Association between heavy metal exposures and the prevalence of pelvic inflammatory disease: a cross-sectional study from the National Health and Nutrition Examination Survey 2013-2018.

Pelvic inflammatory disease (PID) is a common medical condition in women. However, the correlation between exposure to heavy metals, including cadmium (Cd), lead (Pb), manganese (Mn), mercury (Hg), and selenium (Se), and PID, is unclear. Using a large sample size from the National Health and Nutrition Examination Survey, these relationships were studied and verified. PID diagnosis was acquired through a self-reported questionnaire (2013-2018). Heavy metal exposure (Cd, Pb, Mn, Hg, and Se) was measured using mass spectrometry of blood samples. Covariate data were obtained through questionnaires and physical tests. Individuals with complete covariate data were included in the study. The relationship between heavy metal exposure (Cd, Pb, Mn, Hg, and Se) and PID was demonstrated using logistic regression analysis, weighted quantile sum (WQS) regression analysis, and restricted cubic splines (RCS). Overall, 2743 participants were included. Of these, 183 were diagnosed with PID. Through weighted univariate and multivariate regression analyses, the heavy metals of Cd and Pb were positively correlated with the prevalence of PID. However, no significant relationship was observed in the heavy metals of Mn, Hg, and Se. The joint effect of heavy metals further confirmed the important role of Cd and Pb in WQS analysis. After visualizing the RCS, significant curved and linear relationships were observed for Cd and Pb, respectively. Most subgroup analyses confirmed these results. In conclusion, exposure to Cd was nonlinearly correlated with the risk of PID, whereas exposure to Pb showed a linear relationship. Our findings increase the awareness of the environmental effects of exposure to heavy metals in PID. However, further studies are needed to elucidate the causality and underlying mechanisms between heavy metal exposure and the prevalence of PID.

Glioma-Associated Oncogene Family Zinc Finger 2 (GLI2) Activates Wnt Signaling through Transcriptional Inhibition of Neuronal Precursor Cell-Expressed Developmentally Downregulated 4 (NEDD4L) to Promote Androgen-Induced Granulosa Cell Damage.

OBJECTIVE: Being a prevalent endocrine and metabolic disease, polycystic ovary syndrome (PCOS) severely threatens women's physical and mental health. Glioma-associated oncogene family zinc finger 2 (GLI2) expression is up-regulated in granulosa cells of PCOS patients, but its specific role in PCOS remains unclear. METHODS: Following the treatment of human ovarian granulosa cells (KGN) with dihydrotestosterone (DHT), RT-qPCR and western blot were utilized to check GLI2 expression. After GLI2 expression was silenced, cell activity was detected through CCK8 and apoptosis was examined via TUNEL and western blot. Inflammation and oxidative stress were tested utilizing ELISA and western blot. The binding between GLI2 and neuronal precursor cell-expressed developmentally downregulated 4 (NEDD4L) promoter was predicted by JASPAR database and verified by luciferase reporter and ChIP assay. In addition, RT-qPCR and western blot were applied to check the mRNA and protein expressions of NEDD4L. Following the knockdown of NEDD4L in GLI2-silencing cells, CCK8 assay, TUNEL assay, western blot, ELISA and other methods were performed again. Finally, western blot detected the expressions of Wnt pathway-related proteins. RESULTS: GLI2 was up-regulated in DHT-treated KGN cells. Interference with GLI2 increased the viability, decreased the apoptosis, and inhibited the inflammatory response and oxidative stress of DHT-induced KGN cells. GLI2 could bind to NEDD4L promoter and transcriptionally suppress NEDD4L expression. Further experiments testified that NEDD4L depletion reversed the impacts of GLI2 deficiency on the viability, apoptosis, inflammation, oxidative stress and Wnt signaling pathway in DHT-challenged KGN cells. CONCLUSION: GLI2 activated Wnt signaling to promote androgen-induced granulosa cell damage through transcriptional inhibition of NEDD4L.

Synthesis and sonocatalytic property of rod-shape Sr(OH)2·8H2O.

A novel rod-shape sonocatalyst Sr(OH)2·8H2O was prepared by a facile precipitation method, and characterized by X-ray powder diffraction, transmission electron microscopy, Fourier transform infrared spectroscopy and UV-vis absorption spectroscopy. Comparative sonocatalytic degradation experiments were carried out in different conditions under ultrasonic irradiation by using rhodamine B (RhB) as the model substrate, indicating that Sr(OH)2·8H2O was highly sonocatalytic. Total organic carbon experiment demonstrated Sr(OH)2·8H2O with mass mineralization of organic carbon. The effects of catalyst amount, initial RhB concentration and ultrasonic energy of degradation were investigated, and the sonocatalyst could be reused 5 times without significant loss of activity. Furthermore, the potent degrading capability was ascribed to ultrasonic cavitation producing flash light/energy which generated radicals (e.g., OH) with high oxidation activity.

Fabrication and sonocatalytic property of AgPO3 microsphere.

AgPO3 microspheres were prepared by a simple hydrothermal method. The AgPO3 microspheres were characterized by X-ray powder diffraction (XRD), scanning electronic microscopy (SEM), Brunauer-Emmett-Teller (BET), UV-vis absorption spectroscopy (UV-vis), and photoluminescence (PL) measurement. SEM reveals that the AgPO3 microspheres were constructed by the accumulation of small particles. The as-prepared AgPO3 microspheres sonocatalytically degraded Rhodamine B (RhB) excellently under ultrasonic irradiation. The sonocatalytic ability results from the OH radicals induced by AgPO3 microspheres under ultrasonic irradiation. The effects of other conditions on ultrasonic activity were also investigated. The content of OH radicals in the reaction system was determined to further verify the above conclusions.