Health risk in children to fluoride exposure in a typical endemic fluorosis area on Loess Plateau, north China, in the last decade.

Excessive and inadequate intake of fluoride may cause adverse effects in children, such as dental caries and dental fluorosis. This study reports the results of monitoring fluoride concentrations in drinking water from an endemic fluorosis region during the ten-year period (2008 through 2017). The fluoride concentration had a range of 0.03-9.42 mg L-1 (mean = 0.55 ± 0.01 mg L-1). Approximately 10%, 1.3% and 0.06% children are at risk for dental decay, dental fluorosis and skeletal fluorosis, respectively. Probabilistic risks for children were assessed and the fluoride endemic areas were marked by GIS mapping system. On several water consumption points, the hazard quotient (HQ) values for children were higher than 1, indicating potential non-cancer health risks due to fluoride exposure. The results of this study will help governmental agencies to develop better policies for protecting children from exposure to fluoride.

Proteomic analysis of the effects of tumor necrosis factor-? on endothelial cells / 中国病理生理杂志

AIM: To investigate the affected proteins by tumor necrosis factor (TNF)-? in endothelial cells, and further explore the potential molecular mechanism of TNF-? on endothelial cells. METHODS: Nitric oxide (NO) production in the cultured human umbilical vein endothelial cells (HUVECs) was measured by a NO assay kit. Proteomic alterations were analyzed using two-dimensional electrophoresis, and peptide mass fingerprinting with matrix-assisted laser desorption/ionization-time of flight mass spectrometry. RESULTS: NO production in HUVECs decreased significantly after TNF-? treatement. Proteomics analysis showed 21 protein spots were changed including 9 spots that were increased and 11 spots that were decreased after TNF-? stimulation, and 1 spot was only detected in TNF-? activated cell gels. CONCLUSIONS: The decreased expression of ecNOS by TNF-? might result in decrease in NO production. Up-regulated MAP/ERK kinase 3 expression might imply that TNF-? activates the expression of adhesion molecules. Cytoskeletal protein actin is also involved in TNF-? injuried HUVECs. Proteomic analysis can find some clues for identifying new potential target of TNF-?. [