RESUMEN
Objective@#To analyze heavy metal health risks of direct drinking water in primary and secondary schools in Huangpi District, Wuhan, so as to provide reference basis for ensuring drinking water safety of teachers and students.@*Methods@#Cadmium (Cd), Plumbum (Pb) and arsenic (As) in water samples from primary and secondary schools were detected in accordance with the GB/T 5750-2006 "Standard Examination Methods for Drinking Water", water quality was evaluated based on the Quality Standard for Fine Drinking Water(CJ 94-2005). Health risk assessment model was used to evaluate the potential risk of heavy metals in direct drinking water in primary and secondary schools.@*Results@#The unqualified rates of Pb, Cd and As were 0.95%, 1.22% and 0 in 66 primary and secondary schools in Huangpi District, Wuhan. The risk of noncarcinogens related to the direct drinking water of heavy metals (Pb, Cd, As) were less than 1. The range of carcinogenic risks related to the direct drinking water was within the range of 1.07×10 -8 /year -5.58×10 -6 /year which were both within the acceptable level.@*Conclusion@#Concentrations of cadmium, plumbum and arsenic were not found to be significantly elevated as compared to "Quality Standard for Fine Drinking Water" in Huangpi District of Wuhan. Pb and Cd slightly exceeded the standard, with no significant health risk. Water quality and health risk assessment should be strengthened to ensure the safety of drinking water for teachers and students.
RESUMEN
Ischemic heart disease (IHD) is one of the leading causes of death worldwide. C-type lectin domain family 3 member B (CLEC3B) is a C-type lectin superfamily member and is reported to promote tissue remodeling. The serum levels of CLEC3B are downregulated in patients with cardiovascular disease. However, the molecular mechanisms of CLEC3B in IHD is not well-characterized. Therefore, we overexpressed CLEC3B and silenced CLEC3B in H9c2 rat cardiomyocytes for the first time. We then constructed a model of IHD in vitro through culturing H9c2 cardiomyocytes in serum-free medium under oxygen-deficit conditions. Then, Cell Counting Kit-8 (CCK-8), flow cytometry, qRT-PCR, and western blot assays were performed to investigate cell viability, apoptosis, and expression levels of CLEC3B, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), phosphorylated Akt (p-Akt), and cleaved-caspase 3. We observed that the mRNA expression of CLEC3B was decreased in hypoxic H9c2 cardiomyocytes (P<0.05). Overexpression of CLEC3B increased cell viability (P<0.01), inhibited cell apoptosis (P<0.05), upregulated the levels of p-PI3K/PI3K and p-Akt/Akt (P<0.01 or P<0.05), and downregulated expression of cleaved-caspase 3 (P<0.001) in hypoxic H9c2 cardiomyocytes while silencing of CLEC3B caused the opposite results. Inhibition of the PI3K/Akt pathway reversed the protective effect of CLEC3B on hypoxic H9c2 cardiomyocytes. Our study demonstrated that CLEC3B alleviated the injury of hypoxic H9c2 cardiomyocytes via the PI3K/Akt pathway.