Objective:To analyze the iodine content distribution of drinking water in Jingdezhen City, and master the status of prevention and control of iodine deficiency disorders (IDD), so as to provide a basis for adopting targeted control measures and scientific adjustment of control and prevention strategies.Methods:According to the "National Iodine Deficiency Disorders Surveillance Program" and the "National Water Iodine Content Survey Program for Drinking Water", the surveillance of IDD in Jingdezhen City was carried out from 2017 to 2020. Household edible salt samples from pregnant women and students aged 8 to 10 were collected to detect salt iodine content, and urine samples were collected to detect urinary iodine. Thyroid volume of students was measured by B-ultrasonography, and the rate of goiter was calculated. In 2017, the iodine content of drinking water in Jingdezhen City was investigated, and the results were analyzed.Results:From 2017 to 2020, a total of 1 800 students were examined for thyroid gland, and 11 students were found to have goiter, with an goiter rate of 0.61%. A total of 3 201 edible salt samples and 3 201 urine samples were collected from students, the median of salt iodine was 24.96-26.40 mg/kg, the consumption rate of qualified iodized salt was 98.50%-99.50%, and the median of urinary iodine was 172.56-218.35 μg/L. A total of 1 600 edible salt samples and 1 600 urine samples were collected from pregnant women, the median of salt iodine was 24.40-25.38 mg/kg, the consumption rate of qualified iodized salt was 97.25%-98.00%, and the median of urinary iodine was 161.55-205.60 μg/L. In 2017, a total of 667 water samples were collected from 52 villages and towns in 4 counties and districts. The median of water iodine of the 4 counties and districts was 0.6-3.2 μg/L, and that of the 52 villages and towns was 0.3-12.3 μg/L.Conclusions:The iodine nutrition level of students and pregnant women in Jingdezhen City is generally at an appropriate level, but the iodine content of drinking water is low. It is suggested to strengthen the health education and health promotion of IDD among key population, guide the residents to supplement iodine scientifically, and continuously eliminate the harm of IDD.

BACKGROUND:Hyperhomocysteinemia is closely related to the function of islet β cells,but its specific molecular mechanism is not fully understood. OBJECTIVE:To investigate the role of N6 methyltransferase-like 3(METTL3)in homocysteine(Hcy)-induced autophagy of mouse islet β cells. METHODS:The 3rd and 4th generation mouse islet β cells were taken for the experiment.(1)Cell modeling and grouping:cells in control group were not treated with Hcy,while those in homocysteine group were treated with 100 μmol/L Hcy for 48 hours.(2)The mouse islet β-cells were transfected with the plasmids overexpressing Ad-METTL3 and si-METTL3 according to the instructions of LipofectamineTM 2000.Three different interfering fragments were designed,and the one with the best interfering efficiency was verified and screened by PCR.(3)After transfection,the cells were divided into control group,Hcy group,Ad-NC(negative control)+Hcy group,Ad-METTL3+Hcy group,si-NC(negative control)+Hcy group and si-METTL3+Hcy group.(4)qRT-PCR and western blot were used to detect the expression levels of METTL3 and autophagy-related proteins LC3Ⅱ/Ⅰ and p62 in cells.Insulin level was determined by ELISA to evaluate insulin secretion capacity of islet cells.Autophagy-related proteins and insulin level were detected after overexpression and interference with METTL3. RESULTS AND CONCLUSION:Compared with the control group,the expression level of LC3Ⅱ/Ⅰ was increased(P＜0.05),the expression of p62 was significantly reduced(P＜0.05),and the insulin secretion capacity was significantly decreased(P＜0.05)in the Hcy group.Compared with the control group,the protein and mRNA levels of METTL3 were reduced in the Hcy group(P＜0.05).After METTL3 silencing in islet β cells,Hcy further upregulated the expression of LC3Ⅱ/Ⅰ(P＜0.05),significantly dowregulated the expression of p62(P＜0.05),and increased the insulin level(P＜0.05).After overexpression of METTL3,Hcy significantly decreased the LC3Ⅱ/Ⅰ expression and increased the p62 expression in islet β cells(P＜0.05).To conclude,METTL3 is involved in the Hcy-induced autophagy regulation of islet β cells and plays a role in the regulation of insulin secretion.

Objective To study the role of ubiquitin-conjugating enzyme 9(UBC9)in the pyroptosis of homocysteine-induced macrophages mediated by small ubiquitin-like modifier(SUMO)modification.Methods First,the effects of homocysteine at different concentrations(0 μmol/L,50 μ.mol/L,100 μmol/L,150 μmol/L and 200 μmol/L)on the viability and pyrodeath of mouse macrophages(RAW264.7)were detected by CCK-8 and Western blot.Western blot was used to detect the expression levels of UBC9,SUMO-1,and the inflammatory cytokine IL-1β in different groups of cells.qRT-PCR was used to detect the mRNA expression of UBC9 before and after RNA interference and the expression of UBC9,pyrogen-related protein,and SUMO-1 after RNA interference.Results After stimulation with 100 μmol/L homocysteine,the effect of macrophage activity was minimal,and NLRP3 and Caspase-1 were the proteins with the most obvious increase in expression(P＜0.05).Compared with the Control group,the Hcy group's expression of IL-1β and SUMO-1 was increased(P＜0.01).Compared with the Control group,the Hcy group's UBC9 protein and mRNA levels were increased(P＜0.05).The expression of NLRP3,Caspase-1,IL-1β,UBC9,and SUMO-1 was decreased in the si-UBC9+Hcy group compared with the si-NC+Hcy group(P＜0.01).Conclusions Homocysteine induces pyroptosis in macrophages,and its mechanism of action is related to the up-regulation of UBC9 to induce SUMO modification.