AIM:Vascular smooth muscle cell (SMC) proliferation and migration from the arterial wall media into the intima are believed to play a critical role in the pathogenesis of restenosis. Several studies have demonstrated that phosphothioate (PS) oligodeoxynucleotides targeted against genes involved in SMC proliferation inhibits in vitro SMC proliferation and migration. However, the therapeutic effect of antisense ODN on the individual who receives the treatment of delivery of the agent depends on the efficacy of this agent in great degree. We investigated the inhibition effect of a novel agent, insulin-antisense-c-myb-PS-ODN on SMC proliferation in vitro.　METHODS：The rat aortic artery SMCs were cultured in Dulbecco's modified Eagel's medium. The passage 8 to 13 were used as the experiment. Cell surface receptor binding assay was quantified through counting gamma particles emitted from 125　　　　I labeled insulin. SMC rapid proliferation was brought by stimulation of high concentration of fetal bovine serum (FBS). The novel agent of insulin conjugated to the antisense-c-myb-PS-ODN was obtained via incubation of both in condition of certain reagents, pH, temperature, and ion concentration. The characterization and purification of the agent was performed through HPLC. Inhibition of SMC proliferation was reflected by incorporation rate of trillium labeled thymidine deoxyribonucleotide.RESULTS：The binding efficacy of insulin to the receptor was remarkably increased in SMC cultured in supplement of 20% FBS. The inhibition effect of conjugator insulin-c-myb-antisense-PS-ODN was stronger than that of the simple c-myb-antisense-PS-ODN. The inhibition rate of conjugator and simple form on SMC proliferation were 48.34% and 29.54%, respectively. CONCLUSION：The binding efficacy and specificity of c-myb-antisense-PS-ODN to SMC may be enhanced by the insulin receptor mediation through the insulin-insulin receptor interaction. The insulin-receptor targeted method may be a potential and specific therapeutic pathway for restenosis.

Objective:To learn about the iodine nutrition level and its spatial distribution status in key populations in Hubei Province, so as to provide a basis for adjustment of iodine supplementation policy and the realization of scientific and accurate iodine supplementation.Methods:In 2020, a sampling was carried out in Hubei Province according to the "National Iodine Deficiency Disorders Monitoring Plan (2016 Edition)" to monitor the concentration of salt iodine and urinary iodine of key populations (children ages 8 - 10 years old and pregnant women). The spatial distribution of iodine nutrition levels was analyzed by spatial epidemiology.Results:The median salt iodine of 17 263 children's family salt samples was 25.0 mg/kg, and the median urinary iodine (MUI) was 217.0 μg/L. There was significant spatial aggregation in the distribution of urinary iodine level in children at the county level ( Moran's Index = 0.36, P < 0.001). The significant hot spot areas with high urinary iodine level among children were located in Shiyan City and Xiangyang City, while the significant cold spot areas with low urinary iodine level were mainly concentrated in Yichang City. The median salt iodine of 8 618 pregnant women's family salt samples was 25.1 mg/kg, the MUI was 176.3 μg/L. The urinary iodine level among pregnant women at the county level was spatially clustered ( Moran's Index = 0.22, P = 0.003) . The significant hot spot areas with high urinary iodine level among pregnant women were mainly in Enshi Tujia and Miao Autonomous Prefecture, the significant cold spot areas were mainly concentrated in Yichang City. Conclusions:In 2020, the iodine nutrition of children in Hubei Province is at a super appropriate level (200 - 299 μg/L), and the iodine nutrition status of pregnant women is more sensitive, which is close to the lower limit of the appropriate level (150 μg/L). The urinary iodine level of children and pregnant women has significant spatial aggregation at the county level. Targeted intervention will be needed in counties (dictricts) where the urinary iodine level is lower or higher than the normal range, to achieve accurate and scientific iodine supplementation.

Esophageal carcinoma is a malignant disease with a high incidence rate and poor prognosis. The mitochondrial apoptosis pathway plays a pivotal role in the regulation of cell death and has become a focal point in current cancer therapeutics research. Various active components from traditional Chinese medicine （TCM） can target the mitochondrial apoptosis pathway to inhibit esophageal carcinoma， presenting as potential therapeutic agents for this disease. This paper summarizes relevant research on the inhibition of esophageal carcinoma by active components in TCM via targeting the mitochondrial apoptosis pathway. It has been found that flavonoids （casticin， icariin， luteolin， kaempferol， hesperetin， deguelin， etc.）， terpenoids （oridonin， Jaridonin， artesunate， ethyl acetate fraction of pleurotus ferulatus triterpenoid， etc.）， alkaloids （matrine， swainsonine， etc.）， polyphenols （curcumin， epigallocatechin-3-gallate， corilagin， etc.）， steroids （α-hederin， polyphyllin Ⅵ， etc.）， phenols （optimized scorpion venom peptide CT-K3K7， gecko active polypeptide， etc.）， volatile oils （cinnamaldehyde， α -asarone， etc.） and other active components from TCM can target the intrinsic mitochondrial apoptosis pathway， induce apoptosis in esophageal carcinoma cells， and inhibit their proliferation， invasion and migration by regulating oxidative stress， blocking the cell cycle， regulating signaling pathways such as PI3K/Akt and MAPK.