RESUMEN
Background: Maternal education is one of key factors affecting nurturing environment which significantly impacts children's height levels throughout their developmental stages. However, the influence of maternal education on children's height is less studied. This study aims to investigate the dynamic influence of maternal education on children's height among Chinese children aged 0-18 years. Methods: Children undergoing health examinations from January 2021 to September 2023 were included in this study. Clinical information including height, weight, maternal pregnancy history, blood specimens for bone metabolism-related indicators and maternal education level was collected. Children's height was categorized into 14 groups based on age and gender percentiles, following WHO 2006 growth standards. One-way analysis of variance (ANOVA), linear regression, chi-square test and Fisher's exact test were applied for data analysis. Results: A total of 6269 samples were collected, including 3654 males and 2615 females, with an average age of 8.38 (3.97) for males and 7.89 (3.55) for females. Significant correlations between maternal education level, birth weight, birth order, weight percentile, vitamin D, serum phosphorus, alkaline phosphatase levels, and children's height were identified. Birth weight's influence on height varied across age groups. Compared with normal birth weight children, low birth weight children exhibited catch-up growth within the first 6 years and a subsequent gradual widening of the height gap from 6 to 18 years old. Remarkably, the impact of maternal education on height became more pronounced among children above 3-6 years old, which can mitigate the effect of low birth weight on height. Conclusion: We found that weight percentile, birth weight, birth order, bone marker levels, and maternal education level have significant effect on height. Maternal education attenuates the impact of low birth weight on height. The findings indicated that maternal education plays a consistent and critical role in promoting robust and healthy growth.
RESUMEN
AIM: To explore the role of RPL38 on proliferation and apoptosis of gastric cancer cells by regulating miR-374b-5p/VEGF signal pathway. METHODS: qRT-PCR was used to measure the expression of RPL38. CCK8 assay, Matrigel invasion assay, and flow cytometry were used to detect the role of RPL38in MKN-45 cells. Western blot was used to measure the protein expression of VEGF, p-ERK, ERK, p-AKT, AKT in cells. Dual-luciferase assay was performed to verify the relationship between miR-374b-5p and RPL38, miR-374b-5p and VEGF. RESULTS: In our research, we found that RPL38 was upregulation in gastric cancer, loss function of RPL38 could inhibit MKN-45 cell proliferation and invasion, accompany with increasing apoptosis. Then, we verified that RPL38 could interact with miR-374b-5p by performed luciferase assay, there was a negative correlation between RPL38 and miR-374b-5p. Furthermore, we observed that VEGF is a potential target of miR-374b-5p, miR-374b-5p negatively regulated the expression of VEGF, and effected ERK/AKT signal pathways. Next, we found that miR-374b-5p inhibitor or overexpression of VEGF could prevent the anti-tumor function of si-RPL38. CONCLUSION: Knockdown of RPL38 inhibits the proliferation and apoptosis of gastric cancer via miR-374b-5p/VEGF signal pathway.
