Iron parameters in pregnant women with beta-thalassaemia minor combined with iron deficiency anaemia compared to pregnant women with iron deficiency anaemia alone demonstrate the safety of iron supplementation in beta-thalassaemia minor during pregnancy.

In patients with beta-thalassaemia intermedia or major, hepcidin induces iron overload by continuously promoting iron absorption. There have been no studies in pregnant women with beta-thalassaemia minor combined with iron deficiency anaemia (IDA), examining whether hepcidin is inhibited by GDF15, as may occur in patients with beta-thalassaemia intermedia or major, or whether the iron metabolism characteristics and the effect of iron supplementation are consistent with simple IDA in pregnancy. We compared and analysed routine blood parameters, iron metabolism parameters, the GDF15 levels, and the hepcidin levels among four groups, namely the beta-thalassaemia (ß) + IDA, ß, IDA, and normal groups. In addition, the ß + IDA and IDA groups received iron supplementation for four weeks. We found no statistically significant correlation between hepcidin and GDF15 in any group, but a positive correlation was observed between hepcidin and ferritin. After iron supplementation, the routine blood parameters and iron metabolism parameters in the ß + IDA group were improved, and the hepcidin content was significantly increased. These results suggest that in pregnant women with beta-thalassaemia minor, hepcidin functions normally to maintain iron homeostasis, and that iron supplementation is effective and safe.

Claudin 10 acts as a novel biomarker for the prognosis of patients with ovarian cancer.

Ovarian cancer (OC) is one of the most fatal gynecological malignancies in the world and confers a poor 5-year survival rate. The present study was designed to discover novel prognostic markers for patients with OC in order to estimate disease metastasis or recurrence. Based on the large cohorts of transcriptome data from multicenter sources, a comprehensive analysis was performed to explore potential prognostic markers. A total of 269 differentially expressed genes were identified, of which 32 were upregulated and 237 downregulated in OC tissues compared with the corresponding expression in normal tissues. Kaplan-Meier analysis, log-rank test and nomogram analysis were employed to demonstrate that low expression levels of claudin 10 (CLDN10) were associated with a less favorable disease prognosis. The most promising prognostic marker for OC was subsequently selected. Additionally, the prognostic nomogram was constructed in order to assess the 5-year survival rate using CLDN10 expression as a prognostic marker for OC. Furthermore, gene set enrichment analysis and analysis of the tumor-associated competing endogenous RNA network were performed to elucidate the potential biological processes associated with CLDN10 expression. The current results indicated that CLDN10 may influence OC progression via transforming growth factor-ß (TGF-ß)- or WNT/ß-catenin-induced epithelial-to-mesenchymal transition (EMT). The associations among CLDN10, microRNA-486-5p, TGF-ß, WNT/ß-catenin and EMT should be further investigated in future studies.

[Effect of serum restriction on insulin like growth factor-1 expressions and invasiveness in human trophoblast HTR-8/SVneo cells in vitro].

OBJECTIVE: To explore the effect of serum restriction on the invasiveness and expressions of insulin-like growth factor-1 (IGF-1) and matrix metalloproteinase-2 (MMP-2) in human trophoblast HTR-8/SVneo cells in vitro. METHODS: HTR-8/SVneo cells were cultured in the presence of 1%, 5%, or 10% fetal bovine serum (FBS) for 48 h. Fluorescence quantitative PCR and immunofluorescence staining were employed to examine the changes in IGF-1 and MMP-2 expressions at both the mRNA and protein levels in HTR-8/SVneo cells; MTT assay and Transwell invasion assay were used to assess the changes of the cell proliferation and the cell invasion ability, respectively. MMP-2 expression, cell proliferation and invasiveness were also assessed in the cells treated with recombinant human IGF-1. RESULTS: HTR-8/SVneo cells exhibited significantly lowered cell proliferation in cultures containing low concentrations of FBS (P<0.05). The expressions of IGF-1 and MMP-2 at both mRNA and protein levels were significantly down-regulated and the invasiveness was significantly lowered in cells cultured in the medium containing 1% FBS as compared with those of cells cultured in the presence of 5% and 10% FBS (P<0.05). Treatment of the cells with recombinant human IGF-1 significantly up-regulated MMP-2 expression (P<0.05) and increased the cell invasiveness (P<0.05). CONCLUSIONS: FBS restriction down-regulates IGF-1 expression in human trophoblast HTR-8/SVneo cells and suppress the cell invasiveness possibly by suppressing MMP-2 expression. Treatment with recombinant human IGF-1 can up-regulate MMP-2 expression and promote the invasiveness of HTR-8/SVneo cells.