Objective To explore the effect of collaborative health education by both doctors and nurses on parturition?Methods One hundred and sixty primiparas at uterogestation undergoing analgesic parturition were assigned equally into the control and observation groups according to their admission sequence? The control group received routine nursing intervention and the observation group the collaborative health education by both doctors and nurses? The two groups were compared in terms of analgesic effect,vaginal delivery and post-partum hemorrhage? Result The rates of analgesic delivery and vaginal delivery in the observation group were significantly higher and the volume of postpartum hemorrhage was significantly smaller than those of the control group(all P < 0?05)?Conclusion The collaborative health education may be effective in alleviating mental stress of the preimiparas,enhancing the analgesic effect,increasing the rate of vaginal delivery and decreasing the volume of postpartum hemorrhage?

[Summary] To explore the mRNA expression of insulin-like growth factor-Ⅰ (IGF-Ⅰ),extracellular signal regulated kinase (ERK),and glucose transporter 4 (GLUT4) in greater omental adipose tissue of patients with metabolic syndrome and colorectal cancer.The mRNA expression of IGF-Ⅰ,ERK,and GLUT4 in greater omental adipose tissue of the subjects was measured by RT-PCR.(1) The mRNA expression level of IGF-Ⅰ and ERK in the metabolic syndrome group was significantly higher than that in the control group (P＜0.01),while in colorectal cancer subgroup the expression was significantly higher than that in the non-colorectal cancer subgroup (P＜ 0.01).The expression of GLUT4 was obviously lowered (P＜0.01).(2) The expression of ERK was positively correlated with that of IGF-Ⅰ (r =0.608,P＜0.01).The fasting insulin was positively correlated with the expression of ERK and IGF-Ⅰ(r =0.538,0.439,P ＜ 0.01),and negatively with that of GLUT4 (r =-0.457,P ＜ 0.01).There may be relationship between ERK plus IGF-Ⅰ and metabolic syndrome complicated with colorectal cancer.The lowered GLUT4 expression may be related to insulin resistance in metabolic syndrome.

Purpose: Four and a half LIM protein 1 (FHL1) is involved in breast cancer (BC) development, but the regulatory mechanism involved remain unclear. In the present study, we examined the role of FHL1 in BC development. Methods: The expression of FHL1, miR-183-5p, and miR-96-5p in BC tissues was analyzed using StarBase analysis. FHL1 expression in BC tissues, a normal human breast epithelial cell line, and BC cell lines was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The relationship between FHL1 and miR-183-5p/miR-96-5p was analyzed via Pearson's rank correlation, TargetScan, and a dual-luciferase reporter assay. BT549 and MDA-MB-231 cells were transfected with either FHL1 and miR-183-5p mimics, or siFHL1 and a miR-183-5p inhibitor, respectively. The viability, colony number, migration, invasion, and tube length of BT549 and MDA-MB-231 cells were examined using cell counting kit-8, colony formation, wound-healing, Transwell, and tube formation assays, respectively. The levels of FHL1, vascular endothelial growth factor (VEGF), p53, E-cadherin, N-cadherin, and vimentin were quantified using western blotting and qRT-PCR. Results: FHL1 expression was downregulated in BC tissues and cells, whereas miR-183-5p and miR-96-5p were upregulated in BC tissues (negative correlation with FHL1 expression).FHL1 overexpression inhibited the viability, colony number, migration, and invasion of BC cells and the expression of VEGF, N-cadherin, and vimentin, and increased the expression of FHL1, p53, and E-cadherin in BT549 cells. Furthermore, a miR-183-5p mimic reversed these effects of FHL1 overexpression, whereas FHL1 silencing caused opposite results to those observed in MDA-MB-231 cells; however, this was reversed by a miR-183-5p inhibitor. Conclusion Our study suggests that miR-183-5p promotes cell proliferation, metastasis, and angiogenesis by negatively regulating FHL1 in BC.