Objective To explore the effect of artificial femoral head replacement and total hip arthroplasty in treatment of elderly femoral neck fractures. Methods From January 2012 to December 2013 in our hospital 100 cases patients with elderly femoral neck fractures were selected according to the different treatment methods and were randomly divided into two groups, 50 cases in each group, The observation group patients treated with artificial femoral head replace-ment, the control group underwent total hip arthroplasty, the hip function recovery, two groups of patients with operation time, bleeding volume, postoperative drainage volume, duration of hospitalization and early or long-term complications were compared. Results The excellent and good rate of the observation group after treatment was 80.0%, was significantly lower than the control group after treatment (98.0%), the difference was statistically significant (P<0.05). The operative time, hospitalization in observation groups were shorter than the control group, the difference was statistically significant (P<0.05). The bleeding volume, postoperative drainage volume in observation group were significantly less than the control group, there was significant statistical difference (P<0.01). Early complications incidence rate of two groups had no significant statistical difference (10.0% vs 12.0%,P>0.05), long-term complications incidence rate of obser vation group was higher than that of the control group, the difference was statistically significant(12.0%vs 4.0%, P<0.05). Conclusion Artificial femoral head replacement and total hip have their own advantages in treatment of femoral neck fracture, arthroplasty, but the comprehensive effect, artificial femoral head replacement have the advantages of shorter operation time, less trauma, the long-term results after total hip replacement is superior to the artificial replacement of the femoral head, and no acetabular wear and other complications, total hip arthroplasty has certain advantages than ar-tificial femoral arthroplasty.

BACKGROUND: Metastasis is the main cause of tumor-associated death and mainly responsible for treatment failure of breast cancer. Autophagy accelerates tumor metastasis. In our work, we aimed to investigate the possibility of microRNAs (miRNAs) which participate in the regulation of autophagy to inhibit tumor metastasis. METHODS: MiRNA array and comprehensive analysis were performed to identify miRNAs which participated in the regulation of autophagy to inhibit tumor metastasis. The expression levels of miR-3653 in breast cancer tissues and cells were detected by quantitative real-time polymerase chain reaction. In vivo and in vitro assays were conducted to determine the function of miR-3653. The target genes of miR-3653 were detected by a dual luciferase reporter activity assay and Western blot. The relationship between miR-3653 and epithelial-mesenchymal transition (EMT) was assessed by Western blot. Student's t -test was used to analyze the difference between any two groups, and the difference among multiple groups was analyzed with one-way analysis of variance and a Bonferroni post hoc test. RESULTS: miR-3653 was downregulated in breast cancer cells with high metastatic ability, and high expression of miR-3653 blocked autophagic flux in breast cancer cells. Clinically, low expression of miR-3653 in breast cancer tissues (0.054 ± 0.013 vs . 0.131 ± 0.028, t  = 2.475, P  = 0.014) was positively correlated with lymph node metastasis (0.015 ± 0.004 vs . 0.078 ± 0.020, t  = 2.319, P  = 0.023) and poor prognosis ( P  < 0.001). miR-3653 ameliorated the malignant phenotypes of breast cancer cells, including proliferation, migration (MDA-MB-231: 0.353 ± 0.013 vs . 1.000 ± 0.038, t  = 16.290, P  < 0.001; MDA-MB-468: 0.200 ± 0.014 vs . 1.000 ± 0.043, t  = 17.530, P  < 0.001), invasion (MDA-MB-231: 0.723 ± 0.056 vs . 1.000 ± 0.035, t  = 4.223, P  = 0.013; MDA-MB-468: 0.222 ± 0.016 vs . 1.000 ± 0.019, t  = 31.050, P  < 0.001), and colony formation (MDA-MB-231: 0.472 ± 0.022 vs . 1.000 ± 0.022, t  = 16.620, P  < 0.001; MDA-MB-468: 0.650 ± 0.040 vs . 1.000 ± 0.098, t  = 3.297, P  = 0.030). The autophagy-associated genes autophagy-related gene 12 ( ATG12 ) and activating molecule in beclin 1-regulated autophagy protein 1 ( AMBRA1 ) are target genes of miR-3653. Further studies showed that miR-3653 inhibited EMT by targeting ATG12 and AMBRA1 . CONCLUSIONS Our findings suggested that miR-3653 inhibits the autophagy process by targeting ATG12 and AMBRA1 , thereby inhibiting EMT, and provided a new idea and target for the metastasis of breast cancer.
Cell Line, Tumor ; Epithelial-Mesenchymal Transition/genetics* ; MicroRNAs/metabolism* ; Autophagy/genetics* ; Genes, Regulator ; Gene Expression Regulation, Neoplastic/genetics* ; Cell Proliferation/genetics* ; Cell Movement/genetics* ; Neoplasms/genetics*