Objective To investigate the effects of different surgical procedures on clinical outcomes and quality of life(QOL)in patients with breast cancer.Methods The clinical data of 93 patients with breast cancer were retrospectively reviewed.According to the different surgical methods,they were divided into two groups:breast conserving surgery(BCS)group(n =42)and modified radical mastectomy(MRM)group(n =51).Clinical outcomes and QOL score between the two groups were compared.Results Compared with MRM group,the incidence rate of complication in BCS group was significantly lower in subcutaneous exudate[7.1%(3 /42)vs.25.5%(13 /51),χ2 =5.443,P =0.020]and upper limb swelling[14.3%(6 /42)vs.37.3%(19 /51),χ2 =5.443,P =0.020].In the aspect of QOL score,BCS group showed significantly higher score in emotional well -being [(23.14 ±2.71)points vs.(19.98 ±2.69)points,t =5.606,P =0.000],functional well -being[(24.61 ±2.72)points vs.(23.18 ± 2.99)points,t =2.372,P =0.020]and total score of QOL[(116.42 ±12.439)points vs.(111.18 ±10.75)points, t =2.147,P =0.034].BCS group showed significantly lower score in self -rating anxiety scale test[(47.89 ±8.32) points vs.(52.46 ±7.38)points,t =2.767,P =0.007].Conclusion Compared with MRM,BCS can effectively decrease the incidence rate of complications and increase the QOL in breast cancer patients.

Infectious disease hospitals are obliged to cope with public health emergencies such as outbreak of infectious diseases.Such hospitals are required to make early detection,early containment,proper management,reasonable preplans,timely training,targeted drills,reasonable deployment of hospital resources,appropriate protection for hospital staff.General hospitals should also cope with prevention and control of infectious diseases to some extent,and work with infectious disease hospitals hand in hand to better cope with such outbreaks.

Objective To explore the clinical significance of long non-coding RNA(lncRNA)VIM-AS5 expres-sion in human breast cancer tissues and its regulatory mechanism involved in cancer cell proliferation and mi-gration.Methods The Lnc2Cancer 3.0 database was used to analyze the expression of VIM-AS5 in breast cancer tissues and its correlation with the clinical stage and survival time of breast cancer patients.RT-qPCR was used to detect the expression of VIM-AS5 in breast cancer cell lines BT-549,MDA-MB-435,MDA-MB-231 and CAL-51.Plasmid with VIM-AS5 overexpression and negative control were all transfected into CAL-51 cells through liposome recorded as VIM-AS5 group and NC group,respectively.The proliferation and migration of CAL-51 cells were detected by colony formation assay and scratch healing method,respectively.Dual-lucif-erase reporter gene experiment verified the targeting relationship between VIM-AS5 and miR-500a.RT-qPCR was used to detect the expression of miR-500a in CAL-51 cells.Western blot was used to detect the expression of JAK/STAT3 pathway in CAL-51 cells.Results The expression of VIM-AS5 in breast cancer tissues was significantly lower than that in adjacent tissues(P＜0.01).VIM-AS5 expression was negatively correlated with the clinical stage of breast cancer patients(P＜0.01).The survival time of breast cancer patients with low VIM-AS5 expression was significantly shorter than that of breast cancer patients with high VIM-AS5 ex-pression(P＜0.01).Compared with mammary epithelial cell line MCF-10 A cells,VIM-AS5 expression was significantly reduced in breast cancer cells(P＜0.01).The counting number of colony formed in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01).The cell migration rate in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01).Dual-luciferase reporter gene experiment confirmed that miR-500a was the target gene of VIM-AS5(P＜0.01).VIM-AS5 can negatively regulate the expression of miR-500a(P＜0.01).Compared with the NC group,the expression of JAK/STAT3 pathway proteins JAK,p-STAT3,c-Myc,Bcl-2,and CDK3 in CAL-51 cells of the VIM-AS5 group were significantly decreased.Conclusions VIM-AS5 is low-expressed in breast cancer cells,and up-regulation of VIM-AS5 may inhibit the proliferation and migration of breast cancer cells CAL-51 by targeting at miR-500a/JAK/STAT3 pathway.

Objective:To observe the expression of microRNA (miRNA, miR)-5787 in breast cancer tissues and various cell lines, analyze the effect of overexpression of miR-5787 on breast cancer cell invasion and proliferation, and explore its possible molecular mechanism.Methods:Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) method was used to detect the expression of miR-5787 in 47 breast cancer tissues and adjacent tissues, 4 breast cancer cell lines and normal breast epithelial cells. Breast cancer cell lines with the lowest miR-5787 expression were selected and transfected with miR-5787 mimics (experimental group) and control NC mimics (control group), respectively. qRT-PCR was used to detect the expression of miR-5787 in cells of the two groups. Transwell invasion experiment and cell counting kit-8 (CCK-8) were used to detect the effect of miR-5787 overexpression on breast cancer cell invasion and proliferation. Bioinformatics software and dual luciferase reporter gene experiments were used to predict and verify the target genes that miR-5787 could complementally bind. qRT-PCR and Western blot were used to detect the expression of target gene mRNA and protein.Results:Compared with adjacent tissues (5.05±0.82), the expression of miR-5787 in breast cancer tissues (1.32±0.33) was significantly reduced ( P<0.01). Compared with normal breast epithelial cells, the expression of miR-5787 in the four breast cancer cell lines was reduced ( P<0.05), and the expression in HCC1937 cells was the lowest ( P<0.01). After transfection of miR-5787 mimics, the expression of miR-5787 in HCC1937 cells in the experimental group was significantly higher than that in the control group ( P<0.01). Overexpression of miR-5787 could inhibit the invasion ( P<0.05) and proliferation ( P<0.05) of breast cancer HCC1937 cells. Bioinformatics software showed that the target gene of miR-5787 might be heparan sulfate proteoglycan 2 (HSPG2), and miR-5787 could complement HSPG2 mRNA ( P<0.01). qRT-PCR and Western blot indicated that overexpression of miR-5787 could significantly inhibit the expression of HSPG2 gene ( P<0.01), with the decreased expression of Vimentin, N-cadherin, Ki67 and PCNA. Conclusions:miR-5787 expression was low in breast cancer tissues and cell lines. Overexpression of miR-5787 could inhibit the invasion and proliferation of breast cancer HCC1937 cells by interfering with the expression of HSPG2 gene.