Objective To improve the therapeutic effects and to prevent the recurrence of the blepharoptosis. Methods The frontalis muscle was cut to form the ladder shaped frontalis muscle flaps, which was than were transferred under the orbicularis to touch the tarsus with its broad lower part perfectly. The flap was sutured with the tarsus directly. Results All blepharoptosis of twenty four eyes in sixteen patients were treated with excellent results in function and cosmetic appearance. The upper eyelids could be closed effectively. There were no any recurrence and complications in this group. Conclusions The transfer of the ladder shaped frontalis muscle flaps applied in this group benefits the moving of upper eyelid because of its effectiveness in contraction and stable suture with the tarsus. It is more suitable for the treatment of severe blepharoptosis.

Objective: To investigate the effect of long-chain non-coding RNA AL117378.1 on the proliferation and invasion of bladder cancer cells. Methods: From August 2016 to December 2017, the tumor tissues and adjacent tissues of 14 patients with bladder cancer treated by Huangshi Central Hospital of Edong Healthcare Group were selected. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of AL117378.1 in 14 pairs of bladder cancer tissues and corresponding adjacent tissues, bladder cancer cell lines (5637, J82, T24, BIU-87) and corresponding human bladder normal epithelial cells (SV-HUC-1). The negative control plasmid (control group) and the plasmid carrying the AL117378.1 (experimental group) were transfected into the bladder cancer cell line with the lowest expression level. qRT-PCR was used to detect the expression levels of AL117378.1 and non-receptor protein tyrosine phosphatase 9 (PTPN9) mRNA in the transfected cells. The expression levels of PTPN9, E-cadherin, α-SMA, CDK4 and Cyclin A2 protein were detected by Western blotting. MTT assay and Transwell invasion assay were used to detect the cell proliferative capacity and invasive ability of the two groups. Measurement data were expressed as mean± standard deviation(Mean±SD), and comparison between groups used independent sample t test. Results: The expression of AL117378.1 in bladder cancer tissues was lower than that in adjacent tissues (P<0.01). The expression of AL117378.1 in bladder cancer cell lines was lower than that in human bladder normal epithelial cells (P<0.01), and the expression level of AL117378.1 was the lowest in J82 cells (P<0.01). The expression levels of AL117378.1 in the control and experimental groups were 1.02 ± 0.11 and 7.96 ± 1.06, respectively, and the difference was statistically significant (t=6.51, P<0.01). The expression of PTPN9 mRNA was 1.01 ± 0.08 and 4.99 ± 0.50, respectively. the difference was statistically significant (t=7.84, P<0.01). Western blotting results showed that the expression of PTPN9 and E-cadherin increased, and the expression of α-SMA, CDK4 and Cyclin A2 decreased. MTT experiments showed that the proliferation of cells transfected with AL117378.1 was significantly decreased (P<0.05). Transwell invasion experiments showed that the number of invasive cells in the control group and the experimental group were 97.96±13.71 and 38.02±7.51, respectively, and the difference was statistically significant (t=3.84, P<0.01). Conclusions The expression of AL117378.1 was significantly decreased in bladder cancer tissues and cell lines (5637, J82, T24, BIU-87). AL117378.1 can significantly inhibit the proliferation and invasion of bladder cancer cells by positively regulating the expression of PTPN9 gene.

Objective:To observe the expression of long non-coding RNA (lncRNA) PEBP1P2 in renal cell carcinoma (RCC) tissues and its effect on the proliferation and migration of RCC cells.Methods:The expression of PEBP1P2 in 51 RCC tissues and RCC cell lines was detected by real-time quantitative polymerase chain reaction (qPCR). The A498 cells with the lowest expression of PEBP1P2 were transfected, and the cells transfected with PEBP1P2 plasmid were used as the PEBP1P2 group, and the cells transfected with the negative control plasmid were used as the NC group. qPCR was used to detect the expression of PEBP1P2 in the two groups of cells. MTT assay and Transwell migration assay were used to detect the proliferation and migration ability of RCC cells. qPCR and Western blotting were used to detect the expression of caspase recruitment domain family member 10 ( CARD10) gene and NF-κB pathway protein, respectively. Measurement data were expressed as mean±standard deviation ( Mean± SD), and LSD- t test was used for comparison between groups. Results:The expression of PEBP1P2 in RCC tissues was lower than that in adjacent tissues ( t=4.89, P<0.01). The expression of PEBP1P2 in RCC cells was lower than that in normal renal tubular epithelial cells ( P<0.01). The expression of PEBP1P2 in A498 cells of the PEBP1P2 group and NC group was (11.01±1.26) and (1.06±0.19), respectively, and the PEBP1P2 group was significantly higher than that in the NC group ( t=7.81, P<0.01). Overexpression of PEBP1P2 significantly inhibited the proliferation of RCC cells ( P<0.05) and migration ability ( t=3.65, P<0.05). Overexpression of PEBP1P2 significantly suppressed the expression of CARD10 gene in RCC A498 cells ( t=6.83, P<0.01) and inhibited the transduction of NF-κB signaling pathway proteins. Conclusions:PEBP1P2 expression was significantly decreased in RCC tissues. Overexpression of PEBP1P2 significantly inhibited the proliferation and migration of RCC A498 cells. Its molecular mechanism is that PEBP1P2 down-regulates CARD10 gene expression and inhibits NF-κB signaling pathway.

Objective:To investigate the expression of long non-coding RNA (lncRNA) COX10-AS1 in renal cell carcinoma tissues and cell lines and its effect on proliferation and migration of renal cancer cells.Methods:Fluorescence real-time quantitative PCR (qRT-PCR) was used to detect the expression of COX10-AS1 in surgical specimens that have been diagnosed as renal cancer tissues and adjacent tissues by pathology, renal cancer cell lines (786-O, CaKi-1, A498, ACHN) and normal renal tubular epithelium cell line (HK-2). The ACHN cells with the lowest expression were divided into a control group (transfected with a negative control plasmid carrying nonsense sequences) and an experimental group (transfected with a plasmid carrying COX10-AS1 sequences). The expression level of COX10-AS1 was detected by qRT-PCR in two groups of cells. The proliferation and migration ability of ACHN cells were detected by MTS assay and cell scratch assay. The expression of MFN2 mRNA was detected by qRT-PCR. The expressions of MFN2 and Ras-NF-κB signaling pathway proteins were detected by Western blotting. The measurement data were expressed as mean±standard deviation ( Mean± SD), the comparison between the two groups used the t-test, and the comparison among multiple groups adopts the one-way analysis of variance. Results:The expression of COX10-AS1 in renal cell carcinoma was significantly lower than that in adjacent tissues ( P<0.01), The expression of COX10-AS1 in renal cell carcinoma cells was significantly lower than that in renal tubular epithelial cells ( P<0.05), the expression of COX10-AS1 was the lowest in ACHN cells( P<0.01), the above differences were statistically significant compared with the control group, the expression of COX10-AS1 in ACHN cells of experimental group was significantly increased ( P<0.01), the above differences were statistically significant compared with the control cells, the proliferation of ACHN cells in the experimental group was significantly decreased ( P<0.05), and the cell migration ability was significantly decreased ( P<0.01). Compared with the control cells, the expression of MFN2 mRNA in ACHN cells of experimental group was significantly increased ( P<0.01). The expression levels of MFN2 were significantly up-regulated ( P<0.01), and Ras-NF-κB signaling pathway proteins were significantly down-regulated ( P<0.05), the above differences were statistically significant. Conclusions:The expression of COX10-AS1 is decreased in renal cell carcinoma tissues and cell lines. COX10-AS1 may inhibit the proliferation and migration of ACHN cells by promoting the expression of MFN2 gene.