Objective To explore the curative effect of knee flexion deformity on spastic cerebral palsy treatment method.Methods All of 30 patients with spastic cerebral and knee flexion deformity were randomly divided into two groups:traditional operation group and modified operation group,using the commonly used operation (In 15 cases,with traditional hamstring post surgery) and) modified operation (In 15 cases,with modified hamstring post surgery),two groups of patients were treated with Ilizarov external fixation drafting device in the correction of knee flexion deformity after soft tissue release.Adjustment began 7 days after the soft tissue release operation of external fixation,and stretched approximately 0.2 degrees each time,3 times/d,until knee flexion deformity was corrected to hyperextension for 10 degree and maintained for 3 weeks,and the flexion contracture degree of knee joint was measured every 2 weeks;then the Ilizarov external fixation drafting device was removed.Then wear a walking straight leg brace for more than 3 months,until the knee walking function is good.Clinical evaluation included the joint pain index,walking function index,knee flexion deformity degree and range of joint motion score of Dimeglio standard.Results Flexion contracture deformity of knee joint in 30 cases (60 knees) was corrected when Ilizarov external fixator was removed,knee extension to 0 degrees-5 degrees.The two groups of patients had the knee flexion angle range of-1.2 degrees to 13.3 degrees,with an average of (7.32°±3.41°) after removed of the walking straight leg brace,in which 4 cases (8 joints) got recurrent deformity of 10°-15° at the time of removing of the walking straight leg brace.Knee activity significantly was improved at the end of treatment.60 cases of knee joint activity were close to normal,with flexion of 100 degrees to 135 degrees,extension of 0 degrees to 10 degrees.Two groups of patients were statistically significantly improved before and after surgery.Curative effect comparison:The walking function index of the modified operation group was obviously superior to that of the traditional operation group,there was significant statistical difference.There were no statistically significant differences in pain index,knee flexion,and range of joint motion.Conclusion For the treatment of flexion deformity of the knee joint in spastic cerebral palsy,traditional surgery using the semitendinosus and gracilis,post and semimembranosus lysis,combined with the Ilizarov draft external fixation could improve the walking function of the patients,simplify the surgical incision and reduce trauma.As a result,modified hamstring post surgery is an ideal,effective treatment method.

Objective:To investigate the roles of N6-methyladenosine (m 6A) modification in regulating RP11-426A6.5 in the development of laryngeal squamous cell carcinoma (LSCC). Methods:The methylation and expression levels of lncRNAs were identified and important lncRNAs were screened utilizing long non-coding RNA (lncRNA) m 6A methylation microarray. Cancer and para cancer tissue samples were taken from 48 LSCC patients hospitalized to the Department of Otolaryngology-Head and Neck Surgery of the Second Affiliated Hospital of Harbin Medical University between January and September 2017. Expression profiling microarray was performed in 3 of 48 LSCC samples, and methylated RNA immunoprecipitation-quantitative PCR (MeRIP-qPCR) and quantitative real-time fluorescent PCR (qRT-PCR) were performed in the remaining 45 LSCC samples to verify the m 6A modification and expression levels of RP11-426A6.5. Correlations between RP11-426A6.5 and clinical factors were anlysed. Laryngeal cancer cell line with low expression of RP11-426A6.5 was created in vitro using RNA interference (RNAi) technology. The 5-Ethynyl-2′-deoxyuridine (EdU) cell proliferation experiment, wound healing experiment, and transwell invasion experiment were used respectively to measure the proliferation, migration, and invasion of LSCC cells. The effect of RP11-426A6.5 down-regulation on the growth of transplanted tumors in vivo was verified by nude mice tumorigenesis assay. The Cancer Genome Atlas (TCGA) database and sequence-based RNA adenosine methylation site predictor (SRAMP) website were used to predict the enzymes and corresponding methylation sites. MazF digestion was chosen to validate the binding sites. RNAi technology was used to observe the changes in cell function after interfering with the expression of the corresponding genes of the modified enzymes. MeRIP-qPCR was used to detect the level of RP11-426A6.5 m 6A cell line treated with actinomycin D was used to observe the stability of RP11-426A6.5. Results:RP11-426A6.5 methylation and expression levels were significantly higher in LSCC tissues than those in paracancerous tissues (methylation levels: 23.828±4.975 vs 20.280±3.607; expression levels: 1.197±0.314 vs 1.015±0.170, all P values<0.05). RP11-426A6.5 expression levels were closely correlated with T stage (T1-2: 1.081±0.298 vs T3-4: 1.306±0.292, χ 2=5.35, P<0.05). The postoperative survival of patients with high RP11-426A6.5 expressions was significantly lower than that of patients with low RP11-426A6.5 expression ( P=0.046). Assays in vitro and in vivo showed that the downregulation of RP11-426A6.5 significantly decreased the proliferation, migration, and invasion abilities of LSCC cells and the growth of transplanted tumors. The binding of methyltransferase-like 3 (METTL3), an m 6A-modified enzyme, to the corresponding methylation site of RP11-426A6.5 enhanced its stability and mediated its regulation of malignant behaviors of LSCC cells. Conclusions:RP11-426A6.5 can regulate the malignant behaviors of LSCC cells, which is mediated by the m 6A modification process involving in the methyltransferase METTL3.