Objective To analyze and assess the postoperative motor function in children with spastic cerebral palsy (SCP) by surface electromyography (sEMG) and joint angle. Methods Sixteen children with SCP were involved in this study. The sEMG of rectus femoris, biceps femoris, semitendinosus, tibialis anterior, lateral gastrocnemius and medial gastrocnemius muscles and joint angles of the hip, knee and ankle during straight walking were collected preoperatively and postoperatively. In every gait phase, the mean values of joint angles, root mean square and integrated electromyography of sEMG were calculated, to evaluate muscle strength and muscular tension quantitatively. Results The muscle tension of lower limbs was significantly decreased (P<0.05). The muscle strength of rectus femoris and biceps femoris was decreased in the swing phase. At the midswing and terminal swing phase, the strength of tibialis anterior increased significantly (P<0.05). The flexion angle of hip and knee decreased significantly (P<0.05). The dorsiflexion angle of ankle increased significantly (P<0.05), and the varus angle decreased significantly (P<0.05). Conclusions After operation, the crouching gait and clubfoot were improved positively. Therefore, the motor function of children was improved. Combining sEMG and joint angle can evaluate the muscle function of patients quantitatively, and it also can provide references for clinical diagnosis.

Objective: To investigate the effect of long non-coding RNA CDKN2B antisense RNA 1 (CDKN2B-AS1) on malignant biological behaviors of melanoma B16-F10 cells by targeting miR-7-5p. Methods: Melanoma B16-F10 cells were chosen for this study. shRNA CDKN2B-AS1 vector was constructed and transfected into B16-F10 cells. The experimental cells were divided into control group, sh-CDKN2B-AS1 group, miR-7-5p mimic group and miR-7-5p inhibitor group. The expression level of CDKN2B-AS1 mRNA in the transfected B16-F10 cells was detected by RT-PCR; the number of clone formation and the proliferation ability of the cells were detected by Clone formation assay and MTT assay; and the migration and invasion ability of the cells were detected by Scratch-healing assay and Transwell assay. The targeting relationship between CDKN2B-AS1 and miR-7-5p was detected by Luciferase reporter gene assay. The mRNA expression of miR-7-5p and protein expressions of Ki67, cleaved caspase-3, E-cadherin, N-cadherin and Twist1 in B16-F10 cells after transfection with miR-7-5p mimics/inhibitor were detected by RT-PCR and Western blotting, respectively. Results: Compared with the control group, the expression level of CDKN2B-AS1 mRNA in B16-F10 cells of sh-CDKN2B-AS1 group was significantly decreased (P<0.01); the proliferation, migration and invasion ability of cells were significantly decreased (all P<0.01). Luciferase reporter gene assay showed that CDKN2B-AS1 directly targeted miR-7-5p. The mRNAexpression of miR-7-5p, and protein expressions of cleaved caspase-3 and E-cadherininsh-CDKN2B-AS1groupandmiR-7-5pmimic group were significantly up-regulated (all P<0.05), whiletheproteinexpressionsofKi67,N-cadherin,andTwist1weresignificantlydown-regulated (all P<0.05). Conclusion: CDKN2B-AS1 targets miR-7-5p to promote the development of melanoma, and interfering with CDKN2B-AS1 can inhibit the malignant biological behaviors of melanoma B16-F10 cells.