Simulation-Based Arthroscopic Skills Using a Spaced Retraining Schedule Reduces Short-Term Task Completion Time and Camera Path Length.

PURPOSE: To investigate whether acquiring basic knee arthroscopic skills via a spaced retraining schedule could prevent skills deterioration and achieve further skills improvement. METHODS: In the learning phase, 16 residents with no previous hands-on experience in practicing arthroscopic skills were asked to perform basic arthroscopic tasks on a simulator until they attained perfect scores in each task. Immediately after completing the learning phase, a pretest was performed to assess their performance. Next, they were randomly assigned into 2 groups. The spaced retraining group, which undertook a spaced repetitive training phase with a fixed-time interval, returned on days 2, 4 and 6 to repeat the same tasks for 20 minutes per day, whereas the control group did nothing. On day 7, all participants performed a posttest. A 2 × 2 mixed analysis of variance model was used for statistical analysis. RESULTS: Significant differences between the 2 groups were found in task completion time (P = .003) and camera path length (P = .043) but not cartilage injury (P = .186). Residents in the spaced retraining group decreased their task completion time (163.2 ± 23.9 seconds) whereas the task time in the control group increased (351.3 ± 25.5 seconds). The same pattern was found with the camera path length. CONCLUSIONS: Implementing a spaced retraining schedule in 1 week resulted in a reduced task completion time and camera path length but no significant reduction in cartilage injury. It appears that introducing a spaced retraining schedule to retain arthroscopic skills acquired through massed learning may be advantageous. CLINICAL RELEVANCE: In consideration of the training time available to residents and the trend toward massed learning, this spaced retraining schedule may offer a cost-effective and convenient way for residents to maintain and improve their basic arthroscopic skills with no significant increase in time invested.

EPB41L3 is a potential tumor suppressor gene and prognostic indicator in esophageal squamous cell carcinoma.

Although there have been reports about the role of erythrocyte membrane protein band 4.1 like 3 (EPB41L3) in several types of cancer, primarily in non-small-cell lung carcinoma, the molecular function and modulatory mechanisms of EPB41L3 remain unclear. In specific, the functional and clinical significance of EPB41L3 in esophageal squamous cell carcinoma (ESCC) has not been explored to date. In the present study, reduced EPB41L3 expression was demonstrated in ESCC cell lines and tissues, which was due to its high methylation rate. Ectopic expression of EPB41L3 in ESCC cells inhibited cell proliferation in vivo and in vitro. In addition, EPB41L3 overexpression induced apoptosis and G2/M cell cycle arrest by activating Caspase-3/8/9 and Cyclin-dependent kinase 1/Cyclin B1 signaling, respectively. Notably, patients with higher EPB41L3 expression had markedly higher overall survival rates compared with patients with lower EPB41L3 expression. In summary, the present results suggest that EPB41L3 may be a tumor suppressor gene in ESCC development, representing a potential therapeutic target and a prognostic indicator for ESCC.

Epb41l3 suppresses esophageal squamous cell carcinoma invasion and inhibits MMP2 and MMP9 expression.

EPB41L3 may play a role as a metastasis suppressor by supporting regular arrangements of actin stress fibres and alleviating the increase in cell motility associated with enhanced metastatic potential. Downregulation of epb41l3 has been observed in many cancers, but the role of this gene in esophageal squamous cell carcinoma (ESCC) remains unclear. Our study aimed to determine the effect of epb41l3 on ESCC cell migration and invasion. We investigated epb41l3 protein expression in tumour and non-tumour tissues by immunohistochemical staining. Expression in the non-neoplastic human esophageal cell line Het-1a and four ESCC cell lines - Kyse150, Kyse510, Kyse450 and Caes17 - was assessed by quantitative Polymerase Chain Reaction (qPCR) and Western blotting. Furthermore, an EPB41L3 overexpression plasmid and EPB41L3-specific small interfering RNA were used to upregulate EPB41L3 expression in Kyse150 cells and to downregulate EPB41L3 expression in Kyse450 cells, respectively. Cell migration and invasion were evaluated by wound healing and transwell assays, respectively. The expression levels of p-AKT, matrix metalloproteinase (MMP)2 and MMP9 were evaluated. Expression of epb41l3 was significantly lower in tumour tissues than in non-tumour tissues and in ESCC cell lines compared with the Het-1a cell line. Kyse450 and Caes17 cells exhibited higher expression of epb41l3 than Kyse150 and Kyse510 cells. Overexpressing epb41l3 decreased Kyse150 cell migration and invasion, whereas EPB41L3-specific small interfering RNA silencing increased these functions in Kyse450 cells. Furthermore, overexpressing epb41l3 led to downregulation of MMP2 and MMP9 in Kyse150 and Kyse510 cells. Our findings reveal that EPB41L3 suppresses tumour cell invasion and inhibits MMP2 and MMP9 expression in ESCC cells.