Surgical resection is an important method for treating liver cancer,and postoperative liver failure caused by insufficient liver remnant volume is a key factor limiting the success rate of surgical resection.The portal vein embolization(PVE),through artificially obstructing the portal vein,can induce liver volume enlargement,thus,providing theoretical support for preventing postoperative death due to liver failure.In recent years,many innovations and studies on the limitations of PVE,especially on the problem of postoperative insufficient growth rate of liver tissues,have been made by experts both at home and abroad.In view of this,this paper,through summarizing the relevant literature on PVE,makes a detailed review concerning the clinical application and research progress of PVE.

Objective:To design and compile quality evaluation questionnaire on problem-based learning (PBL) of Neurology and to test its reliability and validity.Methods:Referring to the framework of the evaluation system and according to the characteristics of the discipline, we designed the questionnaire on PBL of Neurology. The clinical medical students who participated in neurologic PBL course were taken as the objects of investigation. The reliability of the questionnaire and the reliability of internal consistency were tested. Correlation analysis and exploratory factor analysis were used to evaluate the validity of the questionnaire.Results:The questionnaire on PBL of Neurology included three first-level indicators: teaching plan quality evaluation, teaching method evaluation and teaching quality evaluation, containing 6 second-level indicators and 25 third-level indicators. The correlation coefficient ρ=0.990 ( P<0.01) showed that the retest reliability was good. The cronbach's α coefficient is 0.901, meeting the internal consistency reliability requirement. And the content validity correlation coefficient was 0.307-0.7 ( P<0.05), indicating that each third-level index had a significant correlation with the total score, and the questionnaire item design was good. The three first-level indicators were used as common factors to evaluate the structural validity by exploratory factor analysis and identify the direction of optimization. Conclusion:The questionnaire has good reliability and validity, which can be used as a tool for scientific evaluation on PBL of neurology, and also provide an optimization direction for further research in the future.

Background and purpose:Ethanol has been reported to stimulate progression of breast cancer, yet the underlying mechanism is not fully understood. This study aimed to investigate effects of ethyl alcohol (EtOH) on the calcium-activated neutral protease (CANP)-cyclin E/focal adhesion kinase (FAK) signaling and cell migration in breast cancer cells, as well as the role of epidermal growth factor receptor (EGFR) in the EtOH-stimulated effects, in order to assess the signaling mechanism(s) underlying how EtOH enhances cancer progression.Methods:Human breast cancer cell line MCF-7 was employed as a model system, with MCF-10A mammary epithelial cells as control. In vitro wound healing assay was carried out to evaluate EtOH-induced cell migration. The effects of EtOH or epidermal growth factor on the proteolysis of cyclin E/FAK were detected by Western blot. EGFR inhibitor (EGFR-I) and a speciifc inhibitor for CANP, Calpeptin, were applied to pretreat cultured cells to explore their inlfuences on the cell migration and cyclin E/FAK proteolysis triggered by EtOH.Results:Treatment of model cells with EtOH (0.3%) stimulated significant proteolysis of cyclin E/FAK in a dose-/time-dependent manner and increased migration (+47.30%,P<0.05) in MCF-7 breast cancer cells, but had no signiifcant effect on migration in MCF-10A cells. Pretreatment with Calpeptin (10 μmol/L) signiifcantly reduced EtOH (0.3%)- or EGFR (10 ng/mL)-induced cyclin E/FAK truncation. EGFR-I (3 μmol/L) pro-foundly reduced EtOH-indcued CANP dependent proteolysis of CANP1 and cyclin E/FAK as well as cell migration (-53.00%,P<0.01).Conclusion:EtOH signiifcantly stimulates activation of CANP via EGFR pathway, resulting in proteolysis of cyclin E/FAK and migration in MCF-7 breast cancer cells, suggesting EGFR-CANP signaling to be a potential target for suppression of metastasis in breast cancer.