No abstract

Software engineering is one of the most active fields of entrepreneurship and innovation in the world, and it is also the core field of the information technology industry. Software talents as the foundation and support are an important weight to determine the future direction of my country’s software engineering. How to make colleges and universities cultivate compound software talents with innovative ability and engineering ability and how to guide students to closely combine innovative thinking with social practice are a major challenge faced by the current software process education in colleges and universities in my country. At present, the overall quality of software engineers is poor, which cannot meet the needs of enterprises and training objectives. This paper puts forward the application of the OBE (outcome-based education) model in the training of software talents, which can effectively solve the current problems of talent quality and social demand. The analysis shows that there is a high correlation between collaborative education and satisfaction, and the collaborative education model can effectively improve satisfaction. The investment of scientific research funds can effectively improve the overall quality of scientific research team members. The OBE talent training mode can effectively improve the overall test effect, whether in the experimental set or the test set, the test result of the OBE talent training structure is still the highest, the accuracy rate can reach 94.23%, the recall rate can reach 94.51%, and the F1 value can reach 95.13%. It is fully explained that the identification accuracy is the highest when the OBE talent-training structure is adopted.

As a very important transcription factor, signal transducer and activator of transcription 5a (Stat5a) has been reported to be involved in human reproductive cancers such as breast, prostate and ovarian cancer. However, up to date, the exact role of Stat5a in breast cancer is still not clear. The data reported are conflicting. D5 Stat5a is a variant of Stat5a we cloned recently. This newly cloned variant behave like its full length counterpart in terms of dimerization, being activated by prolactin and nuclear translocation, however it also behave differently in terms of effect on cell proliferation and interaction with other transcription factors. In the present study, we examined its effect on cell proliferation of cultured breast cancer cells (MCF-10A and MCF-7) by using adenovirus-mediated gene transfer and MTS technology. Also, quantitative real time polymerase chain reaction (qRT-PCR), chromatin immunoprecipitation assay (ChIP) and Western blot were used to probe the possible changes of insulin-like growth factor binding protein-7 (IGFBP-7) expression including mRNA and protein, and the epigenetic changes with overexpression of this newly cloned variant. The results clarified that D5 Stat5a (1) behaves as a promoting factor to the cell proliferation of MCF-10A and MCF-7, (2) induces enhancer of zeste homology 2 (EZH2) expression in breast epithelial cells, as well as histone 3 trimethylation of IGFBP-7 promoter region, and (3) lower IGFBP-7 expression was detected in breast cancer tissue. Taking together, we concluded that the mitogenic effect of D5 Stat5a on breast cells is, at least partly, through up-regulation of histone methyltransferase, EZH2, and therefore inhibiting IGFBP-7 expression by increasing H3K27Me3 of IGFBP-7 promoter region.