Model-Driven Derivation of Domain Functional Requirements from Use Cases

Domain analysis is essential to core assets development in software product line engineering. Most existing approaches, however, depend on domain experts’ experience to analyze the commonality and variability of systems in a domain, which remains a manual and intensive process. This paper addresses the issue by proposing a model-driven approach to automating the domain requirements derivation process. The paper focuses on the match between the use cases of existing individual products and the domain functional requirements of a product line. By introducing a set of linguistic description dimensions to differentiate the sub-variations in a use case, the use case template is extended to model variability. To this end, a transformation process is formulated to sustain and deduce the information in use cases, and to match it to domain functional requirements. This paper also presents a prototype which implements the derivation as a model transformation described in a graphical model transformation language MOLA. This approach complements existing domain analysis techniques with less manual operation cost and more efficiency by automating the domain functional requirements development.

Towards Lightweight Requirements Documentation

Most requirements management processes and associated tools are designed for document-driven software development and are unlikely to be adopted for the needs of an agile software development team. We discuss how and what can make the traditional requirements documentation a lightweight process, and suitable for user requirements elicitation and analysis. We propose a reference model for requirements analysis and documentation and suggest what kind of requirements management tools are needed to support an agile software process. The approach and the reference model are demonstrated in Vixtory, a tool for requirements lightweight documentation in agile web application development.

Hsa_Circ_0000826 inhibits the proliferation of colorectal cancer by targeting AUF1

Many circular RNAs(circRNAs)are reported to be abnormally expressed during the progression of various tumors,and these circRNAs can be used as anti-tumor targets.Therefore,it is important to identify circRNAs that can be used effectively for the clinical diagnosis and treatment of colorectal cancer(CRC).Here,we report that hsa_Circ_0000826(Circ_0000826),a circ RNA with significantly reduced expression level in CRC tissues,is associated with a poor prognosis in patients.The silencing of Circ_0000826 promotes the proliferation of CRC cells.Conversely,the overexpression of Circ_0000826 restricted CRC cell proliferation both in vitro and in vivo.Furthermore,Circ_0000826 could target AU-rich element RNA-binding protein 1(AUF1).AUF1,known as heterogeneous nuclear ribonucleoprotein D(hnRNP D),could bind to the c-MYC 3’-UTR and promote c-MYC expression.When Circ_0000826 binds to AUF1,it competitively inhibits the binding of AUF1 to the c-MYC 3’-UTR,which inhibits the c-MYC expression and cell proliferation.These results provide novel insights into the functional mechanism of Circ_0000826 action in CRC progression and indicate its potential use as a therapeutic target in CRC.

Study on the role of transcription factor SPI1 in the development of glioma

Background:Glioma is a common malignant brain tumor.The purpose of this study was to investigate the role of the transcription factor SPI1 in glioma.Methods:SPI1 expression in glioma was identified using qRT-PCR and Western blotting.Cell proliferation was assessed using the CCK8 assay.Transwell and wound healing assays were utilized to evaluate cell migration.Additionally,cell cycle and apoptosis were detected using flow cytometry.Results:We observed that the expression level of SPI1 was up-regulated in glioma tissues,compared to normal tissues.Furthermore,we found that SPI1 is able to promote proliferation and migration of glioma cells in vitro.Flow cytometry results demonstrate that,compared to si-NC cells,si-SPI1 cells stagnated in the G1 phase,and downregulation of SPI1 expression is able to increase rates of apoptosis.Double luciferase activity and chromatin immunoprecipitation assay results indicated that SPI1 can bind to the promoter sites and promote the proliferation and migration of glioma cells by regulating the expression of oncogenic PAICS.Conclusions:Our results suggest that SPI1 can promote proliferation and migration of glioma.Furthermore,SPI1 can be utilized as a potential diagnostic marker and therapeutic target for glioma.