Software fault localization is one of the (if not the) most expensive, tedious and time consuming activities in program debugging. Therefore, there is a high demand for automatic fault localization techniques that can guide programmers to the locations of faults, with minimal human intervention. This demand has led to the proposal and development of various methods, each of which seeks to make the fault localization process more effective in its own unique and creative way. In this article we provide an overview of several such methods and discuss some of the key issues and concerns that are relevant to fault localization.

No abstract

No abstract

Effective debugging is crucial to producing dependable software. Manual debugging is becoming prohibitively expensive, especially due to the growing size and complexity of programs. Given that fault localization is one of the most expensive activities in program debugging, there has been a great demand for fault localization techniques that can help guide programmers to the locations of faults. In this paper a technique named DStar (D * ), which has its origins rooted in similarity coefficient-based analysis, is proposed; which can identify suspicious locations for fault localization automatically without requiring any prior information on program structure or semantics. D * is evaluated across 21 programs and is compared to 16 different fault localization techniques. Both single-fault and multi-fault programs are used. Results indicate that D * is more effective at locating faults than all the other techniques it is compared to.

Tubeimoside-1 (TBMS1), a triterpenoid saponin isolated from the tuber of Bolbostemma paniculatum (Maxim) Franquet, serves an universal suppressive role in multiple cancer types, including lung cancer. However, the mechanism involved in non-small cell lung cancer (NSCLC) cells by which TBMS1 elicits its antitumor effects is not yet completely understood. The present study indicated that 10 µmol/l TBMS1 significantly enhanced apoptosis and notably blocked the migration and invasion of NCI-H1299 cells. These effects were reversed following transfection with miR-126-5p inhibitor into TBMS1-treated NCI-H1299 cells. Vascular endothelial growth factor-A (VEGF-A) is a target gene for miR-126-5p. Notably, results suggested that the downregulated VEGF-A and VEGFR-2 in TBMS1-treated NCI-H1299 cells were upregulated after inhibiting miR-126-5p, and overexpression of VEGF-A or VEGFR-2 could significantly reduce apoptosis and promote the migration and invasion of TBMS1-treated NCI-H1299 cells. Furthermore, TBMS1 combined with TBHQ (an ERK activator) dramatically suppressed TBMS1-induced apoptosis and stimulated TBMS1-reduced migration and invasion in NCI-H1299 cells, suggesting that TBMS1 inhibits the ERK signaling pathway and represses the growth and metastasis of NCI-H1299 cells. Further study demonstrated that either inhibiting miR-126-5p or overexpressing VEGF-A and VEGFR-2 in TBMS1-treated NCI-H1299 cells elevated the mRNA expression levels and phosphorylation levels of MEK1, as well as ERK. To conclude, TBMS1 increases miR-126-5p expression, whereas overexpressing miR-126-5p inactivates VEGF-A/VEGFR-2/ERK signaling pathway, which ultimately actuates the pro-apoptotic and anti-metastatic effects in NCI-H1299 cells. Therefore, the present findings provide a theoretical foundation for TBMS1 as a potential candidate in NSCLC treatment.