The efficient and effective generation of test-data from high-level models is of crucial importance in advanced modern software engineering. Empirical studies have shown that mutation testing is highly effective. This paper describes how search-based automatic test-data generation methods can be used to find mutation adequate test-sets for Matlab/Simulink models.

No abstract

Abstract. The need for effective testing techniques for architectural level descriptions is widely recognised. However, due to the variety of domain-specific architectural description languages, there remains a lack of practical techniques in many application domains. We present a simulation-based testing framework that applies optimisation-based search to achieve high-performance testing for a type of architectural model. The search based automatic test-data generation technique forms the core of the framework. Matlab/Simulink is popularly used in embedded systems engineering as an architectural-level design notation. Our prototype framework is built on Matlab for testing Simulink models. The technology involved should apply to the other architectural notations provided that the notation supports execution or simulation.

Oligodontia is defined as the congenital absence of six or more permanent teeth, excluding the third molars. Oligodontia may contribute to masticatory dysfunction, speech alteration, aesthetic problems and malocclusion. Numerous gene mutations have been association with oligodontia. In the present study, we identified a de novo AXIN2 missense mutation (c.314T>G) in a Chinese individual with non-syndromic oligodontia. This mutation results in the substitution of Val at residue 105 for Gly (p.Val105Gly); residue 105 is located in the highly conserved regulator of G protein signaling (RGS) domain of the AXIN2 protein. This is the first report indicating that a mutation in the RGS domain of AXIN2 is responsible for non-syndromic oligodontia. Our study supports the relationship between AXIN2 mutation and non-syndromic oligodontia and extends the mutation spectrum of the AXIN2 gene.

BackgroundRacial and regional factors are important for the clinical diagnosis of non-syndromic hearing impairment. Comprehensive genetic analysis of deaf patients in different regions of China must be performed to provide effective genetic counseling. To evaluate the mutational spectrum of south Chinese families, we performed genetic analysis for non-syndromic hearing impairment in this population.MethodsComplete clinical evaluations were performed on 701 unrelated patients with non-syndromic hearing impairment from six provinces in south China. Each subject was screened for common mutations, including SLC26A4 c.IVS7-2A > G, c.2168A > G; mitochondrial DNA m.1555A > G, m.1494C > T, m.7444G > A, m.7445A > G; GJB3 c.538C > T, c.547G > A; and WFS1 c.1901A > C, using pyrosequencing. GJB2 and SLC26A4 coding region mutation detection were performed using Sanger sequencing.ResultsGenetic analysis revealed that among the etiology of non-syndromic hearing impairment, GJB2, SLC26A4, and mitochondrial m.1555A > G mutations accounted for 18.0%, 13.1%, and 0.9%, respectively. Common mutations included GJB2 c.235delC, c.109G > A, SLC26A4 c.IVS7-2A > G, c.1229 T > C, and mitochondrial m.1555A > G. The total mutation rate was 45.1% in all patients examined in south China. Overall, the clear contribution of GJB2, SLC26A4, and mitochondrial m.1555A > G to the etiology of the non-syndromic deafness population in south China was 32.0%.ConclusionsOur study is the first genetic analysis of non-syndromic hearing impairment in south China, and revealed that a clear genetic etiology accounted for 32.0% of non-syndromic hearing cases in patients from these regions. The mutational spectrum of non-syndromic hearing impairment in the south Chinese population provides useful and targeted information to aid in genetic counseling.