FlakiMe: Laboratory-Controlled Test Flakiness Impact Assessment

Much research on software testing makes an implicit assumption that test failures are deterministic such that they always witness the presence of the same defects. However, this assumption is not always true because some test failures are due to so-called flaky tests, i.e., tests with non-deterministic outcomes. To help testing researchers better investigate flakiness, we introduce a test flakiness assessment and experimentation platform, called FlakiMe. FlakiMe supports the seeding of a (controllable) degree of flakiness into the behaviour of a given test suite. Thereby, FlakiMe equips researchers with ways to investigate the impact of test flakiness on their techniques under laboratory-controlled conditions. To demonstrate the application of FlakiMe, we use it to assess the impact of flakiness on mutation testing and program repair (the PRAPR and ARJA methods). These results indicate that a 10% flakiness is sufficient to affect the mutation score, but the effect size is modest (2% - 5%), while it reduces the number of patches produced for repair by 20% up to 100% of repair problems; a devastating impact on this application of testing. Our experiments with FlakiMe demonstrate that flakiness affects different testing applications in very different ways, thereby motivating the need for a laboratory-controllable flakiness impact assessment platform and approach such as FlakiMe

Adaptable transition systems

We present an essential model of adaptable transition systems inspired by white-box approaches to adaptation and based on foundational models of component based systems. The key feature of adaptable transition systems are control propositions, imposing a clear separation between ordinary, functional behaviours and adaptive ones. We instantiate our approach on interface automata yielding adaptable interface automata, but it may be instantiated on other foundational models of component-based systems as well. We discuss how control propositions can be exploited in the specification and analysis of adaptive systems, focusing on various notions proposed in the literature, like adaptability, control loops, and control synthesis

Oxysterol-Binding Protein-1 (OSBP1) Modulates Processing and Trafficking of the Amyloid Precursor Protein

BACKGROUND Evidence from biochemical, epidemiological and genetic findings indicates that cholesterol levels are linked to amyloid-β (Aβ) production and Alzheimer's disease (AD). Oxysterols, which are cholesterol-derived ligands of the liver X receptors (LXRs) and oxysterol binding proteins, strongly regulate the processing of amyloid precursor protein (APP). Although LXRs have been studied extensively, little is known about the biology of oxysterol binding proteins. Oxysterol-binding protein 1 (OSBP1) is a member of a family of sterol-binding proteins with roles in lipid metabolism, regulation of secretory vesicle generation and signal transduction, and it is thought that these proteins may act as sterol sensors to control a variety of sterol-dependent cellular processes. RESULTS We investigated whether OSBP1 was involved in regulating APP processing and found that overexpression of OSBP1 downregulated the amyloidogenic processing of APP, while OSBP1 knockdown had the opposite effect. In addition, we found that OSBP1 altered the trafficking of APP-Notch2 dimers by causing their accumulation in the Golgi, an effect that could be reversed by treating cells with OSBP1 ligand, 25-hydroxycholesterol. CONCLUSION These results suggest that OSBP1 could play a role in linking cholesterol metabolism with intracellular APP trafficking and Aβ production, and more importantly indicate that OSBP1 could provide an alternative target for Aβ-directed therapeutic.National Institute on Aging (AG/NS17485

Probabilistic Model Checking for Energy Analysis in Software Product Lines

In a software product line (SPL), a collection of software products is defined by their commonalities in terms of features rather than explicitly specifying all products one-by-one. Several verification techniques were adapted to establish temporal properties of SPLs. Symbolic and family-based model checking have been proven to be successful for tackling the combinatorial blow-up arising when reasoning about several feature combinations. However, most formal verification approaches for SPLs presented in the literature focus on the static SPLs, where the features of a product are fixed and cannot be changed during runtime. This is in contrast to dynamic SPLs, allowing to adapt feature combinations of a product dynamically after deployment. The main contribution of the paper is a compositional modeling framework for dynamic SPLs, which supports probabilistic and nondeterministic choices and allows for quantitative analysis. We specify the feature changes during runtime within an automata-based coordination component, enabling to reason over strategies how to trigger dynamic feature changes for optimizing various quantitative objectives, e.g., energy or monetary costs and reliability. For our framework there is a natural and conceptually simple translation into the input language of the prominent probabilistic model checker PRISM. This facilitates the application of PRISM's powerful symbolic engine to the operational behavior of dynamic SPLs and their family-based analysis against various quantitative queries. We demonstrate feasibility of our approach by a case study issuing an energy-aware bonding network device.Comment: 14 pages, 11 figure

Inhibition of TNF receptor p55 by a domain antibody attenuates the initial phase of acid-induced lung injury in mice

Background: Tumor necrosis factor-α (TNF) is strongly implicated in the development of acute respiratory distress syndrome (ARDS), but its potential as a therapeutic target has been hampered by its complex biology. TNF signals through two receptors, p55 and p75, which play differential roles in pulmonary edema formation during ARDS. We have recently shown that inhibition of p55 by a novel domain antibody (dAb™) attenuated ventilator36 induced lung injury. In the current study we explored the efficacy of this antibody in mouse models of acid-induced lung injury, to investigate the longer consequences of treatment. Methods: We employed two acid-induced injury models, an acute ventilated model and a resolving spontaneously breathing model. C57BL/6 mice were pretreated intratracheally or intranasally with p55-targeting dAb or non-targeting ‘dummy’ dAb, 1 or 4 hours before acid instillation. Results: Acid instillation in the dummy dAb group caused hypoxemia, increased respiratory system elastance, pulmonary inflammation and edema in both the ventilated and resolving models. Pretreatment with p55-targeting dAb significantly attenuated physiological markers of ARDS in both models. p55-targeting dAb also attenuated pulmonary inflammation in the ventilated model, with signs that altered cytokine production and leukocyte recruitment persisted beyond the very acute phase. Conclusions: These results demonstrate that the p55-targeting dAb attenuates lung injury and edema formation in models of ARDS induced by acid aspiration, with protection from a single dose lasting up to 24 hours. Together with our previous data, the current study lends support towards the clinical targeting of p55 for patients with, or at risk of ARDS

Semantic mutation testing

This is the Pre-print version of the Article. The official published version can be obtained from the link below - Copyright @ 2011 ElsevierMutation testing is a powerful and flexible test technique. Traditional mutation testing makes a small change to the syntax of a description (usually a program) in order to create a mutant. A test suite is considered to be good if it distinguishes between the original description and all of the (functionally non-equivalent) mutants. These mutants can be seen as representing potential small slips and thus mutation testing aims to produce a test suite that is good at finding such slips. It has also been argued that a test suite that finds such small changes is likely to find larger changes. This paper describes a new approach to mutation testing, called semantic mutation testing. Rather than mutate the description, semantic mutation testing mutates the semantics of the language in which the description is written. The mutations of the semantics of the language represent possible misunderstandings of the description language and thus capture a different class of faults. Since the likely misunderstandings are highly context dependent, this context should be used to determine which semantic mutants should be produced. The approach is illustrated through examples with statecharts and C code. The paper also describes a semantic mutation testing tool for C and the results of experiments that investigated the nature of some semantic mutation operators for C

Domain Specific Languages for Managing Feature Models: Advances and Challenges

International audienceManaging multiple and complex feature models is a tedious and error-prone activity in software product line engineering. Despite many advances in formal methods and analysis techniques, the supporting tools and APIs are not easily usable together, nor unified. In this paper, we report on the development and evolution of the Familiar Domain-Specific Language (DSL). Its toolset is dedicated to the large scale management of feature models through a good support for separating concerns, composing feature models and scripting manipulations. We overview various applications of Familiar and discuss both advantages and identified drawbacks. We then devise salient challenges to improve such DSL support in the near future

High prevalence of Plasmodium falciparum gametocyte infections in school-age children using molecular detection: patterns and predictors of risk from a cross-sectional study in southern Malawi

Abstract Background In endemic areas, many people experience asymptomatic Plasmodium infections, particularly older children and adults, but their transmission contribution is unknown. Though not the exclusive determinant of infectiousness, transmission from humans to mosquitoes requires blood meals containing gametocytes. Gametocytes often occur at submicroscopic densities, challenging measurement in human populations. More sensitive molecular techniques allow better characterization of gametocyte epidemiologic patterns. Methods Approximately 30 households were selected from each of eight sites in southern Malawi during two cross-sectional surveys. Blood was sampled from 623 people during the dry season and 896 the following rainy season. Among people PCR-positive for Plasmodium falciparum, mature gametocytes were detected by qRT-PCR. Regression models evaluated predictors of gametocyte carriage and density in the total population and among those with PCR-positive infections. Results The prevalence of gametocyte carriage by molecular testing was 3.5% during the dry season and 8.6% during the rainy season, and by microscopy 0.8 and 3.3%, respectively. Nearly half of PCR-positive infections carried gametocytes, regardless of recent symptom status. Among P. falciparum-infected people, only living in unfinished houses and age were significantly associated with gametocyte presence. Infected people in unfinished houses had higher odds of carrying gametocytes (OR 2.24, 95% CI 1.16–4.31), and 31% (95% CI 3–65%) higher gametocyte density than those in finished houses. School-age children (5–15 years), had higher odds than adults (≥16 years) of having gametocytes when infected (OR 2.77, 95% CI 1.47–5.19), but 31% (95% CI 11–47%) lower gametocyte density. Children <5 years did not have significantly higher odds of gametocyte carriage or density when infected than adults. Conclusions School-age children frequently carry gametocytes in communities of southern Malawi and represent an under-recognized reservoir of infection. Malaria elimination strategies should address these frequently asymptomatic reservoirs, especially in highly endemic areas. Improved household construction may also reduce the infectious reservoir.http://deepblue.lib.umich.edu/bitstream/2027.42/134670/1/12936_2016_Article_1587.pd