Prioritization, selection and minimization of test cases are well-known problems in software testing. Test case prioritization deals with the problem of ordering an existing set of test cases, typically with respect to the estimated likelihood of detecting faults. Test case selection addresses the problem of selecting a subset of an existing set of test cases, typically by discarding test cases that do not add any value in improving the quality of the software under test. Most existing approaches for test case prioritization and selection suffer from one or several drawbacks. For example, they to a large extent utilize static analysis of code for that purpose, making them unfit for higher levels of testing such as integration testing. Moreover, they do not exploit the possibility of dynamically changing the prioritization or selection of test cases based on the execution results of prior test cases. Such dynamic analysis allows for discarding test cases that do not need to be executed and are thus redundant. This paper proposes a generic method for prioritization and selection of test cases in integration testing that addresses the above issues. We also present the results of an industrial case study where initial evidence suggests the potential usefulness of our approach in testing a safety-critical train control management subsystem.

These data show the effectiveness of DMF in modulating Th17 cells in addition to Th1/Th2 cells and reflect one of the underlying mechanisms of action of DMF in psoriasis. These findings may also support the possible benefits of using fumarate in the treatment of other autoimmune diseases in the pathogeneses of which Th1 and Th17 cells play major roles.

Abstract. Software testing in industrial projects typically requires large test suites. Executing them is commonly expensive in terms of effort and wall-clock time. Indiscriminately executing all available test cases leads to sub-optimal exploitation of testing resources. Selecting too few test cases for execution on the other hand might leave a large number of faults undiscovered. Limiting factors such as allocated budget and time constraints for testing further emphasizes the importance of test case prioritization in order to identify test cases that enable earlier detection of faults while respecting such constraints. This paper introduces a novel method prioritizing test cases to detect faults earlier. The method combines TOPSIS decision making with fuzzy principles. The method is based on multi-criteria like fault detection probability, execution time, or complexity. Applying the method in an industrial context for testing a train control management subsystem from Bombardier Transportation in Sweden shows its practical benefit.

BackgroundPrevious work has demonstrated immunomodulatory, anti-tumor, anti-metastatic and anti-angiogenic effects of the small molecule quinoline-3-carboxamide tasquinimod in pre-clinical cancer models. To better understand the anti-tumor effects of tasquinimod in transplantable tumor models, we have evaluated the impact of the compound both on recruitment of myeloid cells to tumor tissue and on tumor-induced myeloid cell expansion as these cells are known to promote tumor development.MethodsMice bearing subcutaneous 4 T1 mammary carcinoma tumors were treated with tasquinimod in the drinking water. A BrdU-based flow cytometry assay was utilized to assess the impact of short-term tasquinimod treatment on myeloid cell recruitment to tumors. Additionally, long-term treatment was performed to study the anti-tumor effect of tasquinimod as well as its effects on splenic myeloid cells and their progenitors. Myeloid cell populations were also immune-depleted by in vivo antibody treatment.ResultsShort-term tasquinimod treatment did not influence the proliferation of splenic Ly6Chi and Ly6Ghi cells, but instead reduced the influx of Ly6Chi cells to the tumor. Treatment with tasquinimod for various periods of time after tumor inoculation revealed that the anti-tumor effect of this compound mainly operated during the first few days of tumor growth. Similar to tasquinimod treatment, antibody-mediated depletion of Ly6Chi cells within that same time frame, caused reduced tumor growth, thereby confirming a significant role for these cells in tumor development. Additionally, long-term tasquinimod treatment reduced the splenomegaly and expansion of splenic myeloid cells during a later phase of tumor development. In this phase, tasquinimod normalized the tumor-induced alterations in myeloerythroid progenitor cells in the spleen but had only limited impact on the same populations in the bone marrow.ConclusionsOur results indicate that tasquinimod treatment reduces tumor growth by operating early after tumor inoculation and that this effect is at least partially caused by reduced recruitment of Ly6Chi cells to tumor tissue. Long-term treatment also reduces the number of splenic myeloid cells and myeloerythroid progenitors, but these effects did not influence established rapidly growing tumors.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2481-0) contains supplementary material, which is available to authorized users.

Quinoline-3-carboxamides (Q compounds) are immunomodulatory compounds that have shown efficacy both in autoimmune disease and cancer. We have in here investigated the impact of one such compound, paquinimod, on the development of diabetes in the NOD mouse model for type I diabetes (T1D). In cohorts of NOD mice treated with paquinimod between weeks 10 to 20 of age and followed up until 40 weeks of age, we observed dose-dependent reduction in incidence of disease as well as delayed onset of disease. Further, in contrast to untreated controls, the majority of NOD mice treated from 15 weeks of age did not develop diabetes at 30 weeks of age. Importantly, these mice displayed significantly less insulitis, which correlated with selectively reduced number of splenic macrophages and splenic Ly6Chi inflammatory monocytes at end point as compared to untreated controls. Collectively, these results demonstrate that paquinimod treatment can significantly inhibit progression of insulitis to T1D in the NOD mouse. We propose that the effect of paquinimod on disease progression may be related to the reduced number of these myeloid cell populations. Our finding also indicates that this compound could be a candidate for clinical development towards diabetes therapy in humans.