Are developers fixing their own bugs?: Tracing bug-fixing and bug-seeding committers

This is the post-print version of the Article. The official published version can be accessed from the link below - Copyright @ 2011 IGI GlobalThe process of fixing software bugs plays a key role in the maintenance activities of a software project. Ideally, code ownership and responsibility should be enforced among developers working on the same artifacts, so that those introducing buggy code could also contribute to its fix. However, especially in FLOSS projects, this mechanism is not clearly understood: in particular, it is not known whether those contributors fixing a bug are the same introducing and seeding it in the first place. This paper analyzes the comm-central FLOSS project, which hosts part of the Thunderbird, SeaMonkey, Lightning extensions and Sunbird projects from the Mozilla community. The analysis is focused at the level of lines of code and it uses the information stored in the source code management system. The results of this study show that in 80% of the cases, the bug-fixing activity involves source code modified by at most two developers. It also emerges that the developers fixing the bug are only responsible for 3.5% of the previous modifications to the lines affected; this implies that the other developers making changes to those lines could have made that fix. In most of the cases the bug fixing process in comm-central is not carried out by the same developers than those who seeded the buggy code.This work has been partially funded by the European Commission, under the ALERT project (ICT-258098)

Magnetic resonance imaging in the prenatal diagnosis of neural tube defects

OBJECTIVE: To assess the role of magnetic resonance imaging (MRI) in the prenatal diagnosis of neural tube defects (NTDs). BACKGROUND: NTDs comprise a heterogeneous group of congenital anomalies that derive from the failure of the neural tube to close. Advances in ultrasonography and MRI have considerably improved the diagnosis and treatment of NTDs both before and after birth. Ultrasonography is the first technique in the morphological study of the fetus, and it often makes it possible to detect or suspect NTDs. Fetal MRI is a complementary technique that makes it possible to clear up uncertain ultrasonographic findings and to detect associated anomalies that might go undetected at ultrasonography. The progressive incorporation of intrauterine treatments makes an accurate diagnosis of NTDs essential to ensure optimal perinatal management. The ability of fetal MRI to detect complex anomalies that affect different organs has been widely reported, and it can be undertaken whenever NTDs are suspected. CONCLUSION: We describe the normal appearance of fetal neural tube on MRI, and we discuss the most common anomalies involving the structures and the role of fetal MRI in their assessment. KEY POINTS: • To learn about the normal anatomy of the neural tube on MRI • To recognise the MR appearance of neural tube defects • To understand the value of MRI in assessing NTD

Little effects of Insulin-like Growth Factor-I on testicular atrophy induced by hypoxia

BACKGROUND: Insulin-like Growth Factor-I (IGF-I) supplementation restores testicular atrophy associated with advanced liver cirrhosis that is a condition of IGF-I deficiency. The aim of this work was to evaluate the effect of IGF-I in rats with ischemia-induced testicular atrophy (AT) without liver disease and consequently with normal serum level of IGF-I. METHODS: Testicular atrophy was induced by epinephrine (1, 2 mg/Kg intra-scrotal injection five times per week) during 11 weeks. Then, rats with testicular atrophy (AT) were divided into two groups (n = 10 each): untreated rats (AT) receiving saline sc, and AT+IGF, which were treated with IGF-I (2 μg.100 g b.w.(-1).day(-1), sc.) for 28d. Healthy controls (CO, n = 10) were studied in parallel. Animals were sacrificed on day 29(th). Hypophyso-gonadal axis, IGF-I and IGFBPs levels, testicular morphometry and histopathology, immuno-histochemical studies and antioxidant enzyme activity phospholipid hydroperoxide glutathione peroxidase (PHGPx) were assessed. RESULTS: Compared to controls, AT rats displayed a reduction in testicular size and weight, with histological testicular atrophy, decreased cellular proliferation and transferrin expression, and all of these alterations were slightly improved by IGF-I at low doses. IGF-I therapy increased signifincantly steroidogenesis and PHGPx activity (p < 0.05). Interestingly, plasma IGF-I did not augment in rats with testicular atrophy treated with IGF-I, while IGFBP3 levels, that reduces IGF-I availability, was increased in this group (p < 0.05). CONCLUSION: In testicular atrophy by hypoxia, condition without IGF-I deficiency, IGF-treatment induces only partial effects. These findings suggest that IGF-I therapy appears as an appropriate treatment in hypogonadism only when this is associated to conditions of IGF-I deficiency (such as Laron Syndrom or liver cirrhosis)

Hepatoprotection and neuroprotection induced by low doses of IGF-II in aging rats

<p>Abstract</p> <p>Background</p> <p>GH and IGFs serum levels decline with age. Age-related changes appear to be associated to decreases in these anabolic hormones. We have previously demonstrated that IGF-I replacement therapy improves insulin resistance, lipid metabolism and reduces oxidative damage (in brain and liver) in aging rats. Using the same experimental model, the aim of this work was to study whether the exogenous administration of IGF-II, at low doses, acts analogous to IGF-I in aging rats.</p> <p>Methods</p> <p>Three experimental groups were included in this study: young healthy controls (yCO, 17 weeks old); untreated old rats (O, 103 weeks old); and aging rats treated with IGF-II (O+IGF-II, 2 μg * 100 g body weight^-1* day^-1) for 30 days. Analytical parameters were determined in serum by routine laboratory methods using an autoanalyzer (Cobas Mira; Roche Diagnostic System, Basel, Switzerland). Serum levels of hormones (testosterone, IGF-I and insulin) were assessed by RIA. Serum Total Antioxidant Status was evaluated using a colorimetric assay. Mitochondrial membrane potential was evaluated using rhodamine 123 dye (adding different substrates to determine the different states). ATP synthesis in isolated mitochondria was determined by an enzymatic method.</p> <p>Results</p> <p>Compared with young controls, untreated old rats showed a reduction of IGF-I and testosterone levels with a decrease of serum total antioxidant status (TAS). IGF-II therapy improved serum antioxidant capability without modifying testosterone and IGF-I circulating concentrations. In addition, IGF-II treatment reduced oxidative damage in brain and liver, improving antioxidant enzyme activities and mitochondrial function. IGF-II was also able to reduce cholesterol and triglycerides levels increasing free fatty acids concentrations.</p> <p>Conclusions</p> <p>We demonstrate that low doses of IGF-II induce hepatoprotective, neuroprotective and metabolic effects, improving mitochondrial function, without affecting testosterone and IGF-I levels.</p

Этно-педагогические аспекты формирования интереса у девочек к физической культуре

The evolution of learning can be constrained by trade-offs. As male and female life-histories often diverge, the relationship between learning and fitness may differ between the sexes. However, because sexes share much of their genome, intersexual genetic correlations can prevent males and females from reaching their sex-specific optima resulting in intralocus sexual conflict (IaSC). To investigate if IaSC constraints sex-specific evolution of learning we selected Caenorhabditis remanei nematode females for increased or decreased olfactory learning performance and measured learning, lifespan (in mated and virgin worms), reproduction and locomotory activity in both sexes. Males from downward-selected female lines had higher locomotory activity and longer virgin lifespan but sired fewer progeny than males from upward-selected female lines. In contrast, we found no effect of selection on female reproduction and downward-selected females showed higher locomotory activity but lived shorter as virgins than upward-selected females. Strikingly, selection on learning performance led to the reversal of sexual dimorphism in virgin lifespan. We thus show sex-specific trade-offs between learning, reproduction and lifespan. Our results support the hypothesis that selection on learning performance can shape the evolution of sexually dimorphic life-histories via sex-specific genetic correlations

Effect of the incorporation of interfacial elements on the thermophysical properties of Cu/VGCNFs composites

International audienceVapour grown carbon nanofibres exhibit high mechanical properties and thermal conductivities. Therefore they are potential reinforcements in composites materials for high strength and high thermal conductivity applications. A problem not yet solved is the promotion of an improved copper/carbon interface. Several strategies have been envisaged for the incorporation of alloying elements (Ni, Co, B and Ti) at the interface. These techniques are based on duplex electroless plating coatings (combination of Cu and Ni or Cu and Co), electroless plating of alloys (Cu-B) and addition of metal nanoparticles (Ti) to Cu matrix deposited by electroless plating. The effect of the incorporation of these metallic elements on the microstructure and thermophysical properties is discussed. B and Ti lead to higher interaction at the Cu/C interface over Ni and Co. This allows the reduction of the coefficient of thermal expansion but regarding the thermal conductivity it was not possible to obtain a value higher than that of copper

Dose Dependent Effects on Cell Cycle Checkpoints and DNA Repair by Bendamustine

Bendamustine (BDM) is an active chemotherapeutic agent approved in the U. S. for treating chronic lymphocytic leukemia and non-Hodgkin lymphoma. Its chemical structure suggests it may have alkylator and anti-metabolite activities; however the precise mechanism of action is not well understood. Here we report the concentration-dependent effects of BDM on cell cycle, DNA damage, checkpoint response and cell death in HeLa cells. Low concentrations of BDM transiently arrested cells in G2, while a 4-fold higher concentration arrested cells in S phase. DNA damage at 50, but not 200 µM, was efficiently repaired after 48 h treatment, suggesting a difference in DNA repair efficiency at the two concentrations. Indeed, perturbing base-excision repair sensitized cells to lower concentrations of BDM. Timelapse studies of the checkpoint response to BDM showed that inhibiting Chk1 caused both the S- and G2-arrested cells to prematurely enter mitosis. However, whereas the cells arrested in G2 (low dose BDM) entered mitosis, segregated their chromosomes and divided normally, the S-phase arrested cells (high dose BDM) exhibited a highly aberrant mitosis, whereby EM images showed highly fragmented chromosomes. The vast majority of these cells died without ever exiting mitosis. Inhibiting the Chk1-dependent DNA damage checkpoint accelerated the time of killing by BDM. Our studies suggest that BDM may affect different biological processes depending on drug concentration. Sensitizing cells to killing by BDM can be achieved by inhibiting base-excision repair or disrupting the DNA damage checkpoint pathway