Miracle-dz/UniFAR-FTUs huggingface dataset:
An AST-Based Approach to Classifying Defects

During software development life cycle, a large number of defects could be discovered and reported. Defect classification is essential, as it can help developers better understand the distribution of the defect types and hence help reduce the effort of root cause analysis. In this paper, we proposed an approach to automatically classifying software defects using various features extracted from the Abstract Syntax Tree (AST) of the source code. We evaluated our approach by classifying 1174 defects from MapReduce, Tomcat, and Solr. The experimental results show that the proposed approach can predict interface defects and control/logic defects well.
A point mutation in the human Slo1 channel that impairs its sensitivity to omega-3 docosahexaenoic acid

Long-chain polyunsaturated omega-3 fatty acids such as docosahexaenoic acid (DHA) at nanomolar concentrations reversibly activate human large-conductance Ca2+- and voltage-gated K+ (Slo1 BK) channels containing auxiliary β1 or β4 subunits in cell-free patches. Here we examined the action of DHA on the Slo1 channel without any auxiliary subunit and sought to elucidate the biophysical mechanism and the molecular determinants of the DHA sensitivity. Measurements of ionic currents through human Slo1 (hSlo1) channels reveal that the stimulatory effect of DHA does not require activation of the voltage or Ca2+ sensors. Unlike gating of the hSlo1 channel, that of the Drosophila melanogaster Slo1 (dSlo1) channel is unaltered by DHA. Our mutagenesis study based on the differential responses of human and dSlo1 channels to DHA pinpoints that Y318 near the cytoplasmic end of S6 in the hSlo1 channel is a critical determinant of the stimulatory action of DHA. The mutation Y318S in hSlo1, which replaces Y with S as found in dSlo1, greatly diminishes the channel’s response to DHA with a 22-carbon chain whether β1 or β4 is absent or present. However, the responses to α-linolenic acid, an omegea-3 fatty acid with an 18-carbon chain, and to arachidonic acid, an omega-6 fatty acid with a 20-carbon chain, remain unaffected by the mutation. Y318 in the S6 segment of hSlo1 is thus an important determinant of the electrophysiological response of the channel to DHA. Furthermore, the mutation Y318S may prove to be useful in dissecting out the complex lipid-mediated modulation of Slo1 BK channels.
Fusion of optimized moment based and Gabor texture features for better texture classification

Feature extraction is one of the most vital steps involved in image description. Every feature extraction technique has its own merits and demerits. For a particular application a carefully worked fusion of features, extracted using different techniques, can enhance their image description capabilities. Optimized moment features, obtained from author's previous work, have shown promising results in classifying the textures having reasonable variance in periodicity of patterns and identical second order statistics. Gabor feature extraction is an established technique in describing the texture having features in the range of low frequencies. However, in the presence of periodic variance or impulsive noise, the Gabor filters generate highly variable features at higher frequency. This paper explores the fusion of optimized moment and Gabor energy texture features. The Fisher linear discriminant analysis shows that the discrimination effectiveness of the features increases after fusion. Results have also been validated experimentally through the classification of real texture images.
The Open University ’ s repository of research publications and other research outputs The GAMBAS middleware for smart city applications Book Chapter

The concept of smart cities envisions IoT services that provide distraction-free support for citizens. To realize this vision, the services must adapt to the citizens’ situations, behaviors and intents. This requires them to gather and process the context of their users. Mobile devices provide a promising basis for determining context in an automated manner on a large scale. However, despite the wide availability of mobile platforms, there are only few examples of smart city applications. One reason for this is that existing software platforms only provide limited support for common high-level tasks such as efficient data acquisition, secure and privacypreserving data distribution or interoperable data integration. As shown by the Bus Navigator – a mobile transport application that has been deployed in the city of Madrid – the GAMBAS middleware can flexibly support such tasks and thus, reduce the development effort for a broad spectrum of smart city applications.
The Role of Hypoxia Inducible Factor-1 Alpha in Bypassing Oncogene-Induced Senescence

Oncogene induced senescence (OIS) is a sustained anti-proliferative response acutely induced in primary cells via activation of mitogenic oncogenes such as Ras/BRAF. This mechanism acts as an initial barrier preventing normal cells transformation into malignant cell. Besides oncogenic activation and DNA damage response (DDR), senescence is modulated by a plethora of other factors, and one of the most important one is oxygen tension of the tissue. The aim of this study was to determine the impact of hypoxia on RasV12-induced senescence in human diploid fibroblasts (HDFs). We showed here that hypoxia prevents execution of oncogene induced senescence (OIS), through a strong down-regulation of senescence hallmarks, such as SA- β-galactosidase, H3K9me3, HP1γ, p53, p21CIP1 and p16INK4a in association with induction of hypoxia inducible factor-1α (HIF-1α). In addition, hypoxia also decreased marks of H-RasV12-induced DDR in both cell lines through down-regulation of ATM/ATR, Chk1 and Chk2 phosphorylation as well as decreased γ-H2AX positivity. Utilizing shRNA system targeting HIF-1α we show that HIF-1α is directly involved in down regulation of p53 and its target p21CIP1 but not p16INK4a. In line with this finding we found that knock down of HIF-1α leads to a strong induction of apoptotic response, but not restoration of senescence in Ras expressing HDFs in hypoxia. This indicates that HIF-1α is an important player in early steps of tumorigenesis, leading to suppression of senescence through its negative regulation of p53 and p21CIP1. In our work we describe a mechanism through which hypoxia and specifically HIF-1α preclude cells from maintaining senescence-driven anti proliferative response. These findings indicate the possible mechanism through which hypoxic environment helps premalignant cells to evade impingement of cellular failsafe pathways.
Mitochondrial Membrane Potential and Glutamate Excitotoxicity in Cultured Cerebellar Granule Cells

The relationship between changes in mitochondrial membrane potential (Δψm) and the failure of cytoplasmic Ca2+ homeostasis, delayed Ca2+deregulation (DCD), is investigated for cultured rat cerebellar granule cells exposed to glutamate. To interpret the single-cell fluorescence response of cells loaded with tetramethylrhodamine methyl ester (TMRM+) or rhodamine-123, we devised and validated a mathematical simulation with well characterized effectors of Δψm and plasma membrane potential (ΔψP). Glutamate usually caused an immediate decrease in Δψm of <10 mV, attributable to Ca2+ accumulation rather than enhanced ATP demand, and these cells continued to generate ATP by oxidative phosphorylation until DCD. Cells for which the mitochondria showed a larger initial depolarization deregulated more rapidly. The mitochondria in a subpopulation of glutamate-exposed cells that failed to extrude Ca2+ that was released from the matrix after protonophore addition were bioenergetically competent. The onset of DCD during continuous glutamate exposure in the presence or absence of oligomycin was associated with a slowly developing mitochondrial depolarization, but cause and effect could not be established readily. In contrast, the slowly developing mitochondrial depolarization after transient NMDA receptor activation occurs before cytoplasmic free Ca2+([Ca2+]c) has risen to the set point at which mitochondria retain Ca2+. In the presence of oligomycin no increase in [Ca2+]c occurs during this depolarization. We conclude that transient Ca2+loading of mitochondria as a consequence of NMDA receptor activation initiates oxidative damage to both plasma membrane Ca2+ extrusion pathways and the inhibition of mitochondrial respiration. Depending on experimental conditions, one of these factors becomes rate-limiting and precipitates DCD.
Producer preference for land-based biological carbon sequestration in agriculture: Some implications from a sample of North Dakota farmers

The objective of this study was to develop an understanding of producer preferences for land-based biological carbon (C) sequestration in agriculture. We conducted a mail survey in a US production region to elicit farmers’ willingness to participate in different C credit programs in a hypothetical greenhouse gas mitigation market. We used the survey data to calibrate a behavior model in a benefit-cost framework that characterizes farmers’ decisions about C program participation in relation to preferences and the attributes of both C programs and production. Our empirical analysis suggested that (1) producers would respond to the market incentive for C sequestration; (2) producer responses might be limited, particularly at low C prices; and (3) producers might perceive differentially a cost for C sequestration, depending on individual preferences, production attributes, and specific practices to be adopted. A policy simulation of producer behavior with agricultural census data estimated the potential C offset supply in the study area.
Risk Factors of CVD Mortality among the Elderly in Beijing, 1992 – 2009: An 18-year Cohort Study

Few researchers have examined the effects of multiple risk factors of cardiovascular disease (CVD) mortality simultaneously. This study was to determine the associations of combined lifestyle and other factors with CVD mortality among the elderly (n = 3,257), in Beijing, China, through data mining of the Beijing Longitudinal Study of Aging (BLSA). BLSA is a representative cohort study from 1992 to 2009, hosted by Xuan Wu Hospital. Competing risk survival analysis was conducted to explore the association between risk factors and CVD mortality. The factors focused mainly on lifestyle, physical condition, and the model was adjusted for age and gender. There were 273 of the 1,068 recorded deaths caused by CVD among the 2010 participants. Living in a suburban area (HR = 0.614, 95% CI: 0.410-0.921) was associated with lower CVD mortality. Increasing age (66–75: HR = 1.511, 95% CI: 1.111–2.055; ≥76: HR = 1.847, 95% CI: 1.256–2.717), high blood pressure (HR = 1.407, 95% CI: 1.031–1.920), frequent consumption of meat (HR = 1.559, 95% CI: 1.079–2.254) and physical inactivity (p = 0.046) were associated with higher CVD mortality. The study provides an instructional foundation for the control and prevention of CVD in Beijing, China.
Multi-objective Ensemble Construction , Learning and Evolution

An ensemble of learning machines has been theoretically and empirically shown to generalise better than single learners. Diversity and accuracy are two key properties that ensemble members should possess in order for this generalisation principle to hold. Viewing these properties as objectives, we take the position of rendering multi-objective evolutionary algorithms as effective solution concepts to the problem of ensemble construction and learning.
Three‐dimensional numerical simulation of Martian global dust storms

We present results from the first numerical simulations of simultaneously evolving three-dimensional thermal, dynamical, and radiatively active suspended dust fields in the Martian atmosphere. Simulations of southern summer dust storms (arising from a prescribed southern subtropical surface dust source) conducted with a Mars general circulation model (GCM) illustrate the important role of dust transport by atmospheric eddies. Both traveling and stationary eddies contribute to dust transport to high latitudes in both hemispheres. These hemispheric differences arise from seasonal and topographic effects. Transport into the south polar regions is accomplished primarily by thermally and topographically forced standing eddies. Both traveling and stationary eddies transport dust to middle and high northern (winter) latitudes. Atmospheric wave motions are affected by the developing storms. Thermal tidal amplitudes increase at storm onset, with the calculated pressure response at a model grid point corresponding to the location of the Viking Lander 1 site in good agreement with observations. In qualitative agreement with observations, winter hemisphere baroclinic waves weaken during the early stages of the storm, but as the storm wanes, amplitudes of these waves increase. A slowly westward propagating (9 degrees of longitude per sol) zonal wavenumber one feature in the temperature and geopotential fields at middle northern latitudes amplifies rapidly during the initial sols (Martian solar days) of the simulated storms. This feature is suggestive of the observed north polar warming which occurred during the 1977B global dust storm, but the simulations produce a much weaker polar warming (∼10 K at 0.5 mbar) than was observed (40–50 K). The globally integrated CO2 condensation rate decreases by 15–20% during the simulated dust storm onset and would likely be decreased more if a stronger polar warming were produced. During the initial stages of the simulated storms, surface stress values in the southern subtropics intensify due primarily to the intensification of the Hadley circulation and thermally driven tides. This supports the hypothesis that these components of the general circulation contribute strong positive feedbacks to the developing storms.
The role of behaviour change in eating and physical activity in the battle against childhood obesity

Obesity results from many influences including genetic and environmental. But eating and physical activity are the two fundamental factors which influence obesity development. This work investigates how food consumption choices and the extent of physical activity have an influence on weight, BMI and the prevalence of obesity in a population of children aged 2-15 years. Around forty years ago, the weight profile of the child (or adult) population was not particularly abnormal. But with increases in energy-dense food consumption and reductions in physical activity, weight, BMI and the prevalence of obesity has increased dramatically, especially since the 1990’s. Results from our model can explain these trends. If no interventions are taken to counteract them then these markers will continue to increase in the future with consequential health effects as the children become adults. In an effort to uncover the most effective interventions, this study highlights the role that a system dynamics model can play to help manage the problem in childhood, particularly through considering behavioural changes. Optimisation experiments are conducted to determine whether interventions on the energy intake or energy expenditure sides are likely to be most effective. In anticipated developments of this research it is suggested that the Theory of Planned Behaviour could be used as a framework to identify the motivational factors that influence children in their eating and physical activity habits.
Is there any relationship between serum and urine neopterin and serum interferon‐γ levels in the activity of Behcet's disease?

Background Behcet's disease (BD) is a chronic, inflammatory, multisystem vasculitic disorder. There is no reliable laboratory marker that indicates disease activity. Neopterin is an immunological marker of cellular immune activation, which is secreted by monocytes/macrophages as a result of interferon‐gamma (IFN‐γ) secretion by activated T lymphocytes.
Xenon and Hypothermia Combine Additively, Offering Long-Term Functional and Histopathologic Neuroprotection After Neonatal Hypoxia/Ischemia

Background and Purpose— Hypoxic/ischemic (HI) brain injury affects 1 to 6 per 1000 live human births, with a mortality of 15% to 20%. A quarter of survivors have permanent disabilities. Hypothermia is the only intervention that improves outcome; however, further improvements might be obtained by combining hypothermia with additional treatments. Xenon is a noble anesthetic gas with an excellent safety profile, showing great promise in vitro and in vivo as a neuroprotectant. We investigated combinations of 50% xenon (Xe50%) and hypothermia of 32°C (HT32°C) as a post-HI therapy. Methods— An established neonatal rat HI model was used. Serial functional neurologic testing into adulthood 10 weeks after injury was performed, followed by global and regional brain histopathology evaluation. Results— In the combination Xe50%HT32°C group, complete restoration of long-term functional outcomes was seen. Hypothermia produced improvement on short- (P<0.001) and long- (P<0.001) term functional testing, whereas Xe50% alone predominantly improved long-term function (P<0.05), suggesting that short-term testing does not always predict eventual outcome. Similarly, the Xe50%HT32°C combination produced the greatest (71%) improvement in global histopathology scores, a pattern mirrored in the regional scores, whereas Xe50% and HT32°C individually produced smaller improvements (P<0.05 and P<0.001, respectively). The interaction between the 2 treatments was additive. Conclusions— The xenon/hypothermia combination additively confers greater protection after HI than either treatment alone. The functional improvement is almost complete, is sustained long term, and is accompanied by greatly improved histopathology. The unique safety profile differentiates xenon as an attractive combination therapy with hypothermia to improve the otherwise bleak outcome from neonatal HI.
Selective Deletion of the A1 Adenosine Receptor Abolishes Heart-Rate Slowing Effects of Intravascular Adenosine In Vivo

Objective Intravenous adenosine induces temporary bradycardia. This is due to the activation of extracellular adenosine receptors (ARs). While adenosine can signal through any of four ARs (A1AR, A2AAR, A2BAR, A3AR), previous ex vivo studies implicated the A1AR in the heart-rate slowing effects. Here, we used comparative genetic in vivo studies to address the contribution of individual ARs to the heart-rate slowing effects of intravascular adenosine. Methods and Results We studied gene-targeted mice for individual ARs to define their in vivo contribution to the heart-rate slowing effects of adenosine. Anesthetized mice were treated with a bolus of intravascular adenosine, followed by measurements of heart-rate and blood pressure via a carotid artery catheter. These studies demonstrated dose-dependent slowing of the heart rate with adenosine treatment in wild-type, A2AAR−/−, A2BAR−/−, or A3AR−/− mice. In contrast, adenosine-dependent slowing of the heart-rate was completely abolished in A1AR−/− mice. Moreover, pre-treatment with a specific A1AR antagonist (DPCPX) attenuated the heart-rate slowing effects of adenosine in wild-type, A2AAR−/−, or A2BAR−/− mice, but did not alter hemodynamic responses of A1AR−/− mice. Conclusions The present studies combine pharmacological and genetic in vivo evidence for a selective role of the A1AR in slowing the heart rate during adenosine bolus injection.
Denial of illness; its occurrence in one hundred consecutive cases of hemiplegia.

MANY DESCRIPTIONS of the phenomenon of denial of illness have been published.1The literature contains little, however, concerning the frequency of its occurrence. The purpose of this investigation was to determine the incidence of denial of illness in patients with hemiplegia. We chose hemiplegia because of its prevalence and extensive somatic involvement and for historical reasons. The study also permitted us to observe denial of illness in relation to the mental state of the patient, the side of the body involved, and other factors. The term anosognosia, introduced by Babinski in 1914,1ereferred to two cases of left hemiplegia, but it has subsequently been used by others to denote denial of other illnesses as well. Another phenomenon, the denial of existence of a part of the body, sometimes called autotopagnosia or somatoagnosia,1ghas at times been confused with anosognosia. For the sake of clarity, we decided to
Minimizing the number of actions in parallel planning

In the domain of classical planning one distinguishes plans which are optimal in their number of actions, they are referred as sequential plans, from plans which are optimal in their number of levels, they are referred as parallel plans. Searching optimal sequential plans is generally considered harder than searching optimal parallel plans. Buttner and Rintanen have proposed a search procedure which computes plans whose numbers of levels are fixed and whose numbers of actions are minimal. This procedure is notably used to calculate optimal sequential plans, starting from an optimal parallel plan. In this paper we describe a similar approach, which we have developed from the planner FDP. The idea consists in maintaining two structures, the first one representing the parallel plan and the other representing the sequential plan, performing the choices simultaneously in both structures. The techniques which were developed in FDP to compute sequential plans or parallel plans enable failures detection in the two structures. Experimental results show that this approach is in some cases more efficient than FDP when searching optimal sequential plans.
The Protective Role of Nitric Oxide in a Neurotoxicant- Induced Demyelinating Model1

Demyelination is often associated with acute inflammatory events involving the recruitment-activation of microglia/macrophage, astrocytes, and leukocytes. The ultimate role of inflammatory products in demyelinating disease and in the survival of oligodendrocytes, the myelin forming cells, is unresolved. The current study examines the role of inducible NO synthase (iNOS)-derived NO in a neurotoxicant-induced model of demyelination. NO levels were greatly elevated in the midline corpus callosum during demyelination in genetically intact C57BL/6 mice, and this NO was due solely to the induction of iNOS, as the correlates of NO were not found in mice lacking iNOS. C57BL/6 mice lacking iNOS exhibited more demyelination, but did not display an increased overall cellularity in the corpus callosum, attributable to an unimpeded microglia/macrophage presence. An enhanced course of pathology was noted in mice lacking iNOS. This was associated with a greater depletion of mature oligodendrocytes, most likely due to apoptosis of oligodendrocytes. Microglia and astrocytes did not undergo apoptosis during treatment. Our results suggest a moderately protective role for NO during acute inflammation-association demyelination.