Updating DL-Lite ontologies through first-order queries

In this paper we study instance-level update in DL-LiteA, the description logic underlying the OWL 2 QL standard. In particular we focus on formula-based approaches to ABox insertion and deletion. We show that DL-LiteA, which is well-known for enjoying first-order rewritability of query answering, enjoys a first-order rewritability property also for updates. That is, every update can be reformulated into a set of insertion and deletion instructions computable through a nonrecursive datalog program. Such a program is readily translatable into a first-order query over the ABox considered as a database, and hence into SQL. By exploiting this result, we implement an update component for DLLiteA-based systems and perform some experiments showing that the approach works in practice.Peer ReviewedPostprint (author's final draft

Involvement of autophagy in the effect of exercise on left ventricular hypertrophy induced by high fat diet in rats

Chaired Posters PresentationObjectives: Left ventricular hypertrophy (LVH) associated with obesity increases the morbidity and mortality of cardiovascular disease, which could be attenuated by exercise in overweight and hypertensive patients. The lysosomal degradation pathway − autophagy is reportedly mediated the beneficial effect of exercise on glucose and lipid homeostasis. The present study aimed to investigate the involvement of autophagy in the effect of exercise on LVH induced by high fat diet in rats. Methods: Female adult SD rats were divided into 4 groups namely: (i) high fat diet (HFD), (ii) HFD+exercise, (iii) exercise, (iv) control. Rats in the HFD groups were orally fed with high-fat chow (30% fat) daily for 12 weeks, and rats in the exercise groups had exercise with a motorized wheel in the last 4 weeks. Noninvasive measures of systolic pressure and fat composition were assessed, respectively by tail cuff and MRI. The expression of markers for cardiac hypertrophy and the protein expression in autophagic pathway were determined by quantitative real time-PCR and western blot, respectively. Statistical significance was at p<0.05 with ANOVA analysis followed by post-hoc tests. Results: Rats fed with HFD had LVH (increased heart weight and LV/ RV+septum ratio) with higher levels of body weight, arterial pressures and fat composition than that of the control rat. In addition, the QTc interval and the diameter and disarray of ventricular myocytes were significantly increased in the HFD group, supported by elevated levels of the expression of hypertrophic markers (ANP, BNP, β-MHC). These parameters were attenuated by exercise in the HFD-fed rats. Moreover, we found elevated levels of LC3II in the HFD heart, which were also attenuated by exercise, suggesting an involvement of autophagy in the beneficial effect of exercise. Furthermore, the expression level of AMPKα was also increased in the exercise groups. Conclusion: We demonstrated that exercise lowers the body weight and attenuates the HFD-induced LVH in rats, which probably involves autophagy. Future studies will focus on the role of autophagy in the pathogenesis.published_or_final_versio

Oxidative stress induced by intermittent hypoxia exacerbates lipid accumulation and inflammation in a cell model of non-alcoholic steatohepatitis

Oral PresentationBackground/Aims: The prevalence of obstructive sleep apnea (OSA) is high in patients with non-alcoholic fatty liver disease (NAFLD) and NASH is a progressive hallmark of the pathogenesis of NAFLD. Chronic intermittent hypoxia is associated with recurrent episodes of oxygen desaturation and reoxygenation in OSA patients, leading to excessive production of reactive oxygen species (ROS). The causal link between OSA and NAFLD is not known and the mechanistic effect of intermittent hypoxia (IH) on the pathogenesis of NAFLD remains elusive. Here we tested the hypothesis that IH-induced oxidative stress aggravates lipid accumulation and inflammation induced by sodium palmitate in HepG2 cells. Materials and Methods: HepG2 cells were treated with sodium palmitate or vehicle under normoxia (Nx) or IH condition for 72 hours in the present or absence of a ROS scavenger MnTBAP. Cell viability was detected by MTT assay and intracellular lipid deposit was examined by oil red staining. Lipid peroxidation was measured by malondialdehyde (MDA) assay and levels of reactive oxygen species (ROS) were detected by CM-H2DCFDA staining. The expressions of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), fatty acid uptake-associated genes (caveolin-1 and FATP5), fatty acid synthesis genes (SREBP1 and ACC1) and fatty acid β-oxidation gene ACOX were determined by real-time PCR. Results: Results showed that sodium palmitate increased lipid deposit in the cells and it also decreased cell viability. The effect of sodium palmitate was more prominent in the group co-treated with hypoxia. Levels of MDA and ROS and the expressions of IL-1β, TNF-α, IL-6 and caveolin-1, but not FATP5, were significantly increased in the palmitate- or hypoxia-treated group and were remarkably elevated in the co-treated group. These effects were abolished by MnTBAP treatment. In addition, levels of the expression of ACOX, SREBP1 and ACC1 were significantly lowered in the cells treated with palmitate or hypoxia and the expressions were much less in the cotreated group. Treatment of MnTBAP prevented the decreased expression of ACOX but had no effect on the SREBP1 and ACC1 expression. Conclusion: IH-induced oxidative stress exacerbates lipid accumulation and inflammation induced by sodium palmitate in HepG2 cells, probably mediated by an increase in lipid uptake and a decrease in the fatty acid β-oxidation.published_or_final_versio

On Feedback Vertex Set: New Measure and New Structures

We present a new parameterized algorithm for the {feedback vertex set} problem ({\sc fvs}) on undirected graphs. We approach the problem by considering a variation of it, the {disjoint feedback vertex set} problem ({\sc disjoint-fvs}), which finds a feedback vertex set of size $k$ that has no overlap with a given feedback vertex set $F$ of the graph $G$. We develop an improved kernelization algorithm for {\sc disjoint-fvs} and show that {\sc disjoint-fvs} can be solved in polynomial time when all vertices in $G \setminus F$ have degrees upper bounded by three. We then propose a new branch-and-search process on {\sc disjoint-fvs}, and introduce a new branch-and-search measure. The process effectively reduces a given graph to a graph on which {\sc disjoint-fvs} becomes polynomial-time solvable, and the new measure more accurately evaluates the efficiency of the process. These algorithmic and combinatorial studies enable us to develop an $O^*(3.83^k)$-time parameterized algorithm for the general {\sc fvs} problem, improving all previous algorithms for the problem.Comment: Final version, to appear in Algorithmic

First observation of psi(2S)-->K_S K_L

The decay psi(2S)-->K_S K_L is observed for the first time using psi(2S) data collected with the Beijing Spectrometer (BESII) at the Beijing Electron Positron Collider (BEPC); the branching ratio is determined to be B(psi(2S)-->K_S K_L) = (5.24\pm 0.47 \pm 0.48)\times 10^{-5}. Compared with J/psi-->K_S K_L, the psi(2S) branching ratio is enhanced relative to the prediction of the perturbative QCD ``12%'' rule. The result, together with the branching ratios of psi(2S) decays to other pseudoscalar meson pairs (\pi^+\pi^- and K^+K^-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.Comment: 5 pages, 4 figures, 2 tables, submitted to Phys. Rev. Let

Garlic-derived S-allylmercaptocysteine ameliorates nonalcoholic fatty liver disease in a rat model through inhibition of apoptosis and enhancing autophagy

published_or_final_versio

Study of psi(2S) decays to X J/psi

Using J/psi -> mu^+ mu^- decays from a sample of approximately 4 million psi(2S) events collected with the BESI detector, the branching fractions of psi(2S) -> eta J/psi, pi^0 pi^0 J/psi, and anything J/psi normalized to that of psi(2S) -> pi^+ pi^- J/psi are measured. The results are B(psi(2S) -> eta J/psi)/B(psi(2S) -> pi^+ pi^- J/psi) = 0.098 \pm 0.005 \pm 0.010, B(psi(2S) -> pi^0 pi^0 J/psi)/B(psi(2S) -> pi^+ pi^- J/psi) = 0.570 \pm 0.009 \pm 0.026, and B(psi(2S) -> anything J/psi)/B(psi(2S) -> pi^+ pi^- J/psi) = 1.867 \pm 0.026 \pm 0.055.Comment: 13 pages, 8 figure

Reading faces: differential lateral gaze bias in processing canine and human facial expressions in dogs and 4-year-old children

Sensitivity to the emotions of others provides clear biological advantages. However, in the case of heterospecific relationships, such as that existing between dogs and humans, there are additional challenges since some elements of the expression of emotions are species-specific. Given that faces provide important visual cues for communicating emotional state in both humans and dogs, and that processing of emotions is subject to brain lateralisation, we investigated lateral gaze bias in adult dogs when presented with pictures of expressive human and dog faces. Our analysis revealed clear differences in laterality of eye movements in dogs towards conspecific faces according to the emotional valence of the expressions. Differences were also found towards human faces, but to a lesser extent. For comparative purpose, a similar experiment was also run with 4-year-old children and it was observed that they showed differential processing of facial expressions compared to dogs, suggesting a species-dependent engagement of the right or left hemisphere in processing emotions

Population assessment of future trajectories in coronary heart disease mortality.

Background: Coronary heart disease (CHD) mortality rates have been decreasing in Iceland since the 1980s, largely reflecting improvements in cardiovascular risk factors. The purpose of this study was to predict future CHD mortality in Iceland based on potential risk factor trends. Methods and findings: The previously validated IMPACT model was used to predict changes in CHD mortality between 2010 and 2040 among the projected population of Iceland aged 25–74. Calculations were based on combining: i) data on population numbers and projections (Statistics Iceland), ii) population risk factor levels and projections (Refine Reykjavik study), and iii) effectiveness of specific risk factor reductions (published meta-analyses). Projections for three contrasting scenarios were compared: 1) If the historical risk factor trends of past 30 years were to continue, the declining death rates of past decades would level off, reflecting population ageing. 2) If recent trends in risk factors (past 5 years) continue, this would result in a death rate increasing from 49 to 70 per 100,000. This would reflect a recent plateau in previously falling cholesterol levels and recent rapid increases in obesity and diabetes prevalence. 3) Assuming that in 2040 the entire population enjoys optimal risk factor levels observed in low risk cohorts, this would prevent almost all premature CHD deaths before 2040. Conclusions: The potential increase in CHD deaths with recent trends in risk factor levels is alarming both for Iceland and probably for comparable Western populations. However, our results show considerable room for reducing CHD mortality. Achieving the best case scenario could eradicate premature CHD deaths by 2040. Public health policy interventions based on these predictions may provide a cost effective means of reducing CHD mortality in the future

The iron-chelating drug M30 down-regulates carbon tetrachloride (CCI4)-induced hepatic oxidative stress, inflammation and apoptosis in vitro

Topic: 2 Acute Liver FailureThis journal suppl. entitled: APASL Liver Week 2013BACKGROUND/AIMS: The novel multifunctional brain permeable ironchelator M30 possesses neuroprotective activities against several insults applicable to various neurodegenerative diseases. However, the effect of M30 on CCl4 induced acute liver damage is still unknown. The aim of this study is to investigate whether the multifunctional drug M30 could ameliorate CCl4 induced hepatic injury in human HepG2 cell line. METHODS: HepG2 cells were grown in DMEM supplemented with ...postprin