Dynamic correlation between stock market and oil prices: The case of oil-importing and oil-exporting countries

The paper investigates the time-varying correlation between stock market prices and oil prices for oil-importing and oil-exporting countries. A DCC-GARCH-GJR approach is employed to test the above hypothesis based on data from six countries; Oil-exporting: Canada, Mexico, Brazil and Oil-importing: USA, Germany, Netherlands. The contemporaneous correlation results show that i) although time-varying correlation does not differ for oil-importing and oil-exporting economies, ii) the correlation increases positively (negatively) in respond to important aggregate demand-side (precautionary demand) oil price shocks, which are caused due to global business cycle’s fluctuations or world turmoil (i.e. wars). Supply-side oil price shocks do not influence the relationship of the two markets. The lagged correlation results show that oil prices exercise a negative effect in all stock markets, regardless the origin of the oil price shock. The only exception is the 2008 global financial crisis where the lagged oil prices exhibit a positive correlation with stock markets. Finally, we conclude that in periods of significant economic turmoil the oil market is not a safe haven for offering protection against stock market losses

Share price informativeness and dividend smoothing behavior in GCC markets

This paper examines the dividend smoothing behaviour in Gulf Cooperation Council (GCC) countries, in emerging markets where the response to news and the economic environment are different from those of developed countries. We examine the effect of share price informativeness on dividend smoothing in the (GCC) markets, using an unbalanced panel data for a sample of 628 GCC-listed firms during 1994-2016. For the regression analysis, the hypotheses are tested using panel regressions and GMM estimation. The empirical results can be summarised in the following manner: First, the Lintner model shows that the dividend smoothing degree in GCC firms is comparable to that of a developed market. Second, and importantly, the results reveal that the dividend smoothing in GCC firms is sensitive to private information of share prices. Finally, the findings indicate that information asymmetry and agency-based models affect the tendency to smooth dividends in the GCC markets

INVESTIGATING INTEROPERABILITY CAPABILITIES BETWEEN IFC AND CITYGML LOD 4 – RETAINING SEMANTIC INFORMATION

Applications of 3D City Models range from assessing the potential output of solar panels across a city to determining the best location for 5G mobile phone masts. While in the past these models were not readily available, the rapid increase of available data from sources such as Open Data (e.g. OpenStreetMap), National Mapping and Cadastral Agencies and increasingly Building Information Models facilitates the implementation of increasingly detailed 3D Models. However, these sources also generate integration challenges relating to heterogeneity, storage and efficient management and visualization. CityGML and IFC (Industry Foundation Classes) are two standards that serve different application domains (GIS and BIM) and are commonly used to store and share 3D information. The ability to convert data from IFC to CityGML in a consistent manner could generate 3D City Models able to represent an entire city, but that also include detailed geometric and semantic information regarding its elements. However, CityGML and IFC present major differences in their schemas, rendering interoperability a challenging task, particularly when details of a building’s internal structure are considered (Level of Detail 4 in CityGML). The aim of this paper is to investigate interoperability options between the aforementioned standards, by converting IFC models to CityGML LoD 4 Models. The CityGML Models are then semantically enriched and the proposed methodology is assessed in terms of model’s geometric validity and capability to preserve semantics

Effect of hypoxia on lung gene expression and proteomic profile: insights into the pulmonary surfactant response

Exposure of lung to hypoxia has been previously reported to be associated with significant alterations in the protein content of bronchoalveolar lavage (BAL) and lung tissue. In the present work we have used a proteomic approach to describe the changes in protein complement induced by moderate long-term hypoxia (rats exposed to 10% O2 for 72h) in BAL and lung tissue, with a special focus on the proteins associated with pulmonary surfactant, which could indicate adaptation of this system to limited oxygen availability. The analysis of the general proteomic profile indicates a hypoxia-induced increase in proteins associated with inflammation both in lavage and lung tissue. Analysis at mRNA and protein levels revealed no significant changes induced by hypoxia on the content in surfactant proteins or their apparent oligomeric state. In contrast, we detected a hypoxia-induced significant increase in the expression and accumulation of hemoglobin in lung tissue, at both mRNA and protein levels, as well as an accumulation of hemoglobin both in BAL and associated with surface-active membranes of the pulmonary surfactant complex. Evaluation of pulmonary surfactant surface activity from hypoxic rats showed no alterations in its spreading ability, ruling out inhibition by increased levels of serum or inflammatory proteins.Ministerio de Ciencia BIO2012-30733Ministerio de Ciencia CSD2007-00010Gobierno de la Comunidad de Madrid S2009MAT-1507National Institutes of Health NIH HL3478

The impact of surfactant protein-A on ozone-induced changes in the mouse bronchoalveolar lavage proteome

<p>Abstract</p> <p>Background</p> <p>Ozone is a major component of air pollution. Exposure to this powerful oxidizing agent can cause or exacerbate many lung conditions, especially those involving innate immunity. Surfactant protein-A (SP-A) plays many roles in innate immunity by participating directly in host defense as it exerts opsonin function, or indirectly via its ability to regulate alveolar macrophages and other innate immune cells. The mechanism(s) responsible for ozone-induced pathophysiology, while likely related to oxidative stress, are not well understood.</p> <p>Methods</p> <p>We employed 2-dimensional difference gel electrophoresis (2D-DIGE), a discovery proteomics approach, coupled with MALDI-ToF/ToF to compare the bronchoalveolar lavage (BAL) proteomes in wild type (WT) and SP-A knockout (KO) mice and to assess the impact of ozone or filtered air on the expression of BAL proteins. Using the PANTHER database and the published literature most identified proteins were placed into three functional groups.</p> <p>Results</p> <p>We identified 66 proteins and focused our analysis on these proteins. Many of them fell into three categories: defense and immunity; redox regulation; and protein metabolism, modification and chaperones. In response to the oxidative stress of acute ozone exposure (2 ppm; 3 hours) there were many significant changes in levels of expression of proteins in these groups. Most of the proteins in the redox group were decreased, the proteins involved in protein metabolism increased, and roughly equal numbers of increases and decreases were seen in the defense and immunity group. Responses between WT and KO mice were similar in many respects. However, the percent change was consistently greater in the KO mice and there were more changes that achieved statistical significance in the KO mice, with levels of expression in filtered air-exposed KO mice being closer to ozone-exposed WT mice than to filtered air-exposed WT mice.</p> <p>Conclusion</p> <p>We postulate that SP-A plays a role in reactive oxidant scavenging in WT mice and that its absence in the KO mice in the presence or absence of ozone exposure results in more pronounced, and presumably chronic, oxidative stress.</p

Enhancing e-Infrastructures with Advanced Technical Computing: Parallel MATLAB® on the Grid

MATLAB® is widely used within the engineering and scientific fields as the language and environment for technical computing, while collaborative Grid computing on e-Infrastructures is used by scientific communities to deliver a faster time to solution. MATLAB allows users to express parallelism in their applications, and then execute code on multiprocessor environments such as large-scale e-Infrastructures. This paper demonstrates the integration of MATLAB and Grid technology with a representative implementation that uses gLite middleware to run parallel programs. Experimental results highlight the increases in productivity and performance that users obtain with MATLAB parallel computing on Grids

Survival of Surfactant Protein-A1 and SP-A2 Transgenic Mice After Klebsiella pneumoniae Infection, Exhibits Sex-, Gene-, and Variant Specific Differences; Treatment With Surfactant Protein Improves Survival

Surfactant protein A (SP-A) is involved in lung innate host defense and surfactant-related functions. The human SFTPA1 and SFTPA2 genes encode SP-A1 and SP-2 proteins, and each gene has been identified with numerous genetic variants. SP-A1 and SP-A2 differentially enhance bacterial phagocytosis. Sex differences have been observed in pulmonary disease and in survival of wild type and SP-A knockout (KO) mice. The impact of human SP-A variants on survival after infection is unknown. In this study, we determined whether SP-A variants differentially affect survival of male and female mice infected with Klebsiella pneumoniae. Transgenic (TG) mice, where each carries a different human (h) SP-A1 (6A2, 6A4), SP-A2 (1A0, 1A3) variant or both variants SP-A1/SP-A2 (6A2/1A0, co-ex), and SP-A- KO, were utilized. The hTG and KO mice were infected intratracheally with K. pneumoniae bacteria, and groups of KO mice were treated with SP-A1 or SP-A2 either prior to and/or at the time of infection and survival for both experimental groups was monitored over 14 days. The binding of purified SP-A1 and SP-A2 proteins to phagocytic and non-phagocytic cells and expression of cell surface proteins in alveolar macrophages (AM) from SP-A1 and SP-A2 mice was examined. We observed gene-, variant-, and sex-specific (except for co-ex) differences with females showing better survival: (a) Gene-specific differences: co-ex = SP-A2 &gt; SP-A1 &gt; KO (both sexes); (b) Variant-specific survival co-ex (6A2/1A0) = 1A0 &gt; 1A3 = 6A2 &gt; 6A4 (both sexes); (c) KO mice treated with SPs (SP-A1 or SP-A2) proteins exhibit significantly (p &lt; 0.05) better survival; (d) SP-A1 and SP-A2 differentially bind to phagocytic, but not to non-phagocytic cells, and AM from SP-A1 and SP-A2 hTG mice exhibit differential expression of cell surface proteins. Our results indicate that sex and SP-A genetics differentially affect survival after infection and that exogenous SP-A1/SP-A2 treatment significantly improves survival. We postulate that the differential SP-A1/SP-A2 binding to the phagocytic cells and the differential expression of cell surface proteins that bind SP-A by AM from SP-A1 and SP-A2 mice play a role in this process. These findings provide insight into the importance of sex and innate immunity genetics in survival following infection