61 research outputs found

    Is there a fair allocation of healthcare research funds by the European Union?

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    BackgroundThis study aimed to investigate the distribution of European Union (EU) healthcare research grants across EU countries, and to study the effect of the potential influencing factors on grant allocation.MethodsWe analysed publicly available data on healthcare research grants from the 7th Framework Programme and the Horizon 2020 Programme allocated to beneficiaries between 2007 and 2016. Grant allocation was analysed at the beneficiary-, country-, and country group-level (EU-15 versus newer Member States, defined as EU-13). The investigated country-level explanatory variables included GDP per capita, population size, overall disease burden, and healthcare research excellence. Grant amounts per 100,000 inhabitants were used as an outcome variable in the regression analyses.ResultsResearch funds were disproportionally allocated to EU-15 versus the EU-13, as 96.9% of total healthcare grants were assigned to EU-15 countries. At the beneficiary level, EU funding was positively influenced by participating in previous grants. The average grant amount per beneficiary was higher for EU-15 organizations. In the multiple regression analysis GDP per capita (p = 0.002) and research excellence (pConclusionThe uneven allocation of healthcare research funds across EU countries was influenced by GDP per capita, medical research excellence and population size. Wealthier countries with an average population size and strong research excellence in healthcare had more EU funding for healthcare research. Higher disease burden apparently was not associated with more EU research funding. While our findings are in line with analyses on previous periods, they suggest that the EU did not implement any effective policy measures to improve the unfair allocation of research grants.</div

    The Herschel PACS photometer calibration - A time dependent flux calibration for the PACS chopped point-source photometry AOT mode

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    We present a flux calibration scheme for the PACS chopped point-source photometry observing mode based on the photometry of five stellar standard sources. This mode was used for science observations only early in the mission. Later, it was only used for pointing and flux calibration measurements. Its calibration turns this type of observation into fully validated data products in the Herschel Science Archive. Systematic differences in calibration with regard to the principal photometer observation mode, the scan map, are derived and amount to 5-6%. An empirical method to calibrate out an apparent response drift during the first 300 Operational Days is presented. The relative photometric calibration accuracy (repeatability) is as good as 1% in the blue and green band and up to 5% in the red band. Like for the scan map mode, inconsistencies among the stellar calibration models become visible and amount to 2% for the five standard stars used. The absolute calibration accuracy is therefore mainly limited by the model uncertainty, which is 5% for all three bands.Comment: 20 pages, 7 pages of appendix, 11 figures, accepted to appear in Experimental Astronomy, Special Issue for Herschel Calibrations based on the "Herschel Calibration Workshop: Only the Best Data Products for the Legacy Archive", held at ESAC, 25 - 27 March 2013, http://herschel.esac.esa.int/CalibrationWorkshop5.shtm

    Hydrogen Sulfide Abrogates Hemoglobin-Lipid Interaction in Atherosclerotic Lesion

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    This is the final version of the article. Available from Hindawi Publishing Corporation via the DOI in this record.The infiltration of red blood cells into atheromatous plaques is implicated in atherogenesis. Inside the lesion, hemoglobin (Hb) is oxidized to ferri-and ferrylHb which exhibit prooxidant and proinflammatory activities. Cystathione gamma-lyase-(CSE-) derived H 2 S has been suggested to possess various antiatherogenic actions. Expression of CSE was upregulated predominantly in macrophages, foam cells, and myofibroblasts of human atherosclerotic lesions derived from carotid artery specimens of patients. A similar pattern was observed in aortic lesions of apolipoprotein E-deficient mice on high-fat diet. We identified several triggers for inducing CSE expression in macrophages and vascular smooth muscle cells including heme, ferrylHb, plaque lipids, oxidized low-density lipoprotein, tumor necrosis factor-α, and interleukin-1β. In the interplay between hemoglobin and atheroma lipids, H 2 S significantly mitigated oxidation of Hb preventing the formation of ferrylHb derivatives, therefore providing a novel function as a heme-redox-intermediate-scavenging antioxidant. By inhibiting Hb-lipid interactions, sulfide lowered oxidized Hb-mediated induction of adhesion molecules in endothelium and disruption of endothelial integrity. Exogenous H 2 S inhibited heme and Hb-mediated lipid oxidation of human atheroma-derived lipid and human complicated lesion. Our study suggests that the CSE/H 2 S system represents an atheroprotective pathway for removing or limiting the formation of oxidized Hb and lipid derivatives in the atherosclerotic plaque.The research group is supported by the Hungarian Academy of Sciences (11003). This work was supported by Hungarian Government Grants (OTKA) K112333 (József Balla), K109843 (Péter Nagy), and K116024 (Viktória Jeney) and Marie Curie International Reintegration Grant PIRG08-GA-2010-277006 (Péter Nagy). Péter Nagy is a János Bolyai Research Scholar of the Hungarian Academy of Sciences. Viktória Jeney was supported by Zoltán Magyary Fellowship (TÁMOP 4.2.4.A/2-11/1-2012-0001). László Potor was supported by János Apáczai-Csere Fellowship (TÁMOP 4.2.4.A/2-11/1-2012-0001). The project was cofinanced by the European Union and the European Social Fund (ESF) GINOP-2.3.2-15-2016-00043 IRONHEARTH and EFOP-3.6.2-16-2017-00006 LIVE LONGER
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