Plasma annexin A5 level relates inversely to the severity of coronary stenosis.

Contains fulltext : 51934.pdf (publisher's version ) (Closed access)Exogenous radiolabeled annexin A5 is taken up by atherosclerotic tissue. We measured endogenous plasma annexin A5 and circulating oxidized low-density lipoprotein (oxLDL), a biochemical marker of atherosclerosis, in men with either severe angiographically determined coronary stenosis (n=90) or no or only minor stenosis (n=96). Men without history of cardiac disease or treatment and free of plaques in the carotid artery (by ultrasonography) were taken as controls (n=87). Opposite to oxLDL, annexin A5 decreased at increasing severity of stenosis. OxLDL was lowest and annexin A5 was highest in controls. Percentage differences between groups were higher for annexin A5 than for oxLDL, and highest for oxLDL/annexin A5 ratio. The oxLDL/annexin A5 ratio is a better marker of the severity of coronary stenosis than oxLDL alone, may reflect the presence and extent of the atherosclerotic cardiovascular disease, and might prove useful for preclinical screening purposes

Primary resistance to integrase strand-transfer inhibitors in Europe

Objectives: The objective of this study was to define the natural genotypic variation of the HIV-1 integrase gene across Europe for epidemiological surveillance of integrase strand-transfer inhibitor (InSTI) resistance. Methods: This was a multicentre, cross-sectional study within the European SPREAD HIV resistance surveillance programme. A representative set of 300 samples was selected from 1950 naive HIV-positive subjects newly diagnosed in 2006-07. The prevalence of InSTI resistance was evaluated using quality-controlled baseline population sequencing of integrase. Signature raltegravir, elvitegravir and dolutegravir resistance mutations were defined according to the IAS-USA 2014 list. In addition, all integrase substitutions relative to HXB2 were identified, including those with a Stanford HIVdb score=10 to at least one InSTI. To rule out circulation of minority InSTIresistant HIV, 65 samples were selected for 454 integrase sequencing. Results: For the population sequencing analysis, 278 samples were retrieved and successfully analysed. No signature resistance mutations to any of the InSTIswere detected. Eleven (4%) subjects hadmutations at resistance-associated positions with an HIVdb score =10. Of the 56 samples successfully analysed with 454 sequencing, no InSTI signature mutationsweredetected, whereas integrase substitutionswithanHIVdbscore=10were found in8(14.3%) individuals. Conclusions:No signature InSTI-resistant variantswere circulating in Europe before the introduction of InSTIs. However, polymorphisms contributing to InSTI resistancewere not rare. As InSTI use becomes more widespread, continuous surveillance of primary InSTI resistance is warranted. These data will be key to modelling the kinetics of InSTI resistance transmission in Europe in the coming years. © The Author 2015. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved