The European Convention on Human Rights and the economic crisis : the issue of poverty

Distinguished Lecture delivered on the occasion of the XXIV Human Rights Law course of the Academy of European Law, on 24 June 2013.The European Convention on Human Rights is more than ever our common heritage (patrimoine commun) and we share in this respect a common responsibility at national and international level, between judges and scholars. That is why I really appreciate this kind of meeting since it gives us an opportunity to discuss the rights and freedoms enshrined in the Convention as they are interpreted by the European Court of Human Rights in the context of our contemporary society. That’s really the intelligence of the Convention: through the Court’s interpretation, the rights written in 1950 can have a meaning today in 2013. As legal theorists have observed, the law must be stable yet it cannot stand still. Adaptation and modification have been constant features of the Convention since 1950 and continue to be so today. In this lecture, I will examine the contribution of the European Court of Human Rights to the fight against poverty and social exclusion. I argue in favour of a reading of the European Convention on Human Rights that is aligned with the necessities of the times. In the face of the global financial and economic crisis that developed since 2008, this does not mean sacrificing human rights in the name of austerity and macro-economic discipline; it means improving the protection of the most vulnerable and marginalized segments of the population, in a context in which the rights to access to courts, to housing or to social security have further gained in relevance and importance. I will start by saying a few words about crisis, and particularly economic crisis, and human rights, before examining different aspects of the European Court of Human Rights’ case-law addressing the question of poverty

The European Convention on Human Rights and Church-State Relations. Pluralism vs. Pluralism

SUMMARY: INTRODUCTION: Key Provision – An Indirect Regulation - The Court is Not a Constitutional Court - Judicial Restraint - A Vision of Religious Freedom - Institutional Dimension of Religious Freedom - I. MODELS: No Arbitrary State Interference - State Neutrality and Impartiality - II. COUNTER-MODELS: Islam – Sects

More Women -But Which Women? A Reply to Stéphanie Hennette Vauchez

Abstract Having spent almost 14 years as a judge at the European Court of Huma

Molecular models of human P-glycoprotein in two different catalytic states

P-glycoprotein belongs to the family of ATP-binding cassette proteins which hydrolyze ATP to catalyse the translocation of their substrates through membranes. This protein extrudes a large range of components out of cells, especially therapeutic agents causing a phenomenon known as multidrug resistance. Because of its clinical interest, its activity and transport function have been largely characterized by various biochemical studies. In the absence of a high-resolution structure of P-glycoprotein, homology modeling is a useful tool to help interpretation of experimental data and potentially guide experimental studies.Journal ArticleResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe

Cellular pharmacokinetics of telavancin, a novel lipoglycopeptide antibiotic, and analysis of lysosomal changes in cultured eukaryotic cells (J774 mouse macrophages and rat embryonic fibroblasts)

Background Telavancin is a lipoglycopeptide with multiple mechanisms of action that include membrane-destabilizing effects towards bacterial cells. It shows bactericidal activity against forms of Staphylococcus aureus (phagolysosomal infection) with different resistance phenotypes [methicillin-resistant S. aureus, vancomycin-intermediate S. aureus or vancomycin-resistant S. aureus]. We examine here the uptake, efflux and intracellular distribution of telavancin in eukaryotic cells as well as its potential to induce lysosomal changes (in comparison with vancomycin and oritavancin). Methods J774 macrophages and rat embryo fibroblasts were exposed for up to 24 and 72 h to telavancin (5-90 mg/L). The following studies were performed: measurement of (14)C-labelled telavancin cellular uptake and subcellular distribution (cell fractionation), determination of pericellular membrane integrity (lactate dehydrogenase release), electron microscopy with morphometric analysis of changes in lysosome size and determination of total phospholipid and cholesterol content. Results The uptake of telavancin proceeded linearly as a function of time and concentration in both cell types (clearance rate of approximately 10 mL/g of protein/h). Efflux (macrophages) was approximately 5.7-fold slower. Telavancin subcellular distribution was superimposable on that of a lysosomal marker (N-acetyl-beta-hexosaminidase). It did not cause an increase in the release of lactate dehydrogenase and did not induce significant increases in total phospholipid or cholesterol content. It caused only mild morphological lysosomal alterations (similar to vancomycin and much less than oritavancin by morphometric analysis). Conclusions Telavancin is taken up by eukaryotic cells and localizes in lysosomes, causing mild morphological alterations without evidence of lipid metabolism alterations. These data support our observations that telavancin is active against intracellular S. aureus

Penicillin-binding Proteins (PBP) and Lmo0441 (a PBP-like protein) play a role in Beta-lactam sensitivity of Listeria monocytogenes

While seven penicillin-binding proteins (PBPs) or PBP-like proteins have been identified either by radiolabelled penicillin binding studies or genomic analysis, only PBP3 has been considered of interest for Beta-lactams activity against Listeria monocytogenes. Herein we reveal that both PBP4 and Lmo0441 (a PBP-like protein) play a direct role in cephalosporin activity in L. monocytogenes while PBP4 additionally has a protective affect against both penicillin and carbapenem

Correlation between cytotoxicity induced by Pseudomonas aeruginosa clinical isolates from acute infections and IL-1β secretion in a model of human THP-1 monocytes

Type III secretion system (T3SS) in Pseudomonas aeruginosa is associated with poor clinical outcome in acute infections. T3SS allows for injection of bacterial exotoxins (e.g. ExoU or ExoS) into the host cell, causing cytotoxicity. It also activates the cytosolic NLRC4 inflammasome, activating caspase-1, inducing cytotoxicity and release of mature IL-1β, which impairs bacterial clearance. In addition, flagellum-mediated motility has been suggested to also modulate inflammasome response and IL-1β release. Yet the capacity of clinical isolates to induce IL-1β release and its relation with cytotoxicity have never been investigated. Using 20 clinical isolates from acute infections with variable T3SS expression levels and human monocytes, our aim was to correlate IL-1β release with toxin expression, flagellar motility and cytotoxicity. ExoU-producing isolates caused massive cell death but minimal release of IL-1β, while those expressing T3SS but not ExoU (i.e. expressing ExoS or no toxins) induced caspase-1 activation and IL-1β release, the level of which was correlated with cytotoxicity. Both effects were prevented by a specific caspase-1 inhibitor. Flagellar motility was not correlated with cytotoxicity or IL-1β release. No apoptosis was detected. Thus, T3SS cytotoxicity is accompanied by a modification in cytokine balance for P. aeruginosa clinical isolates that do not express Exo