Euro public debt and the markets: sovereign fundamentals and CDS market dynamics.

At the onset of the crisis, euro area – like all Organisation for Economic Co-operation and Development (OECD) countries – public finances have massively inflated, as is typical in financial crises. The major difference with the past is threefold: the synchronicity across countries of the increase, the debt levels which have been reached; and the existence of credit default swap (CDS) market which has influenced the dynamic of sovereign trading. In this note, we review quickly fundamentals before highlighting the role of the CDS market and the implications for sovereign trading.

Azacytidine Enhances Regulatory T-Cells In Vivo and Prevents Experimental Xenogeneic Graft-Versus-Host Disease

Background The demethylating agent 5-azacytidine (AZA) has proven its efficacy as treatment for myelodysplastic syndrome and acute myeloid leukemia. In addition, AZA can demethylate FOXP3 intron 1 (FOXP3i1) leading to the generation of regulatory T cells (Tregs). Objective We investigated the impact of AZA on xenogeneic graft-versus-host disease (xGVHD) in a humanized murine model of transplantation, and described the impact of the drug on human T cells in vivo. Methods In order to induce xGVHD, human peripheral blood mononuclear cells (huPBMC) were administered intravenously in NOD-scid IL-2Rγnull (NSG) mice. Results AZA successfully improved both survival (p<0.0001) and xGVHD scores (p<0.0001). Further, AZA significantly decreased human T-cell proliferation as well as INF-γ and TNF-α serum levels, and reduced the expression of GRANZYME B and PERFORIN 1 by cytotoxic T cells. In addition, AZA administration significantly increased the function, proliferation and frequency of Tregs through demethylation of FOXP3i1 and higher secretion of IL-2 by conventional T cells due to IL2 gene promoter site 1 demethylation. Interestingly, among AZA-treated mice surviving the acute phase of xGVHD, there was an inverse correlation between the presence of Tregs and signs of chronic GVHD. Finally, Tregs harvested from the spleen of AZA-treated mice were suppressive and stable over time since they persisted at high frequency in secondary transplant experiments. Conclusion These findings emphasize a potential role for AZA as prevention or treatment of GVHD

Hypoxia-induced modulation of apoptosis and BCL-2 family proteins in different cancer cell types

Hypoxia plays an important role in the resistance of tumour cells to chemotherapy. However, the exact mechanisms underlying this process are not well understood. Moreover, according to the cell lines, hypoxia differently influences cell death. The study of the effects of hypoxia on the apoptosis induced by 5 chemotherapeutic drugs in 7 cancer cell types showed that hypoxia generally inhibited the drug-induced apoptosis. In most cases, the effect of hypoxia was the same for all the drugs in one cell type. The expression profile of 93 genes involved in apoptosis as well as the protein level of BCL-2 family proteins were then investigated. In HepG2 cells that are strongly protected against cell death by hypoxia, hypoxia decreased the abundance of nearly all the pro-apoptotic BCL-2 family proteins while none of them are decreased in A549 cells that are not protected against cell death by hypoxia. In HepG2 cells, hypoxia decreased NOXA and BAD abundance and modified the electrophoretic mobility of BIM(EL). BIM and NOXA are important mediators of etoposide-induced cell death in HepG2 cells and the hypoxia-induced modification of these proteins abundance or post-translational modifications partly account for chemoresistance. Finally, the modulation of the abundance and/or of the post-translational modifications of most proteins of the BCL-2 family by hypoxia involves p53-dependent and -independent pathways and is cell type-dependent. A better understanding of these cell-to-cell variations is crucial in order to overcome hypoxia-induced resistance and to ameliorate cancer therapy

Bioactivity and hemocompatibility study of amorphous hydrogenated carbon coatings produced by pulsed magnetron discharge.

Literature contains very few data about the potential biomedical application of amorphous hydrogenated carbon (a-C:H) thin films deposited by reactive pulsed magnetron discharge even so it is one of the most scalable plasma deposition technique. In this article, we show that such a C(2) H(2) pulsed magnetron plasma produces high quality coating with good hemocompatibility and bioactive response: no effect on hemolysis and hemostasis were observed, and proliferation of various cell types such as endothelial, fibroblast, and osteoblast-like cells was not affected when the deposition conditions were varied. Cell growth on a-C:H coatings is proposed to take place by a two-step process: the initial cell contact is affected by the smooth topography of the a-C:H coatings, whereas the polymeric-like structure, together with a moderate hydrophilicity and a high hydrogen content, directs the posterior cell spreading while preserving the hemocompatible behavior. © 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2012

Isoform 111 of vascular endothelial growth factor (VEGF111) improves angiogenesis of ovarian tissue xenotransplantation

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