The XMM-LSS survey: the Class 1 cluster sample over the initial 5 deg(2) and its cosmological modelling

in Monthly Notices of the Royal Astronomical Society (2007), 382(3), 1289-1308

We present a sample of 29 galaxy clusters from the XMM-LSS survey over an area of some 5 deg(2) out to a redshift of z = 1.05. The sample clusters, which represent about half of the X-ray clusters ... [more ▼]

We present a sample of 29 galaxy clusters from the XMM-LSS survey over an area of some 5 deg(2) out to a redshift of z = 1.05. The sample clusters, which represent about half of the X-ray clusters identified in the region, follow well-defined X-ray selection criteria and are all spectroscopically confirmed. For all clusters, we provide X-ray luminosities and temperatures as well as masses, obtained from dedicated spatial and spectral fitting. The cluster distribution peaks around z = 0.3 and T = 1.5 keV, half of the objects being groups with a temperature below 2 keV. Our L-X-T(z) relation points towards self-similar evolution, but does not exclude other physically plausible models. Assuming that cluster scaling laws follow self-similar evolution, our number density estimates up to z = 1 are compatible with the predictions of the concordance cosmology and with the findings of previous ROSAT surveys. Our well-monitored selection function allowed us to demonstrate that the inclusion of selection effects is essential for the correct determination of the evolution of the L-X-T relation, which may explain the contradictory results from previous studies. Extensive simulations show that extending the survey area to 10 deg(2) has the potential to exclude the non-evolution hypothesis, but those constraints on more refined intracluster medium models will probably be limited by the large intrinsic dispersion of the L-X-T relation, whatever be the sample size. We further demonstrate that increasing the dispersion in the scaling laws increases the number of detectable clusters, hence generating further degeneracy [in addition to sigma(8), Omega(m), L-X-T(z)] in the cosmological interpretation of the cluster number counts. We provide useful empirical formulae for the cluster mass-flux and mass-count rate relations as well as a comparison between the XMM-LSS mass sensitivity and that of forthcoming Sunyaev-Zel'dovich surveys. [less ▲]

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Histone deacetylase 7 silencing alters endothelial cell migration, a key step in angiogenesis

in Circulation Research (2007), 101(12), 1237-1246

Global inhibition of class I and II histone deacetylases (HDACs) impairs angiogenesis. Herein, we have undertaken the identification of the specific HDAC(s) with activity that is necessary for the ... [more ▼]

Global inhibition of class I and II histone deacetylases (HDACs) impairs angiogenesis. Herein, we have undertaken the identification of the specific HDAC(s) with activity that is necessary for the development of blood vessels. Using small interfering RNAs, we observed that HDAC7 silencing in endothelial cells altered their morphology, their migration, and their capacity to form capillary tube-like structures in vitro but did not affect cell adhesion, proliferation, or apoptosis. Among several factors known to be involved in angiogenesis, platelet-derived growth factor-B (PDGF-B) and its receptor (PDGFR-beta) were the most upregulated genes following HDAC7 silencing. We demonstrated that their increased expression induced by HDAC7 silencing was partially responsible for the inhibition of endothelial cell migration. In addition, we have also shown that treatment of endothelial cells with phorbol 12-myristate 13-acetate resulted in the exportation of HDAC7 out of the nucleus through a protein kinase C/protein kinase D activation pathway and induced, similarly to HDAC7 silencing, an increase in PDGF-B expression, as well as a partial inhibition of endothelial cell migration. Collectively, these data identified HDAC7 as a key modulator of endothelial cell migration and hence angiogenesis, at least in part, by regulating PDGF-B/PDGFR-beta gene expression. Because angiogenesis is required for tumor progression, HDAC7 may represent a rational target for therapeutic intervention against cancer. [less ▲]

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