Thermal photons in QGP and non-ideal effects

We investigate the thermal photon production-rates using one dimensional boost-invariant second order relativistic hydrodynamics to find proper time evolution of the energy density and the temperature. The effect of bulk-viscosity and non-ideal equation of state are taken into account in a manner consistent with recent lattice QCD estimates. It is shown that the \textit{non-ideal} gas equation of state i.e $\epsilon-3\,P\,\neq 0$ behaviour of the expanding plasma, which is important near the phase-transition point, can significantly slow down the hydrodynamic expansion and thereby increase the photon production-rates. Inclusion of the bulk viscosity may also have similar effect on the hydrodynamic evolution. However the effect of bulk viscosity is shown to be significantly lower than the \textit{non-ideal} gas equation of state. We also analyze the interesting phenomenon of bulk viscosity induced cavitation making the hydrodynamical description invalid. We include the viscous corrections to the distribution functions while calculating the photon spectra. It is shown that ignoring the cavitation phenomenon can lead to erroneous estimation of the photon flux.Comment: 11 pages, 13 figures; accepted for publication in JHE

Genome-wide methylation analysis identifies genes silenced in non-seminoma cell lines

Silencing of genes by DNA methylation is a common phenomenon in many types of cancer. However, the genome wide effect of DNA methylation on gene expression has been analysed in relatively few cancers. Germ cell tumours (GCTs) are a complex group of malignancies. They are unique in developing from a pluripotent progenitor cell. Previous analyses have suggested that non-seminomas exhibit much higher levels of DNA methylation than seminomas. The genomic targets that are methylated, the extent to which this results in gene silencing and the identity of the silenced genes most likely to play a role in the tumours’ biology have not yet been established. In this study, genome-wide methylation and expression analysis of GCT cell lines was combined with gene expression data from primary tumours to address this question. Genome methylation was analysed using the Illumina infinium HumanMethylome450 bead chip system and gene expression was analysed using Affymetrix GeneChip Human Genome U133 Plus 2.0 arrays. Regulation by methylation was confirmed by demethylation using 5-aza-2-deoxycytidine and reverse transcription–quantitative PCR. Large differences in the level of methylation of the CpG islands of individual genes between tumour cell lines correlated well with differential gene expression. Treatment of non-seminoma cells with 5-aza-2-deoxycytidine verified that methylation of all genes tested played a role in their silencing in yolk sac tumour cells and many of these genes were also differentially expressed in primary tumours. Genes silenced by methylation in the various GCT cell lines were identified. Several pluripotency-associated genes were identified as a major functional group of silenced genes