Hydrodynamical analysis of hadronic spectra in the 130 GeV/nucleon Au+Au collisions

We study one-particle spectra and a two-particle correlation function in the 130 GeV/nucleon Au+Au collisions at RHIC by making use of a hydrodynamical model. We calculate the one-particle hadronic spectra and present the first analysis of Bose-Einstein correlation functions based on the numerical solution of the hydrodynamical equations which takes both longitudinal and transverse expansion into account appropriately. The hydrodynamical model provides excellent agreement with the experimental data in the pseudorapidity and the transverse momentum spectra of charged hadrons, the rapidity dependence of anti-proton to proton ratio, and almost consistent result for the pion Bose-Einstein correlation functions. Our numerical solution with simple freeze-out picture suggests the formation of the quark-gluon plasma with large volume and low net-baryon density.Comment: 7 pages, 8 figures, REVTeX4. Numerical results and figures are correcte

Collective flow and two-pion correlations from a relativistic hydrodynamic model with early chemical freeze out

We investigate the effect of early chemical freeze-out on radial flow, elliptic flow and HBT radii by using a fully three dimensional hydrodynamic model. When we take account of the early chemical freeze-out, the space-time evolution of temperature in the hadron phase is considerably different from the conventional model in which chemical equilibrium is always assumed. As a result, we find that radial and elliptic flows are suppressed and that the lifetime and the spatial size of the fluid are reduced. We analyze the p_t spectrum, the differential elliptic flow, and the HBT radii at the RHIC energy by using hydrodynamics with chemically non-equilibrium equation of state.Comment: One subsection and two figures adde

Functional relationships of FANCC to homologous recombination, translesion synthesis and BLM.

Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair