Medium effects in high energy heavy-ion collisions

The change of hadron properties in dense matter based on various theoretical approaches are reviewed. Incorporating these medium effects in the relativistic transport model, which treats consistently the change of hadron masses and energies in dense matter via the scalar and vector fields, heavy-ion collisions at energies available from SIS/GSI, AGS/BNL, and SPS/CERN are studied. This model is seen to provide satisfactory explanations for the observed enhancement of kaon, antikaon, and antiproton yields as well as soft pions in the transverse direction from the SIS experiments. In the AGS heavy-ion experiments, it can account for the enhanced $K^+/\pi^+$ ratio, the difference in the slope parameters of the $K^+$ and $K^-$ transverse kinetic energy spectra, and the lower apparent temperature of antiprotons than that of protons. This model also provides possible explanations for the observed enhancement of low-mass dileptons, phi mesons, and antilambdas in heavy-ion collisions at SPS energies. Furthermore, the change of hadron properties in hot dense matter leads to new signatures of the quark-gluon plasma to hadronic matter transition in future ultrarelativistic heavy-ion collisions at RHIC/BNL.Comment: RevTeX, 65 pages, including 25 postscript figures, invited topical review for Journal of Physics G: Nuclear and Particle Physic

Impact of nuclear data on sodium-cooled fast reactor calculations

Neutron transport and depletion calculations are performed in combination with various nuclear data libraries in order to assess the impact of nuclear data on safety-relevant parameters of sodium-cooled fast reactors. These calculations are supplemented by systematic uncertainty analyses with respect to nuclear data. Analysed quantities are the multiplication factor and nuclide densities as a function of burn-up and the Doppler and Na-void reactivity coefficients at begin of cycle. While ENDF/B-VII.0 / -VII.1 yield rather consistent results, larger discrepancies are observed between the JEFF libraries. While the newest evaluation, JEFF-3.2, agrees with the ENDF/B-VII libraries, the JEFF-3.1.2 library yields significant larger multiplication factors

Regulation of Human MC2-R Gene Expression by CREB, CREM, and ICER in the Adrenocortical Cell Line Y1.

The MC2-Receptor (melanocortin 2 receptor, MC2-R) is a Gs-protein coupled receptor that is upregulated by its own ligand ACTH and by forskolin. The mechanisms regulating MC2-R expression are still unclear. We therefore investigated the role of the stimulatory transcription factors CREB and CREM and the inhibitory factor ICER for regulation of human MC2-R expression. We cotransfected mouse adrenocortical Y1 cells with luciferase reporter gene vectors containing full length and deleted human MC2-R promoter constructs with expression plasmids for CREB, CREBS133A, CREMtau, CREMtauS117A, or ICER. Direct protein-DNA interaction was investigated by EMSA. Wild type CREB did not significantly affect promoter activity due to high endogenous CREB activity. However, CREBS133A decreased forskolin stimulated MC2-R promoter activity by 48+/-5% (mean+/-SEM) while unstimulated values remained unchanged. CREMtau moderately increased basal and forskolin stimulated luciferase activity in a dose-dependent manner (maximum effect 252+/-24% and 186+/-13% VS. control vector, respectively). While this effect required the full length promoter, cAMP stimulation was retained in shorter constructs. ICER reduced basal luciferase activity in Y1 cells by 17+/-28%, but completely abolished forskolin stimulation. Although 5'-deletion constructs mapped the minimum promoter region required for ICER effect to the shortest -64/+40 construct, direct protein DNA interaction in this promoter region could not be identified by EMSA. Moreover, mutation of the SF-1 binding sites, which retained ICER dependent inhibition, excluded SF-1 to be required for this effect. We conclude from these data that transcription factors of the CREB/CREM/ATF family have a moderate effect on human MC2-R promoter activity, but seem to play a minor role in transmitting stimulation of the cAMP pathway to increased MC2-R expression