Break-up mechanisms in heavy ion collisions at low energies

We investigate reaction mechanisms occurring in heavy ion collisions at low energy (around 20 MeV/u). In particular, we focus on the competition between fusion and break-up processes (Deep-Inelastic and fragmentation) in semi-peripheral collisions, where the formation of excited systems in various conditions of shape and angular momentum is observed. Adopting a Langevin treatment for the dynamical evolution of the system configuration, described in terms of shape observables such as quadrupole and octupole moments, we derive fusion/fission probabilities, from which one can finally evaluate the corresponding fusion and break-up cross sections. The dependence of the results on shape, angular momentum and excitation energy is discussed.Comment: submitted to Physical Review

The Dynamical Dipole Mode in Fusion Reactions with Exotic Nuclear Beams

We report the properties of the prompt dipole radiation, produced via a collective bremsstrahlung mechanism, in fusion reactions with exotic beams. We show that the gamma yield is sensitive to the density dependence of the symmetry energy below/around saturation. Moreover we find that the angular distribution of the emitted photons from such fast collective mode can represent a sensitive probe of its excitation mechanism and of fusion dynamics in the entrance channel.Comment: 5 pages, 3 figures, to appear in Phys.Rev.

Nuclear collective dynamics within Vlasov approach

We discuss, in an investigation based on Vlasov equation, the properties of the isovector modes in nuclear matter and atomic nuclei in relation with the symmetry energy. We obtain numerically the dipole response and determine the strength function for various systems, including a chain of Sn isotopes. We consider for the symmetry energy three parametrizations with density providing similar values at saturation but which manifest very different slopes around this point. In this way we can explore how the slope affects the collective response of finite nuclear systems. We focus first on the dipole polarizability and show that while the model is able to describe the expected mass dependence, A^{5/3}, it also demonstrates that this quantity is sensitive to the slope parameter of the symmetry energy. Then, by considering the Sn isotopic chain, we investigate the emergence of a collective mode, the Pygmy Dipole Resonance (PDR), when the number of neutrons in excess increases. We show that the total energy-weighted sum rule exhausted by this mode has a linear dependence with the square of isospin I=(N-Z)/A, again sensitive to the slope of the symmetry energy with density. Therefore the polarization effects in the isovector density have to play an important role in the dynamics of PDR. These results provide additional hints in the investigations aiming to extract the properties of symmetry energy below saturation.Comment: 7 pages, 6 figure

Symmetry Energy Effects on the Mixed Hadron-Quark Phase at High Baryon Density

The phase transition of hadronic to quark matter at high baryon and isospin density is analyzed. Relativistic mean field models are used to describe hadronic matter, and the MIT bag model is adopted for quark matter. The boundaries of the mixed phase and the related critical points for symmetric and asymmetric matter are obtained. Due to the different symmetry term in the two phases, isospin effects appear to be rather significant. With increasing isospin asymmetry the binodal transition line of the (T,\rho_B) diagram is lowered to a region accessible through heavy ion collisions in the energy range of the new planned facilities, e.g. the FAIR/NICA projects. Some observable effects are suggested, in particular an "Isospin Distillation" mechanism with a more isospin asymmetric quark phase, to be seen in charged meson yield ratios, and an onset of quark number scaling of the meson/baryon elliptic flows. The presented isospin effects on the mixed phase appear to be robust with respect to even large variations of the poorly known symmetry term at high baryon density in the hadron phase. The dependence of the results on a suitable treatment of isospin contributions in effective QCD Lagrangian approaches, at the level of explicit isovector parts and/or quark condensates, is finally discussed.Comment: 14 two column pages, 14 figures, new results with other hadron EoS. Accepted for publication in Phys.Rev.

Imbalance of p75(NTR)/TrkB protein expression in Huntington's disease: Implication for neuroprotective therapies

Neuroprotective therapies based on brain-derived neurotrophic factor (BDNF) administration have been proposed for Huntington's disease (HD) treatment. However, our group has recently reported reduced levels of TrkB in HD mouse models and HD human brain suggesting that besides a decrease on BDNF levels a reduction of TrkB expression could also contribute to diminished neurotrophic support in HD. BDNF can also bind to p75 neurotrophin receptor (p75(NTR)) modulating TrkB signaling. Therefore, in this study we have analyzed the levels of p75(NTR) in several HD models, as well as in HD human brain. Our data demonstrates a p75(NTR)/TrkB imbalance in the striatum of two different HD mouse models, Hdh(Q111/111) homozygous knockin mice and R6/1 mice that was also manifested in the putamen of HD patients. The imbalance between TrkB and p75(NTR) levels in a HD cellular model did not affect BDNF-mediated TrkB activation of prosurvival pathways but induced activation of apoptotic cascades as demonstrated by increased JNK phosphorylation. Moreover, BDNF failed to protect mutant huntingtin striatal cells transfected with p75(NTR) against NMDA-mediated excitotoxicity, which was associated with decreased Akt phosphorylation. Interestingly, lack of Akt activation following BDNF and NMDA treatment correlated with increased PP1 levels. Accordingly, pharmacological inhibition of PP1 by okadaic acid (OA) prevented mutant huntingtin striatal cell death induced by NMDA and BDNF. Altogether, our findings demonstrate that the p75(NTR)/TrkB imbalance induced by mutant huntingtin in striatal cells associated with the aberrant activity of PP1 disturbs BDNF neuroprotection likely contributing to increasing striatal vulnerability in HD. On the basis of this data we hypothesize that normalization of p75(NTR) and/or TrkB expression or their signaling will improve BDNF neuroprotective therapies in HD. Cell Death and Disease (2013) 4, e595; doi:10.1038/cddis.2013.116; published online 18 April 201

Heavy Ion Dynamics and Neutron Stars

Some considerations are reported, freely inspired from the presentations and discussions during the Beijing Normal University Workshop on the above Subject, held in July 2007. Of course this cannot be a complete summary but just a collection of personal thougths aroused during the meeting.Comment: 11 pages, no figures, Summary Talk, Int.Workshop on "Nuclear Dynamics in Heavy Ion Collisions and Neutron Stars", Beijing Normal Univ. July 07, to appear in Int.Journ.Modern Physics E (2008