RESUMO
We show that in collisions with neutron-rich heavy ions at energies around the production threshold K0 and K+ yields probe the isospin-dependent part of the nuclear equation of state at high baryon densities. In particular, we suggest the K0/K+ ratio as a promising observable. Results obtained in a covariant relativistic transport approach are presented for Au+Au collisions at 0.8-1.8A GeV. The focus is put on the equation of state influence which goes beyond the collision-cascade picture. The isovector part of the in-medium interaction affects the kaon multiplicities via two mechanisms: (i) a symmetry potential effect, i.e., a larger neutron repulsion in n-rich systems, and (ii) a threshold effect, due to the change in the self-energies of the particles involved in inelastic processes. Genuine relativistic contributions are revealed that could allow one to directly "measure" the Lorentz structure of the effective isovector interaction.
RESUMO
Peloruside A (peloruside), a compound isolated from the marine sponge Mycale hentscheli , inhibits growth of human (HL-60) and mouse (32D-ras) myeloid leukemic cells, as well as non-transformed 32D cells. Using the MTT cell proliferation assay and trypan blue dye exclusion tests, little difference was seen in growth inhibition between 32D and 32D- ras cells; however, peloruside was more cytotoxic to the oncogene-transformed cells. Peloruside also blocked 32D- ras cells more readily in G2/M of the cell cycle, leading to apoptosis. Annexin-V/propidium iodide staining of 32D and 32D- ras cells showed that 1.6 microM peloruside induced significant cell death by 36 hours in 32D cells (16% survival), but to comparable levels as early as 14 hours in 32D- ras cells (11% survival). There was no evidence for activation of either of the initiator caspases-8 or -9 by 0.1 microM peloruside following 12 hours of exposure. Peloruside inhibited T cell proliferation and IL-2 and IFN gamma production in both the mixed lymphocyte reaction and following CD3 cross-linking, and this effect was shown to be a non-specific cytotoxic effect. It is concluded that peloruside preferentially targets oncogene-transformed cells over non-transformed cells by inducing transformed cells to undergo apoptosis.