Proton fraction in neutron stars

The proton fraction in {\sl \beta}-stable neutron stars is investigated within the framework of the Skyrme-Hartree-Fock theory using the extended Skyrme effective interaction for the first time. The calculated results show that the proton fraction disappears at high density, which implies that the pure neutron matter may exist in the interior of neutron stars. The incompressibility of the nuclear equation of state is shown to be more important to determine the proton fraction. Meanwhile, it is indicated that the addition of muons in neutron stars will change the proton fraction. It is also found that the higher-order terms of the nuclear symmetry energy have obvious effects on the proton fraction and the parabolic law of the nuclear symmetry energy is not enough to determine the proton fraction.Comment: 4 Pgaes in REVTex, 2 Figures, 1 Tabl

Contributions of hyperon-hyperon scattering to subthreshold cascade production in heavy ion collisions

Using a gauged flavor SU(3)-invariant hadronic Lagrangian, we calculate the cross sections for the strangeness-exchange reactions YY to N\Xi (Y=\Lambda, \Sigma) in the Born approximation. These cross sections are then used in the Relativistic Vlasov-Uehling-Uhlenbeck (RVUU) transport model to study \Xi production in Ar+KCl collisions at incident energy of 1.76A GeV and impact parameter b=3.5 fm. We find that including the contributions of hyperon-hyperon scattering channels strongly enhances the yield of \Xi, leading to the abundance ratio \Xi^{-}/(\Lambda+\Sigma^{0})=3.38E-3, which is essentially consistent with the recently measured value of $(5.6 \pm 1.2_{-1.7}^{+1.8})\times 10^{-3}$ by the HADES collaboration at GSI.Comment: 8 pages, 5 figure

A Novel Plant Sesquiterpene Lactone Derivative, DETD-35, Suppresses BRAF V600E Mutant Melanoma Growth and Overcomes Acquired Vemurafenib Resistance in Mice

Acquired resistance to vemurafenib develops through reactivation of RAF/MEK/ERK signaling or bypass mechanisms. Recent combination therapies such as a MEK inhibitor combined with vemurafenib show improvement in major clinical end points but the percentage of patients with adverse toxic events is higher than with vemurafenib monotherapy and most patients ultimately relapse. Therefore, there is an urgent need to develop new anti-melanoma drugs and/or adjuvant agents for vemurafenib therapy. In this study, we created a novel semi-organically modified derivative, DETD-35, from deoxyelephantopin (DET), a plant sesquiterpene lactone demonstrated as an anti-inflammatory and anti-mammary tumor agent. Our results show that DETD-35 inhibited proliferation of a panel of melanoma cell lines, including acquired vemurafenib resistance A375 cells (A375-R) established in this study, with superior activities to DET and no cytotoxicity to normal melanocytes. DETD-35 suppressed tumor growth and reduced tumor mass as effectively as vemurafenib in A375 xenograft study. Furthermore, DETD-35 also reduced tumor growth in both acquired (A375-R) and intrinsic (A2058) vemurafenib resistance xenograft models, where vemurafenib showed no anti-tumor activity. Notably, the combination of DETD-35 and vemurafenib exhibited the most significant effects in both in vitro and in vivo xenograft studies due to synergism of the compound and the drug. Mechanistic studies suggested that DETD-35 overcame acquired vemurafenib resistance at least in part through deregulating MEK-ERK, Akt, and STAT3 signaling pathways and promoting apoptosis of cancer cells. Overall, our results suggest that DETD-35 may be useful as a therapeutic or adjuvant agent against BRAFV600E mutant and acquired vemurafenib resistance melanoma