75,286 research outputs found

    Neutrino Capture and r-Process Nucleosynthesis

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    We explore neutrino capture during r-process nucleosynthesis in neutrino-driven ejecta from nascent neutron stars. We focus on the interplay between charged-current weak interactions and element synthesis, and we delineate the important role of equilibrium nuclear dynamics. During the period of coexistence of free nucleons and light and/or heavy nuclei, electron neutrino capture inhibits the r-process. At all stages, capture on free neutrons has a larger impact than capture on nuclei. However, neutrino capture on heavey nuclei by itself, if it is very strong, is also detrimental to the r-process until large nuclear equilibrium clusters break down and the classical neutron-capture phase of the r-process begins. The sensitivity of the r-process to neutrino irradiation means that neutrino-capture effects can strongly constrain the r-process site, neutrino physics, or both. These results apply also to r-process scenarios other than neutrino-heated winds.Comment: 20 pages, 17 figures, Submitted to Physical Review

    Nucleosynthesis in Fast Expansions of High-Entropy, Proton Rich Matter

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    We demonstrate that nucleosynthesis in rapid, high-entropy expansions of proton-rich matter from high temperature and density can result in a wider variety of abundance patterns than heretofore appreciated. In particular, such expansions can produce iron-group nuclides, p-process nuclei, or even heavy, neutron-rich isotopes. Such diversity arises because the nucleosynthesis enters a little explored regime in which the free nucleons are not in equilibrium with the abundant alpha particles. This allows nuclei significantly heavier than iron to form in t he presence of abundant free nucleons early in the expansion. As the temperature drops, nucleons increasingly assemble into alpha particles and heavier nuclei. If the assembly is efficient, the resulting depletion of free neutrons allows disintegrat ion flows to drive nuclei back down to iron and nickel. If this assembly is inefficient, then the large abundance of free nucleons prevents the disintegration flows and leaves a distribution of heavy nuclei after reaction freezeout. For cases in between, an intermediate abundance distribution, enriched in p-process isotopes, is frozen out. These last expansions may contribute to the solar system's supply of the p-process nuclides if mildly proton-rich, high-entropy matter is ejected from proto-neutron stars winds or other astrophysical sites. Also sign ificant is the fact that, because the nucleosynthesis is primary, the signature of this nucleosyn thesis may be evident in metal poor stars.Comment: 11 pages, 2 tables, 1 figure. Submitted to ApJ Letter

    Cancer therapeutic potential of combinatorial immuno- and vaso-modulatory interventions

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    Currently, most of the basic mechanisms governing tumor-immune system interactions, in combination with modulations of tumor-associated vasculature, are far from being completely understood. Here, we propose a mathematical model of vascularized tumor growth, where the main novelty is the modeling of the interplay between functional tumor vasculature and effector cell recruitment dynamics. Parameters are calibrated on the basis of different in vivo immunocompromised Rag1-/- and wild-type (WT) BALB/c murine tumor growth experiments. The model analysis supports that tumor vasculature normalization can be a plausible and effective strategy to treat cancer when combined with appropriate immuno-stimulations. We find that improved levels of functional tumor vasculature, potentially mediated by normalization or stress alleviation strategies, can provide beneficial outcomes in terms of tumor burden reduction and growth control. Normalization of tumor blood vessels opens a therapeutic window of opportunity to augment the antitumor immune responses, as well as to reduce the intratumoral immunosuppression and induced-hypoxia due to vascular abnormalities. The potential success of normalizing tumor-associated vasculature closely depends on the effector cell recruitment dynamics and tumor sizes. Furthermore, an arbitrary increase of initial effector cell concentration does not necessarily imply a better tumor control. We evidence the existence of an optimal concentration range of effector cells for tumor shrinkage. Based on these findings, we suggest a theory-driven therapeutic proposal that optimally combines immuno- and vaso-modulatory interventions
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