The equation of state for neutron matter is calculated within relativistic Hartree-Fock approximation. The tensor couplings of vector mesons to baryons are included, and the change of baryon internal structure in matter is also considered using the quark-meson coupling model. We obtain the maximum neutron-star mass of ∼ 2.0M ⊙ , which is consistent with the recently observed, precise mass, 1.97 ± 0.04M ⊙ . The Fock contribution is very important and, in particular, the inclusion of tensor coupling is vital to obtain such large mass. The baryon structure variation in matter also enhances the mass of a neutron star.

Using relativistic Hartree-Fock approximation, we investigate the properties of the neutron-star matter in detail. In the present calculation, we consider not only the tensor coupling of vector mesons to octet baryons and the form factors at interaction vertexes but also the internal (quark) structure change of baryons in dense matter. The relativistic Hartree-Fock calculations are performed in two ways: one is the calculation with the coupling constants determined by SU(6) (quark model) symmetry, the other is with the coupling constants based on SU(3) (flavor) symmetry. For the latter case, we use the latest Nijmegen (ESC08) model. Then, it is very remarkable that the particle composition of the core matter in SU(3) symmetry is completely different from that in SU(6) symmetry. In SU(6) symmetry, all octet baryons appear in the density region below ∼ 1.2 fm −3 , while, in the ESC08 model, only the Ξ − hyperon is produced. Furthermore, the medium modification of the internal baryon structure hardens the equation of state for the core matter. Taking all these effects into account, we can obtain the maximum neutron-star mass which is consistent with the recently observed mass, 1.97 ± 0.04M ⊙ (PSR J1614-2230). We therefore conclude that the extension from SU(6) symmetry to SU(3) symmetry in the meson-baryon couplings and the internal baryon-structure variation in matter certainly enhance the mass of neutron star. Furthermore, the effects of the form factor at vertex and the Fock contribution including the tensor coupling due to the vector mesons are indispensable to describe the core matter. In particular, the Fock term is very vital in reproducing the preferable value of symmetry energy, a 4 (≃ 30−40 MeV), in nuclear matter.

Within the Dirac-Brueckner-Hartree-Fock approach, using the Bonn potentials, we investigate the properties of dense, asymmetric nuclear matter and apply it to neutron stars. In the actual calculations of the nucleon self-energies and the energy density of matter, we study in detail the validity of an angle-averaged approximation and an averaging of the total momentum squared of interacting two-nucleons in nuclear matter. For practical use, we provide convenient parametrizations for the equation of state for symmetric nuclear matter and pure neutron matter. We also parametrize the nucleon self-energies in terms of polynomials of nucleon momenta. Those parametrizations can accurately reproduce the numerical results up to high densities.

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Fibrodysplasia ossificans progressiva (FOP) is a rare congenital disorder characterized by progressive ossification of soft tissues. FOP is caused by mutations in activin receptorlike kinase 2 (ALK2) that cause its constitutive activation and result in dysregulation of BMP signaling. Here, we show that generation of induced pluripotent stem cells (iPSCs) from FOP-derived skin fibroblasts is repressed because of incomplete reprogramming and inhibition of iPSC maintenance. This repression was mostly overcome by specific suppression of ALK2 expression and treatment with an ALK2 inhibitor, indicating that the inhibition of iPSC generation and maintenance observed in FOP-derived skin fibroblasts results from constitutive activation of ALK2. Using this system, we identified an ALK2 inhibitor as a potential candidate for future drug development. This study highlights the potential of the inhibited production and maintenance of iPSCs seen in diseases as a useful phenotype not only for studying the molecular mechanisms underlying iPS reprogramming but also for identifying drug candidates for future therapies.

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