Limb regeneration is the outcome of a complex sequence of events that are mediated by interactions between cells derived from the tissues of the amputated stump. Early in regeneration, these interactions are mediated by growth factor/morphogen signaling associated with nerves and the wound epithelium. One shared property of these proregenerative signaling molecules is that their activity is dependent on interactions with sulfated glycosaminoglycans (GAGs), heparan sulfate proteoglycan (HSPG) in particular, in the extracellular matrix (ECM). We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. In this study we have identified a subpopulation of cells within the ECM of axolotl skin that express high levels of sulfated GAGs on their cell surface. These cells are dispersed in a grid-like pattern throughout the dermis as well as the loose connective tissues that surround the tissues of the limb. These cells alter their morphology during regeneration, and are candidates for being a subpopulation of connective tissue cells that function as the cells required for pattern-formation during regeneration. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells. In addition, we have identified cells that stain for high levels of expression of sulfated GAGs in mouse limb connective tissue that could have an equivalent function to GRID cells in the axolotl. The identification of GRID cells may have important implications for work in the area of Regenerative Engineering.

Background: Abnormal activation of endochondral bone formation in soft tissues causes significant medical diseases associated with disability and pain. Hyperactive mutations in the bone morphogenetic protein (BMP) type 1 receptor ACVR1 lead to fibrodysplasia ossificans progressiva (FOP), a rare genetic disorder characterized by progressive ossification in soft tissues. However, the specific cellular mechanisms are unclear. In addition, the difficulty obtaining tissue samples from FOP patients and the limitations in mouse models of FOP hamper our ability to dissect the pathogenesis of FOP. Methods. To address these challenges and develop a "disease model in a dish", we created human induced pluripotent stem cells (iPS cells) derived from normal and FOP dermal fibroblasts by two separate methods, retroviral integration or integration-free episomal vectors. We tested if the ability to contribute to different steps of endochondral bone formation was different in FOP vs. control iPS cells. Results: Remarkably, FOP iPS cells showed increased mineralization and enhanced chondrogenesis in vitro. The mineralization phenotypes could be suppressed with a small-molecule inhibitor of BMP signaling, DMH1. Our results indicate that the FOP ACVR1 R206H mutation favors chondrogenesis and increases mineral deposition in vitro. Conclusions: Our findings establish a FOP disease cell model for in vitro experimentation and provide a proof-of-concept for using human iPS cell models to understand human skeletal disorders. © 2013 Matsumoto et al.; licensee BioMed Central Ltd.

Low-lying excited states in P38,40 have been identified in the β decay of Tz=+5,+6, Si38,40. Based on the allowed nature of the Gamow-Teller (GT) decay observed, these states are assigned spin and parity of 1+ and are core-excited 1p1h intruder states with a parity opposite to the ground state. The occurrence of intruder states at low energies highlights the importance of pairing and quadrupole correlation energies in lowering the intruder states despite the N=20 shell gap. Configuration interaction shell model calculations with the state-of-art SDPF-MU effective interaction were performed to understand the structure of these 1p1h states in the even-A phosphorus isotopes. States in P40 with N=25 were found to have very complex configurations involving all the fp orbitals leading to deformed states as seen in neutron-rich nuclei with N≈28. The calculated GT matrix elements for the β decay highlight the dominance of the decay of the core neutrons rather than the valence neutrons.

The structure of 71Zn was investigated by one-neutron transfer and heavy-ion induced complex (deep-inelastic) reactions using the GRETINA-CHICO2 and the Gammasphere setups, respectively. The observed inversion between the 9/2+ and 1/2− states is explained in terms of the role of neutron pairing correlations. Non-collective sequences of levels were delineated above the 9/2+ isomeric state. These are interpreted as being associated with a modest oblate deformation in the framework of Monte-Carlo shell-model calculations carried out with the A3DA-m Hamiltonian in the pfg9/2d5/2 valence space. Similarities with the structure of Ni402868 were observed and the shape-coexistence mechanism in the N=40 region of neutron-rich nuclei is discussed in terms of the so-called Type-II shell evolution, with an emphasis on proton–neutron correlations between valence nucleons, especially those involving the shape-driving g9/2 neutron orbital.

Detailed γ-ray spectroscopy of the exotic neon isotope 28Ne has been performed for the first time using the one-neutron removal reaction from 29Ne on a liquid hydrogen target at 240 MeV/nucleon. Based on an analysis of parallel momentum distributions, a level scheme with spin-parity assignments has been constructed for 28Ne and the negative-parity states are identified for the first time. The measured partial cross sections and momentum distributions reveal a significant intruder p-wave strength providing evidence of the breakdown of the N=20 and N=28 shell gaps. Only a weak, possible f-wave strength was observed to bound final states. Large-scale shell-model calculations with different effective interactions do not reproduce the large p-wave and small f-wave strength observed experimentally, indicating an ongoing challenge for a complete theoretical description of the transition into the island of inversion along the Ne isotopic chain.