The Influence of Chemical Short Range Order on Atomic Diffusion in Al-Ni Melts

We use inelastic neutron scattering and molecular dynamics (MD) simulation to investigate the chemical short range order (CSRO), visible through prepeaks in the structure factors, and its relation to self diffusion in Al-Ni melts. As a function of composition at 1795K Ni self diffusion coefficients from experiment and simulation exhibit a non-linear dependence with a pronounced increase on the Al-rich side. This comes along with a change in CSRO with increasing Al content that is related to a more dense packing of the atoms in Ni-rich Al-Ni systems.Comment: 11 pages, 4 figure

Liver cell therapy: is this the end of the beginning?

The prevalence of liver diseases is increasing globally. Orthotopic liver transplantation is widely used to treat liver disease upon organ failure. The complexity of this procedure and finite numbers of healthy organ donors have prompted research into alternative therapeutic options to treat liver disease. This includes the transplantation of liver cells to promote regeneration. While successful, the routine supply of good quality human liver cells is limited. Therefore, renewable and scalable sources of these cells are sought. Liver progenitor and pluripotent stem cells offer potential cell sources that could be used clinically. This review discusses recent approaches in liver cell transplantation and requirements to improve the process, with the ultimate goal being efficient organ regeneration. We also discuss the potential off-target effects of cell-based therapies, and the advantages and drawbacks of current pre-clinical animal models used to study organ senescence, repopulation and regeneration

Catalytically Active N ‐Heterocyclic Carbene Release from Single‐Chain Nanoparticles Following a Thermolysis‐Driven Unfolding Strategy

International audienc

Isolation and <i>in vitro</i> expansion of CD133^posCD49f^posCD45^neg cells by Magnetic Assisted Cells Separation (MACS) from E12.5 liver enriches for hepatoblast progenitor cells that proliferate in response to FGFR activation.

<p>(A) Phase contrast pictures of <i>in vitro</i> expanded CD133^pos CD49f^pos CD45^neg enriched cells from E12.5 embryonic liver at different time points. Co-immunofluorescence staining for (B) HNF4α and CK19 and (C) ALBUMIN and PCK. (D) Gene expression analysis by RTPCR using RNA isolated from the MACS enriched cells before and after 3-day culture. Negative control = water and positive control = E16.5 whole embryonic cDNA. Scale bar 25 µm. (E) Proliferation indices of CD133^pos CD49f^pos CD45^neg cells treated with rFGF7/10 for 48 hrs and pulse labeled with BrdU (n = 4, *<i>p</i><0.001 compared to control). Data are representative of three or more independent experiments.</p

The murine E12.5 liver is populated with CD133^posCD49f^pos hepatoblast progenitor cells expressing FGFR1 and 2.

<p>(A) Immunofluorescence staining for progenitor cell markers CD133 and CD49f on E12.5 embryonic liver. Yellow cells are double positive cells. DAPI staining (blue) identifies nuclei. (B) Immunostaining of CD133 and Cytokeratin (CK19). (C) Immunostaining for CD133, CD49f and FGFR 1 and (D) FGFR2. White arrows mark triple positive cells and yellow arrows mark positive cells that do not express receptors. Data are representative of three or more independent experiments. Scale bar represents 25 µm.</p

FGFR mediated proliferation of <i>Mat1a</i>

<p><i>^−/−</i><b>cells are mediated in part through PI3K-AKT pathway.</b> Serum-starved <i>Mat1a^−/−</i> cells were treated with rFGF7/10 ± PI3K-AKT inhibitor LY294002 for detection and quantification of (A) pSer 552 β-CATENIN or (B) BrdU. Total and β-CATENIN/BrdU Positive cells were counted from 4–5 HPF images from 3 independent experiments and represented as relative % of control (n = 3, *p<0.001).</p