Pseudorapidity distributions of charged particles from Au+Au collisions at the maximum RHIC energy, Sqrt(s_NN) = 200 GeV

We present charged particle densities as a function of pseudorapidity and collision centrality for the 197Au+197Au reaction at Sqrt{s_NN}=200 GeV. For the 5% most central events we obtain dN_ch/deta(eta=0) = 625 +/- 55 and N_ch(-4.7<= eta <= 4.7) = 4630+-370, i.e. 14% and 21% increases, respectively, relative to Sqrt{s_NN}=130 GeV collisions. Charged-particle production per pair of participant nucleons is found to increase from peripheral to central collisions around mid-rapidity. These results constrain current models of particle production at the highest RHIC energy.Comment: 4 pages, 5 figures; fixed fig. 5 caption; revised text and figures to show corrected calculation of and ; final version accepted for publicatio

YAP/TAZ-Dependent Reprogramming of Colonic Epithelium Links ECM Remodeling to Tissue Regeneration.

Tissue regeneration requires dynamic cellular adaptation to the wound environment. It is currently unclear how this is orchestrated at the cellular level and how cell fate is affected by severe tissue damage. Here we dissect cell fate transitions during colonic regeneration in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is transiently reprogrammed into a primitive state. This is characterized by de novo expression of fetal markers as well as suppression of markers for adult stem and differentiated cells. The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation. In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate. This provides a simple model for tissue regeneration, implicating cellular reprogramming as an essential element.This work was supported by Worldwide Cancer Research (13-1216 to KBJ), Lundbeck Foundation (R105-A9755 to KBJ), the Danish Cancer Society (R56-A2907 and R124-A7724 to KBJ), the Carlsberg Foundation (to KBJ), EMBO Young Investigator programme (to KBJ), AIRC Special Program Molecular Clinical Oncology ‘‘5 per mille’’ (to SP), an AIRC PI-Grant (to SP), Epigenetics Flagship projects (CNR-Miur grants. to SP), the DFF mobilix programme (to SY), Marie Curie fellowship programme (SY and JG), Foundation of Aase and Ejnar Danielsen (OHN), Axel Muusfeldts Foundation (OHN), The Ragnar Söderberg Foundation (CDM). This project has received funding from the European Union’s Horizon 2020 research and innovation programme (grant agreements STEMHEALTH ERCCoG682665 and INTENS 668294 to KBJ and DENOVOSTEM No. 670126 to SP)

YAP/TAZ-Dependent Reprogramming of Colonic Epithelium Links ECM Remodeling to Tissue Regeneration

Tissue regeneration requires dynamic cellular adaptation to the wound environment. It is currently unclear how this is orchestrated at the cellular level and how cell fate is affected by severe tissue damage. Here we dissect cell fate transitions during colonic regeneration in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is transiently reprogrammed into a primitive state. This is characterized by de novo expression of fetal markers as well as suppression of markers for adult stem and differentiated cells. The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation. In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate. This provides a simple model for tissue regeneration, implicating cellular reprogramming as an essential element