1,158 research outputs found

    STELLA Facilitates Differentiation of Germ Cell and Endodermal Lineages of Human Embryonic Stem Cells

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    Stella is a developmentally regulated gene highly expressed in mouse embryonic stem (ES) cells and in primordial germ cells (PGCs). In human, the gene encoding the STELLA homologue lies on chromosome 12p, which is frequently amplified in long-term cultured human ES cells. However, the role played by STELLA in human ES cells has not been reported. In the present study, we show that during retinoic acid (RA)-induced differentiation of human ES cells, expression of STELLA follows that of VASA, a marker of germline differentiation. By contrast, human embryonal carcinoma cells express STELLA at a higher level compared with both karyotypically normal and abnormal human ES cell lines. We found that over-expression of STELLA does not interfere with maintenance of the stem cell state of human ES cells, but following retinoic acid induction it leads to up-regulation of germline- and endodermal-associated genes, whereas neural markers PAX6 and NEUROD1 are down-regulated. Further, STELLA over-expression facilitates the differentiation of human ES cells into BE12-positive cells, in which the expression of germline- and endodermal-associated genes is enriched, and suppresses differentiation of the neural lineage. Taken together, this finding suggests a role for STELLA in facilitating germline and endodermal differentiation of human ES cells

    Stochastic slowdown in evolutionary processes

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    We examine birth--death processes with state dependent transition probabilities and at least one absorbing boundary. In evolution, this describes selection acting on two different types in a finite population where reproductive events occur successively. If the two types have equal fitness the system performs a random walk. If one type has a fitness advantage it is favored by selection, which introduces a bias (asymmetry) in the transition probabilities. How long does it take until advantageous mutants have invaded and taken over? Surprisingly, we find that the average time of such a process can increase, even if the mutant type always has a fitness advantage. We discuss this finding for the Moran process and develop a simplified model which allows a more intuitive understanding. We show that this effect can occur for weak but non--vanishing bias (selection) in the state dependent transition rates and infer the scaling with system size. We also address the Wright-Fisher model commonly used in population genetics, which shows that this stochastic slowdown is not restricted to birth-death processes.Comment: 8 pages, 3 figures, accepted for publicatio

    On the interpretation of spin-polarized electron energy loss spectra

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    We study the origin of the structure in the spin-polarized electron energy loss spectroscopy (SPEELS) spectra of ferromagnetic crystals. Our study is based on a 3d tight-binding Fe model, with constant onsite Coulomb repulsion U between electrons of opposite spin. We find it is not the total density of Stoner states as a function of energy loss which determines the response of the system in the Stoner region, as usually thought, but the densities of Stoner states for only a few interband transitions. Which transitions are important depends ultimately on how strongly umklapp processes couple the corresponding bands. This allows us to show, in particular, that the Stoner peak in SPEELS spectra does not necessarily indicate the value of the exchange splitting energy. Thus, the common assumption that this peak allows us to estimate the magnetic moment through its correlation with exchange splitting should be reconsidered, both in bulk and surface studies. Furthermore, we are able to show that the above mechanism is one of the main causes for the typical broadness of experimental spectra. Finally, our model predicts that optical spin waves should be excited in SPEELS experiments.Comment: 11 pages, 7 eps figures, REVTeX fil

    Microwave Spectroscopy

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    Contains reports on five research projects.United States Army Signal Corps (Contract DA36-039-sc-87376
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