34 research outputs found

    Enhancing Central Nervous System Remyelination in Multiple Sclerosis

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    Recent studies on adult neural stem cells and the developmental biology of myelination have generated the expectation that neural precursors can repair the damaged central nervous system of multiple sclerosis patients where the endogenous remyelination process has failed. As a result, many laboratories are engaged in translational studies in which the goal is to design ways to promote remyelination and repair. Here we raise issues highlighted by prior experimental and human work that should be considered lest these studies become “lost in translation.

    Structural basis of hemadsorbing sites during the formation of syncytia in measles-infected cells

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    The surfaces of cells Infected with measles virus adsorb monkey red blood cells (RBC). In this study, the structure and localization of viral hemadsorbing (HAD) sites and their relationship with antigenic sites and with cell fusion were investigated in measles virus infected Vero cells. Transmission and scanning electron microscopy were combined with immunolabeling, using human anti-measles IgG (Ab) and protein A from Staph, aureus coupled to peroxidase.. In the early syncytia (50-100 2 in diameter), HAD sites were clustered in the center but scattered at the periphery. In contrast, mature giant cells (400 to 500 2) had all HAD sites in the central area which displayed scattered villi. The periphery of the mature giant cells and the mononucleated cells did not hemadsorb but were covered with numerous villi. In the central area, RBC were firmly attached to villi and ridges over nucleocapsids but rarely to viral buds. Villi and ridges under the RBC were covered with antigenic sites which were not detected at the periphery of the mature syncytia. When living cells were treated with Ab at 4°C, complete inhibition of hemadsorption was only observed when RBC were applied to the cells in the cold. In other experiments, cells reacted with Ab at 4°C were washed, brought to 37°C and treated with RBC immediately or after 1-24 hrs. After 1-2 hrs, some HAD sites were present only at the periphery of immature giant cells, suggesting that RBC receptors had already emerged in membrane areas where fusion started again. After 24 hrs, the distribution of HAD and antigenic sites was the same as on cells not exposed to Ab. It seems that when fusion begins, HAD sites appeared on the periphery of the syncytia and then move spontaneously towards the center. With cessation of fusion, HAD sites disappear from the periphery of the giant cell. Receptors for RBC are closely associated with antigenic sites and correlated with viral induced fusion but not with virus production

    ADRENOLEUCODYSTROPHIE LIEE A L'X (MECANISMES ET TRANSFERT DE GENE DANS LE SYSTEME NERVEUX CENTRAL)

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    PARIS-BIUSJ-Physique recherche (751052113) / SudocCentre Technique Livre Ens. Sup. (774682301) / SudocSudocFranceF

    Growth and fate of PSA-NCAM+ precursors of the postnatal brain

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    Oligodendrocyte-type 2 astrocyte (O-2A) lineage cells are derived from multipotential stem cells of the developing CNS. Precursors of O-2A progenitors express the polysialylated (PSA) form of the neural cell adhesion molecule (NCAM) and are detected in neonatal rat brain glial cultures. It is unclear how such PSA-NCAM � “pre-progenitors ” are related to neural stem cells and whether they still have the potential to differentiate along several neural lineages. Here we isolated PSA-NCAM� pre-progenitor cells from glial cultures by immunopanning and found that most of these cells expressed nestin and PDGFreceptor-� but not O-2A antigens. PSA-NCAM � cells synthesized transcripts for fibroblast growth factor (FGF) receptors 1, 2, and 3 and responded to FGF2 by survival and proliferation, growing into large clusters resembling neural spheres. FGF2induced proliferation of PSA-NCAM � pre-progenitors was significantl

    Assembly of enveloped RNA viruses - Chapter 7 Assembly of Coronaviridæ

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    This book is a collection of critical reviews about a diverse group of virus families with two features in common: the stable repository of genetic information in each virus is RNA, and each virus modifies and appropriates a particular patch of the eukaryotic cell membrane system to complete its structure. The reviews take the reader from the level of virus genome structure and expression through the quaternary interactions between virus-specified elements and cellular components that cooperate to produce virus particles. There are spectacular illustrations in this volume, but it is much more than a picture gallery. Reading widely in this book can be an effective antidote to overspecialization: in these pages, you are likely to learn much about viruses and about cells that you didn't know before; you'll discover illuminating parallels between diverse virus families; you'll come away with a sharpened awareness of important things that are still to be learned. Memphis, Tenn. , Summer 1984 David W. Kingsbury Preface This book was written at the suggestion of Dr. David W. Kingsbury made at a work­ shop on viruses organized by the Multiple Sclerosis Society in Aspen, Colorado, U. S. A. , three years ago. Originally, we had thought to focus on the morphological aspects of viral assembly. Later, during our discussions on the process of budding of enveloped RNA viruses, it became evident that we should include biochemical data in our review and correlate them with the structural aspects of virus maturation
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