480 research outputs found

    Dynamical evolution of interplanetary magnetic fields and flows between 0.3 AU and 8.5 AU: Entrainment

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    The radial evolution of interplanetary flows and associated magnetic fields between 0.3 AU and 8.5 was analyzed using data from Helios 1 and Voyager 1, respectively. During a 70 day interval Voyager 1 observed two streams which appeared to be recurrent and which had little fine structure. The corresponding flows observed by Helios 1 were much more complex, showing numerous small streams, transient flows and shocks as well as a few large corotating streams. It is suggested that in moving to 8 AU the largest corotating streams swept up the slower flows (transient and/or corotating streams) and shocks into a relatively thin region in which they coalesced to form a single large amplitude compression wave. This combined process of sweeping and coalescence is referred to as entrainment. The resulting large amplitude compression wave is different from that formed by the steepening of a corotating stream from a coronal hole, because different flows from distinct sources, with possibly different composition and magnetic polarity, are brought together to form a single new structure

    Magnetic fields and flows between 1 AU and 0.3 AU during the primary mission of HELIOS 1

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    The recurrent flow and field patterns observed by HELIOS 1, and the relation between these patterns and coronal holes are discussed. Four types of recurrent patterns were observed: a large recurrent stream, a recurrent slow (quiet) flow, a rapidly evolving flow, and a recurrent compound stream. There recurrent streams were not stationary, for although the sources recurred at approximately the same longitudes on successive rotations, the shapes and latitudinal patterns changed from one rotation to the next. A type of magnetic field and plasma structure characterized by a low ion temperature and a high magnetic field intensity is described as well as the structures of stream boundaries between the sun at approximately 0.3 AU

    Chromatin dynamics during differentiation of myeloid cells

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    Cellular commitment to differentiation requires a tightly synchronized, spatial-temporal interaction of regulatory proteins with the basic DNA and chromatin. A complex network of mechanisms, involving induction of lineage instructive transcription factors, installation or removal of histone modifications and changes in the DNA methylation pattern locally orchestrate the three dimensional chromatin structure and determine cell fate. Maturation of myeloid lineages from haematopoietic stem cells has emerged as a powerful model to study those principles of chromatin mechanisms in cellular differentiation and lineage fate selection. This review summarizes recent knowledge and puts forward novel ideas on how dynamics in the epigenetic landscape of myeloid cells shape the development, immune-activation and leukaemic transformation outcome

    Cross talk between Wnt/β-catenin and Irf8 in leukemia progression and drug resistance

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    Progression and disease relapse of chronic myeloid leukemia (CML) depends on leukemia-initiating cells (LIC) that resist treatment. Using mouse genetics and a BCR-ABL model of CML, we observed cross talk between Wnt/{beta}-catenin signaling and the interferon-regulatory factor 8 (Irf8). In normal hematopoiesis, activation of {beta}-catenin results in up-regulation of Irf8, which in turn limits oncogenic {beta}-catenin functions. Self-renewal and myeloproliferation become dependent on {beta}-catenin in Irf8-deficient animals that develop a CML-like disease. Combined Irf8 deletion and constitutive {beta}-catenin activation result in progression of CML into fatal blast crisis, elevated leukemic potential of BCR-ABL-induced LICs, and Imatinib resistance. Interestingly, activated {beta}-catenin enhances a preexisting Irf8-deficient gene signature, identifying {beta}-catenin as an amplifier of progression-specific gene regulation in the shift of CML to blast crisis. Collectively, our data uncover Irf8 as a roadblock for {beta}-catenin-driven leukemia and imply both factors as targets in combinatorial therapy

    Economic growth in the post-socialist Russian Federation after 1991 : the role of institutions

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    The paper emphasizes the transition in Russia and the role institutions played before and during the process. In Russia, a ?big bang? approach was applied. That is to say, transition was conducted all of a sudden, omitting important underlying reforms. This practice should function as a shock therapy. Hence, the approach should leave no other chance than an abrupt adaption to the new free-market rules. These rules would then lead to fast economic growth and development, as they did in other places. However, since Russian GDP per capita and thereby living standards deteriorated dramatically in the years after the collapse of the Soviet Union, the plan did not work. At any rate, since then Russian economic indicators recovered and partly achieved their pre-1991 levels at the end of the last decade. The paper depicts Russia?s reform efforts and the subsequent developments. The close ties among the political elite, the banking sector and the old nomenklatura are demonstrated. The patrimonial system that persisted for centuries is still observable at the state level. At any rate, Russia can neither evade its historical and institutional development path nor its societal structures that are based on networks and nepotism. Russia?s systemic lack of the rule of law and therewith of secure property, the character of the Russian political system with the patriarch as the head of state and the resulting necessity of corruption and bribes inhibit the realization of its full growth potential

    Molecular Genetics of T Cell Development

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    T cell development is guided by a complex set of transcription factors that act recursively, in different combinations, at each of the developmental choice points from T-lineage specification to peripheral T cell specialization. This review describes the modes of action of the major T-lineage-defining transcription factors and the signal pathways that activate them during intrathymic differentiation from pluripotent precursors. Roles of Notch and its effector RBPSuh (CSL), GATA-3, E2A/HEB and Id proteins, c-Myb, TCF-1, and members of the Runx, Ets, and Ikaros families are critical. Less known transcription factors that are newly recognized as being required for T cell development at particular checkpoints are also described. The transcriptional regulation of T cell development is contrasted with that of B cell development, in terms of their different degrees of overlap with the stem-cell program and the different roles of key transcription factors in gene regulatory networks leading to lineage commitment

    Mutations of the transcription factor PU.1 are not associated with acute lymphoblastic leukaemia

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    The transcription factor PU.1 plays a crucial role during normal haematopoiesis in both myeloid cells and B-lymphocytes. Mice with a disruption in both alleles of the PU.1 locus were found to lack macrophages and B cells and had delayed appearance of neutrophils. In addition, critical decrease of PU.1 expression is sufficient to cause acute myeloid leukaemia (AML) and lymphomas in mice. Recently, we reported that heterozygous mutations in the PU.1 gene are present in some patients with AML. Thus, we hypothesised that PU.1 mutations might also contribute to the development of acute leukaemias of the B-cell lineage. Here, we screened 62 patients with B-cell acute lymphoblastic leukaemia (B-ALL) at diagnosis for genomic mutations by direct sequencing of all five exons of the PU.1 gene. We found no genomic alteration of the PU.1 gene suggesting that PU.1 mutations are not likely to be common in B-ALL
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