Consistent with what has been reported for other organs, platelet-derived growth factor (PDGF)-B is also a key protective factor in noncancerous brain damage,26,27 contributing to blood-brain barrier stability, angiogenesis, and vascular remodeling through the activation of PDGF receptor β (PDGFRβ)-expressing brain pericytes and neuroglial progenitor cells.28,29 During cancer progression PDGFRβ expression has long been associated with tumor-associated stromagenic and angiogenic activities.30 However, its role during brain metastasis development is unknown.
Cover photograph (Copyright 2013, American Society for Microbiology. All Rights Reserved.): Communications between marine Roseobacter bacteria and their unicellular algal hosts. Clockwise from lower left, motile roseobacters (blue bacteria) swim toward algal dimethylsulfoniopropionate, which they use to produce tropodithietic acid (TDA). TDA induces the sessile phase (yellow bacteria) and inhibits nonroseobacters (purple bacteria). Sessile roseobacters produce phenyl acetic acid and indole acetic acid, stimulating algal growth. Ultimately, algal death results in an increase in p-coumaric acid that induces the synthesis of roseobacter motility inducer (RMI), triggering the bacterial motile phase and killing the alga. The swim-or-stick switch is reset, permitting the roseobacters to renew their symbiosis with a fresh algal host. (See related article on page 637.)
Activation Maya 2013 Key
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Abstract:DNA replication in eukaryotes is achieved by the activation of multiple replication origins which needs to be precisely coordinated in space and time. This spatio-temporal replication program is regulated by many factors to maintain genome stability, which is frequently threatened through stresses of exogenous or endogenous origin. Intra-S phase checkpoints monitor the integrity of DNA synthesis and are activated when replication forks are stalled. Their activation leads to the stabilization of forks, to the delay of the replication program by the inhibition of late firing origins, and the delay of G2/M phase entry. In some cell cycles during early development these mechanisms are less efficient in order to allow rapid cell divisions. In this article, we will review our current knowledge of how the intra-S phase checkpoint regulates the replication program in budding yeast and metazoan models, including early embryos with rapid S phases. We sum up current models on how the checkpoint can inhibit origin firing in some genomic regions, but allow dormant origin activation in other regions. Finally, we discuss how numerical and theoretical models can be used to connect the multiple different actors into a global process and to extract general rules.Keywords: DNA replication; replication checkpoint; intra-S phase checkpoint; ATR; Chk1; MBT; initiation rate; numerical; theoretical models
We present a descriptive model for the context of a knowledge worker. This model describes the contextual elements in the work environment of the knowledge worker and how these elements relate to each other. This model is operationalized in an algorithm, the contextual interactive activation model (CIA), which is based on the interactive activation model by Rumelhart and McClelland. It consists of a layered connected network through which activation flows. We have tested CIA in a context identification setting. In this case, the data that we use as input is low-level computer interaction logging data. 2ff7e9595c
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