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In this work, gyrokinetic simulations in edge plasmas of both tokamaks and field reversedconfigurations (FRC) have been carried out using the Gyrokinetic Toroidal Code (GTC) and A New Code (ANC) has been formulated for cross-separatrix FRC simulation.In the tokamak edge, turbulent transport in the pedestal of an H-mode DIII-D plasma isstudied via simulations of electrostatic driftwaves. Annulus geometry is used and simulations focus on two radial locations corresponding to the pedestal top with mild pressure gradient and steep pressure gradient. A reactive trapped electron instability with typical ballooning mode structure is excited in the pedestal top. At the steep gradient, the electrostatic instability exhibits unusual mode structure, peaking at poloidal angles theta=+- pi/2. Simulations find this unusual mode structure is due to steep pressure gradients in the pedestal but not due to the particular DIII-D magnetic geometry. Realistic DIII-D geometry has a stabilizing effect compared to a simple circular tokamak geometry.Driftwave instability in FRC is studied for the first time using gyrokinetic simulation. GTCis upgraded to treat realistic equilibrium calculated by an MHD equilibrium code. Electrostatic local simulations in outer closed flux surfaces find ion-scale modes are stable due to the large ion gyroradius and that electron drift-interchange modes are excited by electron temperature gradient and bad magnetic curvature. In the scrape-off layer (SOL) ion-scale modes are excited by density gradient and bad curvature. Collisions have weak effects on instabilities both in the core and SOL. Simulation results are consistent with density fluctuation measurements in the C-2 experiment using Doppler backscattering (DBS). The critical density gradients measured by the DBS qualitatively agree with the linear instability threshold calculated by GTC simulations.One outstanding critical issue in the FRC is the interplay between turbulence in the FRCcore and SOL regions. While the magnetic flux coordinates used by GTC provide a number of computational advantages, they present unique challenges at the magnetic field separatrix. To address this limitation, a new code, capable of coupled core-SOL simulations, is formulated, implemented, and successfully verified.

Glutamate receptor subunit 4 (GluA4) is highly expressed by neural cells sensitive to excitotoxicity, and is the predominant subunit expressed by oligodendrocyte precursor cells (OPC) during a key period of vulnerability to hypoxic‐ischemic injury. Therefore, transcriptional networks downstream of excitotoxic GluA4 activation represent a promising area for therapeutic intervention. In this work, we identify the CCAAT binding transcription factor NF‐Yb as a novel transcriptional regulator of Gria4 (GluA4 gene), and a controller of excitotoxic death in the oligodendroglial lineage. We describe a novel regulatory region within Gria4 containing CCAAT sequences whose binding by NF‐Yb is regulated by excitotoxicity. Excitotoxicity‐induced alterations in NF‐Yb binding are associated with changes in Gria4 transcription, while knockdown of NF‐Yb alters the transcription of reporter constructs containing this regulatory region. Data from immortalized and primary OPC reveal that RNAi and pharmacological disruption of NF‐Yb alter Gria4 transcription, with the latter inducing apoptosis and influencing a set of apoptotic genes similarly regulated during excitotoxicity. These data provide the first definition of a trans‐acting mechanism regulating Gria4, and identify the NF‐Y network as a potential source of pharmacological targets for promoting OPC survival.

Isoamylase-type debranching enzymes (ISAs) play an important role in determining starch structure. Amylopectin – a branched polymer of glucose – is the major component of starch granules and its architecture underlies the semi-crystalline nature of starch. Mutants of several species lacking the ISA1-subclass of isoamylase are impaired in amylopectin synthesis. Consequently, starch levels are decreased and an aberrant soluble glucan (phytoglycogen) with altered branch lengths and branching pattern accumulates. Here we use TAP (tandem affinity purification) tagging to provide direct evidence in Arabidopsis that ISA1 interacts with its homolog ISA2. No evidence for interaction with other starch biosynthetic enzymes was found. Analysis of the single mutants shows that each protein is destabilised in the absence of the other. Co-expression of both ISA1 and ISA2 Escherichia coli allowed the formation of the active recombinant enzyme and we show using site-directed mutagenesis that ISA1 is the catalytic subunit. The presence of the active isoamylase alters glycogen biosynthesis in E. coli, resulting in colonies that stain more starch-like with iodine. However, analysis of the glucans reveals that rather than producing an amylopectin like substance, cells expressing the active isoamylase still accumulate small amounts of glycogen together with a population of linear oligosaccharides that stain strongly with iodine. We conclude that for isoamylase to promote amylopectin synthesis it needs to act on a specific precursor (pre-amylopectin) generated by the combined actions of plant starch synthase and branching enzyme isoforms and when presented with an unsuitable substrate (i.e. E. coli glycogen) it simply degrades it., PLoS ONE, 8 (9), ISSN:1932-6203

After consolidation, a process that requires gene expression and protein synthesis, memories are stable and highly resistant to disruption by amnestic influences. Recently, consolidated memory has been shown to become labile again after retrieval and to require a phase of reconsolidation to be preserved. New findings, showing that the dependence of reconsolidation on protein synthesis decreases with the age of memory, point to changing molecular requirements for reconsolidation during memory maturation. We examined this possibility by comparing the roles of protein synthesis (a general molecular requirement for memory consolidation) and the activation of protein kinase A (PKA) (a specific molecular requirement for memory consolidation), in memory reconsolidation at two time points after training. Using associative learning in Lymnaea, we show that reconsolidation after the retrieval of consolidated memory at both 6 and 24 h requires protein synthesis. In contrast, only reconsolidation at 6 h after training, but not at 24 h, requires PKA activity, which is in agreement with the measured retrieval-induced PKA activation at 6 h. This phase-dependent differential molecular requirement for reconsolidation supports the notion that even seemingly consolidated memories undergo further selective molecular maturation processes, which may only be detected by analyzing the role of specific pathways in memory reconsolidation after retrieval.