Kinetic instabilities that limit {\beta} in the edge of a tokamak plasma: a picture of an H-mode pedestal

Plasma equilibria reconstructed from the Mega-Amp Spherical Tokamak (MAST) have sufficient resolution to capture plasma evolution during the short period between edge-localized modes (ELMs). Immediately after the ELM steep gradients in pressure, P, and density, ne, form pedestals close to the separatrix, and they then expand into the core. Local gyrokinetic analysis over the ELM cycle reveals the dominant microinstabilities at perpendicular wavelengths of the order of the ion Larmor radius. These are kinetic ballooning modes (KBMs) in the pedestal and microtearing modes (MTMs) in the core close to the pedestal top. The evolving growth rate spectra, supported by gyrokinetic analysis using artificial local equilibrium scans, suggest a new physical picture for the formation and arrest of this pedestal.Comment: Final version as it appeared in PRL (March 2012). Minor improvements include: shortened abstract, and better colour table for figures. 4 pages, 6 figure

Identification of polyubiquitin binding proteins involved in NF-kappaB signaling using protein arrays.

Attachment of ubiquitin to proteins represents a central mechanism for the regulation of protein metabolism and function. In the NF-kappaB pathway, binding of NEMO to polyubiquitinated substrates initiates the pathway in response to cellular stimuli. Other polyubiquitin binding proteins can antagonize this pathway by competing with NEMO for polyubiquitin. We have used protein arrays to identify polyubiquitin binding proteins that regulate NF-kappaB activity. Using polyubiquitin as bait, protein arrays were screened and polyubiquitin binders identified. Novel polyubiquitin binders AWP1, CALCOCO2, N4BP1, RIO3, TEX27, TTC3, UBFD1 and ZNF313 were identified using this approach, while known NF-kappaB regulators including NEMO, A20, ABIN-1, ABIN-2, optineurin and p62 were also identified. Overexpressed AWP1 and RIO3 repressed NF-kappaB activity in a manner similar to optineurin, while siRNAs directed against AWP1 and RIO3 also reduced NF-kappaB activity. TNFalpha-dependent degradation of IkappaBalpha was also suppressed by overexpression of AWP1 and RIO3, possibly due to the polyubiquitin binding activity of these proteins. Protein array screening using polyubiquitin enabled rapid identification of many known and novel polyubiquitin binding proteins and the identification of novel NF-kappaB regulators

Expanding the Substantial Interactome of NEMO Using Protein Microarrays

Signal transduction by the NF-kappaB pathway is a key regulator of a host of cellular responses to extracellular and intracellular messages. The NEMO adaptor protein lies at the top of this pathway and serves as a molecular conduit, connecting signals transmitted from upstream sensors to the downstream NF-kappaB transcription factor and subsequent gene activation. The position of NEMO within this pathway makes it an attractive target from which to search for new proteins that link NF-kappaB signaling to additional pathways and upstream effectors. In this work, we have used protein microarrays to identify novel NEMO interactors. A total of 112 protein interactors were identified, with the most statistically significant hit being the canonical NEMO interactor IKKbeta, with IKKalpha also being identified. Of the novel interactors, more than 30% were kinases, while at least 25% were involved in signal transduction. Binding of NEMO to several interactors, including CALB1, CDK2, SAG, SENP2 and SYT1, was confirmed using GST pulldown assays and coimmunoprecipitation, validating the initial screening approach. Overexpression of CALB1, CDK2 and SAG was found to stimulate transcriptional activation by NF-kappaB, while SYT1 overexpression repressed TNFalpha-dependent NF-kappaB transcriptional activation in human embryonic kidney cells. Corresponding with this finding, RNA silencing of CDK2, SAG and SENP2 reduced NF-kappaB transcriptional activation, supporting a positive role for these proteins in the NF-kappaB pathway. The identification of a host of new NEMO interactors opens up new research opportunities to improve understanding of this essential cell signaling pathway

(G)hosting television: Ghostwatch and its medium

This article’s subject is Ghostwatch (BBC, 1992), a drama broadcast on Halloween night of 1992 which adopted the rhetoric of live non-fiction programming, and attracted controversy and ultimately censure from the Broadcasting Standards Council. In what follows, we argue that Ghostwatch must be understood as a televisually-specific artwork and artefact. We discuss the programme’s ludic relationship with some key features of television during what Ellis (2000) has termed its era of ‘availability’, principally liveness, mass simultaneous viewing, and the flow of the television super-text. We trace the programme’s television-specific historicity whilst acknowledging its allusions and debts to other media (most notably film and radio). We explore the sophisticated ways in which Ghostwatch’s visual grammar and vocabulary and deployment of ‘broadcast talk’ (Scannell 1991) variously ape, comment upon and subvert the rhetoric of factual programming, and the ends to which these strategies are put. We hope that these arguments collectively demonstrate the aesthetic and historical significance of Ghostwatch and identify its relationship to its medium and that medium’s history. We offer the programme as an historically-reflexive artefact, and as an exemplary instance of the work of art in television’s age of broadcasting, liveness and co-presence

3-manifolds which are spacelike slices of flat spacetimes

We continue work initiated in a 1990 preprint of Mess giving a geometric parameterization of the moduli space of classical solutions to Einstein's equations in 2+1 dimensions with cosmological constant 0 or -1 (the case +1 has been worked out in the interim by the present author). In this paper we make a first step toward the 3+1-dimensional case by determining exactly which closed 3-manifolds M^3 arise as spacelike slices of flat spacetimes, and by finding all possible holonomy homomorphisms pi_1(M^3) to ISO(3,1).Comment: 10 page