Sheath parameters for non-Debye plasmas: simulations and arc damage

This paper describes the surface environment of the dense plasma arcs that damage rf accelerators, tokamaks and other high gradient structures. We simulate the dense, non-ideal plasma sheath near a metallic surface using Molecular Dynamics (MD) to evaluate sheaths in the non-Debye region for high density, low temperature plasmas. We use direct two-component MD simulations where the interactions between all electrons and ions are computed explicitly. We find that the non-Debye sheath can be extrapolated from the Debye sheath parameters with small corrections. We find that these parameters are roughly consistent with previous PIC code estimates, pointing to densities in the range $10^{24} - 10^{25}\mathrm{m}^{-3}$. The high surface fields implied by these results could produce field emission that would short the sheath and cause an instability in the time evolution of the arc, and this mechanism could limit the maximum density and surface field in the arc. These results also provide a way of understanding how the "burn voltage" of an arc is generated, and the relation between self sputtering and the burn voltage, while not well understood, seems to be closely correlated. Using these results, and equating surface tension and plasma pressure, it is possible to infer a range of plasma densities and sheath potentials from SEM images of arc damage. We find that the high density plasma these results imply and the level of plasma pressure they would produce is consistent with arc damage on a scale 100 nm or less, in examples where the liquid metal would cool before this structure would be lost. We find that the sub-micron component of arc damage, the burn voltage, and fluctuations in the visible light production of arcs may be the most direct indicators of the parameters of the dense plasma arc, and the most useful diagnostics of the mechanisms limiting gradients in accelerators.Comment: 8 pages, 16 figure

Robust Model Predictive Control for humanoids standing balancing

This paper presents the implementations of Model Predictive Control for the standing balance control of a humanoid to reject external disturbances. The strategies allow the robot to have a compliant behaviour against external forces resulting in a stable and smooth response. The first, ZMP based controller, compensates for the center of mass deviation while the second, attitude controller, regulates the orientation of the body to counterbalance the external disturbances. These two control strategies are combined as an integrated stabilizer, which further increases the effectiveness. Simulation studies on the COMAN humanoid are presented and the data are analysed. The simulations show significant improvements in rejection of external disturbances compared to an existing compliant stabilizer

Modifying the Sum Over Topological Sectors and Constraints on Supergravity

The standard lore about the sum over topological sectors in quantum field theory is that locality and cluster decomposition uniquely determine the sum over such sectors, thus leading to the usual theta-vacua. We show that without changing the local degrees of freedom, a theory can be modified such that the sum over instantons should be restricted; e.g. one should include only instanton numbers which are divisible by some integer p. This conclusion about the configuration space of quantum field theory allows us to carefully reconsider the quantization of parameters in supergravity. In particular, we show that FI-terms and nontrivial Kahler forms are quantized. This analysis also leads to a new derivation of recent results about linearized supergravity.Comment: 17 pages, minor change

Minimal Gaugino Mediation

We propose Minimal Gaugino Mediation as the simplest known solution to the supersymmetric flavor and CP problems. The framework predicts a very minimal structure for the soft parameters at ultra-high energies: gaugino masses are unified and non-vanishing whereas all other soft supersymmetry breaking parameters vanish. We show that this boundary condition naturally arises from a small extra dimension and present a complete model which includes a new extra-dimensional solution to the mu problem. We briefly discuss the predicted superpartner spectrum as a function of the two parameters of the model. The commonly ignored renormalization group evolution above the GUT scale is crucial to the viability of Minimal Gaugino Mediation but does not introduce new model dependence.Comment: LaTeX, 16 pages, 4 figures, running of the bottom and tau Yukawas included, plots revise

Regulation of caspase-3 processing by cIAP2 controls the switch between pro-inflammatory activation and cell death in microglia.

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International Licence. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons licence, users will need to obtain permission from the licence holder to reproduce the material.The activation of microglia, resident immune cells of the central nervous system, and inflammation-mediated neurotoxicity are typical features of neurodegenerative diseases, for example, Alzheimer's and Parkinson's diseases. An unexpected role of caspase-3, commonly known to have executioner role for apoptosis, was uncovered in the microglia activation process. A central question emerging from this finding is what prevents caspase-3 during the microglia activation from killing those cells? Caspase-3 activation occurs as a two-step process, where the zymogen is first cleaved by upstream caspases, such as caspase-8, to form intermediate, yet still active, p19/p12 complex; thereafter, autocatalytic processing generates the fully mature p17/p12 form of the enzyme. Here, we show that the induction of cellular inhibitor of apoptosis protein 2 (cIAP2) expression upon microglia activation prevents the conversion of caspase-3 p19 subunit to p17 subunit and is responsible for restraining caspase-3 in terms of activity and subcellular localization. We demonstrate that counteracting the repressive effect of cIAP2 on caspase-3 activation, using small interfering RNA targeting cIAP2 or a SMAC mimetic such as the BV6 compound, reduced the pro-inflammatory activation of microglia cells and promoted their death. We propose that the different caspase-3 functions in microglia, and potentially other cell types, reside in the active caspase-3 complexes formed. These results also could indicate cIAP2 as a possible therapeutic target to modulate microglia pro-inflammatory activation and associated neurotoxicity observed in neurodegenerative disorders

BUDHIES - III : the fate of HI and the quenching of galaxies in evolving environments

In a hierarchical Universe clusters grow via the accretion of galaxies from the field, groups and even other clusters. As this happens, galaxies can lose and/or consume their gas reservoirs via different mechanisms, eventually quenching their star formation. We explore the diverse environmental histories of galaxies through a multiwavelength study of the combined effect of ram-pressure stripping and group 'processing' in Abell 963, a massive growing cluster at z = 0.2 from the Blind Ultra Deep HI Environmental Survey (BUDHIES). We incorporate hundreds of new optical redshifts (giving a total of 566 cluster members), as well as Subaru and XMM-Newton data from LoCuSS, to identify substructures and evaluate galaxy morphology, star formation activity, and HI content (via HI deficiencies and stacking) out to 3 x R-200. We find that Abell 963 is being fed by at least seven groups, that contribute to the large number of passive galaxies outside the cluster core. More massive groups have a higher fraction of passive and HI-poor galaxies, while low-mass groups host younger (often interacting) galaxies. For cluster galaxies not associated with groups we corroborate our previous finding that HI gas (if any) is significantly stripped via ram-pressure during their first passage through the intracluster medium, and find mild evidence for a starburst associated with this event. In addition, we find an overabundance of morphologically peculiar and/or star-forming galaxies near the cluster core. We speculate that these arise from the effect of groups passing through the cluster (post-processing). Our study highlights the importance of environmental quenching and the complexity added by evolving environments.Peer reviewe

Markers for the identification of late breast cancer recurrence

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited

A Constrained Standard Model from a Compact Extra Dimension

A SU(3) \times SU(2) \times U(1) supersymmetric theory is constructed with a TeV sized extra dimension compactified on the orbifold S^1/(Z_2 \times Z_2'). The compactification breaks supersymmetry leaving a set of zero modes which correspond precisely to the states of the 1 Higgs doublet standard model. Supersymmetric Yukawa interactions are localized at orbifold fixed points. The top quark hypermultiplet radiatively triggers electroweak symmetry breaking, yielding a Higgs potential which is finite and exponentially insensitive to physics above the compactification scale. This potential depends on only a single free parameter, the compactification scale, yielding a Higgs mass prediction of 127 \pm 8 GeV. The masses of the all superpartners, and the Kaluza-Klein excitations are also predicted. The lightest supersymmetric particle is a top squark of mass 197 \pm 20 GeV. The top Kaluza-Klein tower leads to the \rho parameter having quadratic sensitivity to unknown physics in the ultraviolet.Comment: 31 pages, Latex, 2 eps figures, minor correction

Four Generations: SUSY and SUSY Breaking

We revisit four generations within the context of supersymmetry. We compute the perturbativity limits for the fourth generation Yukawa couplings and show that if the masses of the fourth generation lie within reasonable limits of their present experimental lower bounds, it is possible to have perturbativity only up to scales around 1000 TeV. Such low scales are ideally suited to incorporate gauge mediated supersymmetry breaking, where the mediation scale can be as low as 10-20 TeV. The minimal messenger model, however, is highly constrained. While lack of electroweak symmetry breaking rules out a large part of the parameter space, a small region exists, where the fourth generation stau is tachyonic. General gauge mediation with its broader set of boundary conditions is better suited to accommodate the fourth generation.Comment: 27 pages, 5 figure

FTLD-TDP assemblies seed neoaggregates with subtype-specific features via a prion-like cascade

Morphologically distinct TDP-43 aggregates occur in clinically different FTLD-TDP subtypes, yet the mechanism of their emergence and contribution to clinical heterogeneity are poorly understood. Several lines of evidence suggest that pathological TDP-43 follows a prion-like cascade, but the molecular determinants of this process remain unknown. We use advanced microscopy techniques to compare the seeding properties of pathological FTLD-TDP-A and FTLD-TDP-C aggregates. Upon inoculation of patient-derived aggregates in cells, FTLD-TDP-A seeds amplify in a template-dependent fashion, triggering neoaggregation more efficiently than those extracted from FTLD-TDP-C patients, correlating with the respective disease progression rates. Neoaggregates are sequentially phosphorylated with N-to-C directionality and with subtype-specific timelines. The resulting FTLD-TDP-A neoaggregates are large and contain densely packed fibrils, reminiscent of the pure compacted fibrils present within cytoplasmic inclusions in postmortem brains. In contrast, FTLD-TDP-C dystrophic neurites show less dense fibrils mixed with cellular components, and their respective neoaggregates are small, amorphous protein accumulations. These cellular seeding models replicate aspects of the patient pathological diversity and will be a useful tool in the quest for subtype-specific therapeutics