Consistency of the πΔ\pi\Delta interaction in chiral perturbation theory

We analyze the constraint structure of a spin-3/2 particle interacting with a pseudoscalar. Requiring the self consistency of the considered effective field theory imposes restrictions on the possible interaction terms. In the present case we derive two constraints among the three lowest-order $\pi\Delta$ interaction terms. From these constraints we find that the total Lagrangian is invariant under the so-called point transformation. On the other hand, demanding the invariance under the point transformation alone is less stringent and produces only classes of relations among the coupling constants.Comment: 14 pages, no figures, REVTeX

Parameterized Verification of Safety Properties in Ad Hoc Network Protocols

We summarize the main results proved in recent work on the parameterized verification of safety properties for ad hoc network protocols. We consider a model in which the communication topology of a network is represented as a graph. Nodes represent states of individual processes. Adjacent nodes represent single-hop neighbors. Processes are finite state automata that communicate via selective broadcast messages. Reception of a broadcast is restricted to single-hop neighbors. For this model we consider a decision problem that can be expressed as the verification of the existence of an initial topology in which the execution of the protocol can lead to a configuration with at least one node in a certain state. The decision problem is parametric both on the size and on the form of the communication topology of the initial configurations. We draw a complete picture of the decidability and complexity boundaries of this problem according to various assumptions on the possible topologies.Comment: In Proceedings PACO 2011, arXiv:1108.145

Magnetic dipole moment of the Δ(1232)\Delta(1232) in chiral perturbation theory

The magnetic dipole moment of the $\Delta (1232)$ is calculated in the framework of manifestly Lorentz-invariant baryon chiral perturbation theory in combination with the extended on-mass-shell renormalization scheme. As in the case of the nucleon, at leading order both isoscalar and isovector anomalous magnetic moments are given in terms of two low-energy constants. In contrast to the nucleon case, at next-to-leading order the isoscalar anomalous magnetic moment receives a (real) loop contribution. Moreover, due to the unstable nature of the $\Delta (1232)$, at next-to-leading order the isovector anomalous magnetic moment not only receives a real but also an imaginary loop contribution.Comment: 9 pages, 2 figures, REVTeX

Constrained by managerialism : caring as participation in the voluntary social services

The data in this study show that care is a connective process, underlying and motivating participation and as a force that compels involvement in the lives of others, care is at least a micro-participative process. Care or affinity not only persisted in the face of opposition, but it was also used by workers as a counter discourse and set of practices with which to resist the erosion of worker participation and open up less autonomized practices and ways of connecting with fellow staff, clients and the communities they served. The data suggest that while managerialism and taylorised practice models may remove or reduce opportunities for worker participation, care is a theme or storyline that gave workers other ways to understand their work and why they did it, as well as ways they were prepared to resist managerial priorities and directives, including the erosion of various kinds of direct and indirect participation. The degree of resistance possible, even in the highly technocratic worksite in Australia, shows that cracks and fissures exist within managerialism

EGF-induced PIP2 hydrolysis releases and activates cofilin locally in carcinoma cells

Lamellipodial protrusion and directional migration of carcinoma cells towards chemoattractants, such as epidermal growth factor (EGF), depend upon the spatial and temporal regulation of actin cytoskeleton by actin-binding proteins (ABPs). It is generally hypothesized that the activity of many ABPs are temporally and spatially regulated by PIP2; however, this is mainly based on in vitro–binding and structural studies, and generally in vivo evidence is lacking. Here, we provide the first in vivo data that directly visualize the spatial and temporal regulation of cofilin by PIP2 in living cells. We show that EGF induces a rapid loss of PIP2 through PLC activity, resulting in a release and activation of a membrane-bound pool of cofilin. Upon release, we find that cofilin binds to and severs F-actin, which is coincident with actin polymerization and lamellipod formation. Moreover, our data provide evidence for how PLC is involved in the formation of protrusions in breast carcinoma cells during chemotaxis and metastasis towards EGF

Full accounting for verifiable outsourcing

Systems for verifiable outsourcing incur costs for a prover, a verifier, and precomputation; outsourcing makes sense when the combination of these costs is cheaper than not outsourcing. Yet, when prior works impose quantitative thresholds to analyze whether outsourcing is justified, they generally ignore prover costs. Verifiable ASICs (VA)---in which the prover is a custom chip---is the other way around: its cost calculations ignore precomputation. This paper describes a new VA system, called Giraffe; charges Giraffe for all three costs; and identifies regimes where outsourcing is worthwhile. Giraffe’s base is an interactive proof geared to data-parallel computation. Giraffe makes this protocol asymptotically optimal for the prover and improves the verifier\u27s main bottleneck by almost 3x, both of which are of independent interest. Giraffe also develops a design template that produces hardware designs automatically for a wide range of parameters, introduces hardware primitives molded to the protocol’s data flows, and incorporates program analyses that expand applicability. Giraffe wins even when outsourcing several tens of sub-computations, scales to 500x larger computations than prior work, and can profitably outsource parts of programs that are not worthwhile to outsource in full

Committing curriculum time to science literacy: The benefits from science based media resources

Kaposi sarcoma-associated herpesvirus (KSHV) is linked with the development of Kaposi sarcoma and the B lymphocyte disorders primary effusion lymphoma (PEL) and multi-centric Castleman disease. T cell immunity limits KSHV infection and disease, however the virus employs multiple mechanisms to inhibit efficient control by these effectors. Thus KSHV-specific CD4+ T cells poorly recognize most PEL cells and even where they can, they are unable to kill them. To make KSHV-infected cells more sensitive to T cell control we treated PEL cells with the thymidine analogue azidothymidine (AZT), which sensitizes PEL lines to Fas-ligand and TRAIL challenge; effector mechanisms which T cells use. PELs co-cultured with KSHV-specific CD4+ T cells in the absence of AZT showed no control of PEL outgrowth. However in the presence of AZT PEL outgrowth was controlled in an MHC-restricted manner. To investigate how AZT sensitizes PELs to immune control we first examined BJAB cells transduced with individual KSHV-latent genes for their ability to resist apoptosis mediated by stimuli delivered through Fas and TRAIL receptors. This showed that in addition to the previously described vFLIP protein, expression of vIRF3 also inhibited apoptosis delivered by these stimuli. Importantly vIRF3 mediated protection from these apoptotic stimuli was inhibited in the presence of AZT as was a second vIRF3 associated phenotype, the downregulation of surface MHC class II. Although both vFLIP and vIRF3 are expressed in PELs, we propose that inhibiting vIRF3 function with AZT may be sufficient to restore T cell control of these tumor cells

On Sets with Cardinality Constraints in Satisfiability Modulo Theories

Boolean Algebra with Presburger Arithmetic (BAPA) is a decidable logic that can express constraints on sets of elements and their cardinalities. Problems from verification of complex properties of software often contain fragments that belong to quantifier-free BAPA (QFBAPA). Deciding the satisfiability of QFBAPA formulas has been shown to be NP-complete using an eager reduction to quantifier-free Presburger arithmetic that exploits a sparse-solution property. In contrast to many other NP-complete problems (such as quantifier-free first-order logic or linear arithmetic), the applications of QFBAPA to a broader set of problems has so far been hindered by the lack of an efficient implementation that can be used alongside other efficient decision procedures. We overcome these limitations by extending the efficient SMT solver Z3 with the ability to reason about cardinality constraints. Our implementation uses the DPLL(T) mechanism of Z3 to reason about the top-level propositional structure of a QFBAPA formula, improving the efficiency compared to previous implementations. Moreover, we present a new algorithm for automated decomposition of QFBAPA formulas. Our algorithm alleviates the exponential explosion of considering all Venn regions, significantly improving the tractability of formulas with many set variables. Because it is implemented as a theory plugin, our implementation enables Z3 to prove formulas that use QFBAPA constructs alongside constructs from other theories that Z3 supports (e.g. linear arithmetic, uninterpreted function symbols, algebraic data types), as well as in formulas with quantifiers. We have applied our implementation to verification of functional programs; we show it can automatically prove formulas that no automated approach was reported to be able to prove before

A plausibility database summarizing the level of evidence regarding the hazards induced by the exposome on children health

Supplementary data are available online at: https://www.sciencedirect.com/science/article/pii/S143846392300202X#appsec1 .Copyright © 2023 The Authors. Childhood diseases correspond to major public health issues. A large number of studies using different approaches provide evidence regarding effects of environmental exposures, encompassed in the exposome, on children's health. We aimed to summarize the overall level of evidence (LoE) from all streams of evidence regarding exposome effects on child health. For 88 selected chemical and urban factors, we retrieved the conclusions of agency reports or literature reviews published between 2015 and 2021 regarding effects on child health, including cardiovascular, metabolic, neurodevelopmental, respiratory and other health outcomes. Adapted versions of PRISMA flowchart and AMSTAR-2 tool were used to select and assess the quality of the systematic reviews retrieved from PubMed and SCOPUS databases. For each factor-outcome pair, conclusions in three streams of evidence (epidemiological, toxicological and mechanistic, the latter corresponding to in vitro and in silico approaches) were translated into stream-specific LoEs and then combined into an overall LoE ranging from “very unlikely” to “very likely”. The 88 environmental factors were implied in 611 factor-outcome pairs. Forty-four pairs (7%), corresponding to 16 factors, had a very likely overall LoE (≥80%); 127 pairs (21%), corresponding to 49 factors, had a likely or more overall LoE (≥60%). For 81 pairs (13%), no evidence was available in agency reports or published reviews, while for 275 pairs (45%), corresponding to 68 factors, the overall LoE was very unlikely (<20%). Exposure factors with the greatest number of associated health outcomes with a high overall LoE were HCB, PCBs, temperature (8 outcomes), PFOA (7 outcomes), PFOS, cotinine (6 outcomes), arsenic, lead (5 outcomes), bisphenols A and S, PFNA and PM2.5 (4 outcomes), DDT, DDE and DDD, PFHxA, PFDA, green space, UV radiation (3 outcomes). We developed an approach to extract and summarize the existing evidence about effects of environmental factors on health. The plausibility database built for children's health can be used to identify research gaps, conduct quantitative risk assessment studies. It could be expanded to consider a larger fraction of the exposome and other age groups and should be updated on a regular basis.The ATHLETE project was funded by The European Commission, through its Horizon 2020 Framework Program for Research and Innovation (grant agreement 874583). This work was also supported by HERA (Integrating Environment and Health Research: a Vision for the EU) Horizon 2020 project (grant agreement 825417). We acknowledge support from the grant CEX 2018-000806-S funded by MCIN/AEI/10.13039/501100011033, and support from the Generalitat de Catalunya through the CERCA Program

A Gammaherpesvirus Cooperates with Interferon-alpha/beta-Induced IRF2 to Halt Viral Replication, Control Reactivation, and Minimize Host Lethality

The gammaherpesviruses, including Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), establish latency in memory B lymphocytes and promote lymphoproliferative disease in immunocompromised individuals. The precise immune mechanisms that prevent gammaherpesvirus reactivation and tumorigenesis are poorly defined. Murine gammaherpesvirus 68 (MHV68) is closely related to EBV and KSHV, and type I (alpha/beta) interferons (IFNαβ) regulate MHV68 reactivation from both B cells and macrophages by unknown mechanisms. Here we demonstrate that IFNβ is highly upregulated during latent infection, in the absence of detectable MHV68 replication. We identify an interferon-stimulated response element (ISRE) in the MHV68 M2 gene promoter that is bound by the IFNαβ-induced transcriptional repressor IRF2 during latency in vivo. The M2 protein regulates B cell signaling to promote establishment of latency and reactivation. Virus lacking the M2 ISRE (ISREΔ) overexpresses M2 mRNA and displays uncontrolled acute replication in vivo, higher latent viral load, and aberrantly high reactivation from latency. These phenotypes of the ISREΔ mutant are B-cell-specific, require IRF2, and correlate with a significant increase in virulence in a model of acute viral pneumonia. We therefore identify a mechanism by which a gammaherpesvirus subverts host IFNαβ signaling in a surprisingly cooperative manner, to directly repress viral replication and reactivation and enforce latency, thereby minimizing acute host disease. Since we find ISREs 5′ to the major lymphocyte latency genes of multiple rodent, primate, and human gammaherpesviruses, we propose that cooperative subversion of IFNαβ-induced IRFs to promote latent infection is an ancient strategy that ensures a stable, minimally-pathogenic virus-host relationship