Investigation of EMIC wave scattering as the cause for the BARREL 17 January 2013 relativistic electron precipitation event: A quantitative comparison of simulation with observations

Abstract Electromagnetic ion cyclotron (EMIC) waves were observed at multiple observatory locations for several hours on 17 January 2013. During the wave activity period, a duskside relativistic electron precipitation (REP) event was observed by one of the Balloon Array for Radiation belt Relativistic Electron Losses (BARREL) balloons and was magnetically mapped close to Geostationary Operational Environmental Satellite (GOES) 13. We simulate the relativistic electron pitch angle diffusion caused by gyroresonant interactions with EMIC waves using wave and particle data measured by multiple instruments on board GOES 13 and the Van Allen Probes. We show that the count rate, the energy distribution, and the time variation of the simulated precipitation all agree very well with the balloon observations, suggesting that EMIC wave scattering was likely the cause for the precipitation event. The event reported here is the first balloon REP event with closely conjugate EMIC wave observations, and our study employs the most detailed quantitative analysis on the link of EMIC waves with observed REP to date. Key PointsQuantitative analysis of the first balloon REP with closely conjugate EMIC wavesOur simulation suggests EMIC waves to be a viable cause for the REP eventThe adopted model is proved to be applicable to simulating the REP event

Linking Proteomic and Transcriptional Data through the Interactome and Epigenome Reveals a Map of Oncogene-induced Signaling

Cellular signal transduction generally involves cascades of post-translational protein modifications that rapidly catalyze changes in protein-DNA interactions and gene expression. High-throughput measurements are improving our ability to study each of these stages individually, but do not capture the connections between them. Here we present an approach for building a network of physical links among these data that can be used to prioritize targets for pharmacological intervention. Our method recovers the critical missing links between proteomic and transcriptional data by relating changes in chromatin accessibility to changes in expression and then uses these links to connect proteomic and transcriptome data. We applied our approach to integrate epigenomic, phosphoproteomic and transcriptome changes induced by the variant III mutation of the epidermal growth factor receptor (EGFRvIII) in a cell line model of glioblastoma multiforme (GBM). To test the relevance of the network, we used small molecules to target highly connected nodes implicated by the network model that were not detected by the experimental data in isolation and we found that a large fraction of these agents alter cell viability. Among these are two compounds, ICG-001, targeting CREB binding protein (CREBBP), and PKF118–310, targeting β-catenin (CTNNB1), which have not been tested previously for effectiveness against GBM. At the level of transcriptional regulation, we used chromatin immunoprecipitation sequencing (ChIP-Seq) to experimentally determine the genome-wide binding locations of p300, a transcriptional co-regulator highly connected in the network. Analysis of p300 target genes suggested its role in tumorigenesis. We propose that this general method, in which experimental measurements are used as constraints for building regulatory networks from the interactome while taking into account noise and missing data, should be applicable to a wide range of high-throughput datasets.National Science Foundation (U.S.) (DB1-0821391)National Institutes of Health (U.S.) (Grant U54-CA112967)National Institutes of Health (U.S.) (Grant R01-GM089903)National Institutes of Health (U.S.) (P30-ES002109

Proceedings of Abstracts, School of Physics, Engineering and Computer Science Research Conference 2022

© 2022 The Author(s). This is an open-access work distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. For further details please see https://creativecommons.org/licenses/by/4.0/. Plenary by Prof. Timothy Foat, ‘Indoor dispersion at Dstl and its recent application to COVID-19 transmission’ is © Crown copyright (2022), Dstl. This material is licensed under the terms of the Open Government Licence except where otherwise stated. To view this licence, visit http://www.nationalarchives.gov.uk/doc/open-government-licence/version/3 or write to the Information Policy Team, The National Archives, Kew, London TW9 4DU, or email: [email protected] present proceedings record the abstracts submitted and accepted for presentation at SPECS 2022, the second edition of the School of Physics, Engineering and Computer Science Research Conference that took place online, the 12th April 2022

CO emission from an impinging non-premixed flame

Carbon monoxide (CO) results from the incomplete oxidation of hydrocarbon fuels. While CO can be desirable in some syngas processes, it is a dangerous emission from fires, gas heaters, gas stoves, or furnaces where insufficient oxygen in the core reaction prevents complete oxidation of fuel to carbon dioxide and water, particularly when the reaction is interrupted by interaction with relatively cool solid boundaries. This research examines the physico-thermo-chemical processes responsible for carbon monoxide release from a small laminar non-premixed methane/air flame impinging on a nearby surface. We measure the changes in CO emission as correlated with variations in flame structure observed using planar laser induced fluorescence (PLIF of OH and 2-photon CO), and two-line OH PLIF thermometry, as a function of burner-to-plate distance. In particular, this work combines the use of OH and CO PLIF, and PLIF thermometry to describe the relative locations of the CO rich region, the peak heat release zone as indicated by chemiluminescence and OH gradients, and the extended oxidative zone in the impinging flames. The results show that CO release correlates strongly with stagnating flow-driven changes in the location and extent of high concentration regions of OH in surface-impinging diffusion flames

Comprehensive genomic screens identify a role for PLZF-RAR alpha as a positive regulator of cell proliferation via direct regulation of c-MYC

The t(11;17)(q23;q21) translocation is associated with a retinoic acid (RA)–insensitive form of acute promyelocytic leukemia (APL), involving the production of reciprocal fusion proteins, promyelocytic leukemia zinc finger–retinoic acid receptor α (PLZF-RARα) and RARα-PLZF. Using a combination of chromatin immunoprecipitation promotor arrays (ChIP-chip) and gene expression profiling, we identify novel, direct target genes of PLZF-RARα that tend to be repressed in APL compared with other myeloid leukemias, supporting the role of PLZF-RARα as an aberrant repressor in APL. In primary murine hematopoietic progenitors, PLZF-RARα promotes cell growth, and represses Dusp6 and Cdkn2d, while inducing c-Myc expression, consistent with its role in leukemogenesis. PLZF-RARα binds to a region of the c-MYC promoter overlapping a functional PLZF site and antagonizes PLZF-mediated repression, suggesting that PLZF-RARα may act as a dominant-negative version of PLZF by affecting the regulation of shared targets. RA induced the differentiation of PLZF-RARα–transformed murine hematopoietic cells and reduced the frequency of clonogenic progenitors, concomitant with c-Myc down-regulation. Surviving RA-treated cells retained the ability to be replated and this was associated with sustained c-Myc expression and repression of Dusp6, suggesting a role for these genes in maintaining a self-renewal pathway triggered by PLZF-RARα