Hooked flare ribbons and flux-rope related QSL footprints

We studied the magnetic topology of active region 12158 on 2014 September 10 and compared it with the observations before and early in the flare which begins at 17:21 UT (SOL2014-09-10T17:45:00). Our results show that the sigmoidal structure and flare ribbons of this active region observed by SDO/AIA can be well reproduced from a Grad-Rubin non linear force free field extrapolation method. Various inverse-S and -J shaped magnetic field lines, that surround a coronal flux rope, coincide with the sigmoid as observed in different extreme ultraviolet wavelengths, including its multi-threaded curved ends. Also, the observed distribution of surface currents in the magnetic polarity where it was not prescribed is well reproduced. This validates our numerical implementation and set-up of the Grad-Rubin method. The modeled double inverse-J shaped Quasi-Separatrix Layer (QSL) footprints match the observed flare ribbons during the rising phase of the flare, including their hooked parts. The spiral-like shape of the latter may be related to a complex pre-eruptive flux rope with more than one turn of twist, as obtained in the model. These ribbon-associated flux-rope QSL-footprints are consistent with the new standard flare model in 3D, with the presence of a hyperbolic flux tube located below an inverse tear drop shaped coronal QSL. This is a new step forward forecasting the locations of reconnection and ribbons in solar flares, and the geometrical properties of eruptive flux ropes.Comment: Accepted for publication in Ap

A Check on the Validity of Magnetic Field Reconstructions

We investigate a method to test whether a numerically computed model coronal magnetic field B departs from the divergence-free condition (also known as the solenoidality condition). The test requires a potential field B0 to be calculated, subject to Neumann boundary conditions, given by the normal components of the model field B at the boundaries. The free energy of the model field may be calculated using the volume integral of (B-B0)^2, where the integral is over the computational volume of the model field. A second estimate of the free energy is provided by calculating the difference between the volume integral of B^2 and the volume integral of B0^2. If B is divergence-free, the two estimates of the free energy should be the same. A difference between the two estimates indicates a departure from div B = 0 in the volume. The test is an implementation of a procedure proposed by Moraitis et al. (Sol. Phys. 289, 4453, 2014) and is a simpler version of the Helmholtz decomposition procedure presented by Valori et al. (Astron. Astrophys. 553, A38, 2013). We demonstrate the test in application to previously published nonlinear force-free model fields, and also investigate the influence on the results of the test of a departure from flux balance over the boundaries of the model field. Our results underline the fact that, to make meaningful statements about magnetic free energy in the corona, it is necessary to have model magnetic fields which satisfy the divergence-free condition to a good approximation.Australian Research Counci

Effects of flood hazard visualization format on house purchasing decisions

We investigated how decision-making is affected by the visual presentation of flood hazard information. We exposed participants to different formats of flood hazard information while they simulated selecting a property to purchase. We compared three flood hazard formats: (i) maps currently used by the UK Environment Agency, (ii) tables that present flood level and frequency information and (iii) graphical representations depicting the level-frequency combination using a cartoon house image as a physical referent. In the experiment participants were presented, via computer screen, side-by-side information about two houses in a series of trials. Participants made a forced choice preference judgement between 108 different pairs of houses to indicate which they would purchase. Our findings indicate that when hazard information is presented in map format, individuals are less accurate in selecting lower-hazard houses, compared to when the same information is presented as a graphic representation of a house or as a table. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group

High-Throughput Detection of Induced Mutations and Natural Variation Using KeyPoint™ Technology

Reverse genetics approaches rely on the detection of sequence alterations in target genes to identify allelic variants among mutant or natural populations. Current (pre-) screening methods such as TILLING and EcoTILLING are based on the detection of single base mismatches in heteroduplexes using endonucleases such as CEL 1. However, there are drawbacks in the use of endonucleases due to their relatively poor cleavage efficiency and exonuclease activity. Moreover, pre-screening methods do not reveal information about the nature of sequence changes and their possible impact on gene function. We present KeyPoint™ technology, a high-throughput mutation/polymorphism discovery technique based on massive parallel sequencing of target genes amplified from mutant or natural populations. KeyPoint combines multi-dimensional pooling of large numbers of individual DNA samples and the use of sample identification tags (“sample barcoding”) with next-generation sequencing technology. We show the power of KeyPoint by identifying two mutants in the tomato eIF4E gene based on screening more than 3000 M2 families in a single GS FLX sequencing run, and discovery of six haplotypes of tomato eIF4E gene by re-sequencing three amplicons in a subset of 92 tomato lines from the EU-SOL core collection. We propose KeyPoint technology as a broadly applicable amplicon sequencing approach to screen mutant populations or germplasm collections for identification of (novel) allelic variation in a high-throughput fashion

A Novel Cre Recombinase Imaging System for Tracking Lymphotropic Virus Infection In Vivo

BACKGROUND:Detection, isolation, and identification of individual virus infected cells during long term infection are critical to advance our understanding of mechanisms of pathogenesis for latent/persistent viruses. However, current approaches to study these viruses in vivo have been hampered by low sensitivity and effects of cell-type on expression of viral encoded reporter genes. We have designed a novel Cre recombinase (Cre)-based murine system to overcome these problems, and thereby enable tracking and isolation of individual in vivo infected cells. METHODOLOGY/PRINCIPAL FINDINGS:Murine gammaherpesvirus 68 (MHV-68) was used as a prototypic persistent model virus. A Cre expressing recombinant virus was constructed and characterised. The virus is attenuated both in lytic virus replication, producing ten-fold lower lung virus titres than wild type virus, and in the establishment of latency. However, despite this limitation, when the sEGFP7 mouse line containing a Cre-activated enhanced green fluorescent protein (EGFP) was infected with the Cre expressing virus, sites of latent and persistent virus infection could be identified within B cells and macrophages of the lymphoid system on the basis of EGFP expression. Importantly, the use of the sEGFP7 mouse line which expresses high levels of EGFP allowed individual virus positive cells to be purified by FACSorting. Virus gene expression could be detected in these cells. Low numbers of EGFP positive cells could also be detected in the bone marrow. CONCLUSIONS/SIGNIFICANCE:The use of this novel Cre-based virus/mouse system allowed identification of individual latently infected cells in vivo and may be useful for the study and long-term monitoring of other latent/persistent virus infections

The Past and Future of Tuberculosis Research

Renewed efforts in tuberculosis (TB) research have led to important new insights into the biology and epidemiology of this devastating disease. Yet, in the face of the modern epidemics of HIV/AIDS, diabetes, and multidrug resistance—all of which contribute to susceptibility to TB—global control of the disease will remain a formidable challenge for years to come. New high-throughput genomics technologies are already contributing to studies of TB's epidemiology, comparative genomics, evolution, and host–pathogen interaction. We argue here, however, that new multidisciplinary approaches—especially the integration of epidemiology with systems biology in what we call “systems epidemiology”—will be required to eliminate TB

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease