Testing predictors of eruptivity using parametric flux emergence simulations

Solar flares and coronal mass ejections (CMEs) are among the most energetic events in the solar system, impacting the near-Earth environment. Flare productivity is empirically known to be correlated with the size and complexity of active regions. Several indicators, based on magnetic-field data from active regions, have been tested for flare forecasting in recent years. None of these indicators, or combinations thereof, have yet demonstrated an unambiguous eruption or flare criterion. Furthermore, numerical simulations have been only barely used to test the predictability of these parameters. In this context, we used the 3D parametric MHD numerical simulations of the self-consistent formation of the flux emergence of a twisted flux tube, inducing the formation of stable and unstable magnetic flux ropes of Leake (2013, 2014). We use these numerical simulations to investigate the eruptive signatures observable in various magnetic scalar parameters and provide highlights on data analysis processing. Time series of 2D photospheric-like magnetograms are used from parametric simulations of stable and unstable flux emergence, to compute a list of about 100 different indicators. This list includes parameters previously used for operational forecasting, physical parameters used for the first time, as well as new quantities specifically developed for this purpose. Our results indicate that only parameters measuring the total non-potentiality of active regions associated with magnetic inversion line properties, such as the Falconer parameters $L_{ss}$, $WL_{ss}$, $L_{sg}$ and $WL_{sg}$, as well as the new current integral $WL_{sc}$ and length $L_{sc}$ parameters, present a significant ability to distinguish the eruptive cases of the model from the non-eruptive cases, possibly indicating that they are promising flare and eruption predictors.Comment: 46 pages, 16 figures, accepted for publication in Space Weather and Space Climate on June, 8t

La thrombose au cours des néoplasies myéloprolifératives: Influence de la mutation JAK2V617F

Les néoplasies myéloprolifératives (NMP) sans translocation de Philadelphie sont des maladies hématologiques acquises caractérisées par la prolifération d’une ou plusieurs lignées sanguines. Elles regroupent la polyglobulie de Vaquez (PV), la thrombocytémie essentielle (TE) et la myélofibrose primitive (MFP). La survenue de thromboses artérielles ou veineuses est un risque majeur au cours de ces maladies. Les facteurs de risque reconnus actuellement sont un âge supérieur à 60 ans et un antécédent de thrombose. Les mécanismes concourant à ce risque pro-thrombotique augmenté sont cependant multiples et complexes, impliquant l’ensemble des cellules sanguines, des facteurs plasmatiques et le compartiment endothélial. Ces dernières années, de nouveaux mécanismes physiopathologiques ont été révélés. , BCR-ABL negative myeloproliferative neoplasms are acquired hematologic diseases characterized by blood cell proliferation and that include polycythemia vera (PV), essential thrombocytemia (ET) and primary myelofibrosis (PMF). Occurring of venous and arterial thrombosis is the main complication of these diseases. Risk factors for thrombosis are individuals older than 60 and history of thrombosis. The mechanisms leading to thrombosis are complex and involve several blood compartments, plasmatic factors and endothelial cells. Over the last years, new actors of thrombosis have been discovered

Modeling Riparian Restoration Impacts on the Hydrologic Cycle at the Babacomari Ranch, SE Arizona, USA

This paper describes coupling field experiments with surface and groundwater modeling to investigate rangelands of SE Arizona, USA using erosion-control structures to augment shallow and deep aquifer recharge. We collected field data to describe the physical and hydrological properties before and after gabions (caged riprap) were installed in an ephemeral channel. The modular finite-difference flow model is applied to simulate the amount of increase needed to raise groundwater levels. We used the average increase in infiltration measured in the field and projected on site, assuming all infiltration becomes recharge, to estimate how many gabions would be needed to increase recharge in the larger watershed. A watershed model was then applied and calibrated with discharge and 3D terrain measurements, to simulate flow volumes. Findings were coupled to extrapolate simulations and quantify long-term impacts of riparian restoration. Projected scenarios demonstrate how erosion-control structures could impact all components of the annual water budget. Results support the potential of watershed-wide gabion installation to increase total aquifer recharge, with models portraying increased subsurface connectivity and accentuated lateral flow contributions.Walton Family Foundation; Land Change Science (LCS) Program, under the Land Resources Mission Area of the US Geological Survey (USGS); NSF [DBI-0735191, DBI-1265383]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Platelet function studies in myeloproliferative neoplasms patients with Calreticulin or JAK2V617F mutation

Background: JAK2V617F and Calreticulin (CALR) mutations are the most frequent molecular causes of Phi-negative myeloproliferative neoplasms (MPN). Patients with CALR mutations are at lower risk of thrombosis than patients with JAK2V617F. We hypothesized that CALR-mutated blood platelets would have platelet function defects that might explain why these patients are at lower risk of thrombosis. Objectives: Our main objective was to explore and compare platelet function depending on the MPN molecular marker. Methods: We analyzed platelet function in 16 patients with MPN with CALR mutations and 17 patients with JAK2V617F mutation and compared them with healthy controls. None of these patients was taking antiplatelet therapy. We performed an extensive analysis of platelet function and measured plasmatic soluble P-selectin and CD40L levels. Results: We observed significant defects in platelet aggregation, surface glycoprotein expression, fibrinogen binding, and granule content in platelets from patients with MPN compared with that in controls. Moreover, soluble CD40L and P-selectin levels were elevated in patients with MPN compared with that in controls, suggesting an in vivo platelet preactivation. Comparison of platelet function between patients with CALR and JAK2V617F MPN revealed only minor differences in platelets from patients with CALR. However, these results need to be interpreted within the context of absence of an inflammatory environment that could impact platelet function during MPN. Conclusions: These results do not support the hypothesis that calreticulin-mutated platelets have platelet function defects that could explain the lower thrombotic risk of patients with CALR

Single-cell RNA-seq reveals new types of human blood dendritic cells, monocytes, and progenitors

Dendritic cells (DCs) and monocytes play a central role in pathogen sensing, phagocytosis, and antigen presentation and consist of multiple specialized subtypes. However, their identities and interrelationships are not fully understood. Using unbiased single-cell RNA sequencing (RNA-seq) of ~2400 cells, we identified six human DCs and four monocyte subtypes in human blood. Our study reveals a new DC subset that shares properties with plasmacytoid DCs (pDCs) but potently activates T cells, thus redefining pDCs; a new subdivision within the CD1C+ subset of DCs; the relationship between blastic plasmacytoid DC neoplasia cells and healthy DCs; and circulating progenitor of conventional DCs (cDCs). Our revised taxonomy will enable more accurate functional and developmental analyses as well as immune monitoring in health and disease

Identification of a new locus at 16q12 associated with time-to-asthma onset

International audienceBackground: Asthma is a heterogeneous disease in which age-of-onset plays an important role.Objective: We sought to identify the genetic variants associated with time-to-asthma onset.Methods: We conducted a large-scale meta-analysis of nine genome-wide association studies of time-to-asthma onset (total of 5,462 asthmatics with a broad range of age-of-asthma onset and 8,424 controls of European ancestry) performed using survival analysis techniques.Results: We detected five regions associated with time-to-asthma onset at genome-wide significant level (P<5x10-8). We evidenced a new locus in 16q12 region (near cylindromatosis turban tumor syndrome gene (CYLD)) and confirmed four asthma risk regions: 2q12 (IL1RL1), 6p21 (HLA-DQA1), 9p24 (IL33) and 17q12-q21 (ZPBP2-GSDMA). Conditional analyses identified two distinct signals at 9p24 (both upstream of IL33) and at 17q12-q21 (near ZPBP2 and within GSDMA). These seven distinct loci explained together 6.0% of the variance in time-to-asthma onset. In addition, we showed that genetic variants at 9p24 and 17q12-q21 were strongly associated with an earlier onset of childhood asthma (P≤0.002) whereas 16q12 SNP was associated with a later asthma onset (P=0.04). A high burden of disease risk alleles at these loci was associated with earlier age-of-asthma onset (4 years versus 9-12 years, P=10-4).Conclusion: The new susceptibility region for time-to-asthma onset at 16q12 harbors variants that correlate with the expression of CYLD and NOD2 (nucleotide-binding oligomerization domain 2), two strong candidates for asthma. This study demonstrates that incorporating the variability of age-of-asthma onset in asthma modeling is a helpful approach in the search for disease susceptibility genes

First description of an IgM monoclonal antibody causing αIIb β3 integrin activation and acquired Glanzmann thrombasthenia associated with macrothrombocytopenia

BACKGROUND: Acquired Glanzmann thrombasthenia (GT) is a bleeding disorder generally caused by anti-αIIb β3 autoantibodies. OBJECTIVES: We aimed to characterize the molecular mechanism leading to a progressive GT-like phenotype in a patient with chronic immune thrombocytopenia. PATIENT, METHODS AND RESULTS: The patient suffered from repeated episodes of gastrointestinal bleedings and further studies indicated a moderate platelet aggregation defect. Few months later, platelet function showed abolished aggregation using all agonists, but normal agglutination with ristocetin. No platelet-bound antibodies were detected, but the presence of large amounts of an IgM type antibody detected together with αIIb β3 in the patient's permeabilized platelets suggested that this IgM was an autoantibody causing the internalization of the complex. This was confirmed by the fact that the patient's IgM bound to normal platelets but not to platelets from GT type I patients. Moreover, patient's plasma activated αIIb β3 on controls' platelets as evidenced by increased PAC-1 binding. We also demonstrated that the patient's plasma triggered αIIb β3 outside-in signaling, as β3 Tyr773 and FAK were phosphorylated, and increased the rate of actin polymerization in resting platelets reflecting an impairment of cytoskeletal reorganization. As different signs of dysmegakariopoiesis were also observed in our patient, we evaluated the ability of its serum to impair proplatelets formation and showed that it significantly decreased the number of proplatelet-bearing megakaryocytes in controls' bone marrow stem cells culture as compared to normal serum. CONCLUSIONS: We present the case of a patient with a progressive and severely perturbed platelet function associated with the presence of an IgM activating autoantibody directed against αIIb β3 . This article is protected by copyright. All rights reserved

Consistent phenological shifts in the making of a biodiversity hotspot: the Cape flora

Background The best documented survival responses of organisms to past climate change on short (glacial-interglacial) timescales are distributional shifts. Despite ample evidence on such timescales for local adaptations of populations at specific sites, the long-term impacts of such changes on evolutionary significant units in response to past climatic change have been little documented. Here we use phylogenies to reconstruct changes in distribution and flowering ecology of the Cape flora - South Africa's biodiversity hotspot - through a period of past (Neogene and Quaternary) changes in the seasonality of rainfall over a timescale of several million years. Results Forty-three distributional and phenological shifts consistent with past climatic change occur across the flora, and a comparable number of clades underwent adaptive changes in their flowering phenology (9 clades; half of the clades investigated) as underwent distributional shifts (12 clades; two thirds of the clades investigated). Of extant Cape angiosperm species, 14-41% have been contributed by lineages that show distributional shifts consistent with past climate change, yet a similar proportion (14-55%) arose from lineages that shifted flowering phenology. Conclusions Adaptive changes in ecology at the scale we uncover in the Cape and consistent with past climatic change have not been documented for other floras. Shifts in climate tolerance appear to have been more important in this flora than is currently appreciated, and lineages that underwent such shifts went on to contribute a high proportion of the flora's extant species diversity. That shifts in phenology, on an evolutionary timescale and on such a scale, have not yet been detected for other floras is likely a result of the method used; shifts in flowering phenology cannot be detected in the fossil record