36 research outputs found

    On the magnetosphere-ionosphere coupling during the May 2021 geomagnetic storm

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    On 12 May 2021 the interplanetary doppelganger of the 9 May 2021 coronal mass ejection impacted the Earth's magnetosphere, giving rise to a strong geomagnetic storm. This paper discusses the evolution of the various events linking the solar activity to the Earth's ionosphere with special focus on the effects observed in the circumterrestrial environment. We investigate the propagation of the interplanetary coronal mass ejection and its interaction with the magnetosphere-ionosphere system in terms of both magnetospheric current systems and particle redistribution, by jointly analyzing data from interplanetary, magnetospheric, and low Earth orbiting satellites. The principal magnetospheric current system activated during the different phases of the geomagnetic storm was correctly identified through the direct comparison between geosynchronous orbit observations and model predictions. From the particle point of view, we have found that the primary impact of the storm development is a net and rapid loss of relativistic electrons from the entire outer radiation belt. Our analysis shows no evidence for any short-term recovery to pre-storm levels during the days following the main phase. Storm effects also included a small Forbush decrease driven by the interplay between the interplanetary shock and subsequent magnetic cloud arrival

    Resolution of inflammation: a new therapeutic frontier

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    Dysregulated inflammation is a central pathological process in diverse disease states. Traditionally, therapeutic approaches have sought to modulate the pro- or anti-inflammatory limbs of inflammation, with mixed success. However, insight into the pathways by which inflammation is resolved has highlighted novel opportunities to pharmacologically manipulate these processes — a strategy that might represent a complementary (and perhaps even superior) therapeutic approach. This Review discusses the state of the art in the biology of resolution of inflammation, highlighting the opportunities and challenges for translational research in this field

    Transcriptional regulation of the human FPR2/ALX gene : evidence of a heritable genetic variant that impairs promoter activity

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    Lipoxin (LX) A(4), a main endogenous stop-signal of inflammation, activates the G-protein-coupled receptor FPR2/ALX, which triggers potent anti-inflammatory signaling in vivo. Thus, the regulation of FPR2/ALX expression may have pathophysiological and therapeutic relevance. Here, we mapped a nucleotide sequence with strong FPR2/ALX promoter activity. Chromatin immunoprecipitation revealed specificity protein 1 (Sp1) binding to the core promoter. Site-directed mutagenesis of the Sp1 cis-acting element and Sp1 overexpression established that this transcription factor is key for maximal promoter activity, which is instead suppressed by DNA methylation. LXA(4) enhanced FPR2/ALX promoter activity (+74%) and mRNA expression (+87.5%) in MDA-MB231 cells. A single nucleotide mutation (A/G) was detected in the core promoter of one subject with history of cardiovascular disease and of his two daughters. This mutation reduced by 3c35-90% the promoter activity in vitro. Moreover, neutrophils from individuals carrying the A/G variant displayed 3c10- and 3-fold reduction in FPR2/ALX mRNA and protein, respectively, compared with cells from their relatives or healthy volunteers expressing the wild-type allele. These results uncover FPR2/ALX transcriptional regulation and provide the first evidence of mutations that affect FPR2/ALX transcription, thus opening new opportunities for the understanding of the LXA(4)-FPR2/ALX axis in human disease -Simiele, F., Recchiuti, A., Mattoscio, D., De Luca, A., Cianci, E., Franchi, S., Gatta, V., Parolari, A., Werba, J. P., Camera, M., Favaloro, B., Romano, M. Transcriptional regulation of the human FPR2/ALX gene: Evidence of a heritable genetic variant that impairs promoter activity

    Haiti earthquake (Mw 7.2): magnetospheric–ionospheric–lithospheric coupling during and after the main shock on 14 August 2021

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    In the last few decades, the efforts of the scientific community to search earthquake signatures in the atmospheric, ionospheric and magnetospheric media have grown rapidly. The increasing amount of good quality data from both ground stations and satellites has allowed for the detections of anomalies with high statistical significance such as ionospheric plasma density perturbations and/or atmospheric temperature and pressure changes. However, the identification of a causal link between the observed anomalies and their possible seismic trigger has so far been prevented by difficulties in the identification of confounders (such as solar and atmospheric activity) and the lack of a global analytical lithospheric–atmospheric–magnetospheric model able to explain (and possibly forecast) any anomalous signal. In order to overcome these problems, we have performed a multi-instrument analysis of a low-latitude seismic event by using high-quality data from both ground bases and satellites and preserving their statistical significance. An earthquake (Mw = 7.2) occurred in the Caribbean region on 14 August 2021 under both solar quiet and fair weather conditions, thus proving an optimal case study to reconstruct the link between the lithosphere, atmosphere, ionosphere, and magnetosphere. The good match between the observations and novel magnetospheric–ionospheric–lithospheric coupling (M.I.L.C.) modeling of the event confirmed that the fault break generated an atmospheric gravity wave that was able to mechanically perturb the ionospheric plasma density, in turn triggering a variation in the magnetospheric field line resonance frequency

    Electron Signal Induced by GRB 221009A on Charged Particle Telescopes of POES and MetOp Satellites

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    GRB 221009A is a long gamma-ray burst among the most energetic and nearest ( z = 0.151) detected so far. The energy fluence of the burst was so large to cause ionization of the upper layers of Earth’s atmosphere and also observable signals in satellite-borne particle detectors. Electron signals, with the same GRB time development, can arise from the interaction of energetic photons with the particle detector and support structures. This effect was previously reported for the HEPP-L on board the China Seismo-Electromagnetic Satellite. We searched for the same effect on the particle detectors on board five POES and MetOp satellites. Electron signals in coincidence with the gamma-ray emission of the burst were found in three satellites, which were well illuminated by the GRB. The properties of the found electron signals are reported and discussed

    Cystic fibrosis transmembrane conductance regulator (CFTR) expression in human platelets: impact on mediators and mechanisms of the inflammatory response

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    Inflammatory lung disease is a primary cause of morbidity and mortality in cystic fibrosis (CF). Mechanisms of unresolved acute inflammation in CF are not completely known, although the involvement of cystic fibrosis transmembrane conductance regulator (CFTR) in nonrespiratory cells is emerging. Here we examined CFTR expression and function in human platelets (PLTs) and found that they express a biologically active CFTR. CFTR blockade gave an 3c50% reduction in lipoxin A(4) (LXA(4)) formation during PLT/polymorphonuclear leukocytes (PMN) coincubations by inhibiting the lipoxin synthase activity of PLT 12-lipoxygenase. PLTs from CF patients generated 3c40% less LXA(4) compared to healthy subject PLTs. CFTR inhibition increased PLT-dependent PMN viability (33.0\ub15.7 vs. 61.2\ub18.2%; P=0.033), suppressed nitric oxide generation (0.23\ub10.04 vs. 0.11\ub10.002 pmol/10(8) PLTs; P=0.004), while reducing AKT (1.02\ub10.12 vs. 0.71\ub10.007 U; P=0.04), and increasing p38 MAPK phosphorylation (0.650\ub10.09 vs. 1.04\ub10.24 U; P=0.03). Taken together, these findings indicate that PLTs from CF patients are affected by the molecular defect of CFTR. Moreover, this CF PLT abnormality may explain the failure of resolution in CF
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