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To this day, people still face gender discrimination and battle with gender injustices. To change this, we both need accurate knowledge about these injustices and we need to strive for active change. This article provides a theoretical reflection on how social media, by serving as an accessible platform for people to portray their emotions, can be a tool for both of these needs. In terms of the topics it discusses, the article operates at the intersection of the literature on digital activism on the one hand and emotions and social media on the other. However, I approach these topics using a combination of multidisciplinary lenses. I employ the epistemic injustice framework to emphasise the link between gender inequality and the production and distribution of knowledge. In line with the literature on affect theory, I argue both that emotions can generate epistemic novelties and that emotions have collectivising and motivational power. Finally, the article builds on existing research on how social media provide a space for people to portray, distribute, and adopt emotions. The theoretical reflection in this article then combines these insights to demonstrate how social media—by allowing the expression and distribution of emotions—can catalyse both the production of new knowledge and active change. With social media enabling emotions to be heard and seen, this online sphere can contribute to the epistemic empowerment of women and to the fight against gender discrimination and gender injustices.

Coronavirus disease 2019 (COVID-19) pandemic is affecting millions of patients worldwide. The consequences of initial exposure to SARS-CoV-2 go beyond pulmonary damage, with a particular impact on lipid metabolism. Decreased levels in HDL-C were reported in COVID-19 patients. Since HDL particles display antioxidant, anti-inflammatory and potential anti-infectious properties, we aimed at characterizing HDL proteome and functionality during COVID-19 relative to healthy subjects. HDLs were isolated from plasma of 8 severe COVID-19 patients sampled at admission to intensive care unit (Day 1, D1) at D3 and D7, and from 16 sex- and age-matched healthy subjects. Proteomic analysis was performed by LC-MS/MS. The relative amounts of proteins identified in HDLs were compared between COVID-19 and controls. apolipoprotein A-I and paraoxonase 1 were confirmed by Western-blot analysis to be less abundant in COVID-19 versus controls, whereas serum amyloid A and alpha-1 antitrypsin were higher. HDLs from patients were less protective in endothelial cells stiumalted by TNFα (permeability, VE-cadherin disorganization and apoptosis). In these conditions, HDL inhibition of apoptosis was blunted in COVID-19 relative to controls. In conclusion, we show major changes in HDL proteome and decreased functionality in severe COVID-19 patients.

We have demonstrated the capability of laboratory propagation-based microtomography (miroCT) in non-destructive 3D virtual histopathology of human blood clots without any contrast agent. The volumetric information are valuable to understand the mechanical properties of clots which are crucial in selecting the most efficient mechanical thrombectomy method for clot extraction. Different clot types retrieved by mechanical thrombectomy from patient victims of acute ischemic stroke were evaluated through propagation-based microCT. The results were correlated with high-resolution scanning electron microscopy (SEM) images, confirming detected cellular and fibrillary structures. Calcifications appeared as glassy opacity areas with relatively intense signal on microCT images, also proved by energy-dispersive spectroscopy and X-ray diffraction. Hyperintense regions on the microCT corresponded to individual or compact aggregates of red blood cells, whereas fibrin dominated volumes appeared at consistently moderate to low normalized microCT values. Red blood cell shapes and sizes are consistent with the SEM observations. Together with other potential parameters, 3D porosity distribution and volume fraction of structures can be easily measured by microCT data. Further development of automated post-processing techniques for X-ray propagation-based micro/nanoCT, also based on machine learning algorithms, can enable high throughput analysis of blood clot composition and their 3D histological features on large sample cohorts.

The monastic reforms of the 10th century greatly increased the role of the psalter, a biblical book that became the main tool of a monk in personal and collective prayer. The Odbert Psalter, produced in Saint-Bertin around 999, opens with a scene of Pentecost in which we see Christ represented as a king who is static and in a space distinct from the apostles, exhibiting an attitude of meditation. This is not a narrative image: this scene is an indication for the reader of the Psalms. If he follows the example of the apostles, he will arrive at the vision of God, which can only be attained through continuous meditation on the Psalms as it was defined by the reforms. This image serves as a medium for the act of contemplation itself: according to the three modes of vision defined by Saint Augustine, the image of Christ constitutes a pathway from corporeal vision to intellectual vision. By constituting the support of divine contemplation, the psalter and its images are set up here as perfect mediators of the power of the intellect.

Endovascular treatment with stent retriever thrombectomy is a major advancement in the standard of care in acute ischemic stroke (AIS). The modalities through which thrombi embed along stent retriever following mechanical thrombectomy (MTB) have not yet been elucidated. Using scanning electron microscopy (SEM), we analyzed the appearance of thrombi retrieved by MTB from AIS patients, when embedded into the stent retriever. We observed that the organization and structural compactness vary for compositionally different thrombi. The modalities of attachment onto the stent vary according to thrombus composition and organization.

Past cross-national comparisons of socioeconomic segregation have been undercut by lack of comparability in measures, data, and concepts. Using IRIS data from the French Census of 2008 and the French Ministry of Finance as well as tract data from the American Community Survey (2006–2010) and the U.S. Department of Housing and Urban Development Picture of Subsidized Households, and constructing measures to be as similar as possible, we compare socioeconomic segregation in metropolitan areas with a population of more than 1 million in France and the United States. We find much higher socioeconomic segregation in large metropolitan areas in the United States than in France. We also find (1) a strong pattern of low-income neighborhoods in central cities and high-income neighborhoods in suburbs in the United States, but varying patterns across metropolitan areas in France; (2) that high-income persons are the most segregated group in both countries; (3) that the shares of neighborhood income differences that can be explained by neighborhood racial/ethnic composition are similar in France and the United States; and (4) that government-assisted housing is disproportionately located in the poorest neighborhoods in the United States but is spread across many neighborhood income levels in France. We conclude that differences in government provision of housing assistance and levels of income inequality are likely important contributing factors to the Franco-U.S. difference in socioeconomic segregation.

NLRP3 controls the secretion of inflammatory cytokines IL-1β/18 and pyroptosis by assembling the inflammasome. Upon coordinated priming and activation stimuli, NLRP3 recruits NEK7 within hetero-oligomers that nucleate ASC and caspase-1 filaments, but the apical molecular mechanisms underlying inflammasome assembly remain elusive. Here we show that NEK7 recruitment to NLRP3 is controlled by the phosphorylation status of NLRP3 S803 located within the interaction surface, in which NLRP3 S803 is phosphorylated upon priming and later dephosphorylated upon activation. Phosphomimetic substitutions of S803 abolish NEK7 recruitment and inflammasome activity in macrophages in vitro and in vivo. In addition, NLRP3-NEK7 binding is also essential for NLRP3 deubiquitination by BRCC3 and subsequently inflammasome assembly, with NLRP3 phosphomimetic mutants showing enhanced ubiquitination and degradation than wildtype NLRP3. Finally, we identify CSNK1A1 as the kinase targeting NLRP3 S803. Our findings thus reveal NLRP3 S803 phosphorylation status as a druggable apical molecular mechanism controlling inflammasome assembly. Nlrp3 inflammasome activation requires Nek7 recruitment to drive ASC speck formation. Here the authors show how Nlrp3 phosphorylation events control this Nek7 recruitment.

The star β  Pictoris harbors a young planetary system of about 20 million years old, which is characterized by the presence of a gaseous and dusty debris disk, at least two massive planets and many minor bodies. For more than thirty years, exocomets transiting the star have been detected using spectroscopy, probing the gaseous part of the cometary comas and tails. The detection of the dusty component of the tails can be performed through photometric observations of the transits. Since 2018, the Transiting Exoplanet Survey Satellite has observed β  Pic for a total of 156 days. Here we report an analysis of the TESS photometric data set with the identification of a total of 30 transits of exocomets. Our statistical analysis shows that the number of transiting exocomet events ( N ) as a function of the absorption depth ( AD ) in the light curve follows a power law in the form d N ( A D ) ∝ A D - α , where α = 2.3 ± 0.4 . This distribution of absorption depth leads to a differential comet size distribution proportional to R - γ , where γ = 3.6 ± 0.8 , showing a striking similarity to the size distribution of comets in the Solar system and the distribution of a collisionally relaxed population ( γ D = 3.5 ).

BackgroundNo study has evaluated the predictive and prognostic role of CD8 and PD-L1 coexpression in non–small-cell lung cancer (NSCLC).MethodsWe analyzed RNA sequencing and/or immunohistochemistry staining in NSCLC patients from The Cancer Genome Atlas (n = 1016), and 34 metastatic NSCLC samples not treated by immunotherapy as prognostic cohorts. As predictive aspect of CD8 and PD-L1, we used 85 NSCLC patients treated with anti-PD-1. Two validation cohorts were used including 44 NSCLC patients treated with anti-PD-1 and an external cohort with different tumor types.ResultsIn prognostic cohorts, high CD8A expression was associated with longer OS (p = 0.02), while high CD274 mRNA was associated with poor prognosis (p = 0.05). In predictive cohort, high CD8 expression and CD8A mRNA were associated with longer progression-free survival (PFS) (p = 0.0002). There was no significant association between PD-L1 expression and PFS while high CD274 mRNA was associated with longer PFS (p = 0.009). A combination of CD8A and CD274 was highly predictive of outcome. These results were confirmed in the validation cohorts. This two-genes signature demonstrated similar results compared to gold standard signatures.ConclusionCD8 represents both a prognostic and predictive factor of outcomes, while PD-L1 share different prognostic and predictive roles.

Bacterial lipopolysaccharide triggers human caspase-4 (murine caspase-11) to cleave gasdermin-D and induce pyroptotic cell death. How lipopolysaccharide sequestered in the membranes of cytosol-invading bacteria activates caspases remains unknown. Here we show that in interferon-γ-stimulated cells guanylate-binding proteins (GBPs) assemble on the surface of Gram-negative bacteria into polyvalent signaling platforms required for activation of caspase-4. Caspase-4 activation is hierarchically controlled by GBPs; GBP1 initiates platform assembly, GBP2 and GBP4 control caspase-4 recruitment, and GBP3 governs caspase-4 activation. In response to cytosol-invading bacteria, activation of caspase-4 through the GBP platform is essential to induce gasdermin-D-dependent pyroptosis and processing of interleukin-18, thereby destroying the replicative niche for intracellular bacteria and alerting neighboring cells, respectively. Caspase-11 and GBPs epistatically protect mice against lethal bacterial challenge. Multiple antagonists of the pathway encoded by Shigella flexneri , a cytosol-adapted bacterium, provide compelling evolutionary evidence for the importance of the GBP–caspase-4 pathway in antibacterial defense. How lipopolysaccharide embedded in bacterial membranes is sensed by intracellular defense mechanisms has been puzzling. Randow and colleagues show that guanylate-binding proteins assemble on the surface of Gram-negative bacteria to initiate downstream pyroptosis.