Consensus against all odds:explaining the persistence of EU sanctions on Russia

In response to Russia’s actions in Ukraine in 2014, the EU introduced sanctions on Moscow. Despite increasing polarisation among member states after imposition, the sanctions package was consistently renewed. How can sanctions persistence be explained? While scholarly accounts highlight German leadership, commitment to norms, and policymakers’ engagement, the EU’s ability to uphold the sanctions in the face of uneven support among member states remains puzzling. With the help of a two-level game framework, according to which actors make decisions based on the interplay between the domestic and international levels, we argue that the interaction between the Council and domestic politics helped sustaining the consensus. To illustrate this dynamic, in an exploration of domestic factions in Spain and Poland, two member states displaying opposite attitudes towards Russia, we identify the presence of at least one actor whose preference deviates from the core, thereby facilitating consensus

Acute suppression of mitochondrial ATP production prevents apoptosis and provides an essential signal for NLRP3 inflammasome activation

How mitochondria reconcile roles in functionally divergent cell death pathways of apoptosis and NLRP3 inflammasome-mediated pyroptosis remains elusive, as is their precise role in NLRP3 activation and the evolutionarily conserved physiological function of NLRP3. Here, we have shown that when cells were challenged simultaneously, apoptosis was inhibited and NLRP3 activation prevailed. Apoptosis inhibition by structurally diverse NLRP3 activators, including nigericin, imiquimod, extracellular ATP, particles, and viruses, was not a consequence of inflammasome activation but rather of their effects on mitochondria. NLRP3 activators turned out as oxidative phosphorylation (OXPHOS) inhibitors, which we found to disrupt mitochondrial cristae architecture, leading to trapping of cytochrome c. Although this effect was alone not sufficient for NLRP3 activation, OXPHOS inhibitors became triggers of NLRP3 when combined with resiquimod or Yoda-1, suggesting that NLRP3 activation requires two simultaneous cellular signals, one of mitochondrial origin. Therefore, OXPHOS and apoptosis inhibition by NLRP3 activators provide stringency in cell death decisions

Surface subsidence caused by roadway mining as partial extraction in hard coal mining industry

W artykule przedstawiono wyniki geodezyjnych pomiarów deformacji powierzchni, obniżeń i odkształceń poziomych (względnych zmian długości na odcinkach) z dwóch obszarów, gdzie prowadzona jest eksploatacja częściowa przez dwa, jedyne zakłady górnicze w Polsce systemem chodnikowym z pozostawieniem filarów węglowych. Ponadto przedstawiono wartości współczynnika eksploatacyjnego, który charakteryzuje stopień wybrania pokładu (wykorzystania złoża) oraz wykazano jego zależność od stopnia wykorzystania złoża. Wyniki polskich doświadczeń porównano z doświadczeniami kopalni Roadside z eksploatacji komorowo-filarowej w Stanach Zjednoczonych oraz z doświadczeniami kopalni Changxing w Chinach z eksploatacji prowadzonej chodnikami.This paper presents the results of surveys of subsidence and horizontal deformations (relative to changing length between observation points) from two mining areas where only two collieries in Poland extract hard coal seams using gateway mining technology with coal pillars. Furthermore, the operating indicator (exploitation of a deposit) values were presented and its relation from the degree of deposit exploitation demonstrated. The results of subsidence analysis from research areas in Poland were compared with the results of Roadside colliery in the United States, using room and pillar mining technology, and with the results of Changxing colliery in China which applied the roadway backfill coal mining method (RBCM)

Supplementary Material for: Na⁺/H⁺ Exchangers Are Required for the Development and Function of Vertebrate Mucociliary Epithelia

Na+/H+ exchangers (NHEs) represent a highly conserved family of ion transporters that regulate pH homeostasis. NHEs as well as other proton transporters were previously linked to the regulation of the Wnt signaling pathway, cell polarity signaling, and mucociliary function. Furthermore, mutations in the gene SLC9A3 (encoding NHE3) were detected as additional risk factors for airway infections in cystic fibrosis patients. Here, we used the Xenopus embryonic mucociliary epidermis as well as human airway epithelial cells (HAECs) as models to investigate the functional roles of NHEs in mucociliary development and regeneration. In Xenopus embryos, NHEs 1–3 were expressed during epidermal development, and loss of NHE function impaired mucociliary clearance in tadpoles. Clearance defects were caused by reduced cilia formation, disrupted alignment of basal bodies in multiciliated cells (MCCs), and dysregulated mucociliary gene expression. These data also suggested that NHEs may contribute to the activation of Wnt signaling in mucociliary epithelia. In HAECs, pharmacological inhibition of NHE function also caused defective ciliation and regeneration in airway MCCs. Collectively, our data revealed a requirement for NHEs in vertebrate mucociliary epithelia and linked NHE activity to cilia formation and function in differentiating MCCs. Our results provide an entry point for the understanding of the contribution of NHEs to signaling, development, and pathogenesis in the human respiratory tract

miR-34/449 miRNAs are required for motile ciliogenesis by repressing cp110.

The mir-34/449 family consists of six homologous miRNAs at three genomic loci. Redundancy of miR-34/449 miRNAs and their dominant expression in multiciliated epithelia suggest a functional significance in ciliogenesis. Here we report that mice deficient for all miR-34/449 miRNAs exhibited postnatal mortality, infertility and strong respiratory dysfunction caused by defective mucociliary clearance. In both mouse and Xenopus, miR-34/449-deficient multiciliated cells (MCCs) exhibited a significant decrease in cilia length and number, due to defective basal body maturation and apical docking. The effect of miR-34/449 on ciliogenesis was mediated, at least in part, by post-transcriptional repression of Cp110, a centriolar protein suppressing cilia assembly. Consistent with this, cp110 knockdown in miR-34/449-deficient MCCs restored ciliogenesis by rescuing basal body maturation and docking. Altogether, our findings elucidate conserved cellular and molecular mechanisms through which miR-34/449 regulate motile ciliogenesis