How does moving public engagement with research online change audience diversity? Comparing inclusion indicators for 2019 & 2020 European Researchers' night events.

Taking place annually in more than 400 cities, European Researchers' Night is a pan- European synchronized event that aims to bring researchers closer to the public. In this paper audience profiles are compared from events in 2019 and 2020. In 2019, face-to-face events reached an estimated 1.6 million attendees, while in 2020, events shifted online due to the COVID-19 pandemic and reached an estimated 2.3 million attendees. Focusing on social inclusion metrics, survey data is analyzed across two national contexts (Ireland and Malta) in 2019 (n = 656) and 2020 (n = 506). The results from this exploratory, descriptive study shed light on how moving public engagement with research online shifted audience profiles. Based on prior research about the digital divide in access and use of online media, hypotheses were proposed that online European Researchers' Night events would attract audiences with higher educational attainment levels and greater self-reported, subjective economic well-being. While changes were observed from 2019 to 2020, results for each hypothesis show a mixed picture. The first hypothesis was upheld for the highest education levels but failed for the lowest levels suggesting that the pivot to online events simultaneously attracted participants with no formal education and those with postgraduate qualifications, while attracting less of those with undergraduate or lower levels of education. The second hypothesis was not upheld, with online European Researchers' Night events attracting audiences with slightly higher levels of economic well-being compared to face-to-face events. The findings of this study indicate that European Researchers' Night events present a clear opportunity to measure the effects of the digital divide in relation to public engagement with research across Europe.

Investigating diversity in European audiences for public engagement with research: Who attends European Researchers' Night in Ireland, the UK and Malta?

European Researchers' Night is an annual pan-European synchronized event devoted to public engagement with research. It was first held in 2005 and now occurs in over 400 cities across Europe, with the aim of bringing researchers closer to the general public. To investigate social inclusion in these events, we conducted survey research across three national contexts (Ireland, Malta and the UK) and events in seven cities between 2016 and 2019 (n = 1590). The results from this exploratory descriptive study confirmed one hypothesis, namely that event attendees had substantially higher levels of university qualification than the national publics. This is in line with wider patterns of unequal participation in public engagement with research activities based on socio-economic status. However, we also found mixed evidence on the prevalence of ethnic minority representation among event attendees compared to the general population, thus failing to uphold the second hypothesis that predicted an over-representation of white majority participants. This second finding diverges from existing research findings about ethnic diversity amongst science communication audiences, raising the possibility that some public engagement events are over-performing on this dimension of social inclusion. Overall, the findings demonstrate that European Researchers' Night has potential for addressing the critical goal of enhancing the diversity of audiences for public engagement with research, even as it falls short on the key metric of socio-economic diversity.

Invadolysin acts genetically via the SAGA complex to modulate chromosome structure.

Identification of components essential to chromosome structure and behaviour remains a vibrant area of study. We have previously shown that invadolysin is essential in Drosophila, with roles in cell division and cell migration. Mitotic chromosomes are hypercondensed in length, but display an aberrant fuzzy appearance. We additionally demonstrated that in human cells, invadolysin is localized on the surface of lipid droplets, organelles that store not only triglycerides and sterols but also free histones H2A, H2Av and H2B. Is there a link between the storage of histones in lipid droplets and the aberrantly structured chromosomes of invadolysin mutants? We have identified a genetic interaction between invadolysin and nonstop, the de-ubiquitinating protease component of the SAGA (Spt-Ada-Gcn5-acetyltransferase) chromatin-remodelling complex. invadolysin and nonstop mutants exhibit phenotypic similarities in terms of chromosome structure in both diploid and polyploid cells. Furthermore, IX-14(1)/not(1) transheterozygous animals accumulate mono-ubiquitinated histone H2B (ubH2B) and histone H3 tri-methylated at lysine 4 (H3K4me3). Whole mount immunostaining of IX-14(1)/not(1) transheterozygous salivary glands revealed that ubH2B accumulates surprisingly in the cytoplasm, rather than the nucleus. Over-expression of the Bre1 ubiquitin ligase phenocopies the effects of mutating either the invadolysin or nonstop genes. Intriguingly, nonstop and mutants of other SAGA subunits (gcn5, ada2b and sgf11) all suppress an invadolysin-induced rough eye phenotype. We conclude that the abnormal chromosome phenotype of invadolysin mutants is likely the result of disrupting the histone modification cycle, as accumulation of ubH2B and H3K4me3 is observed. We further suggest that the mislocalization of ubH2B to the cytoplasm has additional consequences on downstream components essential for chromosome behaviour. We therefore propose that invadolysin plays a crucial role in chromosome organization via its interaction with the SAGA complex.

Mechanism of sternotomy dehiscence.

OBJECTIVES: Biomechanical modelling of the forces acting on a median sternotomy can explain the mechanism of sternotomy dehiscence, leading to improved closure techniques. METHODS: Chest wall forces on 40 kPa coughing were measured using a novel finite element analysis (FEA) ellipsoid chest model, based on average measurements of eight adult male thoracic computerized tomography (CT) scans, with Pearson's correlation coefficient used to assess the anatomical accuracy. Another FEA model was constructed representing the barrel chest of chronic obstructive pulmonary disease (COPD) patients. Six, seven and eight trans-sternal and figure-of-eight closures were tested against both FEA models. RESULTS: Comparison between chest wall measurements from CT data and the normal ellipsoid FEA model showed an accurate fit (P < 0.001, correlation coefficients: coronal r = 0.998, sagittal r = 0.991). Coughing caused rotational moments of 92 Nm, pivoting at the suprasternal notch for the normal FEA model, rising to 118 Nm in the COPD model (t-test, P < 0.001). The threshold for dehiscence was 84 Nm with a six-sternal-wire closure, 107 Nm with seven wires, 127 Nm with eight wires and 71 Nm for three figure-of-eights. CONCLUSIONS: The normal rib cage closely fits the ellipsoid FEA model. Lateral chest wall forces were significantly higher in the barrel-shaped chest. Rotational moments generated by forces acting on a six-sternal-wire closure at the suprasternal notch were sufficient to cause lateral distraction pivoting at the top of the manubrium. The six-sternal-wire closure may be successfully enhanced by the addition of one or two extra wires at the lower end of the sternotomy, depending on chest wall shape.

Invadolysin, a conserved lipid-droplet-associated metalloproteinase, is required for mitochondrial function in Drosophila.

Mitochondria are the main producers of ATP, the principal energy source of the cell, and reactive oxygen species (ROS), important signaling molecules. Mitochondrial morphogenesis and function depend on a hierarchical network of mechanisms in which proteases appear to be center stage. The invadolysin gene encodes an essential conserved metalloproteinase of the M8 family that is necessary for mitosis and cell migration during Drosophila development. We previously demonstrated that invadolysin is found associated with lipid droplets in cells. Here, we present data demonstrating that invadolysin interacts physically with three mitochondrial ATP synthase subunits. Our studies have focused on the genetic phenotypes of invadolysin and bellwether, the Drosophila homolog of ATP synthase α, mutants. The invadolysin mutation presents defects in mitochondrial physiology similar to those observed in bellwether mutants. The invadolysin and bellwether mutants have parallel phenotypes that affect lipid storage and mitochondrial electron transport chain activity, which result in a reduction in ATP production and an accumulation of ROS. As a consequence, invadolysin mutant larvae show lower energetic status and higher oxidative stress. Our data demonstrate an essential role for invadolysin in mitochondrial function that is crucial for normal development and survival.

The conserved metalloprotease invadolysin localizes to the surface of lipid droplets.

Invadolysin is a metalloprotease conserved in many different organisms, previously shown to be essential in Drosophila with roles in cell division and cell migration. The gene seems to be ubiquitously expressed and four distinct splice variants have been identified in human cells but not in most other species examined. Immunofluorescent detection of human invadolysin in cultured cells reveals the protein to be associated with the surface of lipid droplets. By means of subcellular fractionation, we have independently confirmed the association of invadolysin with lipid droplets. We thus identify invadolysin as the first metalloprotease located on these dynamic organelles. In addition, analysis of larval fat-body morphological appearance and triglyceride levels in the Drosophila invadolysin mutant suggests that invadolysin plays a role in lipid storage or metabolism.