Einbeziehung von Menschen mit geringer Literalität in die Empirische Sozialforschung

This discussion paper deals with the inclusion of people with low literacy skills in empirical social research. The group of authors Nina Weimann-Sandig, Johanna Schneider, Martin Möhring, Götz Schneiderat, Jan Schuhr and Harald Wagner shed light on the social relevance and challenges associated with the inclusion of these vulnerable groups in empirical social research. Low literacy is seen as a phenomenon that encompasses not only individual abilities, but also social conditions. The starting point of the discussion paper is the results of the LitInvolve project, which aimed to analyse the understanding of literacy and its consideration in the various phases of empirical social research. A key finding of the project is that people with low literacy skills are often not adequately rep-resented, leading to a neglect of their perspectives in research and policy-making processes. The discussion paper is divided into several sections. First, the theoretical background is outlined, followed by a detailed analysis of the concepts of low literacy and their relevance for social research. In a next step, the results of the quantitative survey of scientists and the qualitative interviews with low-literate people are presented. The results show that there are a variety of understandings of literacy that are context-dependent and often blurred. This has implications for the way in which research is conducted and how marginalised groups are included. The discussion of the empirical findings makes it clear that considering low literacy in research is not only necessary, but also an ethical obligation to reduce social inequalities

Connexin 43 mediated gap junctional communication enhances breast tumor cell diapedesis in culture

INTRODUCTION: Metastasis involves the emigration of tumor cells through the vascular endothelium, a process also known as diapedesis. The molecular mechanisms regulating tumor cell diapedesis are poorly understood, but may involve heterocellular gap junctional intercellular communication (GJIC) between tumor cells and endothelial cells. METHOD: To test this hypothesis we expressed connexin 43 (Cx43) in GJIC-deficient mammary epithelial tumor cells (HBL100) and examined their ability to form gap junctions, establish heterocellular GJIC and migrate through monolayers of human microvascular endothelial cells (HMVEC) grown on matrigel-coated coverslips. RESULTS: HBL100 cells expressing Cx43 formed functional heterocellular gap junctions with HMVEC monolayers within 30 minutes. In addition, immunocytochemistry revealed Cx43 localized to contact sites between Cx43 expressing tumor cells and endothelial cells. Quantitative analysis of diapedesis revealed a two-fold increase in diapedesis of Cx43 expressing cells compared to empty vector control cells. The expression of a functionally inactive Cx43 chimeric protein in HBL100 cells failed to increase migration efficiency, suggesting that the observed up-regulation of diapedesis in Cx43 expressing cells required heterocellular GJIC. This finding is further supported by the observation that blocking homocellular and heterocellular GJIC with carbenoxolone in co-cultures also reduced diapedesis of Cx43 expressing HBL100 tumor cells. CONCLUSION: Collectively, our results suggest that heterocellular GJIC between breast tumor cells and endothelial cells may be an important regulatory step during metastasis

A computationally designed antigen eliciting broad humoral responses against SARS-CoV-2 and related sarbecoviruses

The threat of spillovers of coronaviruses associated with the severe acute respiratory syndrome (SARS) from animals to humans necessitates vaccines that offer broader protection from sarbecoviruses. By leveraging a viral-genome-informed computational method for selecting immune-optimized and structurally engineered antigens, here we show that a single antigen based on the receptor binding domain of the spike protein of sarbecoviruses elicits broad humoral responses against SARS-CoV-1, SARS-CoV-2, WIV16 and RaTG13 in mice, rabbits and guinea pigs. When administered as a DNA immunogen or by a vector based on a modified vaccinia virus Ankara, the optimized antigen induced vaccine protection from the Delta variant of SARS-CoV-2 in mice genetically engineered to express angiotensin-converting enzyme 2 and primed by a viral-vector vaccine (AZD1222) against SARS-CoV-2. A vaccine formulation incorporating mRNA coding for the optimized antigen further validated its broad immunogenicity. Vaccines that elicit broad immune responses across subgroups of coronaviruses may counteract the threat of zoonotic spillovers of betacoronaviruses

Microfilament organization and wound repair in retinal pigment epithelium

Several systems of microfilaments (MF) associated with adherens-type junctions between adjacent retinal pigment epithelial (RPE) cells and between these cells and the substratum play an important role in maintaining the integrity and organization of the RPE. They include prominent, contractile circumferential MF bundles that are associated with the zonula adherens (ZA) junctions. In chick RPE, these junctions are assembled from smaller subunits thus giving greater structural flexibility to the junctional region. Because the separation of the junctions requires trypsin and low calcium, both calcium-dependent and -independent mechanisms are involved in keeping adjacent RPE cells attached to one another. Another system of MF bundles that crosses the cell at the level of ZA junctions can be induced to form by stretching the epithelium. The MF bundles forming this system are oriented in the direction in which the RPE is stretched, thereby preventing the overextension of the cell in any one direction. The system may be useful as an indicator of the direction in which tension is experienced by RPE during development of the eye, in animal models of disease and during repair of experimentally induced wounds. Numerous single-cell wounds resulting from death of RPE cells by apoptosis at various stages of repair are normally present in developing chick and adult mammalian RPE. These wounds are repaired by the spreading of adjacent RPE cells and by the contraction of MF bundles oriented parallel to the wound edge, which develop during this time. As a result of the spreading in the absence of cell proliferation, the RPE cells increase in diameter with age. Experimentally induced wounds made by removing 5–10 RPE cells are repaired by a similar mechanism within 24 h. In repair of larger wounds, over 125 μm in width, the MF bundles oriented parallel to the wound edge characteristic of spreading cells are later replaced by stress fibers (SFs) that run perpendicularly to the wound edge and interact with the substratum at focal contacts (FCs) as RPE cells start to migrate. Cell proliferation is induced in cells along the wound edge only when the wounds are wide enough to require cell migration. In the presence of antibodies to beta-1-integrins, a component of FCs, cell spreading is not prevented but both cell migration and cell proliferation are inhibited. Thus, only the organization of the cytoskeleton characteristic of migrating RPE cells that have SFs that interact with the substratum at FCs, is associated with the induction of cell proliferation.Key words: retinal pigment epithelium, microfilaments, wound repair.</jats:p

Integrity of the homophilic binding site is required for the preferential localization of NCAM in intercellular contacts

The neural cell adhesion molecule NCAM is a member of the immunoglobulin (Ig) superfamily. NCAM can undergo homophilic binding and heterophilic interactions with cell surface components and is often concentrated at sites of intercellular contact. To investigate the molecular basis of this biased surface distribution, we examined L cell transfectants expressing wild-type or mutant forms of chick NCAM-140 by laser scanning confocal microscopy. Mutant NCAMs that lacked Ig-like domains 1, 2, 4, or 5 were preferentially localized in contact regions. However, the relative concentration of these mutant NCAMs in contact sites was substantially reduced compared with wild-type NCAM. In contrast, NCAM redistribution to intercellular contacts was abolished in cells expressing mutant NCAMs that either lacked Ig-like domain 3 or contained mutations in the homophilic binding site in this domain. In heterotypic contacts between PC12 cells and L cell transfectants, colocalization of rat NCAM and chick NCAM was again dependent on the integrity of the homophilic binding site of the NCAM expressed on L cells. These results provide evidence that homophilic binding is the main mechanism by which NCAM becomes redistributed to intercellular contacts. They also implicate a role for other Ig-like domains in the accumulation of NCAM at cell–cell contacts.Key words: cell–cell adhesion, adhesion molecule, NCAM, homophilic binding, surface distribution.</jats:p