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Research estimating the outcomes of higher education in Germany has widely ignored the private educational sector. This study focuses on labour market returns in terms of the income of graduates from private higher education institutions in Germany. Using data from the National Education Panel Study (NEPS) the results of the Bayesian regression analysis indicate a moderate wage premium for private students compared to students who are enrolled in public higher education institutions regarding the first employment. Despite the predominant role of public universities in Germany, graduates of private higher education institutions receive similar advantages on the labour market as their counterparts in other countries, although private education in other countries is more prestigious.

The break of the epithelial barrier of gingiva has been a subject of minor interest, albeit playing a key role in periodontal pathology, transitory bacteraemia, and subsequent systemic low-grade inflammation (LGI). The significance of mechanically induced bacterial translocation in gingiva (e.g., via mastication and teeth brushing) has been disregarded despite the accumulated knowledge of mechanical force effects on tight junctions (TJs) and subsequent pathology in other epithelial tissues. Transitory bacteraemia is observed as a rule in gingival inflammation, but is rarely observed in clinically healthy gingiva. This implies that TJs of inflamed gingiva deteriorate, e.g., via a surplus of lipopolysaccharide (LPS), bacterial proteases, toxins, Oncostatin M (OSM), and neutrophil proteases. The inflammation-deteriorated gingival TJs rupture when exposed to physiological mechanical forces. This rupture is characterised by bacteraemia during and briefly after mastication and teeth brushing, i.e., it appears to be a dynamic process of short duration, endowed with quick repair mechanisms. In this review, we consider the bacterial, immune, and mechanical factors responsible for the increased permeability and break of the epithelial barrier of inflamed gingiva and the subsequent translocation of both viable bacteria and bacterial LPS during physiological mechanical forces, such as mastication and teeth brushing.

Differences in the tool use of non-human primates and humans are subject of ongoing debate. In humans, representations of object functions underpin efficient tool use. Yet, representations of object functions can lead to functional fixedness, which describes the fixation on a familiar tool function leading to less efficient problem solving when the problem requires using the tool for a new function. In the current study, we examined whether chimpanzees exhibit functional fixedness. After solving a problem with a tool, chimpanzees were less efficient in solving another problem which required using the same tool with a different function compared to a control group. This fixation effect was still apparent after a period of nine months and when chimpanzees had learned about the function of a tool by observation of a conspecific. These results suggest that functional fixedness in our closest living relatives likely exists and cast doubt on the notion that stable function representations are uniquely human.

Nonhuman great apes show remarkable behavioural flexibility. Some individuals are even able to use water as a tool: They spit water into a vertical tube to make a peanut float upwards until it comes into reach (floating peanut task; FPT). In the current study, we used the FPT to investigate how visual feedback, an end-state demonstration and a social demonstration affect task performance in nonhuman great apes in three experiments. Our results indicate that apes who had acquired the solution with a clear tube maintained it with an opaque one. However, apes starting with an opaque tube failed to solve the task. Additionally, facing the peanut floating on a water-filled tube (i.e., an end-state demonstration) promoted success independent on the availability of visual feedback. Moreover, experiencing how water was poured into the tube either by a human demonstrator or by a water tap that had been opened either by the ape or a human did not seem to be of further assistance. First, this study suggests that great apes require visual feedback for solving the FPT, which is no longer required after the initial acquisition. Second, some subjects benefit from encountering the end-state, a finding corroborating previous studies.

Summary Rapid adaptation of weeds to herbicide applications in agriculture through resistance development is a widespread phenomenon. In particular, the grass Alopecurus myosuroides is an extremely problematic weed in cereal crops with the potential to manifest resistance in only a few generations. Target‐site resistances (TSRs), with their strong phenotypic response, play an important role in this rapid adaptive response. Recently, using PacBio's long‐read amplicon sequencing technology in hundreds of individuals, we were able to decipher the genomic context in which TSR mutations occur. However, sequencing individual amplicons are costly and time‐consuming, thus impractical to implement for other resistance loci or applications. Alternatively, pool‐based approaches overcome these limitations and provide reliable allele frequencies, although at the expense of not preserving haplotype information. In this proof‐of‐concept study, we sequenced with PacBio High Fidelity (HiFi) reads long‐range amplicons (13.2 kb), encompassing the entire ACCase gene in pools of over 100 individuals, and resolved them into haplotypes using the clustering algorithm PacBio amplicon analysis (pbaa), a new application for pools in plants and other organisms. From these amplicon pools, we were able to recover most haplotypes from previously sequenced individuals of the same population. In addition, we analysed new pools from a Germany‐wide collection of A. myosuroides populations and found that TSR mutations originating from soft sweeps of independent origin were common. Forward‐in‐time simulations indicate that TSR haplotypes will persist for decades even at relatively low frequencies and without selection, highlighting the importance of accurate measurement of TSR haplotype prevalence for weed management.

A key process in the lifecycle of the malaria parasite Plasmodium falciparum is the fast invasion of human erythrocytes. Entry into the host cell requires the apical membrane antigen 1 (AMA-1), a type I transmembrane protein located in the micronemes of the merozoite. Although AMA-1 is evolving into the leading blood-stage malaria vaccine candidate, its precise role in invasion is still unclear. We investigate AMA-1 function using live video microscopy in the absence and presence of an AMA-1 inhibitory peptide. This data reveals a crucial function of AMA-1 during the primary contact period upstream of the entry process at around the time of moving junction formation. We generate a Plasmodium falciparum cell line that expresses a functional GFP-tagged AMA-1. This allows the visualization of the dynamics of AMA-1 in live parasites. We functionally validate the ectopically expressed AMA-1 by establishing a complementation assay based on strain-specific inhibition. This method provides the basis for the functional analysis of essential genes that are refractory to any genetic manipulation. Using the complementation assay, we show that the cytoplasmic domain of AMA-1 is not required for correct trafficking and surface translocation but is essential for AMA-1 function. Although this function can be mimicked by the highly conserved cytoplasmic domains of P. vivax and P. berghei, the exchange with the heterologous domain of the microneme protein EBA-175 or the rhoptry protein Rh2b leads to a loss of function. We identify several residues in the cytoplasmic tail that are essential for AMA-1 function. We validate this data using additional transgenic parasite lines expressing AMA-1 mutants with TY1 epitopes. We show that the cytoplasmic domain of AMA-1 is phosphorylated. Mutational analysis suggests an important role for the phosphorylation in the invasion process, which might translate into novel therapeutic strategies.

Exposure to airborne ultrafine and nanoparticles has raised increased interest over the recent years as they may cause adverse health effects. A common way to quantify exposure to airborne particles is to measure particle number size distributions through electrical mobility analysis. Four mobility particle sizers have been subject to a detailed intercomparison study, a TSI Fast Mobility Particle Sizer (FMPS), a Grimm Sequential Mobility Particle Sizer (SMPS+C), and two TSI Scanning Mobility Particle Sizers (SMPSs), equipped with two different condensation particle counters (CPC). The instruments were challenged with either NaCl or diesel soot particles. The results indicate that the sizing of all tested instrument was similar with only the FMPS size distributions consistently shifted toward smaller particle sizes. The Grimm SMPS generally measured higher concentrations and broader distributions than the TSI instruments. The two Grimm DMAs agreed well with each other; however, the TSI SMPS results showed a reproducible dependence on the flow rates. While TSI and Grimm SMPS delivered consistent results for sodium chloride (NaCl) and diesel soot, the FMPS seemed to react differently to the changing particle source than the SMPSs, which may be caused by either the different morphology or particle size dependent effects. For NaCl particles, the FMPS delivered the narrowest distributions and concentrations comparable with TSI SMPSs, whereas for diesel soot, it delivered the broadest distributions and higher concentrations than TSI SMPSs.

BackgroundQuantitative serological assays detecting response to SARS-CoV-2 are needed to quantify immunity. This study analyzed the performance and correlation of two quantitative anti-S1 assays in oligo-/asymptomatic individuals from a population-based cohort.MethodsIn total, 362 plasma samples (108 with reverse transcription-polymerase chain reaction [RT-PCR]-positive pharyngeal swabs, 111 negative controls, and 143 with positive serology without confirmation by RT-PCR) were tested with quantitative assays (Euroimmun Anti-SARS-CoV-2 QuantiVac enzyme-linked immunosorbent assay [EI-S1-IgG-quant]) and Roche Elecsys® Anti-SARS-CoV-2 S [Ro-RBD-Ig-quant]), which were compared with each other and confirmatory tests, including wild-type virus micro-neutralization (NT) and GenScript®cPass™. Square roots R of coefficients of determination were calculated for continuous variables and non-parametric tests were used for paired comparisons.ResultsQuantitative anti-S1 serology correlated well with each other (true positives, 96%; true negatives, 97%). Antibody titers decreased over time (< 30 to > 240 days after initial positive RT-PCR). Agreement with GenScript-cPass was 96%/99% for true positives and true negatives, respectively, for Ro-RBD-Ig-quant and 93%/97% for EI-S1-IgG-quant. Ro-RBD-Ig-quant allowed distinct separation between positives and negatives, and less non-specific reactivity versus EI-S1-IgG-quant. Raw values (95% CI) ≥ 28.7 U/mL (22.6–36.4) for Ro-RBD-Ig-quant and ≥ 49.8 U/mL (43.4–57.1) for EI-S1-IgG-quant predicted NT > 1:5 in 95% of cases.ConclusionsOur findings suggest both quantitative anti-S1 assays (EI-S1-IgG-quant and Ro-RBD-Ig-quant) may replace direct neutralization assays in quantitative measurement of immune protection against SARS-CoV-2 in certain circumstances. However, although the mean antibody titers for both assays tended to decrease over time, a higher proportion of Ro-RBD-Ig-quant values remained positive after 240 days.

Dendritic cells (DC) can act tolerogenic at a semi-mature stage by induction of protective CD4(+) T cell and NKT cell responses. Here we studied the role of the co-inhibitory molecule B7-H1 (PD-L1, CD274) on semi-mature DC that were generated from bone marrow (BM) cells of B7-H1(-/-) mice and applied to the model of Experimental Autoimmune Encephalomyelitis (EAE). Injections of B7-H1-deficient DC showed increased EAE protection as compared to wild type (WT)-DC. Injections of B7-H1(-/-) TNF-DC induced higher release of peptide-specific IL-10 and IL-13 after restimulation in vitro together with elevated serum cytokines IL-4 and IL-13 produced by NKT cells, and reduced IL-17 and IFN-gamma production in the CNS. Experiments in CD1d(-/-) and Jalpha281(-/-) mice as well as with type I and II NKT cell lines indicated that only type II NKT cells but not type I NKT cells (invariant NKT cells) could be stimulated by an endogenous CD1d-ligand on DC and were responsible for the increased serum cytokine production in the absence of B7-H1. Together, our data indicate that BM-DC express an endogenous CD1d ligand and B7-H1 to ihibit type II but not type I NKT cells. In the absence of B7-H1 on these DC their tolerogenic potential to stimulate tolerogenic CD4(+) and NKT cell responses is enhanced.