Für wen gebe ich mein Urteil ab? Der systematische Einfluss des Fragebogenadressaten auf Kausalattributionsgewichtungen bei geschlossenen Antwortformaten

Die Fragebogenforschung belegt, dass Respondenten durch Kontextinformationen eines Fragebogens systematisch in ihrem Antwortverhalten beeinflusst werden. So zeigten Norenzayan und Schwarz (1999), dass Probanden bei freier Antwortmöglichkeit eher persönlichkeitsbezogene Ursachen zur Erklärung von Straftaten nennen, wenn der Fragebogen scheinbar von einem Institut für Persönlichkeitsforschung (verglichen mit einem Institut für Sozialforschung) erstellt wurde. Hierzu diskutierte Erklärungen sind einerseits Konversationsmaximen, die einen Bezug zwischen Adressat und Gesagtem induzieren, andererseits kognitive Primings, die selektive kognitive Aktivierungen und damit Verfügbarkeiten bedingen sollen. Die vorliegende Studie untersucht diese Erklärungsalternativen, indem sie erstmals in einem analogen Studiendesign persönlichkeitsbezogene und soziale Gründe in geschlossenen Antwortformaten vorgibt und gewichten lässt. Mögliche Gewichtungsunterschiede sind somit nicht mittels kognitiver Verfügbarkeit erklärbar. Eine Kovarianzanalyse (Alter, Geschlecht und die Big-Five-Persönlichkeitsdimensionen als Kovariaten) belegt im Einklang mit den Konversationsmaximen eine signifikant stärkere Bedeutungszuschreibung für persönlichkeitsbezogene Ursachen unter der Bedingung „Institut für Persönlichkeitsforschung“ im Vergleich zu „Institut für Sozialforschung“ und einer Kontrollbedingung („Institut für Kriminologie“)

Association of Clonal Hematopoiesis of Indeterminate Potential with Inflammatory Gene Expression in Patients with COPD

Chronic obstructive pulmonary disease (COPD) is a disease with an inflammatory pheno type with increasing prevalence in the elderly. Expanded population of mutant blood cells carrying somatic mutations is termed clonal hematopoiesis of indeterminate potential (CHIP). The associ ation between CHIP and COPD and its relevant effects on DNA methylation in aging are mainly unknown. Analyzing the deep-targeted amplicon sequencing from 125 COPD patients, we found enhanced incidence of CHIP mutations (~20%) with a predominance of DNMT3A CHIP-mediated hypomethylation of Phospholipase D Family Member 5 (PLD5), which in turn is positively correlated with increased levels of glycerol phosphocholine, pro-inflammatory cytokines, and deteriorating lung function

Circulating Progenitor Cell Count for Cardiovascular Risk Stratification: A Pooled Analysis

Background: Circulating progenitor cells (CPC) contribute to the homeostasis of the vessel wall, and a reduced CPC count predicts cardiovascular morbidity and mortality. We tested the hypothesis that CPC count improves cardiovascular risk stratification and that this is modulated by low-grade inflammation. Methodology/Principal Findings: We pooled data from 4 longitudinal studies, including a total of 1,057 patients having CPC determined and major adverse cardiovascular events (MACE) collected. We recorded cardiovascular risk factors and high-sensitive C-reactive protein (hsCRP) level. Risk estimates were derived from Cox proportional hazard analyses. CPC count and/or hsCRP level were added to a reference model including age, sex, cardiovascular risk factors, prevalent CVD, chronic renal failure (CRF) and medications. The sample was composed of high-risk individuals, as 76.3% had prevalent CVD and 31.6% had CRF. There were 331 (31.3%) incident MACE during an average 1.7±1.1 year follow-up time. CPC count was independently associated with incident MACE even after correction for hsCRP. According to C-statistics, models including CPC yielded a non-significant improvement in accuracy of MACE prediction. However, the integrated discrimination improvement index (IDI) showed better performance of models including CPC compared to the reference model and models including hsCRP in identifying MACE. CPC count also yielded significant net reclassification improvements (NRI) for CV death, non-fatal AMI and other CV events. The effect of CPC was independent of hsCRP, but there was a significant more-than-additive interaction between low CPC count and raised hsCRP level in predicting incident MACE. Conclusions/Significance: In high risk individuals, a reduced CPC count helps identifying more patients at higher risk of MACE over the short term, especially in combination with a raised hsCRP level

Guidance on Monitoring of Marine Litter in European Seas

This publication is a Reference Report by the Joint Research Centre of the European Commission.The MSFD Technical Subgroup on Marine Litter was tasked to deliver guidance so that European Member States could initiate programmes for monitoring of Descriptor 10 of the MSFD. The present document provides the recommendations and information needed to commence the monitoring required for marine litter, including methodological protocols and categories of items to be used for the assessment of litter on the Beach, Water Column, Seafloor and Biota, including a special section on Microparticles

Quantification of Circulating Endothelial Progenitor Cells Using the Modified ISHAGE Protocol

Circulating endothelial progenitor cells (EPC), involved in endothelial regeneration, neovascularisation, and determination of prognosis in cardiovascular disease can be characterised with functional assays or using immunofluorescence and flow cytometry. Combinations of markers, including CD34+KDR+ or CD133+KDR+, are used. This approach, however may not consider all characteristics of EPC. The lack of a standardised protocol with regards to reagents and gating strategies may account for the widespread inter-laboratory variations in quantification of EPC. We, therefore developed a novel protocol adapted from the standardised so-called ISHAGE protocol for enumeration of haematopoietic stem cells to enable comparison of clinical and laboratory data.In 25 control subjects, 65 patients with coronary artery disease (CAD; 40 stable CAD, 25 acute coronary syndrome/acute myocardial infarction (ACS)), EPC were quantified using the following approach: Whole blood was incubated with CD45, KDR, and CD34. The ISHAGE sequential strategy was used, and finally, CD45(dim)CD34(+) cells were quantified for KDR. A minimum of 100 CD34(+) events were collected. For comparison, CD45(+)CD34(+) and CD45(-)CD34(+) were analysed simultaneously. The number of CD45(dim)CD34(+)KDR(+) cells only were significantly higher in healthy controls compared to patients with CAD or ACS (p = 0.005 each, p<0.001 for trend). An inverse correlation of CD45(dim)CD34(+)KDR(+) with disease activity (r = -0.475, p<0.001) was confirmed. Only CD45(dim)CD34(+)KDR(+) correlated inversely with the number of diseased coronaries (r = -0.344; p<0.005). In a second study, a 4-week de-novo treatment of atorvastatin in stable CAD evoked an increase only of CD45(dim)CD34(+)KDR(+) EPC (p<0.05). CD45(+)CD34(+)KDR(+) and CD45(-)CD34(+)KDR(+) were indifferent between the three groups.Our newly established protocol adopted from the standardised ISHAGE protocol achieved higher accuracy in EPC enumeration confirming previous findings with respect to the correlation of EPC with disease activity and the increase of EPC during statin therapy. The data of this study show the CD45(dim) fraction to harbour EPC

Observations of V592 Cassiopeiae with the Spitzer Space Telescope - Dust in the Mid-Infrared

We present the ultraviolet-optical-infrared spectral energy distribution of the low inclination novalike cataclysmic variable V592 Cassiopeiae, including new mid-infrared observations from 3.5-24 microns obtained with the Spitzer Space Telescope. At wavelengths shortward of 8 microns, the spectral energy distribution of V592 Cas is dominated by the steady state accretion disk, but there is flux density in excess of the summed stellar components and accretion disk at longer wavelengths. Reproducing the observed spectral energy distribution from ultraviolet to mid-infrared wavelengths can be accomplished by including a circumbinary disk composed of cool dust, with a maximum inner edge temperature of ~500 K. The total mass of circumbinary dust in V592 Cas (~10^21 g) is similar to that found from recent studies of infrared excess in magnetic CVs, and is too small to have a significant effect on the long-term secular evolution of the cataclysmic variable. The existence of circumbinary dust in V592 Cas is possibly linked to the presence of a wind outflow in this system, which can provide the necessary raw materials to replenish the circumbinary disk on relatively short timescales, and/or could be a remnant from the common envelope phase early in the formation history of the system.Comment: Accepted for publication in the Astrophysical Journa

Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk.

Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression