Gutenberg Open Science

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ZeitschriftenaufsatzAccess status: Open Access ,
Chronic fatigue: psychometric properties and updated norm values of the Chalder fatigue scale in a cross-sectional sample representative of the German population
(2025) Krakau, Lina; Wicke, Felix; Häuser, Winfried; Beutel, Manfred E.; Brähler, Elmar; Hettich-Damm, Nora
Background The Chalder Fatigue Scale (CFQ) is a commonly used self-report instrument assessing the severity and chronicity of fatigue. We examine the psychometric properties of the CFQ and provide updated normative data for the German general population. Materials and Methods The CFQ was administered to N = 2519 participants (16-96 years). Statistical analyses included the evaluation of the item properties, confirmatory factor analysis and examinig associations with mental health and sociodemographic data. CFQ cut-offs were used to estimate proportions of severe and chronic fatigue scores. We calculated percentile norms for the total sample and stratified by age groups and gender. Results Indicators of internal consistency reliability were high for the CFQ total and subscales (α = 0.84–0.94; ω = 0.86–0.95). We found excellent model fit for a one (χ2 = 196.011, df = 44, p ≤ .001; CFI=.991, RMSEA = 0.037, SRMR = 0.059) and two-factor solution (χ2 = 115.055, df = 42, p ≤ .001; CFI=.996, RMSEA = 0.026, SRMR = 0.045). The CFQ total scale showed low to moderate associations with depression (r = .49, p ≤ .001), anxiety (r = .45, p ≤ .001), and loneliness (r = .26, p ≤ .001), indicating acceptable discriminant validity. Current unemployment was a relevant sociodemographic correlate of fatigue severity (CFQ total: β =.38, se =.09, p ≤ .001). 14.2% of participants reported severe fatigue, while 4.3% reported being fatigued for at least six months (chronic fatigue). Conclusion The CFQ is a brief and reliable instrument for assessing fatigue in general population settings. The results are limited by the lack of comparison with other established fatigue questionnaires.
ZeitschriftenaufsatzAccess status: Open Access ,
Phosphatidylinositol 3-phosphate metabolism impacts cellular a-synuclein localization in Saccharomyces cerevisiae
(2025) Löser, Timo; Bekbulat, Fazilet; Behl, Christian; Schepers, Jana
Alpha-synuclein (αSyn), a hallmark protein of synucleino pathies such as Parkinson’s disease (PD), is likely to be involved in neuronal membrane trafficking and synaptic vesicle dynamics at axon terminals. Its specific binding to anionic phospholipids, such as phosphatidylinositol phos phates that are essential for intracellular signaling and mem brane trafficking, suggests an involvement in vesicular transport processes. In Saccharomyces cerevisiae, a model or ganism for cell biological PD research, human αSyn localizes to the plasma membrane via the secretory machinery. Employing this yeast model, we investigated the impact of αSyn on cellular quality control mechanisms. Additionally, we focused on the effect of αSyn expression in yeast mutants impaired in specific phospholipid biosynthesis and transport pathways, including endovacuolar trafficking and autophagy. In the deletion strains vps34Δ and vps15Δ, lacking phospha tidylinositol 3-phosphate (PI3P) biosynthesis, αSyn mis localizes in the cytosol, and significantly reduces cell viability. In these strains, αSyn species containing an intact lipid binding N terminus also form large perivacuolar, lipid-rich accumulations. In wild type cells, αSyn expression alters the morphology of PI3P-rich membrane structures and upregu lates transcription of SEC4, which encodes a key regulator of the late secretory pathway. Moreover, αSyn colocalizes with overexpressed Sec4 at the emerging cell bud. Our findings demonstrate that PI3P is critical for the targeting of αSyn to the yeast plasma membrane via the secretory pathway, revealing a potential entry point into this complex machinery. Understanding the relationship between αSyn and vesicular trafficking in this system will enhance our knowledge of αSyn trafficking in mammalian cells and, eventually, in PD, offering new research avenues.
ZeitschriftenaufsatzAccess status: Open Access ,
Effects of platelet-rich fibrin on in vitro periodontal ligament cell functions
(2025) Cores Ziskoven, Pablo; Nogueira, Andressa Vilas Boas; Imber, Jean-Claude; Bani, Philipp; Hell, Charlott Luise; Weusmann, Jens; Deschner, James
Background: Periodontitis is a chronic inflammatory disease that leads to tooth loosening and ultimately tooth loss. Regenerative approaches employing bioactive substances aim to restore lost tissues. Platelet-rich fibrin (PRF) is a simple and cost-effective option, but its effects on periodontal ligament (PDL) cells under inflammatory conditions remain unclear. Objectives: This study investigated the stimulating effects of platelet-rich fibrin on molecules crucial for periodontal wound healing and tissue remodelling in periodontal ligament (PDL) cells, under normal and inflammatory conditions mimicked by TNF-α. Methods The stimulating effects of different concentrations of PRF on the gene expression of VEGF, BMP2, COX2, TNF-α, and SPP1 were analysed by real-time PCR and ELISA. In addition, the possible modulating effects of TNF-α, a pro-inflammatory cytokine associated with periodontitis, on PRF-induced effects were studied. Furthermore, cell viability, proliferation, and migration were investigated. Results: A 2–3-fold dose-dependent increase in the expression of all the aforementioned genes by PRF was observed at 24 h and 48 h. Additional incubation with TNF-α did not lead to any significant modulation of PRF-induced expression patterns, indicating that the effects of PRF were not compromised in an inflammatory environment. Functionally, PRF caused a significant 35% increase in cell migration between 24 h and 48 h, which was again not affected by a pro-inflammatory condition. Cell viability and proliferation remained largely unaffected by PRF, irrespective of the presence of TNF-α or not. Conclusions: The results suggest that PRF can promote initial periodontal wound healing even in an inflammatory environment by stimulating the expression of cytokines, growth factors and markers of osteogenic differentiation such as VEGF, BMP2 and SPP1, which are involved in angiogenesis, tissue remodelling, and/or cell migration.