Entwicklung von Vorurteilen im Kindes- und Jugendalter: eine Meta-Analyse zu Altersunterschieden

Ziel dieser Meta-Analyse ist es, internationale Forschungsarbeiten über Altersunterschiede in Vorurteilen bei Kindern und Jugendlichen empirisch zu¬sammen¬zufassen, um dadurch einen (normativen) Verlauf der Vorurteilsentwicklung skizzieren zu können. Insgesamt gingen 140 internationale Doku¬mente mit 147 querschnittlichen und 8 längsschnittlichen Studien in die Analyse ein. Jede dieser Studien untersuchte dabei Vorurteile in mindestens zwei Altersgruppen. Die Altersunterschiede wurden über die verschiedenen Studien systematisch aggregiert. Die Ergebnisse zeigen einen robusten Anstieg von Vorurteilen von der frühen bis mittleren Kindheit und einen leichten Abfall in der späten Kindheit, während im Jugendalter keine systematischen Altersunterschiede gefunden wurden. Differenziertere Analysen erga¬ben jedoch, dass dieser Verlauf maßgeblich bei Vorurteilen in Bezug auf Ethnie und schwarze Hautfarbe zu finden ist, nicht jedoch gegenüber nationalen Gruppen, Behinderten, Ge¬schlechts-gruppen, Homosexuellen oder gegenüber Alten, weshalb nicht von einem allge¬meinen Entwicklungsverlauf von Vorurteilen ausgegangen werden kann. Die Analysen ergaben weiterhin Effekte hinsichtlich methodischer Merkmale der Operationa¬lisierung, wobei insbesondere Unterschiede zwischen expliziten und impliziten Maßen bedeutsam waren. In Bezug auf Merkmale der Stichproben konnten der soziale Status der Fremdgruppe und Kontaktgelegenheiten mit der Fremdgruppe als Moderatoren der Entwick¬lungsverläufe identifiziert werden. So sinken Vorurteile gegenüber statusniedrigeren Gruppen in der späten Kindheit ab, sobald die Kinder Kontakte mit diesen Gruppen haben. Vorurteile gegenüber statushöheren Gruppen steigen jedoch im Verlauf des Grundschulalters an. Insgesamt macht diese Meta-Analyse deutlich, dass sich Vorurteile systematisch mit dem Alter verändern und besonders die späte Kindheit eine sensible Phase im Verlauf der Einstellungsentwicklung darstellt

Metastable Se6 as a ligand for Ag+: from isolated molecular to polymeric 1D and 2D structures

Attempts to prepare the hitherto unknown Se6 2+ cation by the reaction of elemental selenium and Ag[A] ([A]- = [Sb(OTeF5)6]-, [Al(OC(CF3)3)4]-) in SO2 led to the formation of [(OSO)Ag(Se6)Ag(OSO)][Sb(OTeF5)6]2 1 and [(OSO)2Ag(Se6)Ag(OSO)2][Al(OC(CF3)3)4]2 2a. 1 could only be prepared by using bromine as co-oxidant, however, bulk 2b (2a with loss of SO2) was accessible from Ag[Al(OC(CF3)3)4] and grey Se in SO2 (chem. analysis). The reactions of Ag[MF6] (M= As, Sb) and elemental selenium led to crystals of 1/∞{[Ag(Se6)]∞[Ag2(SbF6)3]∞} 3 and {1/∞[Ag(Se6)Ag]∞}[AsF6]2 4. Pure bulk 4 was best prepared by the reaction of Se4[AsF6]2, silver metal and elemental selenium. Attempts to prepare bulk 1 and 3 were unsuccessful. 1–4 were characterized by single-crystal X-ray structure determinations, 2b and 4 additionally by chemical analysis and 4 also by X-ray powder diffraction, FT-Raman and FT-IR pectroscopy. Application of the PRESTO III sequence allowed for the first time 109Ag MAS NMR investigations of 4 as well as AgF, AgF2, AgMF6 and {1/∞[Ag(I2)]∞}[MF6] (M= As, Sb). Compounds 1 and 2a/b, with the very large counter ions, contain isolated [Ag(Se6)Ag]2+ heterocubane units consisting of a Se6 molecule bicapped by two silver cations (local D3d sym). 3 and 4, with the smaller anions, contain close packed stacked arrays of Se6 rings with Ag+ residing in octahedral holes. Each Ag+ ion coordinates to three selenium atoms of each adjacent Se6 ring. 4 contains [Ag(Se6)+]∞ stacks additionally linked by Ag(2)+ into a two dimensional network. 3 features a remarkable 3-dimensional [Ag2(SbF6)3]- anion held together by strong Sb–F … Ag contacts between the component Ag+ and [SbF6]- ions. The hexagonal channels formed by the [Ag2(SbF6)3]- anions are filled by stacks of [Ag(Se6)+]∞ cations. Overall 1–4 are new members of the rare class of metal complexes of neutral main group elemental clusters, in which the main group element is positively polarized due to coordination to a metal ion. Notably, 1 to 4 include the commonly metastable Se6 molecule as a ligand. The structure, bonding and thermodynamics of 1 to 4 were investigated with the help of quantum chemical calculations (PBE0/TZVPP and (RI-)MP2/TZVPP, in part including COSMO solvation) and Born–Fajans–Haber-cycle calculations. From an analysis of all the available data it appears that the formation of the usually metastable Se6 molecule from grey selenium is thermodynamically driven by the coordination to the Ag+ ions

Defective Lipid Droplet-Lysosome Interaction Causes Fatty Liver Disease as Evidenced by Human Mutations in TMEM199 and CCDC115

BACKGROUND &amp; AIMS: Recently, novel inborn errors of metabolism were identified because of mutations in V-ATPase assembly factors TMEM199 and CCDC115. Patients are characterized by generalized protein glycosylation defects, hypercholesterolemia, and fatty liver disease. Here, we set out to characterize the lipid and fatty liver phenotype in human plasma, cell models, and a mouse model.METHODS AND RESULTS: Patients with TMEM199 and CCDC115 mutations displayed hyperlipidemia, characterized by increased levels of lipoproteins in the very low density lipoprotein range. HepG2 hepatoma cells, in which the expression of TMEM199 and CCDC115 was silenced, and induced pluripotent stem cell (iPSC)-derived hepatocyte-like cells from patients with TMEM199 mutations showed markedly increased secretion of apolipoprotein B (apoB) compared with controls. A mouse model for TMEM199 deficiency with a CRISPR/Cas9-mediated knock-in of the human A7E mutation had marked hepatic steatosis on chow diet. Plasma N-glycans were hypogalactosylated, consistent with the patient phenotype, but no clear plasma lipid abnormalities were observed in the mouse model. In the siTMEM199 and siCCDC115 HepG2 hepatocyte models, increased numbers and size of lipid droplets were observed, including abnormally large lipid droplets, which colocalized with lysosomes. Excessive de novo lipogenesis, failing oxidative capacity, and elevated lipid uptake were not observed. Further investigation of lysosomal function revealed impaired acidification combined with impaired autophagic capacity.CONCLUSIONS: Our data suggest that the hyperchole-sterolemia in TMEM199 and CCDC115 deficiency is due to increased secretion of apoB-containing particles. This may in turn be secondary to the hepatic steatosis observed in these patients as well as in the mouse model. Mechanistically, we observed impaired lysosomal function characterized by reduced acidification, autophagy, and increased lysosomal lipid accumulation. These findings could explain the hepatic steatosis seen in patients and highlight the importance of lipophagy in fatty liver disease. Because this pathway remains understudied and its regulation is largely untargeted, further exploration of this pathway may offer novel strategies for therapeutic interventions to reduce lipotoxicity in fatty liver disease.</p