The role of Si impurities in the transient dopant segregation and precipitation in yttrium-doped alumina

Y-doped alumina was sintered at 1500 degrees C for 10 h under ultra-clean experimental conditions without experiencing any abnormal grain growth. The yttrium was fairly homogeneously distributed at the grain boundaries, with a mean value of (Gamma) over bar (Y) = 5.5 at nm(-2). The Y-Al-O precipitates in the clean, Y2O3-doped alumina specimen were the YAP (YAlO3) phase, whereas only the YAG (Y3Al5O12) phase was present in the Y2O3-doped alumina samples contaminated with SiO2. The excess concentrations of Y and Si atoms at the grain boundaries that, at the same time, provoke the formation of structurally complex YAG precipitates and abnormal grain growth were both estimated to be at 4-5 at nm(-2). The compositions of the triple point pocket phases found in the region of the exaggeratedly grown alumina grains indicate the presence of alumino-silicate bulk liquids at the sintering temperature

Soluble versions of outer membrane cytochromes function as exporters for heterologously produced cargo proteins

This study reveals that it is possible to secrete truncated versions of outer membrane cytochromes into the culture supernatant and that these proteins can provide a basis for the export of heterologously produced proteins. Different soluble and truncated versions of the outer membrane cytochrome MtrF were analyzed for their suitability to be secreted. A protein version with a very short truncation of the N-terminus to remove the recognition sequence for the addition of a lipid anchor is secreted efficiently to the culture supernatant, and moreover this protein could be further truncated by a deletion of 160 amino acid and still is detectable in the supernatant. By coupling a cellulase to this soluble outer membrane cytochrome, the export efficiency was measured by means of relative cellulase activity. We conclude that outer membrane cytochromes of S. oneidensis can be applied as transporters for the export of target proteins into the medium using the type II secretion pathway

Podosome-Driven Defect Development in Lamellar Bone under the Conditions of Senile Osteoporosis Observed at the Nanometer Scale

The degradation mechanism of human trabecular bone harvested from the central part of the femoral head of a patient with a fragility fracture of the femoral neck under conditions of senile osteoporosis was investigated by high-resolution electron microscopy. As evidenced by light microscopy, there is a disturbance of bone metabolism leading to severe and irreparable damages to the bone structure. These defects are evoked by osteoclasts and thus podosome activity. Podosomes create typical pit marks and holes of about 300-400 nm in diameter on the bone surface. Detailed analysis of the stress field caused by the podosomes in the extracellular bone matrix was performed. The calculations yielded maximum stress in the range of few megapascals resulting in formation of microcracks around the podosomes. Disintegration of hydroxyapatite and free lying collagen fibrils were observed at the edges of the plywood structure of the bone lamella. At the ultimate state, the disintegration of the mineralized collagen fibrils to a gelatinous matrix comes along with a delamination of the apatite nanoplatelets resulting in a brittle, porous bone structure. The nanoplatelets aggregate to big hydroxyapatite plates with a size of up to 10 x 20 μm2. The enhanced plate growth can be explained by the interaction of two mechanisms in the ruffled border zone: the accumulation of delaminated hydroxyapatite nanoplatelets near clusters of podosomes and the accelerated nucleation and random growth of HAP nanoplatelets due to a nonsufficient concentration of process-directing carboxylated osteocalcin cOC. © 2021 The Authors. Published by American Chemical Society

Zinserhöhung der EZB: Wie groß ist die Inflationsgefahr?

Für Thomas Mayer, Deutsche Bank, erscheint es sinnvoll, dass die EZB den Leitzins auf sein neutrales Niveau hochführt. Noch wichtiger für die Wahrung der Stabilität des Euro wäre es aber, dass sich die EZB aus der Finanzierung von durch Insolvenz bedrohten Staaten und ihren Banken zurückzieht. Holger Schmieding, Berenberg Bank, sieht keine Inflationsgefahr. Er rechnet für Deutschland mit einem jährlichen Preisanstieg von gut 2%. Manfred Jäger-Ambroz.ewicz, Institut der deutschen Wirtschaft Köln, vertritt die Meinung, dass die EZB eine sachgerechte Leitzinspolitik umsetzt und einen angemessenen Leitzinspfad suggeriert. Michael Lamla und Jan-Egbert Sturm, ETH Zürich, betonen, dass die EZB genügend Glaubwürdigkeit und Transparenz besitzt, um die Inflationserwartungen zu beeinflussen und zu homogenisieren. Ihrer Ansicht nach steigen insgesamt die Inflationserwartungen im Euroraum für das nächste Jahr weiterhin an, ohne aber beunruhigende Werte anzunehmen. Auch Ulrich Kater, DekaBank, sieht die Glaubwürdigkeit des Inflationsregimes mit der Geldwertstabilität als wichtigster Zielsetzung unabhängiger Notenbanken nicht gefährdet. Leon Leschus, HWWI, geht davon aus, dass hohe Rohstoffpreise weiterhin zum Inflationsdruck beitragen werden. Es wäre somit wünschenswert, wenn die EZB ihre begonnene restriktive Geldpolitik fortsetzen würde. Hans Wolfgang Brachinger, Universität Fribourg, sieht angesichts teurer Rohstoffe, zunehmender Spekulation und steigender Produktionskosten in China die Inflationsrisiken in Deutschland wachsen, und zwar unabhängig vom Handeln der EZB.Preisniveaustabilität, Geldpolitik, Zins, Zinspolitik, Inflation, Zentralbank, Europäische Wirtschafts- und Währungsunion

Genetics of skin color variation in Europeans: genome-wide association studies with functional follow-up

In the International Visible Trait Genetics (VisiGen) Consortium, we investigated the genetics of human skin color by combining a series of genome-wide association studies (GWAS) in a total of 17,262 Europeans with functional follow-up of discovered loci. Our GWAS provide the first genome-wide significant evidence for chromosome 20q11.22 harboring the ASIP gene being explicitly associated with skin color in Europeans. In addition, genomic loci at 5p13.2 (SLC45A2), 6p25.3 (IRF4), 15q13.1 (HERC2/OCA2), and 16q24.3 (MC1R) were confirmed to be involved in skin coloration in Europeans. In follow-up gene expression and regulation studies of 22 genes in 20q11.22, we highlighted two novel genes EIF2S2 and GSS, serving as competing functional candidates in this region and providing future research lines. A genetically inferred skin color score obtained from the 9 top-associated SNPs from 9 genes in 940 worldwide samples (HGDP-CEPH) showed a clear gradual pattern in Western Eurasians similar to the distribution of physical skin color, suggesting the used 9 SNPs as suitable markers for DNA prediction of skin color in Europeans and neighboring populations, relevant in future forensic and anthropological investigations

Digital Quantification of Human Eye Color Highlights Genetic Association of Three New Loci

Previous studies have successfully identified genetic variants in several genes associated with human iris (eye) color; however, they all used simplified categorical trait information. Here, we quantified continuous eye color variation into hue and saturation values using high-resolution digital full-eye photographs and conducted a genome-wide association study on 5,951 Dutch Europeans from the Rotterdam Study. Three new regions, 1q42.3, 17q25.3, and 21q22.13, were highlighted meeting the criterion for genome-wide statistically significant association. The latter two loci were replicated in 2,261 individuals from the UK and in 1,282 from Australia. The LYST gene at 1q42.3 and the DSCR9 gene at 21q22.13 serve as promising functional candidates. A model for predicting quantitative eye colors explained over 50% of trait variance in the Rotterdam Study. Over all our data exemplify that fine phenotyping is a useful strategy for finding genes involved in human complex traits

Congenital Diarrhea and Cholestatic Liver Disease: Phenotypic Spectrum Associated with MYO5B Mutations

Myosin Vb (MYO5B) is a motor protein that facilitates protein trafficking and recycling in polarized cells by RAB11- and RAB8-dependent mechanisms. Biallelic MYO5B mutations are identified in the majority of patients with microvillus inclusion disease (MVID). MVID is an intractable diarrhea of infantile onset with characteristic histopathologic findings that requires life-long parenteral nutrition or intestinal transplantation. A large number of such patients eventually develop cholestatic liver disease. Bi-allelic MYO5B mutations are also identified in a subset of patients with predominant early-onset cholestatic liver disease. We present here the compilation of 114 patients with disease-causing MYO5B genotypes, including 44 novel patients as well as 35 novel MYO5B mutations, and an analysis of MYO5B mutations with regard to functional consequences. Our data support the concept that (1) a complete lack of MYO5B protein or early MYO5B truncation causes predominant intestinal disease (MYO5B-MVID), (2) the expression of full-length mutant MYO5B proteins with residual function causes predominant cholestatic liver disease (MYO5B-PFIC), and (3) the expression of mutant MYO5B proteins without residual function causes both intestinal and hepatic disease (MYO5B-MIXED). Genotype-phenotype data are deposited in the existing open MYO5B database in order to improve disease diagnosis, prognosis, and genetic counseling.This research was funded by Jubiläumsfonds der Österreichischen Nationalbank, grant no.16678 (to A.R.J.), grant no. 18019 (to G.-F.V.) and Tiroler Wissenschaftsfonds, grant No. 0404/2386 (toG.-F.V.).info:eu-repo/semantics/publishedVersio