Relativistic Multiconfigurational Ab Initio Calculation of Uranyl 3d4f Resonant Inelastic X-ray Scattering

We applied relativistic multiconfigurational all-electron ab initio calculations including the spin−orbit interaction to calculate the 3d4f resonant inelastic X-ray scattering (RIXS) map (3d3/2 →5f5/2 U M 4 absorption edge and 4f5/2 →3d3/2 U M βemission) of uranyl (UO22+). The calculated data are in excellent agreement with experimental results and allow a detailed understanding of the observed features and an unambiguous assignment of all involved intermediate and final states. The energies corresponding to the maxima of the resonant emission and the non-resonant (normal) emission were determined with high accuracy, and the corresponding X-ray absorption near edge structure spectra extracted at these two positions were simulated and agree well with the measured data. With the high quality of our theoretical data, we show that the cause of the splitting of the three main peaks in emission is due to the fine structure splitting of the 4f orbitals induced through the trans di-oxo bonds in uranyl and that we are able to obtain direct information about the energy differences between the 5f and 4f orbitals: Δ5f δ/φ−4f δ/φ, Δ5f π*−4f π, and Δ5f σ*−4f σfrom the 3d4f RIXS map. RIXS maps contain a wealth of information, and ab initio calculations facilitate an understanding of their complex structure in a clear and transparent way. With these calculations, we show that the multiconfigurational protocol, which is nowadays applied as a standard tool to study the X-ray spectra of transition metal complexes, can be extended to the calculation of RIXS maps of systems containing actinides

Sterol regulatory element-binding proteins are regulators of the rat thyroid peroxidase gene in thyroid cells

Sterol regulatory element-binding proteins (SREBPs)-1c and -2, which were initially discovered as master transcriptional regulators of lipid biosynthesis and uptake, were recently identified as novel transcriptional regulators of the sodium-iodide symporter gene in the thyroid, which is essential for thyroid hormone synthesis. Based on this observation that SREBPs play a role for thyroid hormone synthesis, we hypothesized that another gene involved in thyroid hormone synthesis, the thyroid peroxidase (TPO) gene, is also a target of SREBP-1c and -2. Thyroid epithelial cells treated with 25-hydroxycholesterol, which is known to inhibit SREBP activation, had about 50% decreased mRNA levels of TPO. Similarly, the mRNA level of TPO was reduced by about 50% in response to siRNA mediated knockdown of both, SREBP-1 and SREBP-2. Reporter gene assays revealed that overexpression of active SREBP-1c and -2 causes a strong transcriptional activation of the rat TPO gene, which was localized to an approximately 80 bp region in the intron 1 of the rat TPO gene. In vitro- and in vivo-binding of both, SREBP-1c and SREBP-2, to this region in the rat TPO gene could be demonstrated using gel-shift assays and chromatin immunoprecipitation. Mutation analysis of the 80 bp region of rat TPO intron 1 revealed two isolated and two overlapping SREBP-binding elements from which one, the overlapping SRE+609/InvSRE+614, was shown to be functional in reporter gene assays. In connection with recent findings that the rat NIS gene is also a SREBP target gene in the thyroid, the present findings suggest that SREBPs may be possible novel targets for pharmacological modulation of thyroid hormone synthesis

The dual of pure non-Abelian lattice gauge theory as a spin foam model

We derive an exact duality transformation for pure non-Abelian gauge theory regularized on a lattice. The duality transformation can be applied to gauge theory with an arbitrary compact Lie group G as the gauge group and on Euclidean space-time lattices of dimension d >= 2. It maps the partition function as well as the expectation values of generalized non-Abelian Wilson loops (spin networks) to expressions involving only finite-dimensional unitary representations, intertwiners and characters of G. In particular, all group integrations are explicitly performed. The transformation maps the strong coupling regime of non-Abelian gauge theory to the weak coupling regime of the dual model. This dual model is a system in statistical mechanics whose configurations are spin foams on the lattice.Comment: 28 pages, LaTeX + PicTeX; typographical errors correcte

The role of Austrian Airlines within the Lufthansa Group

12th International Conference on Air Transport – INAIR 2023, The Future of Aviation – is the Sky the Limit? 15-17 November 2023, Tartu, EstoniaAustrian Airlines is a relatively small but important part of the Lufthansa Group, and is to some extent overshadowed by its much larger German owner, together with its higher profile Swiss International Airlines compatriot and neighbour. Even so, Austrian is not as small as the group's other network carrier member Brussels Airlines. The group's low-cost point-to-point carrier Eurowings is not closely considered in this paper as the primary focus here is on a network carrier analysis, with Austrian positioned as the main case study subject. In this regard, Austrian delivers a hub-and-spoke network out of Vienna International Airport (VIE) which both compliments and strengthens the overall group's scale, scope and density. Austrian contributes a substantial boost to the Lufthansa Group in Central and Eastern Europe, though this has been reduced as a result of the ongoing war in Ukraine, including Russian air space closure. Austrian's future prospects are closely aligned with events in Ukraine, with an end to the war likely to see the airline well positioned to resume services quite quickly to Ukraine, Belarus and Russia. The study here finds that Austrian Airlines clearly maintains a symbiotic relationship with its parent company, rather than a dependency on the wider group for its survival, though it would likely be a smaller airline if it was not part of the Lufthansa Group. They compliment each other

High-Fat Diet Induces Unexpected Fatal Uterine Infections in Mice with aP2 -Cre-mediated Deletion of Estrogen Receptor Alpha

Estrogen receptor alpha (ERα) is a major regulator of metabolic processes in obesity. In this study we aimed to define the relevance of adipose tissue ERα during high-fat diet (HFD)-induced obesity using female aP2-Cre−/+/ERαfl/fl mice (atERαKO). HFD did not affect body weight or glucose metabolism in atERαKO- compared to control mice. Surprisingly, HFD feeding markedly increased mortality in atERαKO mice associated with a destructive bacterial infection of the uterus driven by commensal microbes, an alteration likely explaining the absence of a metabolic phenotype in HFD-fed atERαKO mice. In order to identify a mechanism of the exaggerated uterine infection in HFD-fed atERαKO mice, a marked reduction of uterine M2-macrophages was detected, a cell type relevant for anti-microbial defence. In parallel, atERαKO mice exhibited elevated circulating estradiol (E2) acting on E2-responsive tissue/cells such as macrophages. Accompanying cell culture experiments showed that despite E2 co-administration stearic acid (C18:0), a fatty acid elevated in plasma from HFD-fed atERαKO mice, blocks M2-polarization, a process known to be enhanced by E2. In this study we demonstrate an unexpected phenotype in HFD-fed atERαKO involving severe uterine bacterial infections likely resulting from a previously unknown negative interference between dietary FAs and ERα- signaling during anti-microbial defence

Acyl-CoA Dehydrogenase Drives Heat Adaptation by Sequestering Fatty Acids

Cells adapt to temperature shifts by adjusting levels of lipid desaturation and membrane fluidity. This fundamental process occurs in nearly all forms of life, but its mechanism in eukaryotes is unknown. We discovered that the evolutionarily conserved C. elegans gene acdh-11 (acyl CoAdehydrogenase, ACDH) facilitates heat adaptation by regulating the lipid desaturase FAT-7. Human ACDH deficiency causes the most common inherited disorders of fatty acid oxidation, with syndromes that are exacerbated by hyperthermia. Heat up-regulates acdh-11 expression to decrease fat-7 expression. We solved the high-resolution crystal structure of ACDH-11 and established the molecular basis of its selective and high-affinity binding to C11/C12-chain fatty acids. ACDH-11 sequesters C11/C12-chain fatty acids and prevents these fatty acids from activating nuclear hormone receptors and driving fat-7 expression. Thus, the ACDH-11 pathway drives heat adaptation by linking temperature shifts to regulation of lipid desaturase levels and membrane fluidity via an unprecedented mode of fatty acid signaling.National Institutes of Health (U.S.) (Grants GM24663 and K99HL11665)Charles A. King Trust (Postdoctoral Fellowship