Numerical proceeding to calculate impurity states in 2D semiconductor heterostructures.

The article provides and discusses details of numerical proceeding for the expansion method to calculate energy positions and wave functions of the localized and resonant electronic states emerging in quantum well-type semiconductor nanostructures because of perturbation of confined states by the Coulomb potential of the hydrogenic impurity center. Effective mass approximation is used. Several excited both resonant and non-resonant states are calculated and classified for the case of a simple rectangular GaAs/AlGaAs quantum well.

Remodeling of the chromatin landscape in peripheral blood cells in patients with severe Delta COVID-19.

COVID-19 is characterized by systemic pro-inflammatory shifts with the development of serious alterations in the functioning of the immune system. Investigations of the gene expression changes accompanying the infection state provide insight into the molecular and cellular processes depending on the sickness severity and virus variants. Severe Delta COVID-19 has been characterized by the appearance of a monocyte subset enriched for proinflammatory gene expression signatures and a shift in ligand-receptor interactions.

Pulmonary maternal immune activation does not cross the placenta but leads to fetal metabolic adaptation.

The fetal development of organs and functions is vulnerable to perturbation by maternal inflammation which may increase susceptibility to disorders after birth. Because it is not well understood how the placenta and fetus respond to acute lung- inflammation, we characterize the response to maternal pulmonary lipopolysaccharide exposure across 24 h in maternal and fetal organs using multi-omics, imaging and integrative analyses. Unlike maternal organs, which mount strong inflammatory immune responses, the placenta upregulates immuno-modulatory genes, in particular the IL-6 signaling suppressor Socs3.

TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1.

Limitation of excessive inflammation due to selective degradation of pro-inflammatory proteins is one of the cytoprotective functions attributed to autophagy. In the current study, we highlight that selective autophagy also plays a vital role in promoting the establishment of a robust inflammatory response. Under inflammatory conditions, here TLR3-activation by poly(I:C) treatment, the inflammation repressor TNIP1 (TNFAIP3 interacting protein 1) is phosphorylated by Tank-binding kinase 1 (TBK1) activating an LIR motif that leads to the selective autophagy-dependent degradation of TNIP1, supporting the expression of pro-inflammatory genes and proteins.

Identification of ester-linked ubiquitylation sites during TLR7 signalling increases the number of inter-ubiquitin linkages from 8 to 12.

The E3 ligase HOIL-1 forms ester bonds in vitro between ubiquitin and serine/threonine residues in proteins. Here, we exploit UbiSite technology to identify serine and threonine residues undergoing HOIL-1 catalysed ubiquitylation in macrophages stimulated with R848, an activator of the TLR7/8 heterodimer. We identify Thr12, Thr14, Ser20 and Thr22 of ubiquitin as amino acid residues forming ester bonds with the C-terminal carboxylate of another ubiquitin molecule.