Assessing the stability of psychobiological stress reactivity during adolescence: mixed-effect modelling of cortisol responses to laboratory stressors.

Background: Puberty has been historically considered as a time of risk and vulnerability for young people. It is associated with rapid development in the hypothalamus, which is central in the production of both stress and sex steroids. While patterns of stress reactivity are calibrated in early life, this time of rapid development may provide a means for these patterns to change.

Probing and manipulating the Mexican hat-shaped valence band of InSe.

Ferroelectrics based on van der Waals semiconductors represent an emergent class of materials for disruptive technologies ranging from neuromorphic computing to low-power electronics. However, many theoretical predictions of their electronic properties have yet to be confirmed experimentally and exploited. Here, we use nanoscale angle-resolved photoemission electron spectroscopy and optical transmission in high magnetic fields to reveal the electronic band structure of the van der Waals ferroelectric indium selenide (α-InSe).

A dual role of Cohesin in DNA DSB repair.

Cells undergo tens of thousands of DNA-damaging events each day. Defects in repairing double-stranded breaks (DSBs) can lead to genomic instability, contributing to cancer, genetic disorders, immunological diseases, and developmental defects. Cohesin, a multi-subunit protein complex, plays a crucial role in both chromosome organization and DNA repair by creating architectural loops through chromatin extrusion.

Discovery of a DNA methylation profile in individuals with Sifrim-Hitz-Weiss syndrome.

Pathogenic heterozygous variants in CHD4 cause Sifrim-Hitz-Weiss syndrome, a neurodevelopmental disorder associated with brain anomalies, heart defects, macrocephaly, hypogonadism, and additional features with variable expressivity. Most individuals have non-recurrent missense variants, complicating variant interpretation. A few were reported with truncating variants, and their role in disease is unclear.

STAT5B leukemic mutations, altering SH2 tyrosine 665, have opposing impacts on immune gene programs.

STAT5B is a vital transcription factor for lymphocytes. Here, function of two STAT5B mutations from human T cell leukemias: one substituting tyrosine 665 with phenylalanine (STAT5B), the other with histidine (STAT5B) was interrogated. modeling predicted divergent energetic effects on homodimerization with a range of pathogenicity.