Long non-coding RNAs direct the SWI/SNF complex to cell type-specific enhancers.

The coordination of chromatin remodeling is essential for DNA accessibility and gene expression control. The highly conserved and ubiquitously expressed SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex plays a central role in cell type- and context-dependent gene expression. Despite the absence of a defined DNA recognition motif, SWI/SNF binds lineage specific enhancers genome-wide where it actively maintains open chromatin state.

Adaptive emotion regulation might prevent burnout in emergency healthcare professionals: an exploratory study.

Background: Emergency department (ED) professionals face a high risk of physical, mental, and emotional strain, which can lead to burnout. Burnout arises from chronic work-related stress, which negatively impacts ED professionals, the healthcare system, as well as patient outcomes. Effective adaptive emotion regulation strategies (ERS) are crucial for handling stress in healthcare workplaces and mitigating the risk of burnout.

RUNX1 interacts with lncRNA SMANTIS to regulate monocytic cell functions.

Monocytes, the circulating macrophage precursors, contribute to diseases like atherosclerosis and asthma. Long non-coding RNAs (lncRNAs) have been shown to modulate the phenotype and inflammatory capacity of monocytes. We previously discovered the lncRNA SMANTIS, which contributes to cellular phenotype expression by controlling BRG1 in mesenchymal cells.

[The role of mental health support for medical students.].

Introduction: The mental health of medical students is of critical importance during their medical studies, which can be a long and challenging period. Academic expectations, high workload, and emotional stress can contribute to mental burden and burnout among medical students, placing an increased burden on the healthcare system in the future. Therefore, psychological support and mental health services play a crucial role in medical education.

Long non-coding RNA PCAT19 safeguards DNA in quiescent endothelial cells by preventing uncontrolled phosphorylation of RPA2.

In healthy vessels, endothelial cells maintain a stable, differentiated, and growth-arrested phenotype for years. Upon injury, a rapid phenotypic switch facilitates proliferation to restore tissue perfusion. Here we report the identification of the endothelial cell-enriched long non-coding RNA (lncRNA) PCAT19, which contributes to the proliferative switch and acts as a safeguard for the endothelial genome.