Biology subjects

Iseler, J.

Publications and source records attributed to Iseler, J..

2 recordsLinked to original sources

bioRxiv2025

Burnout in nurses and biomarkers of stress, inflammation and neuroplasticity.

Burnout is an occupational challenge to the health, performance, and retention of healthcare personnel. The objective of this cross-sectional study was to further our understanding of the association between burnout, work, coping, and cognitive impairment as it relates to neuroendocrine, inflammatory, and neuroplastic disease mechanisms. One hundred hospital- based registered nurses responded to a validated survey addressing employment and work characteristics, coping, and cognitive impairment, and a one-item, burnout scale. In addition, they all provided blood samples. Nineteen percent of the nurses reported symptoms of evolving burnout and an additional 12% reported established burnout. Severity of burnout was inversely associated with self-rated energy (p<.001), ability to concentrate (p<.001), and positively associated with stressed at work (p<.001), but not with workplace cognitive impairment. The anti-inflammatory and pro-energetic biomarker interleukin-10 was elevated in respondents in the combined two highest burnout categories (mean 2.81, S.E.M. 0.26 pg/mL) vs. a median of 2.09 pg/mL in the no-burnout category (p<.02). When biomarkers in blood were regressed on severity of burnout, concentration of the anabolic hormone dehydroepiandrosterone-sulfate (standardized beta -.73, p=.007) and the neuronal strain biomarker neurofilament light chain (-.79, p=.01) inversely predicted burnout. In contrast, the ability to cope with a tough situation at work was positively associated with burnout (.75, p=.02). The study not only confirms the association between burnout and self-reported individual and work-related adverse outcomes but, importantly, burnout-relevant neuroendocrine, inflammatory, and neuronal biomarkers. Nurses suffering from burnout might exhibit dysfunctional coping resulting in decreased recognition of low energy, which accelerates the burnout process. It is proposed that assessment of biological disease mechanisms should play a larger role in both scholarly and clinical burnout work.

neuroscience↗

bioRxiv2023

Mechanosensitive recruitment of Vinculin maintains junction integrity and barrier function at epithelial tricellular junctions

Apical cell-cell junctions, including adherens junctions (AJs) and tight junctions (TJs), adhere epithelial cells to one another and regulate selective permeability at both bicellular junctions (BCJs) and tricellular junctions (TCJs). Although several specialized proteins are known to localize at TCJs, it remains unclear how actomyosin-mediated tension transmission at TCJs contributes to the maintenance of junction integrity and barrier function at these sites. Here, utilizing gastrula-stage Xenopus laevis embryos as a model system, we describe a mechanism by which Vinculin, a mechanosensitive protein, anchors the actomyosin network at TCJs, thus maintaining TJ stability and barrier function. Using an optogenetic approach, we found that acutely increasing junctional tension results in robust recruitment of Vinculin to apical junctions immediately surrounding TCJs. In Vinculin knockdown (KD) embryos, junctional actomyosin intensity is decreased and becomes disorganized at TCJs. Using fluorescence recovery after photobleaching (FRAP), we show that loss of Vinculin results in reduced Actin stability at TCJs. Vinculin knockdown also destabilizes Angulin-1, a key protein involved in regulating barrier function at TCJs. When Vinculin KD embryos are subjected to increased tension, TCJs cannot maintain their proper morphology. Finally, using a live imaging barrier assay, we detect increased barrier leaks at TCJs in Vinculin KD embryos. Together, our findings show that Vinculin-mediated actomyosin organization is required to maintain junction integrity and barrier function at TCJs and reveal new information about the interplay between adhesion and barrier function at TCJs. HighlightsO_LIVinculin is mechanosensitively recruited to tricellular junctions C_LIO_LIVinculins actin-binding function is needed for tricellular actomyosin organization C_LIO_LITricellular tight junctions are unstable when Vinculin is knocked down C_LIO_LIVinculin is required to maintain barrier function at tricellular junctions C_LI

cell biology↗