Biology subjects

Wilhelm, I.

Publications and source records attributed to Wilhelm, I..

4 recordsLinked to original sources

bioRxiv2026

REM Sleep Iota Oscillations Across the Lifespan

Iota oscillations are a newly discovered marker of wakefulness and rapid eye movement (REM) sleep. So far, iota in REM sleep has only been reported in the surface electroencephalography (EEG) of a small sample of young adults and in intracranial recordings of epileptic patients. Here, we investigated the presence of these oscillations in a large dataset (N=937) of high-density sleep EEG recordings from individuals 7 to 70 years old. We found that iota spectral peaks during REM sleep were between 25 and 40 Hz, slightly faster than in wake (25-35 Hz). Iota power was significantly associated with REM sleep architecture, increasing with both REM duration and across progressive sleep cycles. Iota peaks were observed in individuals of all ages, although the prevalence decreased gradually with age, from 88% in children to 44% in older adults. Most iota spectral peak properties (frequency, amplitude, timing, topography) likewise shifted with age. The most striking effect, however, was in bandwidth, such that children had narrow iota peaks, older adults had broad iota peaks, and 20-30 year olds could have either. It remains unclear whether narrowband and broadband iota are functionally equivalent. On shorter time scales (< 1 year), iota properties remained stable across measurements. Analyses of a separate dataset of monozygotic and dizygotic twins revealed high heritability of all iota peak properties except bandwidth. Overall, these results establish iota as a genetically determined trait-like marker of REM sleep with unique age-related changes. Iota oscillations open new avenues to investigate the interaction between sleep, genetics, development, and aging.

neuroscience↗

bioRxiv2026

Extracellular vesicles from triple negative breast cancer cells disrupt the blood-brain barrier via miR-146a-5p- and TGF-β1-mediated downregulation of endothelial Paqr5

Brain metastases are a common and often fatal complication of certain cancer types, such as triple-negative breast cancer. However, the molecular pathways driving brain metastasis formation, including the migration of cancer cells from the bloodstream to the brain parenchyma across the blood-brain barrier, are not yet fully defined. Therefore, using highly relevant mouse and human model systems, the mechanisms by which triple-negative breast cancer cells and their released extracellular vesicles modulate the blood-brain barrier-forming endothelium to increase its permissiveness to tumour cell entry into the brain are investigated. It is observed that extracellular vesicles derived from tumour cells are taken up by cerebral endothelial cells, where they induce miR-146a-5p- and TGF-{beta}1-mediated downregulation of PAQR5/mPR{gamma}, a membrane progesterone receptor. This, in turn, leads to disruption of interendothelial tight junctions, particularly through repression of claudin-5 expression, a critical protein for maintaining barrier function. Altogether this identifies a novel mechanism by which triple-negative breast cancer-derived extracellular vesicles compromise blood-brain barrier integrity, thereby facilitating transendothelial migration of cancer cells and promoting brain metastasis development. Moreover, this study is the first to highlight the role of membrane progesterone receptors in regulating the blood-brain barrier. Table of contents O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=136 SRC="FIGDIR/small/701753v2_ufig1.gif" ALT="Figure 1"> View larger version (46K): org.highwire.dtl.DTLVardef@113c0a8org.highwire.dtl.DTLVardef@1cd5625org.highwire.dtl.DTLVardef@1d2b3c2org.highwire.dtl.DTLVardef@178a97_HPS_FORMAT_FIGEXP M_FIG Extracellular vesicles from triple-negative breast cancer cells induce miR-146a-5p- and TGF-1-mediated downregulation of PAQR5/mPR{gamma}, a membrane progesterone receptor, in blood-brain barrier-forming endothelial cells. This results in disruption of interendothelial tight junctions, thereby promoting enhanced migration of cancer cells into the brain. This mechanism highlights the role of membrane progesterone receptors in regulating the blood-brain barrier. C_FIG

cancer biology↗

bioRxiv2020

Selective REM-Sleep Suppression Increases Next-Day Negative Affect and Amygdala Responses to Social Exclusion

Healthy sleep, positive general affect, and the ability to regulate emotional experiences are fundamental for well-being. In contrast, various mental disorders are associated with altered rapid eye movement (REM) sleep, negative affect, and diminished emotion regulation abilities. However, the neural processes mediating the relationship between these different phenomena are still not fully understood. In the present study of 42 healthy volunteers, we investigated the effects of selective REM sleep suppression (REMS) on general affect, as well as on feelings of social exclusion, emotion regulation, and their neural underpinnings. Using functional magnetic resonance imaging we show that REMS increases amygdala responses to experimental social exclusion, as well as negative affect on the morning following sleep deprivation. There was no evidence that emotional responses to experimentally induced social exclusion or their regulation using cognitive reappraisal were impacted by diminished REM sleep. Our findings indicate that general affect and amygdala activity depend on REM sleep, while specific emotional experiences possibly rely on additional psychological processes and neural systems that are less readily influenced by REMS.

neuroscience↗

bioRxiv2019

Pseudomonas aeruginosa lectin LecB impairs keratinocyte fitness by abrogating growth factor signalling

Lectins are glycan-binding proteins with no catalytic activity and ubiquitously expressed in nature. Numerous bacteria employ lectins to efficiently bind to epithelia, thus facilitating tissue colonisation. Wounded skin is one of the preferred niches for Pseudomonas aeruginosa, which has developed diverse strategies to impair tissue repair processes and promote infection.\n\nHere, we analyse the effect of the P. aeruginosa fucose-binding lectin LecB on human keratinocytes and demonstrate that it triggers events in the host, upon binding to fucosylated residues on cell membrane receptors, that extend beyond its role as an adhesion molecule. We found that LecB associates with several growth factor receptors and dampens their signalling pathways, leading to the arrest of cell cycle. Additionally, we describe a novel LecB-triggered mechanism to downregulate host cell receptors by showing that LecB leads to insulin-like growth factor receptor 1 internalisation, without receptor activation, and subsequent missorting towards intracellular endosomal compartments.\n\nOverall, these data highlight that LecB is a multitask virulence factor that, through subversion of several host pathways, has a profound impact on keratinocyte proliferation and survival.

cell biology↗