Biology subjects

Davenport, A.

Publications and source records attributed to Davenport, A..

3 recordsLinked to original sources

bioRxiv2025

Magnetoencephalography Reveals Neuroprotective Effects of COVID-19 Vaccination in Non-Human Primates

SUMMARY PARAGRAPHCOVID-19, caused by the SARS-CoV-2 virus, can lead to widespread neurological complications, including cognitive deficits and neurodegenerative symptoms, even in the absence of significant structural brain abnormalities. The potential neuroprotective effects of SARS-CoV-2 vaccination remain underexplored. Here, we demonstrate the neuroprotective effects of a psoralen-inactivated SARS-CoV-2 vaccine in a non-human primate model using resting-state magnetoencephalography (MEG), a non-invasive neurophysiological recording technique with sub-millisecond temporal and submillimeter spatial resolution. MEG scans demonstrated substantial preservation of neural activity across multiple brain regions in vaccinated subjects compared to unvaccinated controls following viral challenge. This approach not only underscores the role of vaccination in mitigating severe neurological outcomes but also highlights the capability of MEG to detect subtle yet significant changes in brain function that may be overlooked by other imaging modalities. These findings advance our understanding of vaccine-induced neuroprotection and establish MEG as a powerful tool for monitoring brain function in the context of viral infections.

neuroscience↗

bioRxiv2024

Low maternal plasma apelin in the second trimester is associated with adverse pregnancy outcome in severe, early-onset fetal growth restriction

ContextFetal growth restriction increases adverse pregnancy outcomes such as preterm birth and intrauterine fetal death. Apelin is a secreted peptide expressed in placental syncytiotrophoblast and downregulated in fetal growth restriction. ObjectivesWe tested the hypothesis that adverse pregnancy outcome is associated with low maternal plasma apelin at diagnosis of early-onset fetal growth restriction. MethodsPlasma samples and fetomaternal blood flow Doppler velocimetry measurements were obtained from pregnant women (n=59) at diagnosis of early-onset fetal growth restriction in the second trimester. Plasma apelin was determined by ELISA and pregnancy outcome was recorded. Placental gene expression was analysed after birth by qRT-PCR, compared to term placentas from women with late-onset fetal growth restriction or with appropriate-for-gestational age infants. ResultsAt diagnosis of early-onset fetal growth restriction, plasma apelin concentration was significantly lower in women who delivered extremely preterm (<28 weeks gestation) or had an intrauterine fetal death, compared to women who had a livebirth[≥]28 weeks (P<0.05). Plasma apelin correlated directly with uterine artery volume flow rate and inversely with pulsatility index. Placental gene expression of apelin, but not the apelin receptor or elabela, was lower in women with early-onset fetal growth restriction delivering preterm than in appropriate-for-gestational-age, term control women. ConclusionLow maternal circulating apelin during the second trimester is associated with impaired uteroplacental perfusion and subsequent adverse pregnancy outcome in severe, early-onset fetal growth restriction. Placental apelin deficiency may contribute mechanistically to the pathogenesis of early-onset fetal growth restriction.

physiology↗

bioRxiv2024

Vestigial like 4 regulates the adipogenesis of classical brown adipose tissue

Brown adipose tissue (BAT) is mammals primary non-shivering thermogenesis organ, and the molecular mechanisms regulating BAT growth and adipogenesis are largely unknown. The Hippo-YAP pathway has been well-known for controlling organ size, and Vestigial like 4 (VGLL4) is a transcriptional regulator that modulates the Hippo-YAP pathway by competing against YAP for binding to TEAD proteins. In this study, we dissected the function of VGLL4 in regulating BAT development. We generated a conventional Vgll4 mutant mouse line, in which the two Tondu (TDU) domains of VGLL4 were disrupted. We found that deletion of the TDU domains of VGLL4 resulted in perinatal lethality and paucity of the interscapular BAT. Histological and magnetic resonance imaging studies confirmed that the adipogenesis of BAT was impaired in Vgll4 mutants. Adeno-associated virus (AAV) mediated, brown adipocyte-specific overexpression of VGLL4 increased BAT volume and protected the adult male mice from acute cold stress. Genomic studies suggest that VGLL4/TEAD1 complex directly regulates the myogenic and adipogenic gene expression programs of BAT. In conclusion, our data identify VGLL4 as a previously unrecognized adipogenesis factor that regulates classical BAT development.

developmental biology↗