Helen N Jones

This study shows that maternal cortisol elevation due to stress mediates fetal growth restriction in undernourished guinea pigs, beyond just nutrient limitation.

This study examines extracellular vesicles and miRNA profiles in maternal and umbilical cord plasma from pregnancies with fetal congenital heart defects compared to controls, finding altered EV counts and miRNA levels.

This study shows repeated nanoparticle-mediated IGF1 treatment corrects aberrant placental structure in a guinea pig model of fetal growth restriction, improving fetal growth and placental function.

This study examines the effects of trophoblast stress and hIGF1 nanoparticle gene therapy on gene and protein expression in fetal liver and kidney cells using a co-culture model.

This study shows that placental hIGF1 nanoparticle treatment in guinea pigs reduces FGR-related kidney structural and signaling pathway changes.

This study shows that placental hIGF1 nanoparticle gene therapy in guinea pigs reduces FGR-associated liver metabolic dysregulation in a fetal sex-specific manner.

This study investigates placental IGF1 signaling and nutrient transport in a guinea pig model of FGR with nanoparticle-mediated IGF1 treatment, showing sex-specific changes and supporting therapeutic potential.

This study examines placental transcriptome changes in a guinea pig model of placental insufficiency with and without hIGF1 nanoparticle treatment, identifying key signaling and metabolic pathways affected.

This paper demonstrates that placental nanoparticle-mediated IGF1 gene therapy corrects fetal growth restriction in a guinea pig model by improving fetal weight, blood glucose, and reducing cortisol levels.

This study identifies transcriptome changes in the sub-placenta/decidua associated with placental insufficiency and shows that hIGF1 nanoparticle treatment alters gene expression related to trophoblast invasion and homeostasis.

The paper constructs a genome-scale transcriptional regulatory network of the human placenta using genomic and transcriptomic data, identifying key regulators of preterm birth.

This study delivers hIGF1-loaded nanoparticles to the placenta of a pregnant rhesus macaque via uterine artery catheterization, showing successful placental uptake and expression of hIGF1.

This study shows that HAND1 knockdown affects gene expression in trophoblast cells but not endothelial cells, highlighting the importance of extra-embryonic tissue in CHD research.

The paper identifies potential targeting moieties for placental therapeutics by comparing proteomes of normal and intrauterine growth restricted placentas.

This study shows that Hand1 deficiency in mice leads to impaired placental labyrinth formation and vascularization, causing embryonic lethality and linking Hand1 to placental development in CHD.

The paper identifies unique transcriptomic signatures in idiopathic spontaneous and infection-related preterm births compared to normal term births, highlighting differences in IGF signaling and inflammation.