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Biomedical subjects

Rachel Moore

Publications and source records attributed to Rachel Moore.

2 recordsLinked to original sources

A comparison of fetal organ measurements by echo-planar magnetic resonance imaging and ultrasound.

OBJECTIVES: To compare fetal organ size measured using echo-planar magnetic resonance imaging and 2D ultrasound. To determine the relative accuracy with which each technique can predict fetal growth restriction. DESIGN: A cross sectional, observational study comparing two different measurement techniques against a gold standard, in a normal clinical population and an abnormal population. SETTING AND POPULATION: Seventy-four pregnant women (33 who were ultimately found to be normal and 37 with fetal growth restricted fetuses) were recruited from the City Hospital Nottingham UK to be scanned once (at various gestations). METHODS: Each fetus had a standard ultrasound biometry assessment followed by magnetic resonance imaging measurement of organ volumes. MAIN OUTCOME MEASURES: For each measurement for both techniques, the normal population was plotted with 90% confidence intervals. Fetal growth restricted subjects were compared with the normal population using this plot; 2 x 2 tables were created for each measurement. This was used to calculate the relative sensitivities and positive predictive value of the different measurements. A Bland-Altman plot was used to compare the ultrasound and magnetic resonance imaging measurements of fetal weight. RESULTS: Brain sparing was seen in ultrasonic head circumference measurements, but an overall reduction in fetal growth restriction brain volume was apparent using magnetic resonance imaging at late gestations. Across the whole range of gestational ages, ultrasound assessment of fetal weight was the best predictor of fetal growth restriction. CONCLUSION: Ultrasound fetal weight assessment appears to identify more fetuses with fetal growth restriction than abdominal circumference. The brain sparing apparent in ultrasonic head circumference measurements of fetuses with fetal growth restriction masks a reduction in brain volume observed with magnetic resonance imaging.

Abdomen↗

Blocking endogenous FGF-2 activity prevents cranial osteogenesis.

Normal growth and morphogenesis of the cranial vault reflect a balance between cell proliferation in the sutures and osteogenesis at the margins of the cranial bones. In the clinical condition craniosynostosis, the sutures fuse prematurely as a result of precocious osteogenic differentiation and craniofacial malformation results. Mutations in several fibroblast growth factor receptor (FGFR) genes have now been identified as being responsible for the major craniosynostotic syndromes. We have used a grafting technique to manipulate the levels of endogenous FGF-2 ligand in embryonic chick cranial vaults and thereby perturb morphogenesis. Implantation of beads loaded with FGF-2 did not affect normal cranial development at physiological concentrations, although they elicited a morphogenetic response in the limb. Implantation of beads loaded with a neutralising antibody to FGF-2 generated a concentration-dependent response. When a single bead was implanted, the grafts grew to a massive size as a result of increased cell division in the tissue. With greater inactivation of FGF-2 protein (two to three beads implanted), all further bone differentiation and cell proliferation was blocked. These data further support the emerging idea that the intensity of FGF-mediated signalling determines the developmental fate of the skeletogenic cells in the cranial vault. High and low levels correlate with differentiation and proliferation, respectively. A balance between the two ensures normal cranial vault morphogenesis. This is consistent with the observation that several FGFR mutations causing craniosynostosis result in constitutive activation of the receptor.

Animals↗