Elizabeth Dyson

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We have established a targeted loss-of-function mutation in the RXR alpha gene in the mouse germ line that results in embryonic lethality between E13.5 and E16.5 when bred to homozygosity. The major defect responsible for lethality is hypoplastic development of the ventricular chambers of the heart, which is manifest as a grossly thinned ventricular wall(More)
We have recently characterized a cardiac model of ventricular chamber defects in retinoid X receptor alpha (RXR alpha) homozygous mutant (-/-) gene-targeted mice. These mice display generalized edema, ventricular chamber hypoplasia, and muscular septal defects, and they die at embryonic day 15. To substantiate our hypothesis that the embryos are dying of(More)
BACKGROUND With the emphasis on the need for clinical governance and evidence-based practice in the healthcare industry there is increasing pressure on researchers to provide tangible research evidence of the effectiveness of new treatments, interventions and services. Recruiting an adequate size of sample is an important factor in the success or otherwise(More)
To study the molecular mechanisms that control patterning of the heart tube during early cardiogenesis, we have used the ventricular myosin regulatory light chain (MLC-2v), which is expressed in the ventricular segment of the primitive heart tube, as a genetic marker for ventricular specification in rodents. To assess whether the atrial isoform, MLC-2a,(More)
Primary care in England is being restructured and reorganized around primary care groups and primary care trusts, and a new system of clinical governance has been put in place to standardise levels of clinical care. There has been little exploration of the effect of these changes on the working practices of nurses in primary care. Telephone interviews were(More)
The vitamin A metabolite retinoic acid (RA) is utilized as a signalling molecule in wide variety of developmental processes, defined by defects which occur after nutritional vitamin A deficiency or after exposure to excess vitamin A. We have initiated a genetic analysis of RA function through the establishment of lines of mice which carry germline mutations(More)
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