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Biomedical subjects

G E Moore

Publications and source records attributed to G E Moore.

At least 361 records · Page 20Linked to original sources
PubMedDate not supplied

The effects of distension of the small intestine on myocardial blood flow in anaesthetised cats: possible relevance to coronary vasospasm.

The haemodynamic effects of distending the small intestine (with a balloon in the lumen) were examined in cats anaesthetised with chloralose. Particular attention was paid to blood flow changes in localised areas of the left ventricular wall (as assessed using the heated thermocouple technique). Intestinal distension led to an increase in systemic blood pressure but usually to a reduction in myocardial blood flow; no cardiac dysrhythmias were observed. When the effect of increased systemic (perfusion) pressure on blood flow was eliminated (using partial correlation coefficients) flow then bore a negative relationship to intestinal pressure, probably indicating constriction of the myocardial blood vessles. This may indicate that distension of hollow organs can lead to a visceral-cardiac reflex. The resulting coronary vasospasm might be one cause of pain in certain patients with angina pectoris.

Animals↗
PubMedDate not supplied

Linkage of an X-chromosome cleft palate gene.

Many congenital malformations, such as cleft palate and neural tube defects, have a multifactorial origin involving both environmental and genetic factors. Conditions such as these may be exclusively monogenic, polygenic or environmental, but in most cases both genetic and environmental factors are involved. This study describes the sub-chromosomal localization of a single gene defect causing cleft palate and ankyloglossia (tongue-tied) in a large Icelandic family. This defect is a model for the analysis of other neural-crest malformations that show a more complex multifactorial inheritance pattern.

Cleft Palate↗
PubMedDate not supplied

Human EGFR, a candidate gene for the Silver-Russell syndrome, is biallelically expressed in a wide range of fetal tissues.

Maternal uniparental disomy of chromosome 7 (mUPD7) has been reported in around 10% of cases of Silver-Russell syndrome (SRS). This suggests that at least one gene on chromosome 7 is imprinted and involved in the pathogenesis of this condition. One candidate is epidermal growth factor receptor (EGFR) which maps to chromosome 7p12, a region homologous to an imprinted region on mouse chromosome 11. Using a restriction fragment length polymorphism, biallelic expression of EGFR was found in a range of normal human fetal tissues. Expression was also demonstrated in fibroblasts and lymphoblasts from SRS patients with mUPD7. Thus no evidence that EGFR is imprinted was found, making its involvement in SRS unlikely. However, EGFR was shown to be widely expressed in the human fetus, evidence that this gene plays an important role in early development.

Abnormalities, Multiple↗