Preterm birth (birth before week 37 of gestation) occurs in approximately 5-10% of all pregnancies. This value may be higher in certain population groups and has not decreased over the past 20-30 years. Although some preterm births may be elective, approximately 30% occur in association with an underlying infectious process, and about 50% are idiopathic preterm births of unknown cause. Preterm birth is associated with 70% of neonatal deaths, and up to 75% of neonatal morbidity. Infants born preterm have an increased incidence of blindness, deafness, cerebral palsy, neurological disorders and pulmonary disorders (Morrison, 1990;

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Cholesteryl ester transfer protein gene polymorphisms are associated with an increased risk of FLD in adolescent females. The effect is independent of adiposity in homozygotes, thereby placing lean individuals at a significant risk of FLD.

The amplitude, frequency and rate of rise of intra-uterine pressure cycles in rats (postpartum, ovariectomized) were unaffected by treatment with progesterone. Amplitude was also unaffected by a combination of treatments with progesterone and oestradiol-17 beta, which was adequate to ensure the survival of 84% of foetuses in ovariectomized pregnant rats. The failure of progesterone to influence myometerial activity could not be attributed to a lack of "true" progesterone receptors since these were present in the myometria of the test animals in concentrations exceeding those of oestrous animals. Evidence was obtained which suggested that a high-affinity binding protein, different from the "true" receptor may predominate in the myometrium of the pregnant rat. Oestradiol-17 beta in single or repeated doses of from 0.25 to 5 microgram, however, was found to reduce the frequency of pressure cycles but to increase significantly their rate of rise of pressure. There was a latency of 6--8 h in these effects of oestradiol. The possibility that inhibition of the myometrium by oestrogen may play a part in the preparation for parturition is discussed.

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