Abstract

Preterm labour continues to be a major contributor to neonatal and infant morbidity. Recent data from the USA indicate that the number of preterm deliveries (including those associated with preterm labour) has risen in the last 20 years by 30%. This increase is despite considerable efforts to introduce new therapies for the prevention and treatment of preterm labour and highlights the need to assess research in this area from a fresh perspective. In this paper we discuss i) the limitations of our knowledge concerning prediction, prevention and treatment of preterm labour and ii) future multidisciplinary strategies for improving our approach.

Highlights

  • Preterm labour continues to be a major contributor to neonatal and infant morbidity

  • Recent data from the USA indicate that the number of preterm deliveries has risen in the last 20 years by 30% [1,2], with the highest rates still affecting ethnic and racial minorities and women of low socio-economic status

  • We have demonstrated a significant increase in TRPC3, 4 and 6 protein in myometrial tissue from women in labour and have subsequently investigated potential stimuli responsible for inducing such changes [26]

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Summary

Background

Preterm labour continues to be a major contributor to neonatal and infant morbidity. Recent data from the USA indicate that the number of preterm deliveries (including those associated with preterm labour) has risen in the last 20 years by 30% (from 9.4% to 12.5%) [1,2], with the highest rates still affecting ethnic and racial minorities and women of low socio-economic status. Our current strategy has resulted in the development of common research themes and collaborative translational studies to address scientific and clinical questions concurrently One such theme is the understanding the role that inflammatory mediators play in preterm labour (Figure 2). Our recent studies have clearly demonstrated that IL1B, at concentration found in high vaginal swabs from women in preterm labour, increases the excitability of human uterine cells [28] within 24 hours of treatment. This timing is consistent with in vivo observations that IL1B induces contractions in animals within a similar timeframe [29]. A variety of 'omic' based technologies will be employed to provide insight into the temporal nature of biochemical events and potentially identify novel biomarkers for prediction of risk

Conclusion
Tribe RM
13. Jones G
Findings
23. Minke B

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