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Vol. 7 No. 3, March 2006
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NeoReviews Vol.7 No.3 2006 e151
© 2006 American Academy of Pediatrics

Understanding the Timing of Birth

The Continuing Challenge to Prevent Prematurity

Jeffrey D. Roizen*
Louis J. Muglia, MD, PhD*

* Department of Pediatrics, Washington University School of Medicine, St. Louis, Mo

Abbreviations: CRH: corticotropin-releasing hormone • COX: cyclooxygenase • cPLA2: cytosolic phospholipase A2 • FP receptor: PGF2alpha receptor • HKE: heat-killed Escherichia coli • HPA axis: hypothalamic-pituitary-adrenal axis • KO: knockout • LH: luteinizing hormone • PG: prostaglandin • SCN: suprachiasmatic nucleus • 15-PGDH: 15-prostaglandin dehydrogenase • 20 alpha-HSD: 20 alpha-hydroxysteroid dehydrogenase

The first 300 words of the full text of this article appear below.


    Objectives
 
After completing this article, readers should be able to:

  1. Delineate the frequency and increasing incidence of preterm birth.
  2. Describe models for determining the timing of birth based on interacting interval and circadian timers.
  3. Explain differences in mechanisms for labor induction between humans and nonprimate mammals.
  4. Describe conserved pathways for labor in humans and nonprimate mammals.
  5. Delineate promising avenues for future study of human preterm birth.


    Introduction
 
Preterm birth is the primary cause of neonatal morbidity and mortality, occurring in approximately 10% of all births and affecting almost 500,000 infants in the United States annually. Although medical progress over the past 30 years has dramatically improved survival for these infants, their birth occurring at a time of central nervous system, pulmonary, and gastrointestinal immaturity still predisposes them to long-term cognitive and physical impairments. Intervention focusing on preventing preterm birth is an ideal strategy for alleviating this problem. However, despite receiving considerable attention, the mechanisms underlying the timing of normal labor and the pathogenesis of preterm labor remain obscure. Progress has been made in identifying the roles of infection, uterine structural anomalies, and fetal or maternal stress in prematurity, but the preterm birth rate has increased 27% since 1981 in the United States. Approximately 50% of human preterm births have no clear medical causes, but racial disparities in preterm labor rates independent of geographic, maternal medical, and socioeconomic factors suggest a significant genetic contribution to the timing of labor. The grouping of the timing of births in different pregnancies in the same mother strengthens the suggestion of a significant genetic contribution to the timing of labor. In this article, we review data regarding the timing of term labor and preterm labor, with a specific focus on relevance to human labor.


    The Causes of Prematurity
 
Many identifiable factors contribute to human preterm birth. Placental abruption, multiple gestation pregnancy, . . . [Full Text of this Article]







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