Placental and Cord Blood Markers Associated With Premature Birth and Disorders of Premature Birth in Newborn Infants
Condition: Premature Birth
MeSH terms: Premature Birth
Study type: Observational

Summary: 
      The purpose of this study is to determine if changes in specific gene products in the
      placenta or cord/infant blood affect a baby's birth weight, increase the risk of premature
      birth, or increase the risk of developing diseases of prematurity. We would also like to
      characterize whether placental epigenetic changes or placental markers of environmental
      exposures are associated with premature birth.
    

Detailed description: 
      Prematurity, diseases of prematurity and growth-disorders of newborn infants contribute
      significantly to morbidity and mortality seen in newborn infants [1,2,3]. One out of eight
      newborn infants in the USA is born premature (gestational age less than 37 completed weeks).
      In 2004, of the 27,860 infants dying within the first year of life, greater than 16,000 were
      born premature [2]. Moreover, premature infants who survive the neonatal period are at
      increased risk of cerebral palsy, developmental delays, growth impairment and long-term
      respiratory disability [3-5]. Additionally, fetal growth restriction and fetal growth excess
      results in infants being delivered as small for gestational age infants or large for
      gestational age infants, respectively. Infants born with such growth-disorders are at
      increased risk of perinatal morbidity and mortality and as adults are at significant risk of
      obesity, type II diabetes and heart disease [6,7].

      While the etiology of preterm birth and growth-disorders can be ascribed to maternal
      conditions, chromosomal defects or specific maternal environmental exposures in some newborn
      infants, for a majority the etiology remains unknown [8,9]. There is increasing evidence
      pointing to the role of genetic susceptibility factors in the causation of prematurity and
      growth-disorders of the newborn infant [8, 10-12]. Further, epigenetic changes in growth
      regulating or inflammatory genes in the placenta can program the fetus for premature birth,
      growth-disorders and other diseases in the postnatal period.

      The overall objective of this application is four-fold.

        1. To determine whether altered placental or fetal expression of imprinted genes is
           associated with disorders of growth, prematurity or other postnatal diseases in newborn
           infants.

        2. To determine whether altered placental expression of genes that regulate the innate
           immune response is associated with premature birth or other postnatal diseases in
           newborn infants.

        3. To determine whether placental markers of environmental exposure (such as Polycyclic
           Aromatic Hydrocarbons or PAH) or epigenetic changes in placental inflammatory genes or
           growth genes are associated with prematurity or postnatal diseases in newborn infants.

        4. To determine whether cord blood immune responses and markers of immune-cell function are
           different between preterm and term infants and are associated with postnatal diseases in
           preterm infants.
    

Observational model: Case-Control
Time perspective: Prospective
Sampling method: Probability Sample
Study population: 
        Infants who are born both premature (less than 37 weeks gestation) and full term infants
        (greater than 37 weeks gestation).
      
Biospecimen description: 
      whole blood, placenta
    
Keywords: Placenta; Cord Blood; PAH; Environmental Markers; Toll-Like Receptors