Placental and Cord Blood Markers Associated With Premature Birth and Disorders of Premature Birth in Newborn Infants
| Status: | Completed |
|---|---|
| Conditions: | Women's Studies |
| Therapuetic Areas: | Reproductive |
| Healthy: | No |
| Age Range: | Any |
| Updated: | 4/21/2016 |
| Start Date: | June 2009 |
| End Date: | August 2015 |
Study of Environmental Toxicants and Inflammatory Markers in Prematurity and Diseases of Prematurity
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.
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.
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.
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.
Inclusion Criteria:
- all infants born alive
Exclusion Criteria:
- infants who are born with no signs of life
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