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Investigators: Andrew Gill External collaborators: Assoc Prof David Tingay (Murdoch Children's Research Institute) The POLAR trial is an MRFF-funded
Since the first description of bronchopulmonary dysplasia (BPD), multiple definitions to diagnose BPD and its grading have been published. Several studies have compared the predictive performance of these definitions for long-term outcomes. The objective was to identify the BPD definition with the optimal predictive performance for long-term respiratory and neurological outcomes in preterm infants.
Jane Pillow BMedSci (Dist) MBBS, PhD (Dist) FRACP Head, Developmental Chronobiology jane.pillow@thekids.org.au Head, Developmental Chronobiology
Understand how bronchopulmonary dysplasia (BPD) and antenatal and postnatal factors influence diaphragmatic functional effectiveness in very preterm infants.
A Cochrane 2016 review indicated cycled light might benefit neonatal health in hospital. We systematically reviewed chronobiological factors for neonatal health in hospital units, identifying 56 relevant studies on light-dark cycles, feeding, noise, massage therapy, rooming-in, incubators vs. cribs, neonatal units vs. homes, and time-of-day of birth. Empirical evidence for benefits from chronobiology is weaker than expected, including light.
Preterm infants are often vitamin A deficient, and vitamin A has functions that could mitigate the processes that lead to bronchopulmonary dysplasia. Therefore, supplementation of preterm infants with vitamin A to reduce the risk of bronchopulmonary dysplasia makes inherent sense.
Lung inflammation and impaired alveolarization precede bronchopulmonary dysplasia (BPD). Glucocorticoids are anti-inflammatory and reduce ventilator requirements in preterm infants. However, high-dose glucocorticoids inhibit alveolarization. The effect of glucocorticoids on lung function and structure in preterm newborns exposed to antenatal inflammation is unknown. We hypothesise that postnatal low-dose dexamethasone reduces ventilator requirements, prevents inflammation and BPD-like lung pathology, following antenatal inflammation.
Perinatal inflammation increases the risk for bronchopulmonary dysplasia in preterm neonates, but the underlying pathophysiological mechanisms remain largely unknown. Given their anti-inflammatory and regenerative capacity, multipotent adult progenitor cells (MAPC) are a promising cell-based therapy to prevent and/or treat the negative pulmonary consequences of perinatal inflammation in the preterm neonate.
The extent of lung hypoplasia impacts the survival and severity of morbidities associated with congenital diaphragmatic hernia.
Laboratory models provide an important tool in helping to understand the cellular and molecular drivers of respiratory disease. Many animal models exist that model the neonatal outcomes of preterm birth.