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Vitamin A and bronchopulmonary dysplasia: the next steps

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.

Multipotent adult progenitor cells prevent functional impairment and improve development in inflammation driven detriment of preterm ovine lungs

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.

Elevated leukotriene B4 and 8-isoprostane in exhaled breath condensate from preterm-born infants

Inflammation and oxidative stress play a key role in the development of bronchopulmonary dysplasia (BPD), possibly contributing to persistent respiratory morbidity after preterm birth. We aimed to assess if inflammatory markers were elevated in exhaled breath condensate (EBC) of infants born very prematurely (< 32 weeks gestation) at 12-16 corrected months of age, and if increased levels were associated with BPD diagnosis and respiratory morbidity.

Positive End-Expiratory Pressure Levels during Resuscitation of Preterm Infants at Birth: The POLAR Trial

Investigators: Andrew Gill External collaborators: Assoc Prof David Tingay (Murdoch Children's Research Institute) The POLAR trial is an MRFF-funded

Living with lung disease: experimental models to assess the long-term effects of prematurity

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.

Airway smooth muscle thickness and contraction are enhanced by intra-amniotic lipopolysaccharide in an ovine model of premature birth

Abnormalities of the airway smooth muscle (ASM) layer in asthma may develop before birth. We hypothesize that antenatal inflammation causes physiological abnormalities of the ASM that predisposes asthma. This study determined the short-term effects of antenatal inflammation on the developing ASM.

Impact of fetal treatments for congenital diaphragmatic hernia on lung development

The extent of lung hypoplasia impacts the survival and severity of morbidities associated with congenital diaphragmatic hernia.

Vitamin A supplementation in very-preterm or very-low-birth-weight infants to prevent morbidity and mortality: A systematic review and meta-Analysis of randomized trials

A previous systematic review showed that intramuscular vitamin A supplementation reduced the risk of bronchopulmonary dysplasia (BPD) in very-low-birth-weight (VLBW) infants. However, more recent studies have questioned this finding.

Effect of Enteral Vitamin A on Fecal Calprotectin in Extremely Preterm Infants: A Nested Prospective Observational Study

Vitamin A has anti-inflammatory and immune-modulating properties. We aimed to assess whether enteral water-soluble vitamin A supplementation in extremely preterm infants decreases fecal calprotectin, a marker of intestinal inflammation.

Lung recruitment before surfactant administration in extremely preterm neonates with respiratory distress syndrome (IN-REC-SUR-E): a randomised, unblinded, controlled trial

The importance of lung recruitment before surfactant administration has been shown in animal studies. Well designed trials in preterm infants are absent. We aimed to examine whether the application of a recruitment manoeuvre just before surfactant administration, followed by rapid extubation (intubate-recruit-surfactant-extubate [IN-REC-SUR-E]), decreased the need for mechanical ventilation during the first 72 h of life compared with no recruitment manoeuvre (ie, intubate-surfactant-extubate [IN-SUR-E]).