Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease in infants and is associated with increased mortality, respiratory morbidity, neurodevelopmental impairment, and increased healthcare costs. In parallel with advances made in the field of neonatal intensive care, the phenotype of BPD has evolved from a fibrocystic disease affecting late preterm infants to one of impaired parenchymal development and dysregulated vascular growth predominantly affecting infants born before 29 weeks’ gestational age. BPD has been shown to have significant lifelong consequences. Adults with BPD have been found to have abnormal lung function tests, reduced exercise tolerance, and may be at increased risk for developing chronic obstructive pulmonary disease. Evidence shows that BPD occurs secondary to genetic-environmental interactions in an immature lung. In this review, we evaluate the various clinical definitions, imaging modalities, and biomarker data that are helpful in making an early diagnosis of BPD. In addition, we evaluate recent evidence about the prevention and treatment of BPD. We discuss the invasive and non-invasive ventilation strategies and pharmacological agents used in the early, evolving, and established phases of BPD.

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Given that neonatal sepsis remains an important factor contributing to mortality and morbidity in neonates, identification of accurate biomarkers to aid in its timely and accurate diagnosis is critical. In this review, we discuss the current evidence behind the use of biomarkers commonly used in clinical practice, as well as presenting recent developments in this area of research. Besides summarizing information regarding "traditional" biomarkers (eg, hematological indices, CRP, and other acute-phase reactants, cytokines), we provide the latest clinical status on some relatively "newer" biomarkers (eg, PCR-and "-omic" technology-based, biophysical biomarkers) in the diagnosis of neonatal sepsis. We believe that certain biophysical (RALIS, core-peripheral temperature differences) in combination with selective biochemical (procalcitonin, nCD64, presepsin) markers offer the best likelihood of being adopted for clinical use in the detection of neonatal sepsis in the near future. In addition, serial measurements of selective biochemical markers (procalcitonin, nCD64) offer promise in the decision to initiate and/or control the duration of antibiotic therapy. It is important to conduct adequately powered prospective multicenter studies to continue to establish the accuracy and safety of utilizing such biomarkers of neonatal sepsis so that appropriate and adequate therapy is tailored to each infant for optimal outcomes.

Background: Macrophage migration inhibitory factor (MIF) has been implicated as a protective factor in the development of bronchopulmonary dysplasia (BPD) and is known to be regulated by . The aim of this study was to evaluate the role of miR-451 and the MIF signaling pathway in in vitro and in vivo models of BPD. Methods: Studies were conducted in mouse lung endothelial cells (MLECs) exposed to hyperoxia and in a newborn mouse model of hyperoxia-induced BPD. Lung and cardiac morphometry as well as vascular markers were evaluated. Results: Increased expression of miR-451 was noted in MLECs exposed to hyperoxia and in lungs of BPD mice. Administration of a miR-451 inhibitor to MLECs exposed to hyperoxia was associated with increased expression of MIF and decreased expression of angiopoietin (Ang) 2. Treatment with the miR-451 inhibitor was associated with improved lung morphometry indices, significant reduction in right ventricular hypertrophy, decreased mean arterial wall thickness and improvement in vascular density in BPD mice. Western blot analysis demonstrated preservation of MIF expression in BPD animals treated with a miR-451 inhibitor and increased expression of vascular endothelial growth factor-A (VEGF-A), Ang1, Ang2 and the Ang receptor, Tie2. Conclusion: We demonstrated that inhibition of miR-451 is associated with mitigation of the cardio-pulmonary phenotype, preservation of MIF expression and increased expression of several vascular growth factors.