Somatic growth is significantly impaired after NP but recovers steadily following S2P, as the patient transitions toward separated series circulation. Earlier S2P may lead to earlier resumption of normal growth in this critical period of early infancy.

In contrast to the LV, 2D echocardiographic indices of RV size and function, with the exception of TAM, do not correlate with MRI data.

Exposure to high concentration of oxygen (hyperoxia) leads to lung injury in experimental animal models and plays a role in the pathogenesis of diseases such as Acute Respiratory Distress Syndrome (ARDS) and Bronchopulmonary dysplasia (BPD) in humans. The mechanisms responsible for sex differences in the susceptibility towards hyperoxic lung injury remain largely unknown. The major goal of this study was to characterize the changes in the pulmonary transcriptome following hyperoxia exposure and further elucidate the sex-specific changes. Male and female (8–10 wk) wild type (WT) (C57BL/6J) mice were exposed to hyperoxia (FiO2>0.95) and gene expression in lung tissues was studied at 48 h. A combination of fold change ≥1.4 and false discovery rate (FDR)<5% was used to define differentially expressed genes (DEGs). Overrepresentation of gene ontology terms representing biological processes and signaling pathway impact analysis (SPIA) was performed. Comparison of DEG profiles identified 327 genes unique to females, 585 unique to males and 1882 common genes. The major new findings of this study are the identification of new candidate genes of interest and the sex-specific transcriptomic changes in hyperoxic lung injury. We also identified DEGs involved in signaling pathways like MAP kinase and NF-kappa B which may explain the differences in sex-specific susceptibility to hyperoxic lung injury. These findings highlight changes in the pulmonary transcriptome and sex-specific differences in hyperoxic lung injury, and suggest new pathways, whose components could serve as sex-specific biomarkers and possible therapeutic targets for acute lung injury (ALI)/acute respiratory distress (ARDS) in humans.

Tachyarrhythmias form a significant majority of the cardiac emergencies encountered in the pediatric age group. While the initial management often depends on the hemodynamic status of the patient at presentation, a systematic approach that follows the stabilization of the patient with the tools available at bedside, specifically the surface electrocardiogram often results in optimal treatment response that is tailored towards the mechanism and severity of the arrhythmia. The goal of this review is to provide the pediatric cardiologist with such an approach based on clinical history and analysis of the electrocardiogram (ECG). Illustrative examples are used to explain this approach towards the more common tachyarrhythmias. A general overview of the initial anti-arrhythmic interventions will be provided.