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Objective: Determine the contemporary incidence of pathogenic tracheal aspirate (TA) cultures when obtained within 12 h of birth, and to associate TA culture results with specific clinical conditions that increase the risk of infection.Study Design: A retrospective study over a 6-month period of admissions to a single outborn neonatal intensive care unit when a TA sample was collected within 12 h of birth (n ¼ 139).Result: In total, 9 of 139 (6.5%) TA cultures were positive for pathogenic bacterial growth. Maternal fever (relative risk (RR) ¼ 7.7, P<0.04) and clinical chorioamnionitis (RR ¼ 6.4, P<0.02) were significantly associated with pathogenic TA culture results. Infants with a pathogenic TA culture had lower white blood cell counts (7 500 vs 13 900 mm À3 , P<0.05) when compared with infants with a negative culture. In eight of the nine patients with pathogenic cultures, either the mother or the infant received antibiotics before TA sample collection. Conclusion:Early TA culture is a helpful tool in diagnosing pneumonia, especially in certain clinical scenarios, including maternal fever, clinical chorioamnionitis and leukopenia. Administration of antibiotics before sample collection does not seem to preclude culture growth.

Background: Protein-calorie restriction in humans is associated with changes in iron metabolism that differ from dietary iron-deficiency. Dietary iron absorption and tissue iron distribution and are regulated by the hepatocellular peptide hormone hepcidin, which mediates a decrease in circulating iron concentrations and increase in cellular iron stores. Hepcidin is upregulated in response to increased serum and tissue iron, upregulated in response to ER-stress via the transcription factor CREB-H, and down-regulated in response to erythroid iron demand via the circulating signaling molecule erythroferrone/myonectin (ERFE). An overnight fast was reported to decrease expression of skeletal muscle ERFE in mice. Objective: The aim of this study was to investigate the regulation of hepcidin in the hypoferremia of fasting. Design/Methods: We analyzed parameters of iron homeostasis in five 5 week old male AKR mice fasted for 18 hours overnight (and allowed access to water) compared with mice with access to chow ad libitum. Serum and tissue iron concentrations were measured. Liver hepcidin mRNA was quantified by real-time RT-PCR and verified by Northern blot analysis. Marrow ERFE and liver CREB-H mRNA expression was quantified by RT-PCR and normalized to beta actin. Results: As anticipated, fasted mice had significantly lower serum iron concentrations (203 vs 321 mcg/dL, P<0.001) and transferrin saturations (64.4 vs 79.6%, P<0.05). Duodenal iron concentrations were increased in fasted mice, 2.3-fold (P<0.01). Histochemical staining demonstrated iron retention in the absorptive enterocytes. Liver (916 vs 735 mcg/g, P=0.1) and splenic (480 vs 414 mcg/g, P=0.001) iron concentrations were modestly higher in the fasted mice. Despite hypoferremia, the fasted mice demonstrated increased liver hepcidin expression (1.9 fold, P < 0.05). Liver CREB-H mRNA expression was increased ~10 fold, P<0.01; however there was no change in liver XBP-1 processing (marker of ER stress). Marrow ERFE expression was downregulated by approximately one third (P<0.01). Conclusions: The fasting state in mice is associated with increased hepcidin expression, iron retention in absorptive enterocytes, and decreased circulating iron. These observations suggest that the hypoferremia of fasting is not consequent to limited iron availability, but rather to hepcidin-mediated retention of iron in the duodenum and storage tissues. They moreover support a role for nutritional state, independent of iron status, as a regulator of hepcidin and mediated by changes in expression of ERFE and CREB-H. Disclosures No relevant conflicts of interest to declare.

We describe three preterm neonates with bronchopulmonary dysplasia, pulmonary hypertension and ventricular hypertrophy who incurred subendocardial infarctions, as evidenced by electrocardiographic, laboratory or autopsy findings. We propose that cardiac hypertrophy contributed to the risk for subendocardial ischemia and infarction, and suggest diligence for this complication.