Publications by authors named "Bodil Salvesen"

Objective: To evaluate epidemiology and outcomes among very preterm infants (<32 weeks' gestation) with culture-positive and culture-negative late-onset sepsis (LOS).

Design: Cohort study using a nationwide, population-based registry.

Setting: 21 neonatal units in Norway.

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Background: Sepsis is a leading cause of neonatal morbidity and mortality. Clinical suspicion may lead to overuse of antibiotics. The objective of this study was to assess the epidemiology of early-onset sepsis (EOS) and antibiotic exposure during the first week of life in Norwegian term infants.

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Background: Meconium displaces surfactant from the alveolar surface and inhibits its function. The development of active synthetic surfactants is complicated, especially to synthesize the hydrophobic surfactant proteins SP-B and SP-C. A synthetic surfactant, CHF5633 containing SP-B and SP-C analogs, has been designed to act similarly to the natural surfactant poractant alfa.

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Objective: Meconium, the first intestinal discharge of the newborn, contains material accumulated during fetal life. Meconium activates complement and CD14 and may induce a systemic inflammatory response. Toll-like receptors are classical pattern-recognition receptors recognizing both exogenous and host-derived ligands.

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Background: The complement system is an important part of innate immunity. Complement deficiencies or inappropriate activation of complement may cause severe diseases. The complement functional test, Wielisa, assesses all three complement activation pathways in humans.

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Objective: Meconium aspiration syndrome is still a serious condition with high mortality and morbidity. No specific treatment is yet available, although surfactant is known to reduce the need for extracorporeal membrane oxygenation and surfactant lavage has shown promising results in animal studies. Our group has previously shown reduced oxygenation index in an experimental model of meconium aspiration syndrome in newborn pigs when mixing albumin with meconium before endotracheal instillation.

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Background: Meconium aspiration syndrome has a complex pathophysiology. Meconium activates the complement system and meconium-induced cytokine formation is differentially mediated by complement and CD14. C1-inhibitor (C1-INH) regulates complement and contact-system activation mainly by protease inhibition, but may reduce inflammation by other mechanisms as well.

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Objective: Meconium aspiration syndrome has a complex, poorly defined pathophysiology. Meconium is a potent activator of complement in vitro and in vivo; the latter is associated with a systemic inflammatory response. The complement system and Toll-like receptors are 2 important upstream components of the innate immune system that act partly independently in the inflammatory network.

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