The neonatal brain is not protected by osteopontin peptide treatment after hypoxia-ischemia.

Neonatal encephalopathy due to perinatal hypoxia-ischemia (HI) is a severe condition, and current treatment options are limited. Expression of endogenous osteopontin (OPN), a multifunction glycoprotein, is strongly upregulated in the brain after neonatal HI. Intracerebrally administered OPN has been shown to be neuroprotective following experimental neonatal HI and adult stroke.

Development of cerebral gray and white matter injury and cerebral inflammation over time after inflammatory perinatal asphyxia.

Antenatal inflammation is associated with increased severity of hypoxic-ischemic (HI) encephalopathy and adverse outcome in human neonates and experimental rodents. We investigated the effect of lipopolysaccharide (LPS) on the timing of HI-induced cerebral tissue loss and gray matter injury, white matter injury and integrity, and the cerebral inflammatory response. On postnatal day 9, mice underwent HI by unilateral carotid artery occlusion followed by systemic hypoxia which resulted in early neuronal damage (MAP2 loss) at 3 h that did not increase up to day 15.

Hypotension in preterm neonates: low blood pressure alone does not affect neurodevelopmental outcome.

Objective: To compare neurodevelopmental outcome, mean arterial blood pressure (MABP), and regional cerebral oxygenation (rSco2) between preterm neonates treated for hypotension and controls.

Study Design: Preterm neonates (N = 66) with a gestational age (GA) ≤32 weeks, without a patent ductus arteriosus, treated for hypotension (dopamine ≥5 μg/kg/min) were included. Neonates were matched to controls for GA, birth weight, sex, and year of birth.

Mitochondrial JNK phosphorylation as a novel therapeutic target to inhibit neuroinflammation and apoptosis after neonatal ischemic brain damage.

Neonatal encephalopathy is associated with high mortality and life-long developmental consequences. Therapeutic options are very limited. We assessed the effects of D-JNKi, a small peptide c-Jun N-terminal kinase (JNK) MAP kinase inhibitor, on neuroinflammation, mitochondrial integrity and neuronal damage in a neonatal rat model of ischemic brain damage.

Effect of antihypotensive treatment on cerebral oxygenation of preterm infants without PDA.

Background: Preterm infants with hypotension (mean arterial blood pressure [MABP] < gestational age [GA]) are treated with volume expansion and/or dopamine to ensure adequate cerebral perfusion/oxygenation. We used near-infrared spectroscopy to analyze the effects of volume expansion and dopamine on cerebral oxygenation in hypotensive preterm infants without patent ductus arteriosus (PDA).

Patients And Methods: Among 390 infants, 71 (GA < 32 weeks) were hypotensive and eligible for inclusion.

Upper and lower airway cultures in children with cystic fibrosis: do not neglect the upper airways.

Background: Airways of cystic fibrosis (CF) patients are colonised with bacteria early in life. We aimed to analyse differences between results of simultaneously taken upper airway (UAW) and lower airway (LAW) cultures, to describe clinical characteristics of patients with positive versus negative cultures and to follow up the patients with P. aeruginosa positive UAW cultures.