Brain regions and functional interactions supporting early word recognition in the face of input variability

Perception and cognition in infants have been traditionally investigated using habituation paradigms, assuming that babies' memories in laboratory contexts are best constructed after numerous repetitions of the very same stimulus in the absence of interference. A crucial, yet open, question regards how babies deal with stimuli experienced in a fashion similar to everyday learning situations-namely, in the presence of interfering stimuli. To address this question, we used functional near-infrared spectroscopy to test 40 healthy newborns on their ability to encode words presented in concomitance with other words. The results evidenced a habituation-like hemodynamic response during encoding in the left-frontal region, which was associated with a progressive decrement of the functional connections between this region and the left-temporal, right-temporal, and right-parietal regions. In a recognition test phase, a characteristic neural signature of recognition recruited first the right-frontal region and subsequently the right-parietal ones. Connections originating from the right-temporal regions to these areas emerged when newborns listened to the familiar word in the test phase. These findings suggest a neural specialization at birth characterized by the lateralization of memory functions: the interplay between temporal and left-frontal regions during encoding and between temporo-parietal and right-frontal regions during recognition of speech sounds. Most critically, the results show that newborns are capable of retaining the sound of specific words despite hearing other stimuli during encoding. Thus, habituation designs that include various items may be as effective for studying early memory as repeated presentation of a single word.European Research Council under European Union 269502 CONICYT-Chile Program PIA/BASAL FB0003 "Progetto strategico NEURAT" from the University of Padua CONICYT-Chile Program PAI/Academia 7913002

Effect of allopurinol in addition to hypothermia treatment in neonates for hypoxic-ischemic brain injury on neurocognitive outcome (ALBINO):Study protocol of a blinded randomized placebo-controlled parallel group multicenter trial for superiority (phase III)

Background: Perinatal asphyxia and resulting hypoxic-ischemic encephalopathy is a major cause of death and long-term disability in term born neonates. Up to 20,000 infants each year are affected by HIE in Europe and even more in regions with lower level of perinatal care. The only established therapy to improve outcome in these infants is therapeutic hypothermia. Allopurinol is a xanthine oxidase inhibitor that reduces the production of oxygen radicals as superoxide, which contributes to secondary energy failure and apoptosis in neurons and glial cells after reperfusion of hypoxic brain tissue and may further improve outcome if administered in addition to therapeutic hypothermia. Methods: This study on the effects of ALlopurinol in addition to hypothermia treatment for hypoxic-ischemic Brain Injury on Neurocognitive Outcome (ALBINO), is a European double-blinded randomized placebo-controlled parallel group multicenter trial (Phase III) to evaluate the effect of postnatal allopurinol administered in addition to standard of care (including therapeutic hypothermia if indicated) on the incidence of death and severe neurodevelopmental impairment at 24 months of age in newborns with perinatal hypoxic-ischemic insult and signs of potentially evolving encephalopathy. Allopurinol or placebo will be given in addition to therapeutic hypothermia (where indicated) to infants with a gestational age ≥ 36 weeks and a birth weight ≥ 2500 g, with severe perinatal asphyxia and potentially evolving encephalopathy. The primary endpoint of this study will be death or severe neurodevelopmental impairment versus survival without severe neurodevelopmental impairment at the age of two years. Effects on brain injury by magnetic resonance imaging and cerebral ultrasound, electric brain activity, concentrations of peroxidation products and S100B, will also be studied along with effects on heart function and pharmacokinetics of allopurinol after iv-infusion. Discussion: This trial will provide data to assess the efficacy and safety of early postnatal allopurinol in term infants with evolving hypoxic-ischemic encephalopathy. If proven efficacious and safe, allopurinol could become part of a neuroprotective pharmacological treatment strategy in addition to therapeutic hypothermia in children with perinatal asphyxia. Trial registration: NCT03162653, www.ClinicalTrials.gov, May 22, 2017.</p

Chest ultrasound in children

Sebbene per molti anni il polmone sia stato erroneamente considerato non esplorabile con gli ultrasuoni, nell\u2019ultimo decennio l\u2019ecografia toracica (ET) \ue8 stata applicata allo studio della patologia pleurica, degli addensamenti parenchimali e dell\u2019interstizio polmonare nel paziente adulto. L\u2019ET pu\uf2 risultare utile per chiarire la natura e la pertinenza anatomica di reperti radiografici dubbi, permettendo di distinguere tra addensamenti, atelettasie e versamenti pleurici; inoltre \ue8 la metodica di scelta per la valutazione longitudinale di queste condizioni. Il basso costo, la rapidit\ue0 di esecuzione e la ripetibilit\ue0 dell\u2019indagine, oltre alle ovvie ragioni radioprotezionistiche, fanno s\uec che l\u2019ET in campo pediatrico - soprattutto se direttamente eseguibile dal clinico al letto del paziente - si proponga come metodica di grande interesse, degna di approfondimenti e sviluppi

Lung Ultrasound Diagnostic Accuracy in Neonatal Pneumothorax

Background. Pneumothorax (PTX) still remains a common cause of morbidity in critically ill and ventilated neonates. At the present time, lung ultrasound (LUS) is not included in the diagnostic work-up of PTX in newborns despite of excellent evidence of reliability in adults. The aim of this study was to compare LUS, chest X-ray (CXR), and chest transillumination (CTR) for PTX diagnosis in a group of neonates in which the presence of air in the pleural space was confirmed. Methods. In a 36-month period, 49 neonates with respiratory distress were enrolled in the study. Twenty-three had PTX requiring aspiration or chest drainage (birth weight 2120 ± 1640 grams; gestational age = 36 ± 5 weeks), and 26 were suffering from respiratory distress without PTX (birth weight 2120 ± 1640 grams; gestational age = 34 ± 5 weeks). Both groups had done LUS, CTR, and CXR. Results. LUS was consistent with PTX in all 23 patients requiring chest aspiration. In this group, CXR did not detect PTX in one patient while CTR did not detect it in 3 patients. Sensitivity and specificity in diagnosing PTX were therefore 1 for LUS, 0.96 and 1 for CXR, and 0.87 and 0.96 for CTR. Conclusions. Our results confirm that also in newborns LUS is at least as accurate as CXR in the diagnosis of PTX while CTR has a lower accuracy

A 16q deletion involving FOXF1 enhancer is associated to pulmonary capillary hemangiomatosis

BACKGROUND: Pulmonary capillary hemangiomatosis (PCH) is an uncommon pulmonary disorder, with variable clinical features depending on which lung structure is affected, and it is usually linked to pulmonary arterial hypertension. Congenital PCH has been very rarely described and, so far, the only causative gene identified is EIF2AK4, which encodes for a translation initiation factor. However, not all PCH cases might carry a mutation in this gene. CASE PRESENTATION: We report the clinical and cytogenetic characterization of a patient (male, newborn, first child of healthy non-consanguineous parents) died after three days of life with severe neonatal pulmonary hypertension, due to diffuse capillary hemangiomatosis diagnosed post mortem. Conventional karyotyping, Microarray-Based Comparative Genomic Hydridization (CGHa) and quantitative PCR were performed. CGHa revealed a heterozygous chromosome 16q23.3q24.1 interstitial deletion, spanning about 2.6 Mb and involving a FOXF1 gene enhancer. Quantitative PCR showed that the proband’s deletion was de novo. Microsatellite analysis demonstrate that the deletion occurred in the maternal chromosome 16. CONCLUSION: FOXF1 loss of function mutation have been so far identified in alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV), a lung disease different from PCH. Our data suggest the hypothesis that disruption of the FOXF1 gene enhancer could be a genetic determinant of PCH. Moreover, our findings support the idea that FOXF1 is a paternally imprinted gene. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12881-015-0241-7) contains supplementary material, which is available to authorized users