Prevention, Reduction and Repair of Brain Injury of the Preterm Infant.
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ABSTRACT:
SUBMITTER: van Bel F
PROVIDER: S-EPMC6435588 | biostudies-literature | 2019
REPOSITORIES: biostudies-literature
Publications
Prevention, Reduction and Repair of Brain Injury of the Preterm Infant.
van Bel Frank F Vaes Josine J Groenendaal Floris F
Frontiers in physiology 20190320
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Project description:Preterm birth is associated with a high risk of morbidity and mortality including brain damage and cerebral palsy. The development of brain injury in the preterm infant may be influenced by many factors including perinatal asphyxia, infection/inflammation, chronic hypoxia and exposure to treatments such as mechanical ventilation and corticosteroids. There are currently very limited treatment options available. In clinical trials, magnesium sulfate has been associated with a small, significant reduction in the risk of cerebral palsy and gross motor dysfunction in early childhood but no effect on the combined outcome of death or disability, and longer-term follow up to date has not shown improved neurological outcomes in school-age children. Recombinant erythropoietin has shown neuroprotective potential in preclinical studies but two large randomized trials, in extremely preterm infants, of treatment started within 24 or 48 h of birth showed no effect on the risk of severe neurodevelopmental impairment or death at 2 years of age. Preclinical studies have highlighted a number of promising neuroprotective treatments, such as therapeutic hypothermia, melatonin, human amnion epithelial cells, umbilical cord blood and vitamin D supplementation, which may be useful at reducing brain damage in preterm infants. Moreover, refinements of clinical care of preterm infants have the potential to influence later neurological outcomes, including the administration of antenatal and postnatal corticosteroids and more accurate identification and targeted treatment of seizures.
| S-EPMC7915709 | biostudies-literature
Project description:BackgroundT cells have been implicated in various neurological conditions, yet their role in neonatal brain injuries remains unclear. This study aimed to investigate the impact of perinatal factors on frequencies of T cell subsets in preterm infants and to explore the differences in blood genome expression profiles between preterm infants with and without brain injury.Materials and methodsThree cohorts of preterm infants were used. Blood samples were collected soon after birth for the first cohort and late timepoint for the second and third cohorts. In the first cohort (88 infants), flow cytometry measured the proportions of αβT and γδT cell subsets in peripheral blood, analyzing associations with gestational age, birth weight, sex, delivery type, and maternal conditions. The second cohort focused on the relationship between T cell subsets and brain injury. In the third cohort, transcriptome sequencing identified differentially expressed genes and pathways in infants with brain injury, highlighting immune-related changes.ResultsInfants born at 29-30 weeks or with a birth weight of 1000-1500 g had significantly higher proportions of Vδ2+ T cells compared to those born at 30-32 weeks or with a birth weight > 1500 g, while no significant difference was found between infants born at < 29 weeks or with a birth weight < 1000 g. A negative correlation was observed between gestational age and Vδ2+ T cell frequency. No significant associations were found between Vδ2+ T cell proportions and perinatal factors other than gestational age or brain injury. Blood transcriptome analysis revealed 173 differentially expressed genes, characterized by downregulated interferon signaling and upregulated antimicrobial and neutrophil pathways in infants with brain injury.ConclusionsGestational age and birth weight influence Vδ2+ T cell proportions in preterm infants, likely reflecting immune maturation. While no direct link to brain injury was found, altered immune pathways suggest potential biomarkers for prognosis, warranting further research into their roles and therapeutic implications in neonatal brain injuries.
| S-EPMC11607874 | biostudies-literature
Project description:Microglia are the resident phagocytic cells of the central nervous system. During brain development they are also imperative for apoptosis of excessive neurons, synaptic pruning, phagocytosis of debris and maintaining brain homeostasis. Brain damage results in a fast and dynamic microglia reaction, which can influence the extent and distribution of subsequent neuronal dysfunction. As a consequence, microglia responses can promote tissue protection and repair following brain injury, or become detrimental for the tissue integrity and functionality. In this review, we will describe microglia responses in the human developing brain in association with injury, with particular focus on the preterm infant. We also explore microglia responses and mechanisms of microglia toxicity in animal models of preterm white matter injury and in vitro primary microglia cell culture experiments.
| S-EPMC4155935 | biostudies-literature
Project description:IntroductionWhite matter injury (WMI) is now the major disease that seriously affects the quality of life of preterm infants and causes cerebral palsy of children, which also causes periventricular leuko-malacia (PVL) in severe cases. The study aimed to develop a method based on cranial ultrasound images to evaluate the risk of WMI.MethodsThis study proposed an ultrasound radiomics diagnostic system to predict the WMI risk. A multi-task deep learning model was used to segment white matter and predict the WMI risk simultaneously. In total, 158 preterm infants with 807 cranial ultrasound images were enrolled. WMI occurred in 32preterm infants (20.3%, 32/158).ResultsUltrasound radiomics diagnostic system implemented a great result with AUC of 0.845 in the testing set. Meanwhile, multi-task deep learning model preformed a promising result both in segmentation of white matter with a Dice coefficient of 0.78 and prediction of WMI risk with AUC of 0.863 in the testing cohort.DiscussionIn this study, we presented a data-driven diagnostic system for white matter injury in preterm infants. The system combined multi-task deep learning and traditional radiomics features to achieve automatic detection of white matter regions on the one hand, and design a fusion strategy of deep learning features and manual radiomics features on the other hand to obtain stable and efficient diagnostic performance.
| S-EPMC10157025 | biostudies-literature
Project description:Development of the gut microbiota is greatly impacted in preterm infants. Despite increasing knowledge about microbiota composition in preterm infants, knowledge about the functional signatures of the intestinal microbiota remains limited. The aim was to study transitions in microbiota activity during the first six postnatal weeks in ten preterm infants. A total of 64 stool samples were measured by LC-MS/MS.
2017-07-14 | PXD005574 | Pride
Project description:Longitudinal stool metagenomics from preterm infants within the first month after birth
| PRJEB52938 | ENA
Project description:Development of the intestinal microbiota in preterm infants during the first six postnatal weeks determined by 454 pyrosequencing of the 16S rRNA gene.
| PRJEB18915 | ENA
Project description:BackgroundExtremely preterm infants often receive mechanical ventilation (MV), which can contribute to bronchopulmonary dysplasia (BPD). However, the effects of MV alone on the extremely preterm lung and the lung's capacity for repair are poorly understood.AimTo characterise lung injury induced by MV alone, and mechanisms of injury and repair, in extremely preterm lungs and to compare them with very preterm lungs.MethodsExtremely preterm lambs (0.75 of term) were transiently exposed by hysterotomy and underwent 2 h of injurious MV. Lungs were collected 24 h and at 15 d after MV. Immunohistochemistry and morphometry were used to characterise injury and repair processes. qRT-PCR was performed on extremely and very preterm (0.85 of term) lungs 24 h after MV to assess molecular injury and repair responses.Results24 h after MV at 0.75 of term, lung parenchyma and bronchioles were severely injured; tissue space and myofibroblast density were increased, collagen and elastin fibres were deformed and secondary crest density was reduced. Bronchioles contained debris and their epithelium was injured and thickened. 24 h after MV at 0.75 and 0.85 of term, mRNA expression of potential mediators of lung repair were significantly increased. By 15 days after MV, most lung injury had resolved without treatment.ConclusionsExtremely immature lungs, particularly bronchioles, are severely injured by 2 h of MV. In the absence of continued ventilation these injured lungs are capable of repair. At 24 h after MV, genes associated with injurious MV are unaltered, while potential repair genes are activated in both extremely and very preterm lungs.
| S-EPMC3660361 | biostudies-literature
Project description:Early childhood poverty is a risk factor for lower school achievement, reduced earnings, and poorer health, and has been associated with differences in brain structure and function. Whether poverty causes differences in neurodevelopment, or is merely associated with factors that cause such differences, remains unclear. Here, we report estimates of the causal impact of a poverty reduction intervention on brain activity in the first year of life. We draw data from a subsample of the Baby's First Years study, which recruited 1,000 diverse low-income mother-infant dyads. Shortly after giving birth, mothers were randomized to receive either a large or nominal monthly unconditional cash gift. Infant brain activity was assessed at approximately 1 y of age in the child's home, using resting electroencephalography (EEG; n = 435). We hypothesized that infants in the high-cash gift group would have greater EEG power in the mid- to high-frequency bands and reduced power in a low-frequency band compared with infants in the low-cash gift group. Indeed, infants in the high-cash gift group showed more power in high-frequency bands. Effect sizes were similar in magnitude to many scalable education interventions, although the significance of estimates varied with the analytic specification. In sum, using a rigorous randomized design, we provide evidence that giving monthly unconditional cash transfers to mothers experiencing poverty in the first year of their children's lives may change infant brain activity. Such changes reflect neuroplasticity and environmental adaptation and display a pattern that has been associated with the development of subsequent cognitive skills.
| S-EPMC8812534 | biostudies-literature
Project description:ObjectiveMagnetic resonance spectroscopy (1H-MRS) may provide clinically relevant data regarding metabolic processes that govern the course of preterm brain injury.Study design46 very preterm infants (VP) were evaluated by magnetic resonance imaging and 1H-MRS at term-equivalent age. Brain injury was assessed according to the Kidokoro scale. Moreover, 17 term-born infants with hypoxic-ischemic encephalopathy (HIE) were scanned. The metabolic profile of the central nervous system was obtained from the bilateral thalamus.ResultThe Lipids/Creatine, Choline/Creatine, N-acetyl aspartate/Choline, Lactate/N-acetyl aspartate, and Lactate/Creatine ratios differed between VP infants with moderate+severe brain damage and those without brain injury. Moreover, VP infants with moderate+severe brain damage had higher Lactate/ N-acetyl aspartate and Lactate/Creatine ratios than HIE group.ConclusionThere were significant differences in the cerebral metabolite profile at TEA between VP infants with and without brain injury. The 1H-MRS profile of VP infants with moderate+severe brain damage may reflect profound chronic metabolic alterations.
| S-EPMC11825355 | biostudies-literature