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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to pursue peculiarities of fetal metabolism, fluorometric measurements of intracellular nicotinamide adenine dinucleotide (NAD) were made in perfused adult and fetal guinea pig livers following the administration of various agents before and after anoxia loadings. Oxygen and glucose concentrations of the drainage from perfused livers were also measured. The following results were obtained: (1) NAD reduction, oxygen uptake and glucose production were observed to be lower in fetal livers in response to lactate, pyruvate, octanoate and ethanol than the adult ones, suggesting immaturity of fetal intracellular metabolism. (2) However, on the basis of NAD reduction following norepinephrine (NE) administration, fetal plasma membraneous receptors were considered to be similarly active, although induced glucose production was lower than the adult ones. Sequential NE administrations yielded consecutive changes in NAD reduction and glucose production, suggesting active response of fetal plasma membrane to NE. (3) After one hour and three hours of anoxia loadings, adult NAD reduction rates by NE were decreased remarkably to 37% and 11%, respectively, of the control values on average, while fetal rates were reduced to only 61% and 45% of the control values, suggesting anoxic tolerance of fetal plasma membrane. (4) After three hours of anoxia loading, NAD reduction was observed following succinate administration in adult livers, indicating membraneous damage due to anoxia. No such changes were observed in fetal livers. (5) Scanning spectrophotometric studies demonstrated activities of mitochondrial cytochromes in perfused adult and fetal livers, indicating the efficacy of non-destructive in vivo measurements.
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PMID:[Comparative studies on perfused adult and fetal guinea pig liver metabolism before and after anoxia loadings, with special reference to intracellular redox state]. 687 38

The reported incidence of Bronchopulmonary dysplasia (BPD) varies from 5% to 68%. The different criteria used to define BPD are responsable for these discrepancies: some Authors include only patients with a clinical and radiological picture that fits the stage IV, as originally described by Northway, others use a more liberal approach and include all patients with manifestations of chronic pulmonary disease. We observed BPD in 12 of 22 (54%) survivors infants of very low birth weight (mean 1115 gm) and gestational age (mean 29,2 weeks). The infants were all born between November 1979 and March 1981. According to Ehrenkranz et al., we classified the radiological findings as severe, moderate and mild. We believe that the etiology of BPD in very low birth weight infants is multifactorial. However, pulmonary oxygen toxicity and immaturity are the most important causes.
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PMID:[Bronchopulmonary dysplasia in very low birth weight infants]. 692 45

In addition to their role in oxygen transport and ventilation, the lungs serve as an important defense function consisting of nonspecific and specific components. The nonspecific factors include aerodynamic filtration, mucociliary apparatus, bronchoalveolar fluid flow and lymphohematogenous drainage (anatomic systems) as well as phagocytosis and inflammation; the specific factors include B-cell immunity (IgG, A, M, D and E) and T-cell immunity (cell-mediated immunity). In the lungs, specialized lymphoid tissues in contact with epithelium (bronchus-associated lymphoid tissues; BALT) function in local antibody (secretory IgA) and cell-mediated immunity responses to foreign antigens. Based upon these considerations, a number of therapeutic interventions have been developed to enhance various components of lung defense. These include substances which enhance both nonspecific elements (leukocyte transfusion, plasma, nonspecific immunostimulants, e.g., immunoactive bacterial extracts) as well as specific elements (vaccines, intravenous gammaglobulin, plasma, interferons, cytokines). The need for further development and utilization of new immune interventions is underscored by the large number of infants and children who suffer from recurrent respiratory infections, who have either maturational immaturity (e.g. small for gestational age newborn), genetically determined (e.g. cystic fibrosis) or acquired defects (e.g. AIDS) of lung defense mechanisms. The emergence of antibiotic-resistant bacterial organisms, e.g. Streptococcus pneumoniae, poses an additional need for new immune interventions.
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PMID:Current concepts of immune interventions in children with respiratory diseases. 752 41

We have developed 1H-chemical shift imaging (CSI) and functional magnetic resonance imaging (FMRI) methods on a clinical MRI system, in which metabolic and functional information can be obtained from the brain. 31P- and 1H-CSI are in clinical use. Using 1H-CSI, the peaks of N-acetylaspartate (NAA), choline (Cho) and creatine (Cr) are clearly detected in multiple small voxels. In normal children, the ratio of NAA/Cho increased after birth in different manners in different parts of the brain. The peak of NAA decreased in some disorders with brain damage or neuronal immaturity. It has been shown recently that functional activation of the cortex can be visualized with MR imaging with a blood oxygen level dependent (BOLD) effect. At an activated area, the ratio of deoxyhemoglobin to oxyhemoglobin decreased in the capillary and venous beds. Therefore, with a decrease of the effect of the T2 susceptibility from deoxyhemoglobin, the signal intensity of the activated area increased. CSI and FMRI have a unique possibility in the field of non-invasive brain analysis.
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PMID:[Metabolic and functional magnetic resonance imaging of the brain: clinical application to pediatric brain diseases]. 772 56

Chronic oxygen dependence is associated with immaturity, male sex and low birthweight, but amongst that high risk group further criteria are necessary to predict those most at risk. We previously developed a chest radiograph scoring system which, when used at 1 month of age, proved useful in predicting chronic oxygen dependency at 36 weeks post-conceptional age (PCA). We have now assessed whether the scoring system, if applied at 24 h of age, added predictive value to readily available demographic and ventilatory data. 50 infants, birthweight less than 1200 g and ventilated from birth, were examined. They had a median gestational age of 27 weeks (range 23-34), birthweight of 886 g (range 470-1172) and chest radiograph score of 7 (range 2-13). Univariate analysis revealed that oxygen dependency at 28 days and 36 weeks PCA was significantly associated with low gestational age, male sex and high ventilatory requirements, in addition to a high chest radiograph score. Stepwise regression analysis, however, demonstrated that a high chest radiograph score predicted oxygen dependence at 28 days, independent of immaturity, low birthweight, male sex and high ventilatory requirements. A chest radiograph score of more than 5 rendered an infant four times more likely to be oxygen dependent at 28 days than those with lower scores. We conclude the chest radiograph appearance at 24 h of age could be used as a criterion to institute interventional strategies aimed at reducing chronic oxygen dependence.
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PMID:Chest radiograph appearance at 24 h of age--prediction of chronic oxygen dependency. 773 62

We studied Ureaplasma urealyticum colonization in 93 intubated infants (gestational ages 23-40 weeks) in our neonatal intensive care unit by obtaining cultures from endotracheal aspirate and nasopharynx during their first week of life. Eighteen infants had positive cultures, giving a colonization rate of 19%. No infant more than 30 weeks' gestation had a positive culture. The infants with positive cultures had a significantly lower gestational age and birth weight (p < 0.009 and p < 0.005), with a colonization rate of 33% in infants less than 1000 g. Among the infants with positive cultures, 10 of 17 developed chronic lung disease in contrast with 21 of 72 infants with negative cultures. The development of chronic lung disease and duration of oxygen requirement was strongly associated with immaturity but only weakly with Ureaplasma urealyticum.
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PMID:Neonatal Ureaplasma urealyticum colonization and chronic lung disease. 781 88

When compared to adults, muscle mass in children is lower and the relative development of aerobic and anaerobic pathways is different. The main consequences are the following: 1) The aerobic metabolism, evaluated by measurement of maximal oxygen uptake (VO2max), is either the same as in adults or more developed when VO2 max is related to body mass or lean body mass. 2) The maximal anaerobic power developed during force-velocity test and Wingate test is lower than in adults even if it is expressed by total or lean body mass unit. Blood lactate concentration is also lower. This immaturity of the anaerobic metabolism, especially the "lactic pathway" may result from lower anaerobic enzyme activities (lactico-dehydrogenase, phosphofructokinase, etc) and glycogen content. During puberty, "lactic metabolism" starts to develop significantly, simultaneously with muscle mass. It has been suggested that sexual hormones (testosterone in boys, oestrogens in girls) and other factors, such as growth factors, are implicated in this phenomenon. During this period, the aerobic metabolism remains unchanged. In prepubertal children there is neither aerobic nor anaerobic specialization: the highest anaerobic performance is associated with the highest VO2 max. Moreover, it seems that before puberty, bioenergetic profile is not modified by training. 3) Despite a high VO2 max, performance in endurance events is not as high in children as in adults because of a lower running economy. Cardiovascular responses are characterized by higher maximal and infra-maximal heart rates, and lower systolic stroke volume and arterial blood pressures than in adults. During prolonged exercise, the hormonal adaptations for energy substrate utilization is quite different from adults: a lower decrease in insulin and increase in catecholamines and glucagon in response to exercise could be responsible for a less effective regulation of glycemia with a risk of hypoglycemia. Therefore, an adequate carbohydrate intake is recommended.
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PMID:[Physiology of muscular exercise in children]. 784 28

In recent years increasing experimental and clinical data have provided compelling evidence for the involvement of oxygen free radicals in the 3 main disorders of prematurity--chronic lung disease, retinopathy of prematurity and intraventricular haemorrhage. Infants born prior to 30 weeks gestation or weighing less than 1500 g at birth appear to be most at risk. They are very underdeveloped and as a consequence of the immaturity of their lungs often require intense respiratory support, including the provision of supplemental oxygen. The theoretical basis for free radical involvement in these disorders is that oxygen centred radicals and related reactive oxygen metabolites are formed too rapidly to be detoxified by the antioxidant defence mechanisms in specific tissues. In the case of chronic lung disease, the evidence currently favours excess oxygen (hyperoxia) as the cause of the greater oxygen free radical production, whereas in retinopathy of prematurity and intraventricular haemorrhage, it is proposed that low oxygen tensions (hypoxia) followed by periods of reoxygenation is the more likely stimulus for excess radical formation.
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PMID:Free radical disorders of preterm infants. 822 Oct 31

The premature infant is more vulnerable to the NICU environment than a full-term infant due to neurologic immaturity and physiologic instability. Studies have been done on the effects of long-term decreases in environmental light, but none have been done on the immediate effects. The purpose of this study was to determine the relationship between immediate changes in environmental illumination and oxygen saturation in preterm neonates and whether these were affected by gestational and postnatal age. The oxygen saturations of 27 sleeping infants (2 to 56 days of age) between 26 and 37 weeks gestation were continuously recorded for 40 minutes utilizing a Nellcor N200 oximeter. After recording baseline saturations for 5 minutes with the room lights at 100 footcandles, the illumination level was lowered to 5 footcandles. At the end of 30 minutes, lights were increased to the previous level. Oxygen saturations were recorded at one and five minutes after illumination decreases and increases. There was a statistically significant interaction between repeated measures of saturation at baseline and one and five minutes after lights were increased and covariates gestational, corrected gestational, and postnatal age (p = .02, p = .008, p = .005). Repeated measure analysis of covariance (ANCOVA) revealed no statistically significant changes in oxygen saturations after the lights had been lowered for babies who were younger in gestational or postnatal age. The results of this study suggest that rapidly increasing illumination may be a cause of stress to the younger gestationally and postnatally preterm neonate.
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PMID:The effect of environmental lighting on the oxygen saturation of preterm infants in the NICU. 835 Aug 54

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2


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