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

Early investigators suggested that endurance training had little influence upon the aerobic function of the prepubescent child. It is shown that the twin explanations of this supposed phenomenon (a high intrinsic level of physical activity and an immaturity of biochemical systems) have little foundation. Moreover, critical examination of the original experiments shows a number of problems of experimental design, often including an inadequate sample size, a lack of control group, an inappropriate pattern of training relative to the initial fitness of the child, and too short a period of observation. Recent, well-designed studies all show a response in prepubescent children. Comparison with adults is hampered by difficulties in matching training intensity, but there is no immediate evidence that the training response of the prepubescent child is less than in an older person. The main basis for the increase of oxygen transport seems an increase of cardiac stroke volume. Plainly, the development of athletic performance and the attack upon cardiac risk factors can be begun before puberty, although in the average prepubescent it may be more important for the school programmes to develop positive, lifelong attitudes, than to maximise aerobic function.
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PMID:Effectiveness of training programmes for prepubescent children. 157 77

To determine if external ventricular constraint significantly limits fetal left ventricular (LV) stroke volume and can thus account for the plateau of the fetal ventricular function curve, we studied nine fetal lambs (142 to 144 days' gestation) after partial delivery by cesarean section (halothane anesthetic). LV stroke volume (electromagnetic flow probe), LV end-diastolic pressure, and external ventricular constraint (intrapericardial pressure [liquid-filled balloon]) were measured over a range of end-diastolic pressures under two conditions: with a closed chest and closed pericardium and with an open chest and open pericardium. Stroke volume recorded during open chest and open pericardium exceeded those recorded during closed chest and closed pericardium at any given end-diastolic pressure (p less than 0.01). Decreases in external ventricular constraint significantly increased LV transmural pressure (preload) and substantially increased fetal LV stroke volume. Thus the plateau of the fetal ventricular function curve was largely a result of external ventricular constraint limiting LV preload, not necessarily a result of myocyte immaturity.
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PMID:Effects of external constraint on the fetal left ventricular function curve. 159 42

Right ventricular Starling responses to acute volume infusion in newborn lambs were compared to those in older groups of lambs. When peak stroke volume/kg was reached during infusion, right ventricular end-diastolic pressures for the newborn group were significantly lower (p less than 0.001) than those obtained for older groups, in spite of significantly higher resting and peak stroke volumes in the two younger groups. Newborn lambs developed tricuspid regurgitation and right-to-left foraminal shunting, demonstrated by echocardiography, at a mean end-diastolic pressure of 7.5 mm Hg. No right-to-left shunting was noted in older lambs. This study demonstrated a blunted Starling response in the newborn lamb's right ventricle. The response to volume loading improved with maturation, but was still less than that reported for the left ventricle. Clinical implications regarding right ventricular immaturity and inadequate response to altered hemodynamic situations are raised.
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PMID:Hemodynamic responses of the acutely stressed neonatal right ventricle: a maturational study in lambs. 395 98

This discussion addresses the questions of the parinatal, neonatal, and infant health and development of children born to adolescent mothers as related to other biologic and social factors. Medical and legislative plans for adolescent mothers and their infants must be based on assessment of both mortality and morbidity of the infants born to adolescent mothers. Focus here is on neonatal data on 55,711 pregnancies collected by the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke; neonatal data from the University of Kansas Medical Center covering 4000 pregnancies, 770 of which were gestations in teenage mothers; and obstetric, perinatal, and neonatal data concerning 6087 pregnancies in 1976, 1977, and 1978 at the Regional Perinatal Center at the University of Rochester. Ample evidence suggests a strong association between maternal age and birth weight. In particular, Hardy and Mellits found a higher frequency of low birth weight infants born to young black women. Interactions with other variables, including parity, clearly illustrate that firstborn infants are lighter than subsequent infants up to a maternal age of 35. Hoffman et al. have demonstrated that American women 18 years and under show a tendency to have infants of shorter gestational age than women 19-24 years of age. Cigarette smoking, alcohol and drug abuse, prolonged rupture of membranes, seizure disorders, and gonorrhea were significantly more frequently diagnosed in teenage mothers. The studies showed that behavioral and medical complications in the mothers were more powerful determinants of infants born with weight of less than 2500 gm than maternal age alone. In sum, when maternal and fetal growth retarding factors are taken into account among mothers of specific age categories, no biologic disadvantage appears unique to adolescent mothers. Findings fail to support the often expressed view that the mother's biologic immaturity is the main factor responsible for excessive fetal and neonatal deaths in infants born to very young mothers. Proportionately more infants born to adolescent mothers required admission to the intensive care or special care nurseries at the University of Rochester hospital than did infants born to mothers in their 20s (15.77% versus 13.9%). The data suggest that the mothering skills and child rearing practices of adolescent childbearing women have yet to be evaluated adequately.
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PMID:The infants of adolescent mothers. 736 May 10

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

The blood-brain barrier (BBB) is a diffusion barrier, which impedes influx of most compounds from blood to brain. Three cellular elements of the brain microvasculature compose the BBB-endothelial cells, astrocyte end-feet, and pericytes (PCs). Tight junctions (TJs), present between the cerebral endothelial cells, form a diffusion barrier, which selectively excludes most blood-borne substances from entering the brain. Astrocytic end-feet tightly ensheath the vessel wall and appear to be critical for the induction and maintenance of the TJ barrier, but astrocytes are not believed to have a barrier function in the mammalian brain. Dysfunction of the BBB, for example, impairment of the TJ seal, complicates a number of neurologic diseases including stroke and neuroinflammatory disorders. We review here the recent developments in our understanding of the BBB and the role of the BBB dysfunction in CNS disease. We have focused on intraventricular hemorrhage (IVH) in premature infants, which may involve dysfunction of the TJ seal as well as immaturity of the BBB in the germinal matrix (GM). A paucity of TJs or PCs, coupled with incomplete coverage of blood vessels by astrocyte end-feet, may account for the fragility of blood vessels in the GM of premature infants. Finally, this review describes the pathogenesis of increased BBB permeability in hypoxia-ischemia and inflammatory mechanisms involving the BBB in septic encephalopathy, HIV-induced dementia, multiple sclerosis, and Alzheimer disease.
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PMID:The blood-brain barrier: an overview: structure, regulation, and clinical implications. 1520 56

Survivors of premature birth have a predilection for perinatal brain injury, especially to periventricular cerebral white matter. Periventricular white matter injury (PWMI) is now the most common cause of brain injury in preterm infants and the leading cause of chronic neurological morbidity. The spectrum of chronic PWMI includes focal cystic necrotic lesions (periventricular leukomalacia) and diffuse myelination disturbances. Recent neuroimaging studies support that the incidence of periventricular leukomalacia is declining, whereas focal or diffuse noncystic injury is emerging as the predominant lesion. In a significant number of infants, PWMI appears to be initiated by perturbations in cerebral blood flow that reflect anatomic and physiological immaturity of the vasculature. Ischemic cerebral white matter is susceptible to pronounced free radical-mediated injury that particularly targets immature stages of the oligodendrocyte lineage. Emerging experimental data supports that pronounced ischemia in the periventricular white matter is necessary but not sufficient to generate the initial injury that leads to PWMI. The developmental predilection for PWMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible oligodendrocyte progenitors. Injury to oligodendrocyte progenitors may contribute to the pathogenesis of PWMI by disrupting the maturation of myelin-forming oligodendrocytes. There has been substantial recent progress in the understanding of the cellular and molecular pathogenesis of PWMI. The oligodendrocyte progenitor is a key target for preventive strategies to reduce ischemic cerebral white matter injury in premature infants.
Stroke 2007 Feb
PMID:Maturation-dependent vulnerability of perinatal white matter in premature birth. 1726 26

The immature brain is prone to hypoxic-ischemic encephalopathy and stroke. The incidence of arterial stroke in newborns is similar to that in the elderly. However, the pathogenesis of ischemic brain injury is profoundly affected by age at the time of the insult. Necrosis is a dominant type of neuronal cell death in adult brain, whereas widespread neuronal apoptosis is unique for the early postnatal synaptogenesis period. The inflammatory response, in conjunction with excitotoxic and oxidative responses, is the major contributor to ischemic injury in both the immature and adult brain, but there are several areas where these responses diverge. We discuss the contribution of various inflammatory mechanisms to injury and repair after cerebral ischemia in the context of CNS immaturity. In particular, we discuss the role of lower expression of selectins, a more limited leukocyte transmigration, undeveloped complement pathways, a more rapid microglial activation, differences in cytokine and chemokine interplay, and a different threshold to oxidative stress in the immature brain. We also discuss differences in activation of intracellular pathways, especially nuclear factor kappaB and mitogen-activated protein kinases. Finally, we discuss emerging data on both the supportive and adverse roles of inflammation in plasticity and repair after stroke.
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PMID:Does inflammation after stroke affect the developing brain differently than adult brain? 1967 67

A best evidence topic (BET) in cardiac surgery was written according to a structured protocol. The question addressed was whether ABO-incompatible (ABO-I) heart transplant recipients have a similar survival rate as an ABO-compatible (ABO-C) transplant in the pediatric population <1 year of age. Altogether more than 112 papers were found using the reported search, of which 10 represented the best evidence to answer the clinical question. Generally, ABO-I transplantation has been associated with the neonatal population because of the relative immaturity of the immune system for the first year of life. In the BET the search-term 'pediatric' was used as a method to ensure retrieval all relevant papers. However, the vast majority of the patients reviewed were <1 year of age with specific techniques undertaken to modulate preoperative, intraoperative and postoperative isohemagglutinin titer levels with rejection monitoring. Therefore, the BET conclusions should not be applied to the pediatric group as a broad age classification. Two large series are of particular interest. Patel et al. reviewed all primary heart transplantation recipients < or =1 year of age in the United Network for Organ Sharing/Organ Procurement and Transplantation Network (UNOS/OPTN) registry (ABO-I=35 vs. ABO-C=556). There was no difference in 30-day mortality (ABO-I=5.9% vs. ABO-C=8.8%; P=0.55); one-year mortality (ABO-I=16.6% vs. ABO-C=14.7%; P=0.77); graft rejection (ABO-I=1 vs. ABO-C=0); and graft failure (ABO-I=24% vs. ABO-C=24%; P>0.99). Three-year Kaplan-Meier survival was 70% (P=0.85). Propensity score adjusted analysis did not implicate ABO-I as a predictor of mortality [hazard ratio (HR)=3.6, confidence interval (CI): 0.2-49.0; P=0.33]. The ABO-I group demonstrated an increased need for pacemaker (ABO-I=3.1% vs. ABO-C=0.4%; P=0.03) and higher stroke rate (ABO-I=12.9% vs. ABO-C=1.3%; P<0.0001). Dipchand et al. published the results of the Toronto cohort from 1992 to 2006 (ABO-I=16 vs. ABO-C=38). The median age at transplantation (ABO-I=88 days vs. ABO-C=84 days; P=0.82) and the number of neonatal transplant recipients (ABO-I=17% vs. ABO-C=22%; P=0.59) was similar. The freedom from post-transplantation death or retransplantation was equivalent at one year (ABO-I=77% vs. ABO-C=84%) and seven years (ABO-I=74% vs. ABO-C=74%; P=0.87). No significant difference was observed for the five-year freedom from: rejection (ABO-I=60% vs. ABO-C=45%; P=0.41); renal dysfunction (ABO-I=67% vs. ABO-C=72%; P=0.70); allograft vasculopathy (ABO-I=87% vs. ABO-C=78%; P=0.45); and post-transplantation lymphoproliferative disorder (PTLD) (ABO-I=87% vs. ABO-C=86%; P=0.93). We conclude that ABO-I transplantation is comparable to ABO-C transplantation, with several retrospective papers concluding there is no difference in mortality, morbidity or graft failure in the pediatric population <1 year of age.
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PMID:Does ABO-incompatible and ABO-compatible neonatal heart transplant have equivalent survival? 2030 66

Cell transplantation has been proposed as a potential approach to the treatment of neurological disorders. One cell population of interest consists of human umbilical cord blood (hUCB) cells, which have previously been shown to be useful for reparative medicine in haematological diseases. However, hUCB cells are also capable of differentiating into various non-haematopoietic cells, including those of the neural lineage. Moreover, hUCB cells can secrete numerous neurotrophic factors and modulate immune function and inflammatory reaction. Several studies on animal models of ischemic brain injury have demonstrated the potential of hUCB cells to minimize damage and promote recovery after ischemic brain injury.This review focuses on the treatment of both stroke and perinatal hypoxic-ischemic brain injury using hUCB cells. We discuss the therapeutic effects demonstrated after hUCB cell transplantation and emphasize possible mechanisms counteracting pathophysiological events of ischemia, thus leading to the generation of a regenerative environment that allows neural plasticity and functional recovery. The therapeutic functional effects of hUCB cells observed in animal models make the transplantation of hUCB cells a promising experimental approach in the treatment of ischemic brain injury. Together with its availability, low risk of transplantation, immaturity of cells, and simple route of application, hUCB transplantation may stand a good chance of being translated into a clinical setting for the therapy of ischemic brain injury.
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PMID:Umbilical cord blood cell transplantation after brain ischemia--from recovery of function to cellular mechanisms. 2151 22


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