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Results for “Neurodevelopment”

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At least 649 records · Page 36Linked to original sources

PubMed1999

Pediatric experience with intradialytic parenteral nutrition and supplemental tube feeding.

Good nutrition is necessary to maximize the potential for growth and development in the pediatric age-group, but children, like adults with chronic renal failure and end-stage renal disease, may be anorectic and eat poorly. Infants and adolescents are at special risk because of the intense demands of growth during the first 2 years of life and again during puberty. Neurodevelopment is also adversely affected by poor nutrition, especially in infants. Approximately two-thirds of pediatric dialysis patients are treated with chronic peritoneal dialysis, which results in significant protein losses in the dialysis effluent that can contribute to protein-calorie malnutrition. Meeting the nutritional needs of pediatric patients usually requires supplemental sources, such as intradialytic parenteral nutrition (IDPN) or tube feeding. Little is known about the effectiveness or desirability of IDPN in pediatric patients. More studies, especially of amino acid-based dialysis fluids for chronic peritoneal dialysis, need to be done before making IDPN a standard for pediatrics. Supplemental nasogastric or gastrostomy tube feedings have been very successful in maintaining and improving growth in infants, but no studies are available to evaluate their success in older children and adolescents. Recombinant growth hormone therapy, in addition to good nutrition and control of other growth factors such as acidosis, renal osteodystrophy, and chronic volume depletion, may be necessary for most growth-retarded children with chronic renal failure to achieve normal adult height.

Adolescent↗

PubMed1998

The role of gender differences in the reduction of etiologic heterogeneity in schizophrenia.

Recent research has shown a resurgence of interest in the study of gender differences in schizophrenia. Accumulated evidence suggests that, compared with women, men have a higher incidence of schizophrenia, earlier age of onset, poorer course and medication response, poorer premorbid social and intellectual functioning, fewer affective symptoms, lower family morbid risk of schizophrenia and affective disorders, more evidence of obstetric complications in their mothers, and greater structural brain abnormalities. The roles of estrogen, neurodevelopment, and family history of affective disorder are evaluated as co-contributors to the observed gender differences in schizophrenia. Particular emphasis is given to evaluating the hypothesis that men are more prone to a hypothesized poor-prognosis, neurodevelopmental subtype of schizophrenia, for which early environmental brain insults play an important etiologic role, whereas women may be more prone to a hypothesized good-prognosis, affective subtype that is genetically related to the affective disorders. This hypothesis is evaluated in terms of (a) its ability to account for gender differences in schizophrenia, (b) its ability to link differences in clinical presentation to proposed differences in etiology; and (c) its potential to generate testable predictions for future schizophrenia research.

Adult↗

PubMedDate not supplied

Cognitive and motor development in children with vertically transmitted HIV infection.

This study was designed to examine mental and motor development in infants with vertically transmitted human immunodeficiency virus (HIV) infection. Early neurodevelopment was examined in 25 young children with HIV infection acquired through vertical transmission. Compared with 25 children born to HIV-positive mothers but not infected with the virus, and after controlling for developmental risk factors, the HIV-infected group showed impairments in mental and motor development. Mental and motor development were assessed using the Bayley Scales of Infant Development. On the mental scale (MDI), the HIV-infected infants obtained significantly lower scores than the uninfected infants. On the performace scale (PDI), the HIV-infected infants obtained significantly lower standard scores than the uninfected infants. CT scan results were available for 20 of the HIV-infected children. CT abnormalities were associated with developmental delays, particularly for motor development. The results point to the importance of early abnormalities in myelination and of subcortical lesions of cognitive and motor development.

Brain↗

PubMed2003

Outcome in preterm small for gestational age infants compared to appropriate for gestational age preterms at the age of 2 years: a prospective study.

OBJECTIVES: To investigate the effects of small for gestational age (SGA) in preterm infants on growth and development until the age of 22 months. STUDY DESIGN: Seventy-four preterm infants being born SGA (birth weight <10th percentile) were compared with 74 appropriate for gestational age (AGA) infants matched prospectively according to gestational age with respect to growth parameters and neurodevelopment (using Griffiths developmental scores) at the age of 22 months corrected age. RESULTS: Birth weight was significantly lower in SGA-infants compared to AGA-infants (1503 g (430-2205 g) versus 1995 g (680-3300 g); P<0.0001 (median and range)). There were no significant differences regarding the median gestational age (34 weeks), gender distribution, mode of delivery, umbilical artery pH, and APGAR-scores. Mean Griffiths-scores did not differ significantly between both groups (96.7% versus 97.6%). Developmental retardation was diagnosed in 9 SGA-infants versus 10 AGA-infants. Within the total group a positive correlation was observed between gestational age and developmental scoring. Body weight, head circumference, and height were significantly lower in SGA-infants at 22 months corrected age. CONCLUSION: No significant differences regarding neurodevelopmental outcome at 22 months were observed between SGA- and AGA-infants. SGA-infants did not show catch-up growth.

Apgar Score↗

PubMed2003

Placental insufficiency and its consequences.

Placental insufficiency is a process leading to progressive deterioration in placental function and a decrease in transplacental transfer of oxygen and nutrients to the fetus. The resulting fetal hypoxemia is the major stimulus involved in the reduction in fetal growth as an attempt to reduce metabolic demands by the growing fetus. Fetal growth restriction (FGR) is the second cause of perinatal death after prematurity and can complicate up to 6% of all pregnancies. It is becoming apparent that its occurrence has major impacts on the fetus and placenta with consequences on the cardiovascular, metabolic and neurological development up to adulthood. We are just starting to unveil some of the basic mechanisms involved in this complex adaptation that may lead to reprogramming of fetal organs development mostly the heart, pancreas, lungs and brain. It is becoming clear that future research is needed to develop strategies to improve antenatal detection of FGR, in addition to reduce the risk of abnormal neurodevelopment during childhood, and onset of common diseases in adulthood following pregnancies complicated with placental insufficiency.

Animals↗

PubMed1998

Outcome of 88 pregnancies with absent or reversed end-diastolic blood flow (ARED flow) in the umbilical arteries.

OBJECTIVES: To investigate both perinatal and postneonatal morbidity and mortality in fetuses with absent or reversed end-diastolic flow (ARED flow) in the umbilical artery. STUDY DESIGN: A 5 year prospective follow-up of 88 fetuses with ARED flow. RESULTS: Sixteen stillbirths, 16 neonatal deaths, six postneonatal deaths and one death at 2 years of age were noted. Out of the 42 fetuses born alive, 36 showed a normal neurological development whereas six were mentally handicapped. Adverse prognosis was more frequently found in the group with absent end-diastolic flow at first examination and then reversed flow until delivery, compared to the groups of always absent or always reversed end-diastolic flows. CONCLUSIONS: Prompt delivery is recommended in these high-risk pregnancies in order to prevent long-term sequelae, obviously depending on the local limits of viability. Further studies appropriately designed for assessing long-term neurodevelopment of fetuses with ARED flow, although demanding, are mandatory.

Female↗

PubMed1998

A gene essential to brain growth and development maps to the distal arm of rat chromosome 12.

A recently discovered, spontaneous, autosomal recessive mutation in rats, flathead (fh), results in greatly reduced brain growth beginning in late fetal development. In this study we have mapped the fh mutation by determining the pattern of segregation of polymorphic microsatellite markers with respect to fh in 51 affected F2 offspring from a single interstrain intercross. Two markers on chromosome 12, D12Rat80 and D12Mgh6, cosegregated with the fh mutation in all 51 affected animals. The distribution of six additional markers in 40 informative meioses further localizes fh approximately 2 cM teleomeric to nos1. There are no known mutations in homologous regions of either mouse or human genomes that result in deficits in late neurodevelopment similar to that observed in fh/fh animals. The unique phenotype of fh/fh animals and the location of fh suggests the presence of a novel gene essential to normal brain development on the distal end of rat chromosome 12.

Aging↗

PubMed2002

Hippocampal heterotopia with molecular and electrophysiological properties of neocortical neurons.

Cortical malformations resulting from aberrant brain development can be associated with mental retardation, dyslexia, and intractable forms of epilepsy. Despite emerging interest in the pathology and etiology of cortical malformations, little is known about the phenotype of cells within these lesions. In utero exposure to the DNA methylating agent methylazoxymethanol acetate (MAM) during a critical stage in neurodevelopment results in animals with distinct clusters of displaced neurons in hippocampus, i.e. nodular heterotopia. Here we examined the molecular and electrophysiological properties of cells within hippocampal heterotopia using rats exposed to MAM during gestation. Molecular analysis revealed that heterotopic cells do not express mRNA markers normally found in hippocampal pyramidal cells or dentate granule cells (SCIP, Math-2, Prox-1, neuropilin-2). In contrast, Id-2 mRNA, normally abundant in Layer II-III supragranular neocortical neurons but not in CA1 pyramidal neurons, was prominently expressed in hippocampal heterotopia. Current-clamp analysis of the firing properties of heterotopic neurons revealed a striking similarity with supragranular cortical neurons. In particular, both cells were characterized by small hyperpolarizing 'sag' potentials, high input resistance values, slow spike-train afterhyperpolarizations, and the absence of a depolarizing afterpotential. Normotopic CA1 pyramidal neurons (e.g. pyramidal cells with normal lamination adjacent to a heterotopia) in the MAM brain exhibited molecular and electrophysiological properties that were nearly identical to those of age-matched CA1 pyramidal neurons from control rats. We conclude that neuronal heterotopiae in the hippocampus of MAM-exposed rats are comprised of neurons with a Layer II-III supragranular cortex phenotype. The MAM model, therefore, may serve as a useful tool in examination of the factors influencing aberrant brain development and epilepsy.

Action Potentials↗

PubMed1998

Hippocampal and cortical growth-associated protein-43 messenger RNA in schizophrenia.

Growth-associated protein-43 is involved in maturational and plasticity-associated processes, and changes in growth-associated protein-43 expression are a marker of altered plasticity following experimental and neuropathological lesions. Using in situ hybridization, we have investigated growth-associated protein-43 mRNA in the medial temporal lobe and cerebral cortex in 11 normal subjects and 11 matched subjects with schizophrenia, a disorder in which perturbed neurodevelopment and aberrant plasticity are implicated. In the schizophrenia group, growth-associated protein-43 messenger RNA was decreased in the medial temporal lobe, primary visual cortex and anterior cingulate gyrus, but was unaltered in the superior temporal and dorsolateral prefrontal cortices. Correlations of growth-associated protein-43 messenger RNA signal between areas were stronger and more numerous in the schizophrenics than in the controls, suggesting a more global regulation of growth-associated protein-43 expression. Finally, the ratio of growth-associated protein-43 messenger RNA to synaptophysin messenger RNA--a putative index of the production of new synapses--was decreased in the medial temporal lobe in the schizophrenics. Our findings imply that neuronal plasticity as indexed by growth-associated protein-43 expression is impaired, and perhaps aberrantly regulated, in schizophrenia. The data support the emerging view that the disease pathophysiology is one which affects the hippocampal and cortical circuitry and that the abnormalities are reflected in the altered expression of specific neuronal genes.

Adult↗

PubMed2001

Neurotoxicity and molecular effects of methylmercury.

The neurotoxicity of high levels of methylmercury (MeHg) and the high susceptibility of the developing brain are well established both in humans and experimental animals. Prenatally poisoned children display a range of effects varying from severe cerebral palsy to subtle developmental delays. Still unknown is the lowest dose that impairs neurodevelopment. The primary source of human exposure is the fish. The data obtained so far from epidemiological studies on fish-eating populations are not consistent. A reference dose of 0.1 microg MeHg/kg per day has been established by the U.S. Environmental Protection Agency based on a study on Iraqi children exposed to MeHg in utero. However, these exposures occurred at high level for a limited period of time, and consequently were not typical of lower chronic exposure levels associated with fish consumption. Major obstacles for estimation of a threshold dose for MeHg include the delayed appearance of the neurodevelopmental effects following prenatal exposure and limited knowledge of cellular and molecular processes underlying these neurological changes. In this respect, a strategy which aims at identifying sensitive molecular targets of MeHg at environmentally relevant levels may prove particularly useful to risk assessment. Here some examples of MeHg molecular effects occurring at low doses/concentrations are presented.

Animals↗

PubMed2001

The relationship between age and the fatty acid composition of cerebral cortex and erythrocytes in human subjects.

The important role that neural tissue fatty acid composition plays in neurodevelopment and various pathological states is increasingly recognized. However, there are limited data regarding the fatty acid composition of normal human brain at various ages. The purpose of this study was to describe human cerebral cortex fatty acid composition from ages 2 to 88 years. The relationship between cerebral cortex and erythrocyte fatty acid composition was also investigated. Samples of frontal cerebral cortex and of erythrocytes were obtained from 58 human subjects on whom autopsies were performed. The mean age of subjects was 40 +/- 29 years, with a range of 2 to 88 years. The fatty acid composition of tissues was determined, and linear regression models were used to describe the relationship between age and the fatty acid composition of cerebral cortex and erythrocytes. The data were bilinear, with changes occurring after the approximate age of 18 years. Therefore, the cohort was divided into subjects with ages < or =18 and >18 years. In the younger group, the polyunsaturated fatty acids generally decreased with age, with the exception of 22:6n3, which demonstrated a significant increase. The level of mono-unsaturated fatty acids, in contrast, generally increased to the age of 18 years. Several of the polyunsaturated fatty acids also decreased with age in the older cohort, particularly 20:4n6. The levels of 18:2n6, however, increased significantly with age in the older cohort. Among subjects < or =18 years of age, there was no significant relationship between cerebral cortex and erythrocyte fatty acid levels. In the older cohort, there was a significant relationship between brain and erythrocyte levels for several fatty acids, particularly 16:0. These data demonstrate that levels of cerebral cortex fatty acids change from early childhood through late adulthood, and indicate that the levels of several erythrocyte fatty acids may be useful in predicting brain fatty acid levels in adults.

Adolescent↗

PubMed2001

Biochemical, behavioral, physiologic, and neurodevelopmental changes in mice deficient in monoamine oxidase A or B.

The availability of mutant mice that lack either MAO A or MAO B has created unique profiles in the central and peripheral availability of serotonin, norepinephrine, dopamine, and phenylethylamine. This paper summarizes some of the current known phenotypic findings in MAO A knock-out mice and contrast these with those of MAO B knock-out mice. Differences are discussed in relation to the biochemical, behavioral, and physiologic changes investigated to date, as well as the role played by redundancy mechanisms, adaptational responses, and alterations in neurodevelopment.

Animals↗

PubMed1999

Localization of the Norrie disease gene mRNA by in situ hybridization.

Norrie disease is a rare X-linked recessive neurodevelopmental disorder. The affected males manifest congenital blindness, which is often associated with hearing loss, mental retardation and psychiatric problems. Genetic linkage studies have localized the gene to the short arm of the X-chromosome and the gene has been isolated recently. The encoded protein is a member of the superfamily of growth factors containing a cystine knot motif and may be involved in cell adhesion and neurodevelopment. Molecular genetic analysis revealed a large number of missense, nonsense, deletion, and splice-site mutations among Norrie patients. In order to further determine the role of the Norrie disease gene, we studied the distribution pattern of its mRNA in the retina and in brain by in situ hybridization. The results show abundant hybridization signals in outer nuclear, inner nuclear, and ganglion cell layers of the retina in all three species (mice, rabbit, and human) examined. There was no significant expression in the vitreous body, lens, and rod outer segment. High expression levels were also observed in the cerebellar granular layer, hippocampus, olfactory bulb, cortex, and epithelium of the rabbit brain. These data suggest that the Norrie disease gene could play a critical role in the differentiation or maintenance of the differentiated state of the retina.

Animals↗

PubMed1999

Enteral feeding in the preterm infant.

In planning enteral feeding in the preterm infant, decisions need to be made regarding the feeding schedule, choice of milk, and the route of administration. Feeds should be commenced within a week after birth beginning with subnutritional quantities. Preterm human milk from the infant's own mother is the milk of choice. When full enteral feeding is established, supplementation with human milk fortifier is recommended. Donor human milk and preterm formula are alternatives. Early establishment of enteral nutrition and maintenance of optimal nutrition during infancy are important as dietary manipulations in preterm infants have potential long-term influences on their health, growth and neurodevelopment.

Enteral Nutrition↗

PubMed2001

Rett syndrome: clinical correlates of the newly discovered gene.

The recent identification of mutations in the gene, MECP2, in girls with Rett syndrome (RS) firmly establishes the molecular genetic basis of this X-linked dominant disorder. This discovery, with ramifications far beyond establishing the gene for RS, represents a dramatic conclusion to an intensive, decade-long search. MECP2 encodes a methyl-CpG-binding protein (MeCP2) involved in transcriptional silencing of a yet to be defined number and type of genes. The clinical spectrum of resultant disorders extends well beyond RS. Indeed, the clinical phenotypes for MECP2 mutations range from mild disability in the mother of a girl with RS to rapidly progressive encephalopathy in her brother. Further, the recent identification of MECP2 mutations in boys with phenotypes quite different from RS adds yet another element to the mix. Within the classic RS group, clinical severity varies remarkably, depending at least in part on the degree of non-random X-inactivation. Those with clinical patterns in the border zones of RS remain to be examined fully for less severe mutational events. Further, the pathobiology of RS and the role of transcriptional silencing as a disease-producing mechanism could be a prototype for other disorders of neurodevelopment. Thus, the identification of mutations in MECP2 creates completely new vistas as to fundamental neurobiologic processes, to disease mechanisms in the neurodevelopmental disabilities, and to potential new therapeutic strategies for RS and related disorders.

Adolescent↗

PubMed1985

The cephalization index: a screening device for brain maturity and vulnerability in normal and intrauterine growth retarded newborns.

Predictive estimates of future neurological maldevelopment as a result of vascular induced intrauterine injury are based on the assumption that the body is more affected than the brain resulting in asymmetrical intrauterine growth retarded (IUGR) newborns. The higher the brain:body ratio, the more severe the IUGR process and the greater the risk for the brain to be affected. This prompted us to study in human newborns, a cephalization index based on the ratio of head circumference to body weight to express the degree of brain maturity and possible vulnerability in relation to gestational age. The newborn cephalization index was correlated with neurodevelopment. A trend could be delineated; in the later gestational age, the higher the cephalization index reflecting a greater degree of brain vulnerability, the more severe the clinical pathology; especially the likelihood of cerebral palsy and severe psychomotor retardation. The cephalization index may serve as an additional screening device for high risk intrauterine growth retarded newborns.

Body Weight↗

PubMed2000

Congenital unilateral hydrocephalus--CT findings.

Congenital unilateral hydrocephalus is extremely uncommon with 18 cases previously reported in the English literature. Two additional newborns with unilateral hydrocephalus are presented. The second baby also presented a mega cisterna magna. This unusual association between Dandy-Walker variant and unilateral hydrocephalus has not been previously reported. Following ventriculo-peritoneal shunt, the babies had a normal cognitive neurodevelopment. The role of cranial computed tomography (CT) in diagnosis and follow-up is emphasized.

Brain↗

PubMed1997

Cytokine regulation of embryonic rat dopamine and serotonin neuronal survival in vitro.

Interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) are cytokines with pleiotropic effects in the central nervous system (CNS), including an emerging role in neurodevelopment. This study measured the effects of cytokines on the survival of tyrosine hydroxylase (TH) immunoreactive dopamine neurons from the substantia nigra (SN), and 5-hydroxytryptamine (5-HT) immunoreactive serotonin neurons from the rostral raphe (RR), using cultures from embryonic day 14 (E14) rat brain. IL-1beta, IL-6, and TNF-alpha were added to cell cultures at 1, 10 and 100 U/ml. After 3 days in vitro, TH and 5-HT neurons were counted. The survival of 5-HT neurons was significantly reduced by 20-30% at 10 U/ml of IL-6. IL-1beta and TNF-alpha at doses of 1 and 10 U/ml appeared to have a similar effect on the survival of these neurons, but this effect was not statistically significant. Comparable non-significant reductions of survival also occurred for TH neurons at the lower doses of IL-6 and TNF-alpha. In separate experiments, SN and RR cultures were exposed to the cytokines at a higher dose (1000 U/ml), causing a significant 30-40% decrease in the survival of TH neurons, but little or no change in 5-HT neuronal survival. Taken together, these results show that IL-1beta, IL-6, and TNF-alpha can affect developing monoamine neurons at physiologically relevant concentrations, and that high doses differentially inhibit the survival of TH and 5-HT neurons after short exposures.

Animals↗