Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is an increasing concern about HIV infection in paediatric age, due to its increasing incidence in some countries, especially in Europe, and due to its social aspects. HIV infection has particular features, while occurring during paediatric age: infection of child frequently occurs during pregnancy (perinatal form of HIV infection), a period characterized by the immaturity of the immune system of the host. Encephalopathy is a frequent manifestation of the disease, recurrent fever episodes have a different pathogenesis than in adults, LIP (lymphocytic interstitial pneumonia) is a common manifestation of the disease and there is a higher progression rate to AIDS. Antiretroviral therapy, as zidovudine (AZT) in paediatric age is still on clinical trials, and only few preliminary data are available.
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PMID:[The acquired immunodeficiency syndrome (AIDS) in childhood]. 196 93

Despite the immaturity of the newborn brain, the neonatal period is reported to have a very high frequency of seizures. This review concludes that many of the neonatal events that are called seizures probably originate from subcortical structures, have little in common with cortical seizures seen in older individuals, and may not benefit from conventional anticonvulsant treatment. Many studies of anticonvulsants in the newborn have important methodologic problems, compounded by the fact that the seizures tend to spontaneously remit with the resolution of the acute hypoxic-ischemic encephalopathy that is most often the cause. Randomized trials of anticonvulsants in this setting have not been carried out. Even in many of these seizures do not originate in the cortex, they still imply profound cortical disturbance and are associated with high mortality and morbidity. It is unknown if the type and duration of treatment influence the long-term, overall outcome. The seizures usually stop in the newborn period, and anticonvulsants beyond hospital discharge seem unwarranted because they are unlikely to prevent subsequent epilepsy. Newer investigations, including video-EEG and nuclear magnetic resonance studies, may clarify the real significance of neonatal seizures.
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PMID:Neonatal seizures: a commentary on selected aspects. 330 17

Hypoxic encephalopathy during the late gestation and perinatal period occupies a large part as a cause of mentally and physically handicaps. An extensive study on the pathogenesis and pathophysiology of the hypoxic brain damage is, therefore, the matter of urgency to minimize the occurrence of handicapped children. The main factors and/or processes relating to hypoxic or hypoxic-ischemic brain damage are (1) structural and functional immaturity of the brain vascular system and (2) a metabolic cascade triggered by hypoxia. As the following metabolic cascade subsequent to hypoxia has been partly made clear; (a) disturbance of the energy metabolism, (b) excessive release of excitatory amino acids and subsequent activation of NMDA and K/Q receptors at the cell membrane, (c) collapse of the membrane ion pump, and (d) increase in turnover of membrane phospholipids.
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PMID:[Pathogenesis of hypoxic encephalopathy during pre- and peri-natal periods]. 813 81

The paper presents the analysis of unfavourable ante- and intranatal factors as well as the data of neurosonography of 109 children with the fits during the first year of life and of 58 children with hypoxic-ischemic encephalopathy without convulsions. The high degree of the correlation was found between complications of the first half of pregnancy and the disturbances of growth and development of a child. Frequency of a trauma in the course of a delivery correlated with frequency of asphyxia. A persistence of a germinative matrix and signs of functional immaturity of the brain suggested the important role of both focal and multifocal cerebral dysplasias in the genesis of epileptic fits at the early stages of ontogenesis. In children with nonmalignant neonatal and idiopathic fits there were some nonvisualized cortical disorders that became pronounced under hypoxic-dysmetabolic conditions in the first case and during a period of the following maturation of axon-dendritic bounds and of the increase of neuronal activity in the second case.
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PMID:[On the etiology of epileptic seizures in children of the first year of life]. 1020 33

The paper presents the results of somatic, neurologic and neurophysiologic examination of 614 children which had hypoxic-ischemic encephalopathy of a moderate degree during the period from the birth till 3 years old. A period of gestation was characterised by some signs of fetoplacental insufficiency in 44.3% of children. Disorders in labor activity were revealed in 83.7% of mothers. Delay in nervous-mental development (77.3%), deviations in forming rhythmic EEG activity (75%), signs of morphologic immaturity of brain (38.8%) testified to inhibition of postnatal neuroontogenesis. All that together with high frequency of motor disorders (73.3%) and disorders in cerebral blood flow (43.8%) during the 1-st year of life were found to underlie development of psychoneurologic diseases in children of early age and necessitates early rehabilitation of these children.
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PMID:[Nervous-mental health of children who had perinatal damage of the nervous system]. 1075 51

In order to grasp the characteristics and outcomes with infants hospitalized long-term in NICUs, we reviewed all summary charts of 18 perinatal medical centers in Tokyo for the period from January 1989 to December 1998. We sampled 3,000 infants who required neonatal intensive care over 90 consecutive days out of 46,309 registered cases during the decade. The duration of hospital stay, making a comparative analysis of the number of days for the 50 percentile, was as follows. As a whole the infants required 125 days until discharge. Infants with 29-30 weeks gestation and infants with birth weights 1,000-1,499 g required shorter stays (106 days in both cases). The "discharge with complications" group required 136 days, and the "discharge on remission" group 119 days. Within the 31-32 weeks gestation group, those with "discharge with complications" required 107 days. Within the 29-30 weeks gestation group, those with "discharge on remission" required 104 days. Infants with 1,000-1,499 g birth weights for the "discharge with complications" and "discharge on remission" groups required 116 and 104 days respectively. Focusing on birthplace, the group of "inside-born" (born at perinatal medical centers) infants required 124 days, and the "outside-born" (born at non-perinatal medical centers) required 127 days. Respiratory distress syndrome (RDS), bronchopulmonary dysplasia (BPD) and chronic lung disease (CLD) were often seen in patients under 29 weeks gestation and under 1,000 g birth weight. Hypoxic ischemic encephalopathy (HIE), convulsions, congenital malformations and chromosomal abnormalities were frequent in the groups over 31 weeks and over 1,500 g. Apnoea and transient tachypnoea of newborn (TTN) often occurred in these at 29-30 weeks and 1,000-1,499 g. Also, apnoea and TTN were often seen in the "discharge on remission" group. RDS, apnoea and TTN occurRed frequently in the "inside-born" infants with over 31 weeks of gestation and over 1,500 g birth weight. There were many cases of HIE and convulsions in the "outside-born" infants of these groups. We found infants who required long-term intensive care to comprise three main groups. The first group consisted of infants of 29-30 weeks gestation and 1,000-1,499 g birth weight and demonstrated mild or few complications. The second consisted of under 29 weeks and under 1,000 g and exhibited complications of chronic lung diseases caused by immaturity of respiratory organs. The third was the group of over 31 weeks and over 1,500 g who had complications due to central nervous system disease, congenital malformations and chromosomal abnormalities.
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PMID:[A survey of infants requiring long-term neonatal intensive care in Tokyo: 1989-1998]. 1240 75

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

We have conducted a case-control retrospective study to determine the risk of Intra Uterine Growth Retardation (IUGR) in pregnant women with preeclampsia. We have found that IUGR is one of the most prominent features of preeclampsia and occurs in 27% of cases (Odds Ratio 1.20). IUGR occurs during fetal-placental insufficiency (ultrasound structural changes of placenta such as aging and calcifications take place in 67.8% of cases, oligohydramnia in 42.8% of cases, changes of hemodynamics in maternal -- fetal placental unit -- in 82.3% of cases; deviation from the norm of resistance index and pulse index was 1.5-2 times higher). IUGR was accompanied with the poor functional state of the fetus (85.7% according to the cardiotocographic monitoring); morphological investigation of placenta showed dystrophic and destructive changes, which finally leads to the high rate of morbidity during neonatal period (hypoxic-ischemic encephalopathy -- 66%, respiratory distress syndrome -- 36%, pneumonia and atelectasis --14%) and fetal functional immaturity confirmed by EEG.
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PMID:[Risk of iugr syndrome development during preeclampsia of the pregnant]. 1636 54

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

An aim of the study was to specify peculiarities of the clinical dynamics of organic psychic infantilism and psychopathological presentations of this disorder in adolescence. A significant prevalence of psychic infantilism caused by organic CNS damage in patients seeking psychiatric help in adolescence and a negative effect of this disorder on social adaptation in this period of life were found. Sixty-seven patients, aged 15-18 years, (ICD-10 diagnosis F06) with signs of psychic infantilism were studied. In these cases, psychic infantilism encompassed all aspects of mental activity and manifested itself as a constant personality trait that caused the infantile type of reaction to the most of life situations. The clinical heterogeneity of organic infantilism determined by the different degree of psychic immaturity in some areas of psychic activity and concomitant encephalopathy symptoms was noted. This allowed to single out 3 groups of patients: with domination of psychic infantilism in volition (28 patients), in emotional sphere (21 patients) and immaturity of cognitive functions (20 patients). The clinical heterogeneity of psychic infantilism likely reflects the character of CNS damage (localization and time of the damage) and specifics of related organic dysontogenesis.
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PMID:[Peculiarities of organic psychic infantilism in adolescents]. 2003 50


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