Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sharp rise in the caesarean section rate, over the past years has been causing lot of concerns. It is to be evaluated whether the decrease in perinatal mortality rate is due to the rising rate of caesarean section. Five hundred consecutive patients were selected on whom caesarean section had been performed. Both mother and baby were followed till they are discharged from the hospital. Foetal distress was the commonest indication in primigravidae who underwent caesarean section. The other indications of caesarean section in this study were breech, severe pre-eclampsia, eclampsia, cord prolapse, elderly primi, postdated, premature rupture of membrane, twin, compound presentation, meconium stained liquor. The occurrence of perinatal morbidity in caesarean section was 10% compared to 12% in vaginal delivery. Common causes of perinatal morbidity were asphyxia, prematurity, diarrhoea, septicaemia, jaundice, conjunctivitis and scalp injury. The occurrence of perinatal mortality in caesarean section was 3.8% compared to 3% in vaginal delivery. Causes of perinatal mortality were stillbirth, meconium aspiration syndrome, hypoxic ischaemic encephalopathy, prematurity and congenital malformation. In spite of safety of vaginal birth after caesarean section it continues to be underutilised. Good perinatal care proper screening and use of newer effective pharmacological agents improve the maternal progress as well as perinatal outcome without increasing the caesarean section rate.
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PMID:Impact of increased rate of caesarean section on perinatal outcome: sociolegal evaluation. 2218 63

Translational research in preterm brain injury depends upon the delineation of the human neuropathology in order that animal models faithfully reiterate it, thereby ensuring direct relevance to the human condition. The major substrate of human preterm brain injury is the encephalopathy of prematurity that is characterized by gray and white matter lesions reflecting combined acquired insults, altered developmental trajectories, and reparative phenomena. Here we highlight the key features of human preterm brain development and the encephalopathy of prematurity that are critical for modeling in animals. The complete mimicry of the complex human neuropathology is difficult in animal models. Many models focus upon mechanisms related to a specific feature, for example, loss of premyelinating oligodendrocytes in the cerebral white matter. Nevertheless, animal models that simultaneously address oligodendrocyte, neuronal, and axonal injury carry the potential to decipher shared mechanisms and synergistic treatments to ameliorate the global consequences of the encephalopathy of prematurity.
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PMID:Modeling the encephalopathy of prematurity in animals: the important role of translational research. 2268 53

In the study of 887 new born infants with prenatal and perinatal risk factors for brain damage, 11 children with West syndrome that progressed into Lennox-Gastaut syndrome and another 4 children with Lennox-Gastaut syndrome that had not been preceded by West syndrome were found. In this study we present the main findings of these 15 subjects. In all infants multifactor antecedents were detected. The most frequent risk factors were prematurity and severe asphyxia; however placenta disorders, sepsis, and hyperbilirubinemia were also frequent. In all infants MRI direct or secondary features of periventricular leukomalacia were observed. Followup of all infants showed moderate to severe neurodevelopmental delay as well as cerebral palsy. It is concluded that prenatal and perinatal risk factors for brain damage are very important antecedents that should be taken into account to follow up those infants from an early age in order to detect and treat as early as possible an epileptic encephalopathy.
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PMID:Epileptic encephalopathy in children with risk factors for brain damage. 2295 40

High angular resolution diffusion imaging (HARDI) demonstrates transient radial coherence of telencephalic white matter in the human fetus. Our objective was to define the neuroanatomic basis of this radial coherence through correlative HARDI- and postmortem tissue analyses. Applying immunomarkers to radial glial fibers (RGFs), axons, and blood vessels in 18 cases (19 gestational weeks to 3 postnatal years), we compared their developmental profiles to HARDI tractography in brains of comparable ages (n = 11). At midgestation, radial coherence corresponded with the presence of RGFs. At 30-31 weeks, the transition from HARDI-defined radial coherence to corticocortical coherence began simultaneously with the transformation of RGFs to astrocytes. By term, both radial coherence and RGFs had disappeared. White matter axons were radial, tangential, and oblique over the second half of gestation, whereas penetrating blood vessels were consistently radial. Thus, radial coherence in the fetal white matter likely reflects a composite of RGFs, penetrating blood vessels, and radial axons of which its transient expression most closely matches that of RGFs. This study provides baseline information for interpreting radial coherence in tractography studies of the preterm brain in the assessment of the encephalopathy of prematurity.
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PMID:Radial coherence of diffusion tractography in the cerebral white matter of the human fetus: neuroanatomic insights. 2313 6

CEACAM1 is the founder molecule of the family of 'carcinoembryonic antigen-related cell adhesion molecules' and part of the immunoglobulin superfamily. Due to its role as a coreceptor to many other receptors (e.g. Toll-like receptor 2, Toll-like receptor 4, T-cell receptor, B-cell receptor, epidermal growth factor receptor and vascular endothelial growth factor receptor) and its different isoforms, CEACAM1 is a multifunctional protein with an impact on proliferation and differentiation of multiple cell types. Although different modes of action in other tissues are described, the role of CEACAM1 in the developing brain remains elusive. Here we report for the first time that CEACAM1 is expressed ontogenetically in oligodendrocytes of the developing rat brain, and that CEACAM1 expression has a spatiotemporal relation to myelination. In addition, CEACAM1 expression is altered in a model of hyperoxia- and inflammation-induced encephalopathy of prematurity, a myelination disorder of children born preterm. Furthermore, primary oligodendrocytes stimulated with CEACAM1 show increased myelination. Therefore, we postulate that CEACAM1 is, at least in part, involved in hyperoxia- and inflammation-induced disruption of myelination, but may also play a role in intact myelination as it is ontogenetically expressed in myelinating oligodendrocytes.
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PMID:CEACAM1 expression in oligodendrocytes of the developing rat brain shows a spatiotemporal relation to myelination and is altered in a model of encephalopathy of prematurity. 2365 19

We studied a model of hemorrhagic encephalopathy of prematurity (EP) that closely recapitulates findings in humans with hemorrhagic EP. This model involves tandem insults of 20 min intrauterine ischemia (IUI) plus an episode of elevated venous pressure induced by intraperitoneal glycerol on post-natal day (P) 0. We examined Sur1 expression, which is upregulated after focal ischemia but has not been studied after brief global ischemia including IUI. We found that 20 min IUI resulted in robust upregulation of Sur1 in periventricular microvessels and tissues. We studied tandem insult pups from untreated or vehicle-treated dams (TI-CTR), and tandem insult pups from dams administered a low-dose, non-hypoglycemogenic infusion of the Sur1 blocker, glibenclamide, for 1 week after IUI (TI-GLIB). Compared to pups from the TI-CTR group, pups from the TI-GLIB group had significantly fewer and less severe hemorrhages on P1, performed significantly better on the beam walk and accelerating Rotarod on P35 and in tests of thigmotaxis and rapid learning on P35-49, and had significantly greater body and brain weights at P52. We conclude that low-dose glibenclamide administered to the mother at the end of pregnancy protects pups subjected to IUI from post-natal events of elevated venous pressure and its consequences.
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PMID:The protective effect of glibenclamide in a model of hemorrhagic encephalopathy of prematurity. 2366 41

In recent decades, there has been a general increase in survival rates of preterm and low birth weight infants, but this overall decrease in perinatal mortality has not been accompanied by a decrease in long-term physical and mental disability. In order to reduce the long-term sequelae of prematurity and to establish preventive measures, it is important to identify risk factors since the main determinant of specific vulnerability to different types of lesions is gestational age. The regional tissue vulnerability at a given gestational age is probably determined by the local metabolic requirements together with specific cell characteristics and their level of maturation. In this article, we discuss the most common neonatal cerebral lesions (cerebellar haemorrhage, germinal matrix intraventricular haemorrhage, periventricular leukomalacia, arterial ischaemic stroke, cerebral vein sinus thrombosis and hypoxic-ischaemic encephalopathy) related to the gestational age-dependent vulnerability of the premature brain.
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PMID:Different gestational ages and changing vulnerability of the premature brain. 2396 92

This case report concerns a newborn with bilateral adrenal massive hemorrhage complicated by inferior cava vein thrombosis, hypertension and encephalopathy to elaborate diagnostic and therapeutic problem of neonatal thromboembolic events. Increasing of risk population (extreme prematurity), improvement of imaging, laboratory and neonatologist care enhanced in recent years the diagnosis of this group of diseases. Even if literature about this subject is poor, we remark the significant effort of neonatologist to revise and update neonatal guidelines and the relevance of the institution of the National Registry of Neonatal Thrombosis (RITI).
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PMID:[An unusual case of "complicated" adrenal hemorrhage]. 2405 77

Brief but severe asphyxia in late gestation or at the time of birth may lead to neonatal hypoxic ischemic encephalopathy and is associated with long-term neurodevelopmental impairment. We undertook this study to examine the consequences of transient in utero asphyxia in late gestation fetal sheep, on the newborn lamb after birth. Surgery was undertaken at 125 days gestation for implantation of fetal catheters and placement of a silastic cuff around the umbilical cord. At 132 days gestation (0.89 term), the cuff was inflated to induce umbilical cord occlusion (UCO), or sham (control). Fetal arterial blood samples were collected for assessment of fetal wellbeing and the pregnancy continued until birth. At birth, behavioral milestones for newborn lambs were recorded over 24 h, after which the lambs were euthanased for brain collection and histopathology assessments. After birth, UCO lambs displayed significant latencies to (i) use all four legs, (ii) attain a standing position, (iii) find the udder, and (iv) successfully suckle--compared to control lambs. Brains of UCO lambs showed widespread pathologies including cell death, white matter disruption, intra-parenchymal hemorrhage and inflammation, which were not observed in full term control brains. UCO resulted in some preterm births, but comparison with age-matched preterm non-UCO control lambs showed that prematurity per se was not responsible for the behavioral delays and brain structural abnormalities resulting from the in utero asphyxia. These results demonstrate that a single, brief fetal asphyxic episode in late gestation results in significant grey and white matter disruption in the developing brain, and causes significant behavioral delay in newborn lambs. These data are consistent with clinical observations that antenatal asphyxia is causal in the development of neonatal encephalopathy and provide an experimental model to advance our understanding of neuroprotective therapies.
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PMID:Experimental modelling of the consequences of brief late gestation asphyxia on newborn lamb behaviour and brain structure. 2422 20

First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. During the last decade, glibenclamide has received renewed attention due to its pleiotropic protective effects in acute CNS injury. Acting via inhibition of the recently characterized Sur1-Trpm4 channel (formerly, the Sur1-regulated NCCa-ATP channel) and, in some cases, via brain KATP channels, glibenclamide has been shown to be beneficial in several clinically relevant rodent models of ischemic and hemorrhagic stroke, traumatic brain injury, spinal cord injury, neonatal encephalopathy of prematurity, and metastatic brain tumor. Glibenclamide acts on microvessels to reduce edema formation and secondary hemorrhage, it inhibits necrotic cell death, it exerts potent anti-inflammatory effects and it promotes neurogenesis-all via inhibition of Sur1. Two clinical trials, one in TBI and one in stroke, currently are underway. These recent findings, which implicate Sur1 in a number of acute pathological conditions involving the CNS, present new opportunities to use glibenclamide, a well-known, safe pharmaceutical agent, for medical conditions that heretofore had few or no treatment options.
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PMID:Glibenclamide for the treatment of acute CNS injury. 2427 50


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