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

Eleven globes of seven anencephalic infants with a gestational age of 36 to 41 weeks were examined pathologically. Atrophy of the ganglion cell and nerve fibre layers of the retina was found in all cases; optic nerve atrophy was noted in all 10 specimens in which the optic nerve was identified. In addition to findings attributable to immaturity, including persistent pupillary membrane (in 10 globes) and incomplete formation of the anterior chamber angle (in 5), we noted retinal dysplasia (in 4), colobomata (in 2) and proliferative retinopathy (in 1). Uncommon or previously undescribed abnormalities in association with anencephaly included cystic malformations of the meninges, sclera and globe (in one case each).
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PMID:Ocular anomalies in anencephaly: a clinicopathological study of 11 globes. 193 64

Identification of a suitable animal model is essential for the continued study of retinopathy of prematurity (ROP). Since 1984 we have used the newborn rat for the study of oxygen-induced retinopathy (OIR). The rat retina is highly immature at birth. Like those of humans, the retinal vessels arise from mesenchymal precursors, but contrary to that which occurs in humans, canalization of the rats inner retinal vessels is not related to the presence of cystoid spaces. In addition, only immature Stage I photoreceptors are present around the optic disk at birth. This extreme immaturity makes the rat retina highly susceptible to direct damage from oxygen. Oxygen-induced retinopathy can be produced by exposing the newborn rat to 80% oxygen for the first 7-10 days of life. We have demonstrated that OIR does not develop when oxygen is administered under conditions of moderate hyperbarism (+1.8 atm). It is possible that hyperbarism exerts a protective effect on the immature retinal vessels by inducing a vasoconstrictive response which reduces the amount of oxygen transported from the choroid to the inner retina during hypoxia. I recently hypothesized that this vasoconstriction might also affect the ciliary body, thus reducing the quality of aqueous produced, and we are currently studying the relationship between development of the immature retinal vessels in the rat and production and drainage of the aqueous. The question we are attempting to answer is whether a condition of relatively increased intraocular pressure is capable of promoting the development of OIR.
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PMID:Oxygen-induced retinopathy in the rat model. 220 74

This chapter presents a strategy for integration of the current thinking about the causes of ROP. Application of these concepts assumes that results of any etiologic study are derived from valid methods. Discussion of principles of validity in epidemiologic studies is beyond the scope of this paper. However, reference was made to two sources of invalidity in studies of the causes of ROP: 1) the empirical or operational definition and measurement of the conceptual cause, and 2) confounding by degree of immaturity of retinal vasculatures, particularly with regard to interpretation of duration of ventilatory support as a cause of ROP. The distinction was made between an agent that initiates or promotes disease mechanism and a cause. Failure to appreciate this distinction has contributed to the confusion about the role of oxygen in the pathogenesis of retinopathy. Apart from settings of oxygen mismanagement, oxygen per se is part of the mechanism for development of disease. Certainly there are other biochemical requirements in addition to oxygen that set the stage for full-blown disease. Factors that are associated with the disruption of normal development of retinal vasculature and are susceptible to manipulation (either by reduction or elimination) during the prenatal and postnatal period may be more useful component causes to investigate.
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PMID:Causes of retinopathy of prematurity: an epidemiologic perspective. 290 85

Our preliminary data show high levels of adenosine in the blood of very low birth weight (VLBW) infants, positively correlating to their prematurity (i.e. body weight class). This prompted us to look for a mechanism promoting such impressive adenosine increase. We hypothesized a correlation with oxygen challenge. In fact, it is recognized that either oxygen lack or its excess contribute to the pathogenesis of the injuries of prematurity, such as retinopathy (ROP) and periventricular white matter lesions (PWMI). The optimal concentration of oxygen for resuscitation of VLBW infants is currently under revision. We propose that the elevated adenosine blood concentrations of VLBW infants recognizes two sources. The first could be its activity-dependent release from unmyelinated brain axons. Adenosine in this respect would be an end-product of the hypometabolic VLBW newborn unmyelinated axon intensely firing in response to the environmental stimuli consequent to premature birth. Adenosine would be eventually found in the blood due to blood-brain barrier immaturity. In fact, adenosine is the primary activity-dependent signal promoting differentiation of premyelinating oligodendrocyte progenitor cells (OPC) into myelinating cells in the Central Nervous System, while inhibiting their proliferation and inhibiting synaptic function. The second, would be the ecto-cellular ATP synthesized by the endothelial cell plasmalemma exposed to ambient oxygen concentrations due to premature breathing, especially in lung. ATP would be rapidly transformed into adenosine by the ectonucleotidase activities such as NTPDase I (CD39), and NT5E (CD73). An ectopic extra-mitochondrial aerobic ATP synthetic ability was reported in many cell plasma-membranes, among which endothelial cells. The potential implications of the cited hypotheses for the neonatology area would be great. The amount of oxygen administration for reviving of newborns would find a molecular basis for its assessment. VLBW infants may be regarded as those in which premature exposure to ambient oxygen concentrations and oxidative stress causes a premature functioning of the extra-mitochondrial oxidative phosphorylation primarily in axons and endothelium. Adenosine may become a biomarker of prematurity risk, whose implications further studies may assess.
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PMID:Why do premature newborn infants display elevated blood adenosine levels? 2706 86