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10.1016/S0140-6736(13)60178-6 http://scihub22266oqcxt.onion/10.1016/S0140-6736(13)60178-6 C4389630!4389630!23782686     free     free     free       Lancet 2013 ; 382 (9902): 1445-57 Nephropedia Template TP {{tp|p=23782686|t=2013. Retinopathy of prematurity |pdf=|usr=}}{{23782686}} gab.com Text Retinopathy of prematurity JO: Lancet http://www.kidney.de/pget.php?&tw=1&pmid=23782686 #FOAvip The immature retinas of preterm neonates are susceptible to insults that disrupt neurovascular growth, leading to retinopathy of prematurity. Suppression of growth factors due to hyperoxia and loss of the maternal?fetal interaction result in an arrest of retinal vascularisation (phase 1). Subsequently, the increasingly metabolically active, yet poorly vascularised, retina becomes hypoxic, stimulating growth factor-induced vasoproliferation (phase 2), which can cause retinal detachment. In very premature infants, controlled oxygen administration reduces but does not eliminate retinopathy of prematurity. Identification and control of factors that contribute to development of retinopathy of prematurity is essential to prevent progression to severe sight-threatening disease and to limit comorbidities with which the disease shares modifiable risk factors. Strategies to prevent retinopathy of prematurity will depend on optimisation of oxygen saturation, nutrition, and normalisation of concentrations of essential factors such as insulin-like growth factor 1 and ?-3 polyunsaturated fatty acids, as well as curbing of the effects of infection and inflammation to promote normal growth and limit suppression of neurovascular development. Twit Text FOAVip Retinopathy of prematurity ????Lancet http://www.kidney.de/pget.php?&tw=1&pmid=23782686 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23782686 #FOAvip English Wikipedia <ref>{{Cite pmid|23782686}}</ref> Retinopathy of prematurity #MMPMID23782686 Hellström A; Smith LEH; Dammann O Lancet 2013[Oct]; 382 (9902): 1445-57 PMID23782686show ga The immature retinas of preterm neonates are susceptible to insults that disrupt neurovascular growth, leading to retinopathy of prematurity. Suppression of growth factors due to hyperoxia and loss of the maternal?fetal interaction result in an arrest of retinal vascularisation (phase 1). Subsequently, the increasingly metabolically active, yet poorly vascularised, retina becomes hypoxic, stimulating growth factor-induced vasoproliferation (phase 2), which can cause retinal detachment. In very premature infants, controlled oxygen administration reduces but does not eliminate retinopathy of prematurity. Identification and control of factors that contribute to development of retinopathy of prematurity is essential to prevent progression to severe sight-threatening disease and to limit comorbidities with which the disease shares modifiable risk factors. Strategies to prevent retinopathy of prematurity will depend on optimisation of oxygen saturation, nutrition, and normalisation of concentrations of essential factors such as insulin-like growth factor 1 and ?-3 polyunsaturated fatty acids, as well as curbing of the effects of infection and inflammation to promote normal growth and limit suppression of neurovascular development. äRetinopathy of prematurity (epmc).pdf DeepDyve Pubget Overpricing