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    Incidence and severity of retinopathy of prematurity in Turkey
    (BMJ Publishing Group, 2015) Bas A.Y.; Koc E.; Dilmen U.; Oguz S.S.; Ovali F.; Demirel N.; Zenciroglu A.; Tekin N.; Caner I.; Arslanoglu S.; Celik Y.; Öztürk A.; Cömert S.; Bulbul A.; Kultursay N.; Koklu E.; Duman N.; Koksal N.; Salihoglu O.; Coban A.; Demirel G.; Bolat F.; Gökalp A.; Satar M.; Ipek M.S.; Bas E.K.; Narli N.; Mutlu M.; Cetinkaya M.; Akman I.; Yigit S.; Narter F.; Sivasli E.; Ahrabi A.F.; Atalay Y.; Tanyeri B.; Arsan S.; Perk Y.; Ors R.; Tuncer O.; Ecevit A.; Oygur N.; Ozdemir O.M.; Hakan N.; Aliefendioglu D.; Acunas B.; Cetin H.; Ozek E.; Tunc T.; Turkmen M.; Aydemir C.; Takci S.
    Background: The purpose of this study was to estimate the current incidence of retinopathy of prematurity (ROP) and the need for treatment in preterm infants in Turkey. Methods: The study included preterm infants who had been screened for ROP between 2011 and 2013 in 49 neonatal intensive care units. Infants with birth weight (BW) ?1500 g or ?32 weeks' gestational age and those with BW >1500 g or >32 weeks' GA with an unstable clinical course were included. The incidence of any ROP or severe ROP and treatment modalities were determined. Results: The study population included 15 745 preterm infants: 11 803 (75%) with GA ?32 weeks, and 3942 (25%) with GA >32 weeks. Overall, 30% were found to have any stage of ROP, and 5% had severe ROP. Severe ROP was diagnosed in 8.2% of infants with BW ?1500 g and 0.6% of infants with BW >1500 g. Of all infants diagnosed with ROP, 16.5% needed laser photocoagulation, and 20 patients born at >32 weeks' GA required this treatment modality. Vitroretinal surgery was performed in 28 infants with severe ROP: 23 with GA ?28 weeks and 5 with GA 29-32 weeks. Conclusions: The findings of our study have the important implication that more mature babies are at risk of severe ROP requiring treatment. An effective programme for detecting and treating ROP should be established in Turkey.
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    Transient Tachypnea of the Newborn (TTN): A Role for Polymorphisms of Surfactant Protein B (SP-B) Encoding Gene? [Transiente Tachypnoe des Neugeborenen (TTN): Spielen Polymorphismen im Surfactant-Protein-B-Gen (SP-B) eine Rolle?]
    (2003) Tutdibi E.; Hospes B.; Landmann E.; Gortner L.; Satar M.; Yurdakök M.; Dellagrammaticas H.; Örs R.; Ilikkan B.; Ovali F.; Sarman G.; Kumral A.; Arslanoglu S.; Koc H.; Yildiran A.
    Background: Transient tachypnea of the newborn (TTN) is usually a benign self-limiting respiratory disorder in the immediate neonatal period. The lipophilic surfactant-associated protein B (SP-B) was demonstrated to be the most relevant structural component of the surfactant system for immediate postnatal pulmonary adaptation. We hypothesized genetic variations of surfactant protein B (heterozygous 121 ins 2 mutation er intron 4 polymorphisms) to be related to TTN. Patients and Method: We screened genomic DNA of 83 healthy term neonates (gestational age: 39 (37-41) completed weeks [median and range]; birth weight: 3325 ± 541 grams [mean ± SD]) and 75 infants presenting with TTN (gestational age: 38 (37-41) completed wecks [median and range]; birth weight: 3091 ± 435 grams [mean ± SD]) by means of PCR-amplification, fragment length and sequence analysis. TTN was diagnosed an the basis of the clinical signs with respiratory rate > 60 breaths/minute, fraction of inspired oxygen > 0.21, and characteristic radiographic findings within less than 24 hours after birth. Newborns with any infection, pulmonary or cardiac congenital malformations, postnatal asphyxia and infants born to diabetic mothers were excluded. Results: In TTN-group the frequency of male infants (68.4% versus 44.6%, p < 0.05) and caeserian section were significantly higher (68.4% versus 30.1%, p < 0.05). We did not find any statistical difference in frequency of intron 4 variations between controls and TTN-group (8.4% versus 10.7%). None of the infants were heterozygous for the 121ins2 SP-B mutation. Conclusions: WC conclude polymorphisms of intron 4 and heterozygous 121 ins 2 mutation not to associated with TTN.