Browsing by Author "Kuscu K."
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Item The concentration of insulin-like growth factor-1 and insulin-like growth factor-binding protein-3 in maternal sera during pregnancy with normal and growth retarded fetuses; [Normal ve yetersiz fetal gelisim gosteren gebelerde gebelik suresince serum insulin benzeri buyume faktoru-1 (IGF-1) ve insulin benzeri buyume faktoru baglayici protein-3 (IGFBP-3) konsantrasyonlari](2000) Lacin S.; Oruc S.; Kuscu K.; Ersoy B.; Tansug N.; Uyanik B.S.; Yildirim Y.; Koyuncu F.Objective: To determine the concentrations of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 in maternal sera of pregnancies with normal and growth retarded fetuses and investigate the relationship between these substances and fetal growth. Materials and Methods: Blood samples of 148 pregnant women were collected at 14-16 and 30-31 weeks and during delivery. Also cord blood samples were obtained during delivery. For the determination of IGF-1 and IGFBP-3, double-sided IRMA method was used. Infants were divided into two groups as normal and growth retarded fetuses based upon their patterns of growth using the percentile curves and the serum levels were compared. Correlation analysis and Mann-Whitney U test were used as statistical calculations. Results: Both IGF-1 and IGFBP-3 levels increased while approaching term in all pregnant women. In growth retarded cases, maternal IGF-1 levels were found to be significantly lower than pregnancies with normal fetuses (p< 0.005), but maternal IGFBP-3 levels were not different between two groups. IGF-1 levels in cord blood during delivery were not different while IGFBP-3 levels were significantly higher in growth retarded fetuses. Conclusion: Our study did not support the hypothesis that fetal growth retardation is due to IGF-1 deficiency. High binding protein levels may cause a relative free IGF-1 deficiency, but the levels of binding protein is probably secondary to metabolic changes or placental insufficiency. Low levels of IGF-1 and high levels of binding proteins implies the necessity of further investigation of placental transfer.Item α-Lipoic Acid Vaginal Administration Contrasts Inflammation and Preterm Delivery in Rats(SAGE Publications Inc., 2019) Micili S.C.; Goker A.; Kuscu K.; Ergur B.U.; Fuso A.α-Lipoic acid (ALA) is a safe natural molecule involved in the immunomodulation of many physiological processes. Orally administered ALA has been reported to treat several inflammatory pathologies and support pregnancy. Our study aimed at testing ALA vaginal administration in female Wistar rats evaluating its tissue distribution (experiment I), impact on implantation process (experiment II), and effectiveness in contrasting induced preterm birth (experiment III). In experiment I, rats were intravaginally treated with 50 mg/kg or 500 mg/kg ALA, or with a physiologic solution, for 4 days. α-Lipoic acid distribution in uterus and cervical tissues was evaluated by immunohistochemical analyses. In experiment II, rats received intravaginally the above treatments for 5 days, then they were mated and, if pregnant, included in the experiment to evaluate both implantation rate and the content of implantation mediators in uterus tissues. In experiment III, pregnant rats were pretreated with placebo or with vaginal ALA for 4 days and then induced to delivery with mifepristone plus PGE2 on the 19th day of pregnancy. The delivery time was recorded, and the messenger RNA (mRNA) levels of pro-inflammatory cytokines were detected in the uterine tissues by real-time polymerase chain reaction. Immunohistochemistry was also performed. Results showed that vaginal ALA was well absorbed and distributed. The treatment did not affect the implantation process and was able to significantly revert mifepristone plus prostaglandin E2 effects, delaying the timing of delivery and significantly decreasing mRNA synthesis and release of pro-inflammatory cytokines. We provide for the first time new information on vaginal ALA use, even during pregnancy, opening a perspective for further studies. © The Author(s) 2018.