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BACKGROUND: Circulating endothelial progenitor cells (EPCs) may be necessary throughout pregnancy by ensuring proper placentation and embryonic growth. The lack of standardized EPC quantification techniques has prevented conclusive proof of an increase in EPC during pregnancy. OBJECTIVES: The purpose of this study was to determine whether EPC levels change for healthy and idiopathic fetal growth restriction (FGR) pregnancies. MATERIALS AND METHODS: The study population consisted of 48 healthy pregnant females with no previous history of IUGR (10 in the first trimester, 15 in the second, and 23 in the third), 48 women with pregnancy complicated by idiopathic FGR, and 15 non-pregnant women. By using flow cytometry, EPCs in maternal blood were recognized as CD45dim/CD34/KDR cells. ELISA was used to measure plasmatic cytokines. RESULTS: We ascertained a progressive rise in EPCs in healthy pregnancies that was apparent in the first but more pronounced in the third trimester. At comparable gestational ages, FGR-complicated pregnancies had impaired EPC growth. Placental growth factor and stromal-derived factor-1 levels in the blood were significantly lower in FGR than in healthy pregnancies, which may have contributed to the degradation of the EPCs. CONCLUSION: The count in EPCs might hold considerable promise toward developing a peculiar authentication marker for observing pregnancies, and could be the focus of cutting-edge tactics for the prognosis and treatment of FGR pregnancies.

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Objective: A common and serious pregnancy issue known as intrauterine growth restriction (IUGR) occurs when the fetus is unable to reach its full growth potential. Mitochondria are crucial to the development of the fetus and the placenta. We aimed to elucidate the role of oxidative stress parameters and markers of DNA damage. The integrity of the mitochondrial DNA (mtDNA) was studied. Materials and Methods: Blood samples were collected from 48 females (cases and controls, respectively). Oxidative stress parameters were analyzed. DNA was extracted followed by high-performance liquid chromatography to study 8-OH-dG and mt DNA by real-time polymerase chain reaction. Western blot analysis was performed for nuclear-encoded mitochondrial proteins and DNA damage markers. Results: When pregnant women were compared to non-pregnant women in their first, second, and third trimesters, a highly significant progressive drop in circulating mtDNA was found. In addition, mtDNA was considerably higher in mothers carrying IUGR fetuses than in healthy pregnancies. Sirtuin-3 protein expression was considerably suppressed in the IUGR placenta (P = 0.027), whereas Nrf1 expression was not statistically different from the control group in the IUGR. Increased oxidative stress led to greater DNA damage in IUGR. The highest concentrations of 8-OH-dG were found in IUGR with levels significantly higher than those in the non-pregnant group. Conclusion: Our research sets the path for further investigation into mitochondrial anomalies in IUGR pregnancies and offers evidence for disturbed mitochondrial homeostasis. The mtDNA might offer a fresh perspective on the processes involved in physiological gestation. In addition, the presence of mtDNA may aid in the diagnosis of IUGR during pregnancy.

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OBJECTIVE: The aim of the present study was to examine the relation between the PON1 polymorphisms and recurrent pregnancy loss (RPL). METHODS: In a cross-sectional study, blood samples were collected from 100 females. DNA was extracted and PON1 genotypes were determined by polymerase chain reaction (PCR) amplification. RESULTS: Regarding PON1 L55M, the mutated allele (M) frequency was found in 70.5% in RPL and in 53.5% in controls; the M allele was significantly associated with an increased risk of RPL (adjusted odds ratio [ORadj] = 2.07; 95% confidence interval [CI]; p < 0.001). However, regarding PON1 Q192R, the R mutated allele frequency was found in 28.5% in RPL and in 33% in controls. The R allele did not show any risk for RPL (ORadj 0.81; 95%CI; p = 0.329). CONCLUSION: The present study suggests that there is an effect of genetic polymorphism on RPL and provides additional evidence that combines with the growing information about the ways in which certain PON1 genotypes can affect the development of the fetus in the uterus.

OBJETIVO: O objetivo deste estudo foi examinar a relação entre os polimorfismos PON1 e perda recorrente de gravidez PRG. MéTODOS: Em um estudo transversal, foram coletadas amostras de sangue de 100 mulheres. O DNA foi extraído e os genótipos PON1 foram determinados por amplificação por PCR. RESULTADOS: Com relação ao PON1 L55M, a frequência do alelo mutado (M) foi encontrada em 70,5% no PRG e em 53,5% nos controles; o alelo M foi significativamente associado a um risco aumentado de PRG (odds radio ajustado [ORadj] =2,07; intervalo de confiança [IC] 95%; p < 0,001). No entanto, em relação ao PON1 Q192R, a frequência do alelo mutado R foi encontrada em 28,5% no PRG e em 33% nos controles. O alelo R não mostrou qualquer risco para PRG (ORadj 0,81; IC 95; p = 0,329). CONCLUSãO: O presente estudo sugere que há um efeito do polimorfismo genético sobre PRG e fornece evidências adicionais que se combinam com as informações crescentes sobre as maneiras pelas quais certos genótipos PON1 podem afetar o desenvolvimento do feto no útero.

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Abstract Objective The aim of the present study was to examine the relation between the PON1 polymorphisms and recurrent pregnancy loss (RPL). Methods In a cross-sectional study, blood samples were collected from 100 females. DNA was extracted and PON1 genotypes were determined by polymerase chain reaction (PCR) amplification. Results Regarding PON1 L55M, the mutated allele (M) frequency was found in 70.5% in RPL and in 53.5% in controls; theMallele was significantly associated with an increased risk of RPL (adjusted odds ratio [ORadj]=2.07; 95% confidence interval [CI]; p<0.001). However, regarding PON1 Q192R, the R mutated allele frequency was found in 28.5% in RPL and in 33% in controls. The R allele did not show any risk for RPL (ORadj 0.81; 95%CI; p=0.329). Conclusion The present study suggests that there is an effect of genetic polymorphism on RPL and provides additional evidence that combines with the growing information about the ways in which certain PON1 genotypes can affect the development of the fetus in the uterus.

Resumo Objetivo O objetivo deste estudo foi examinar a relação entre os polimorfismos PON1 e perda recorrente de gravidez PRG. Métodos Em um estudo transversal, foramcoletadas amostras de sangue de 100 mulheres. O DNA foi extraído e os genótipos PON1 foram determinados por amplificação por PCR. Resultados Com relação ao PON1 L55M, a frequência do alelo mutado (M) foi encontrada em 70,5% no PRG e em 53,5% nos controles; o alelo M foi significativamente associado a um risco aumentado de PRG (odds radio ajustado [ORadj] =2,07; intervalo de confiança [IC] 95%; p<0,001). No entanto, em relação ao PON1 Q192R, a frequência do alelo mutado R foi encontrada em 28,5% no PRG e em 33% nos controles. O alelo R não mostrou qualquer risco para PRG (ORadj 0,81; IC 95; p=0,329). Conclusão O presente estudo sugere que há um efeito do polimorfismo genético sobre PRG e fornece evidências adicionais que se combinam com as informações crescentes sobre asmaneiras pelas quais certos genótipos PON1 podemafetar o desenvolvimento do feto no útero.

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AIM: To evaluate the comparative outcome of induced labor by intracervical Foley catheter with misoprostol versus misoprostol alone. MATERIALS & METHODS: A total of 1306 women were enrolled over 4 years, induced with either intracervical Foley with misoprostol or misoprostol alone and compared in terms of induction-delivery interval, mode of delivery, the presence of uterine tachysystole, postpartum hemorrhage and perinatal outcome. RESULTS: Induction to delivery interval, the duration between induction to active labor was significantly reduced, deliveries within 24 h were significantly higher and the number of misoprostol doses used was significantly less in Foley with misoprostol group. CONCLUSION: The outcome of combination of intracervical Foley catheter and misoprostol is superior for labor induction, without affecting maternal or perinatal outcome.

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INTRODUCTION: Vitamin D is now known to be essential to Mycobacterium tuberculosis containment and killing through activation of 25-hydroxyvitamin-D receptors (VDRs) present on all immune cells or obtained from dietary food stuffs as either vitamin D3 or vegetable vitamin D2 (also known as ergocalciferol). AIM: To evaluate the association of serum vitamin D level between the Female Genital Tuberculosis (FGTB) cases and healthy controls. MATERIALS AND METHODS: Total 120 cases and 120 controls enrolled for the study following inclusion and exclusion criteria. Detailed clinical history was taken from each subjects. Total of 3 ml of the blood was collected in EDTA vial from each subject (case and control). Quantification of serum vitamin D level was measured by active human vitamin D ELISA kit using an ELISA reader. Statistical analysis was done using Statistical Package for Social Science (SPSS) version 21.0. A p-value <0.05 was considered as significant. RESULTS: A total of 120 confirmed FGTB cases and 120 healthy control enrolled for study. Out of 120 women 97.5%, 10.0%, 3.3%, 3.3% were detected positive for M. tuberculosis respectively. Comparing the mean demographic value of age and BMI were (29.03±3.127, 28.03±3.00) and (22.92±3.33, 24.15±3.97) respectively with the p=0.012* and p=0.010* found to be significant among cases and controls. The mean serum vitamin D level was 14.96±8.81 in cases and 23.00±8.83 in controls with p-value<0.001. There was a significant positive association found in low serum vitamin D level among FGTB cases than controls. CONCLUSION: Vitamin D is important for normal immune cell function, as well as regression of FGTB disease. FGTB may be controlled by regulating the serum vitamin D level concentration. This study suggests that, vitamin D deficiency and BMI is strongly associated with the progression of active FGTB disease which alters the expression of antimicrobial peptide and lead to the persistence of TB infection. Therefore, serum vitamin D level may play an important role in treatment of FGTB.