Relationship of Placental and Serum Lipoprotein-Associated Phospholipase A2 Levels with Hypertensive Disorders of Pregnancy.

Background: A series of studies has shown that lipoprotein-associated phospholipase A2 (Lp-PLA2) is closely associated with abnormal lipid metabolism and vascular endothelial cell injury, but its role in hypertensive disorders of pregnancy (HDP) remains unclear. This study aims to determine the relationship between placental and serum LP-PLA2 levels and HDP, and to provide a feasible method for predicting HDP. Methods: The placental and serum Lp-PLA2 levels of 63 patients with HDP (20, 25, and 18 cases with gestational hypertension, mild preeclampsia, and severe preeclampsia, respectively) and 20 women with normal pregnancies (control group) were measured via a combination of tissue microarray and immunohistochemistry, real-time quantitative RT-PCR and enzyme-linked immunosorbent assay (ELISA). Results: 1) The gene and protein expression levels of placental LP-PLA2: the HDP group had significantly higher levels than those of the control group (P < 0.05). The mild preeclampsia group had significantly higher levels than those of the control group (P < 0.05); the severe preeclampsia group had significantly higher levels than those of the mild preeclampsia group (P < 0.05). 2) Serum levels of Lp-PLA2: the HDP group had significantly higher levels than those of the control group (P < 0.05). The Lp-PLA2 levels increased gradually with the progression of the HDP; there were significant differences in the four groups using pair-wise comparisons (P < 0.05). 3) Serum levels of LP-PLA2 were positively correlated with placental LP-PLA2 levels in the HDP group (r = 0.435, P < 0.05). Conclusion: Elevated Lp-PLA2 levels may be associated with the occurrence of HDP, and changes of Lp-PLA2 levels in the maternal blood may be regarded as a monitoring indicator for this disease.

Value of fasting plasma glucose to screen gestational diabetes mellitus before the 24th gestational week in women with different pre-pregnancy body mass index.

BACKGROUND: Gestational diabetes mellitus (GDM) is usually diagnosed between 24th and 28th gestational week using the 75-g oral glucose tolerance test (OGTT). It is difficult to predict GDM before 24th gestational week because fast plasma glucose (FPG) decreases as the gestational age increases. It is controversial that if FPG ≥5.1 mmol/L before 24th gestational week should be intervened or not. The aim of this study was to evaluate the value of FPG to screen GDM before 24th gestational week in women with different pre-pregnancy body mass index (BMI). METHODS: This was a multi-region retrospective cohort study in China. Women who had a singleton live birth between June 20, 2013 and November 30, 2014, resided in Beijing, Guangzhou and Chengdu, and received prenatal care in 21 selected hospitals, were included in this study. Pre-pregnancy BMI, FPG before the 24th gestational week, and one-step GDM screening with 75 g-OGTT at the 24th to 28th gestational weeks were extracted from medical charts and analyzed. The pregnant women were classified into four groups based on pre-pregnancy BMI: Group A (underweight, BMI < 18.5 kg/m), Group B (normal, BMI 18.5-23.9 kg/m), Group C (overweight, BMI 24.0-27.9 kg/m) and Group D (obesity, BMI ≥28.0 kg/m). The trend of FPG before 24th week of gestation was described, and the sensitivity and specificity of using FPG before the 24th gestational week to diagnose GDM among different pre-pregnancy BMI groups were reported. Differences in the means between groups were evaluated using independent sample t-test and analysis of variance. Pearson Chi-square test was used for categorical variables. RESULTS: The prevalence of GDM was 20.0% (6806/34,087) in the study population. FPG decreased gradually as the gestational age increased in all pre-pregnancy BMI groups until the 19th gestational week. FPG was higher in women with higher pre-pregnancy BMI. FPG before the 24th gestational week and pre-pregnancy BMI could be used to predict GDM. The incidence of GDM in women with FPG ≥5.10 mmol/L in the 19th to 24th gestational weeks and pre-pregnancy overweight or obesity was significantly higher than that in women with FPG ≥5.10 mmol/L and pre-pregnancy BMI <24.0 kg/m (78.5% [62/79] vs. 52.9% [64/121], χ = 13.425, P < 0.001). CONCLUSIONS: FPG decreased gradually as the gestational age increased in all pre-pregnancy BMI groups until the 19th gestational week. Pre-pregnancy overweight or obesity was associated with an increased FPG value before the 24th gestational week. FPG ≥5.10 mmol/L between 19 and 24 gestational weeks should be treated as GDM in women with pre-pregnancy overweight and obesity.

Moderate prenatal alcohol exposure suppresses the TLR4-mediated innate immune response in the hippocampus of young rats.

Prenatal alcohol exposure (PAE) could lead to developmental disorders of the central nervous system (CNS) and mental retardation. Toll-like receptor (TLR) 4 plays an important role in PAE-induced neurodevelopmental defects. However, how PAE affects TLR4 response in the brain remains controversial. Using a moderate PAE model by feeding pregnant rats with liquid ethanol diet, we investigated the TLR4-mediated response to intraventricular injection of lipopolysaccharide (LPS) in the hippocampus of PEA rats at postnatal day (PND) 30. The results showed that PAE significantly up-regulated the expression of Toll-Interleukin-1 Receptor (TIR)-domain-containing adaptor protein inducing interferon (IFN)-ß (TRIF), TNF-α, and IL-1ß in the rat hippocampus in the absence of LPS, indicated by western blot assay. LPS treatment dramatically up-regulated the expressions of TLR4 and its downstream molecules in the hippocampus of paired-food and control groups. But no such significant changes of those molecules were found in the hippocampus of PAE animals. Moreover, the LPS stimulation even down-regulated the levels of TLR4 and TRIF in the PAE group. These data suggest that the relatively moderate level of PAE may lead to a mild neuroinflammation and a suppression of TLR4-mediated response to LPS in the hippocampus of young rats. As innate immunity plays crucial roles in CNS development, moderate PAE-induced suppression of TLR4-mediated response may serve as a new candidate mechanism of CNS developmental defects.

Analysis of correlation factors and pregnancy outcomes of hypertensive disorders of pregnancy - a secondary analysis of a random sampling in Beijing, China.

OBJECTIVE: We aimed to assess the prevalence and risk factors for hypertensive disorders and to study the main pregnancy outcomes in the Beijing area of China. STUDY DESIGN: This study randomly sampled 15 hospitals in Beijing from Jun 2013 to Nov 2013 and evaluated 15 194 deliveries. Logistic regression analysis was used to study the association between risk factors and hypertensive disorders. Pregnancy outcomes included preterm birth, cesarean delivery and small for gestational age (SGA). RESULTS: The prevalence of hypertensive disorders, preeclampsia (PE) and severe PE was 4.4, 2.7 and 1.8%, respectively. The risk factors for hypertensive disorders and severe PE were maternal body mass index before pregnancy, gestational weight gain (GWG), gestational diabetes and pre-gestational diabetes, and third trimester cholesterol (CHOL) levels. First trimester high-density lipoprotein was a protective factor for severe PE. The incidence of hypertensive disorders increased with maternal age. Preterm delivery, cesarean delivery and small infant size for gestational age were more prevalent in the severe PE group compared with the non-hypertensive group. CONCLUSIONS: In the Beijing area of China, maternal body mass index before pregnancy, GWG, maternal complications of gestational diabetes and pre-gestational diabetes, and third trimester CHOL levels are risk factors for both hypertensive disorders of pregnancy and severe PE. First trimester high-density lipoprotein is a protective factor for severe PE. Severe preeclampsia leads to a higher incidence of preterm delivery, cesarean delivery and SGA infants.

Association between X-Ray Repair Cross-Complementing Group 1 Arg399Gln Polymorphism and Cervical Cancer Risk: A Meta-Analysis in the Chinese Population.

BACKGROUND: Many studies have examined the association of X-ray repair cross-complementing group 1 (XRCC1) Arg399Gln polymorphism with cervical cancer susceptibility. However, the results of these studies are inconsistent. To further assess the effects of XRCC1 Arg399Gln polymorphism on the risk of cervical cancer in the Chinese population, a meta-analysis was performed. METHODS: Relevant studies were identified using PubMed, Springer Link, Ovid, Chinese Wanfang Data Knowledge Service Platform, Chinese National Knowledge Infrastructure, and Chinese Biology Medicine through December 2015. Pooled ORs and 95% CIs were used to assess the strength of the associations. RESULTS: This meta-analysis identified 7 studies, including 1,589 cases and 2,235 controls. In the total analyses, a significantly elevated risk of cervical cancer was associated with variants of XRCC1 Arg399Gln (GA vs. GG: OR 1.30, 95% CI 1.13-1.49; AA + GA vs. GG: OR 1.27, 95% CI 1.02-1.58). In the subgroup analyses stratified by geographic areas and histopathology type, it revealed the significant result in South China. CONCLUSIONS: This meta-analysis showed that the XRCC1 Arg399Gln GA variant might be risk alleles for cervical cancer susceptibility in the Chinese population, and further studies in other ethnic groups are required to arrive at definite conclusions.

Relationship of Liver X Receptors α and Endoglin Levels in Serum and Placenta with Preeclampsia.

BACKGROUND: Liver X receptor alpha (LXRα) and endoglin have been postulated to play roles in trophoblast invasion and lipid metabolic disturbances. However, the relationship between LXRα and endoglin levels in serum and placenta of patients with preeclampsia remains poorly understood. The objective of this study was to identify correlations between LXRα, endoglin and preeclampsia and provide new feasible methods of clinical prediction and treatment for preeclampsia. METHODS: We enrolled 45 patients with preeclampsia (24 with moderate preeclampsia and 21 with severe preeclampsia) and 15 normal pregnant women (control group) who were admitted to the Department of Obstetrics of the General Hospital of Beijing Command between October 2012 and July 2013 in this study. Serum and placental LXRα and endoglin levels were analyzed by enzyme-linked immunosorbent assay, real-time quantitative PCR, tissue microarray and immunohistochemistry. RESULTS: Serum and placental LXRα and endoglin levels were significantly higher in patients with preeclampsia than those in control group (P<0.05, each). Moreover, patients with severe preeclampsia displayed significantly higher LXRα and endoglin levels than those with moderate preeclampsia (P<0.05, each). The LXRα sensitivity, specificity and positive and negative predictive values were 66.00%, 80.00%, 89.19% and 48.48%, respectively, while those of endoglin levels were 62.00%, 85.00%, 91.18% and 47.22%, respectively. LXRα and endoglin levels in serum and placenta from patients with preeclampsia were positively correlated (serum: r = 0.486, P<0.01; placenta: r = 0.569, P<0.01). CONCLUSIONS: Elevated LXRα and endoglin levels may be associated with preeclampsia pathogenesis and development and could be used as potential predictors for this disorder.

Risk of adverse pregnancy outcomes stratified for pre-pregnancy body mass index.

OBJECTIVE: To estimate the risk of adverse maternal and perinatal outcomes in women with different pre-pregnancy body mass index (BMI). METHODS: We conducted a cohort study with 14 451 singleton pregnancies in 15 medical centers in Beijing between 20 June 2013 and 30 November 2013 using cluster random sampling. We divided participants into four groups based on pre-pregnancy BMI: Group A (underweight): BMI < 18.5 kg/m(2), Group B (normal): 18.5-23.9 kg/m(2), Group C (overweight): 24-27.9 kg/m(2), Group D (obesity): ≥28 kg/m(2). We used multivariate analysis to evaluate the association of the risk of adverse pregnancy outcomes and pre-pregnancy BMI. RESULTS: The prevalence of maternal overweight and obesity was 14.82% (2142/14 451) and 4.71% (680/14 451) in the study population, respectively. Higher pre-pregnancy BMI is associated with higher prevalence of gestational diabetes (GDM), macrosomia, Cesarean section (C-section), preeclampsia and postpartum hemorrhage. Pre-pregnancy overweight or obesity increases the risk of adverse pregnancy outcomes, regardless of GDM status. CONCLUSIONS: Pre-pregnancy overweight or obesity is associated with increased risk of adverse pregnancy outcomes. Nutrition counseling is recommended before pregnancy in women who have overweight or obesity.

TP53 codon 72 polymorphism and susceptibility to cervical cancer in the Chinese population: an update meta-analysis.

BACKGROUND: Although many epidemiologic studies investigated the TP53 codon 72 polymorphism and its association with cervical cancer (CC), definite conclusions cannot be drawn. AIM OF THE STUDY: To evaluate the association between TP53 codon 72 polymorphism and risk of cervical cancer in the Chinese population. METHODS: A computerized literature search was carried out in PubMed, Springer Link, Ovid, Chinese Biomedical Database (CBM), Chinese National Knowledge Infrastructure (CNKI), and Chinese Wanfang Database to collect relevant articles. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to calculate the strength of association. RESULTS: A total of 16 studies including 1684 CC cases and 1178 controls were involved in this meta-analysis. Overall, significant increased association was found between the Pro/Pro carriers and CC risk when all studies in Chinese population pooled into the meta-analysis (heterozygous model: OR = 1.22, 95% CI: 1.01-1.46). In subgroup analyses stratified by ethnicity and source of controls, the same results were observed in Han and in hospital-based studies. CONCLUSION: Our results suggest that the TP53 codon 72 polymorphism may be potential biomarkers for CC risk in the Chinese population, especially for Han Chinese, and studies with wider spectrum of population are required for definite conclusions.

Deregulation of miR-128 in ovarian cancer promotes cisplatin resistance.

OBJECTIVE: Platinum-based chemotherapy is the standard treatment in advanced ovarian cancer, but most patients will relapse with drug-resistant disease. MicroRNAs have been demonstrated to function in chemoresistance in cancers. In this study, we focused on the role of miR-128 in cisplatin-resistant ovarian cancer. MATERIALS AND METHODS: The expression of miR-128 RNA and its targeted genes, the polycomb ring finger oncogene Bmi-1 and ATP-binding cassette subfamily C member 5 (ABCC5), were investigated in the epithelial ovarian cancer cells and ovarian carcinomas. RESULTS: miR-128 expression was significantly reduced in the cisplatin-resistant human epithelial ovarian cancer cell line SKOV3/CP compared with parental SKOV3 cells and decreased upon treatment with cisplatin in a concentration-dependent manner in SKOV3, OVCAR3, and PEO14 cells. Overexpression of miR-128 resensitized SKOV3/CP cells to cisplatin and reduced the expression of cisplatin-resistant-related proteins ABCC5 and Bmi-1, whereas miR-128 inhibitors increased cisplatin resistance in SKOV3 cells. Cisplatin combined with miR-128 agomirs inhibited the growth of SKOV3/CP xenograft tumors more effectively than cisplatin alone. Diminished expression of ABCC5 and Bmi-1 and higher cisplatin concentrations were observed in tumor tissue of mice treated with miR-128 agomirs in addition to cisplatin. CONCLUSIONS: Taken together, our findings suggest that miR-128 may act as a promising therapeutic target for improvement of tumor sensitivity to cisplatin.

Systemic injection of low-dose lipopolysaccharide fails to break down the blood-brain barrier or activate the TLR4-MyD88 pathway in neonatal rat brain.

We aimed to investigate whether peripheral low-dose lipopolysaccharide (LPS) induces the breakdown of the blood-brain barrier (BBB) and/or the activation of toll-like receptor 4 (TLR4) in the neonatal rat brain. Neonatal rats received intraperitoneal injections of low-dose LPS (0.3 mg/kg∙bw), and the BBB compromise was detected by Evans Blue extravasation and electron microscopy. Meanwhile, TLR4, adaptin myeloid differentiation factor 88 (MyD88), nuclear transcription factor kappa-B (NF-κB) p50 and tumor necrosis factor alpha (TNFα) in the neonatal rat brain were determined by quantitative real-time polymerase chain reaction (PCR) and Western Blot. Immunohistochemistry was used to determine the distribution and activation of microglia in the brain after LPS administration. It was demonstrated that Evans Blue extravasation was not observed in the brain parenchyma, and that tight junctions of cerebral endothelial cells remained intact after systemic injections of LPS in neonatal rats. Although intracerebroventricular injections of LPS activated microglia and up-regulated the expression of TLR4, MyD88, NF-κB p50 and TNFα in the neonatal rat brain, systemic LPS did not induce these responses. These findings indicate that while the neonatal rat brain responds to the direct intra-cerebral administration of LPS through robust TLR4 activation, systemic low-dose LPS does not induce the innate immune reaction or compromise the BBB in neonatal rats.

[Study on the effect of di-(2-ethylhexyl) phthalate on pregnant rats and the protection of zinc against it in pregnancy].

OBJECTIVE: To investigate the effect of di-(2-ethylhexyl) phthalate (DEHP) on pregnant rat and the protection of zinc. METHODS: Fifty rats were randomized equally into 5 groups consisting of blank (given 1 ml 0.9% sodium chloride), corn oil (given 1 ml corn oil), zinc (given 1 ml zinc gluconate including 1.2 mg zinc), DEHP (given 50 mg×kg(-1)×d(-1) DEHP) and DEHP + zinc (given 50 mg×kg(-1)×d(-1) DEHP + zinc gluconate). At the beginning of the experiment (about 7 d before pregnancy), the female rats were administered with corresponding drugs everyday. The pregnant rats were killed and the fetal rats were removed on 19th day. The following results in each group were recorded: the body weight and the organic weight of the female rats, the number and the weight of fetus rats and the placental weight. RESULTS: The weight and the coefficient of female rats' kidney/body, spleen/body, brain/body, and heart/body in DEHP group compared with other groups were not statistical significance (all P > 0.05). The coefficient of female rats' liver/body, uterus/body, and ovary/body of blank group were (4.4 ± 0.7)%, (1.26 ± 0.09)%, (0.083 ± 0.009)% respectively, corn oil group were (4.5 ± 0.6)%, (1.29 ± 0.10)%, (0.084 ± 0.008)%, zinc group were (4.4 ± 0.4)%, (1.26 ± 0.08)%, (0.084 ± 0.009)%, DEHP group were (5.4 ± 1.0)%, (1.11 ± 0.08)%, (0.074 ± 0.012)%, and DEHP + zinc group were (4.4 ± 1.0)%, (1.28 ± 0.10)%, (0.082 ± 0.007)%; in DEHP group the coefficient of female rats' liver/body, uterus/body, and ovary/body compared with other groups was statistical significance (P < 0.05). The fetal quantity, fetal weight and placental weight of female rats of blank group were 12.8 ± 2.7, (6.03 ± 0.16) g, (1.00 ± 0.03) g respectively, corn oil group were 13.6 ± 3.1, (6.07 ± 0.20) g, (1.00 ± 0.04) g, zinc group were 13.3 ± 3.1, (6.16 ± 0.18) g, (1.00 ± 0.05) g, DEHP group were 9.2 ± 4.1, (4.03 ± 0.09) g, (0.95 ± 0.03) g, and zinc + DEHP group were 12.1 ± 2.9, (6.09 ± 0.17) g, (0.99 ± 0.03) g. In DEHP group the fetal quantity, fetal weight and placental weight of female rats compared with other groups were statistical significance (P < 0.05). CONCLUSION: DEHP can damage female rats and fetal rats in gestation period. Zinc supplied before pregnancy can relieve the influence by DEHP.

Relationship of adiponectin and resistin levels in umbilical serum, maternal serum and placenta with neonatal birth weight.

OBJECTIVE: Adiponectin and resistin have been postulated to play a role in the regulation of energy metabolism during pregnancy. However, relationship of adiponectin and resistin levels in umbilical serum, maternal serum and placenta with neonatal birth weight remains to be poorly understood. The purpose of the study was to clarify the correlations between adiponectin and resistin levels and neonatal birth weight. METHODS: Enzyme immunoassay was used to measure the adiponectin and resistin levels in maternal and umbilical serum from 40 normal pregnant women (control group), 30 women with macrosomia (macrosomia group) and 30 women with fetal growth restriction (FGR group). Immunohistochemistry was used to measure adiponectin and resistin levels in placenta. RESULTS: Serum adiponectin and resistin levels were significantly increased in control women compared with that in macrosomia mothers, but significantly decreased compared with that in FGR mothers. The levels of adiponectin and resistin in control babies were significantly higher than that in macrosomic babies, whereas significantly lower than that in FGR babies. The placental expressions of adiponectin and resistin in macrosomia, control and FGR group were gradually elevated, and there was a significant difference between them. Umbilical serum adiponectin levels and placental adiponectin expression were inversely correlated with birth weight. Umbilical serum levels and placental expression of resistin had positive correlation with maternal serum resistin and negative correlation with birth weight. In addition, maternal serum resistin levels were inversely correlated with birth weight. CONCLUSION: It is suggested that adiponectin and resistin play an important role in controlling body weight and may be related to the occurrence of fetal macrosomia and FGR.

[Effects of di-(2-ethylexyl) phthalate on apoptosis of cytotrophoblasts in early pregnancy].

OBJECTIVE: To investigate the influence of di-(2-ethylexyl) phthalate (DEHP) on cell apoptosis and expression of Bcl-2 and bax in cultured human first trimester cytotrophoblasts. METHODS: Human first trimester cytotrophoblasts were cultured with DEHP at concentration of 0, 25, 50, 100 µmol/L for 24 hours. Cell apoptosis was detected by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) and flow cytometer method. The expression of apoptosis-associated genes, including Bcl-2 and bax, were detected by reverse transcription (RT)-PCR in cultured cytotrophoblast cells. The protein expression of Bcl-2 and bax in cytotrophoblast cells was measured by western blot. RESULTS: (1) The expression of Bcl-2: when incubated with DEHP at concentration of 0, 25, 50 and 100 µmol/L, the expression of Bcl-2 were 1.00 ± 0.05, 1.03 ± 0.04, 1.04 ± 0.03, 1.04 ± 0.04, which did not show statistical difference (P > 0.05). The expression of Bcl-2 protein were 0.11 ± 0.02, 0.11 ± 0.04, 0.12 ± 0.02, 0.12 ± 0.03, which also didn't reach statistical difference (P > 0.05). (2) The expression of bax: when incubated with DEHP at concentration of 50 and 100 µmol/L, the expression of bax protein were 0.63 ± 0.04 and 0.81 ± 0.04, which were significantly higher than 0.23 ± 0.05 with DEHP at 0 µmol/L (P < 0.05). The expression of bax mRNA were 0.96 ± 0.04 and 1.02 ± 0.04, which was significantly higher than 0.81 ± 0.05 with DEHP at 0 µmol/L (P < 0.05). (3) Apoptosis: when incubated with DEHP at concentration of 50 and 100 µmol/L for 24 hours, the apoptotic cell ratio were (18.8 ± 2.6) % and (20.3 ± 2.0) % by annexin V-FITC/PI staining, which were significantly higher than (10.6 ± 1.4) % at 0 µmol/L and (18.1 ± 4.6) % and (19.5 ± 1.2) % by TUNEL staining, which were significantly higher than (11.2 ± 3.1) % at 0 µmol/L of DEHP (P < 0.05). CONCLUSION: DEHP could induce apoptosis of cytotrophoblast cells by increasing bax gene expression, but had no effect on Bcl-2 expression.

Relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomia.

AIM: Adiponectin and resistin are novel hormones secreted by human adipocytes and mononuclear cells, which have been postulated to play roles in the regulation of energy metabolism during pregnancy. However, correlations between adiponectin and resistin levels in umbilical and maternal serum and fetal macrosomia remain poorly understood. The purpose of this study was to clarify the relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomia. METHODS: Serum adiponectin and resistin levels were prospectively measured by enzyme immunoassay in 70 mothers and their 70 neonates. The study group included 30 neonates with macrosomia and the control group included 40 neonates that were appropriate for gestational age. The correlations of cord serum adiponectin and resistin with maternal serum adiponectin and resistin, birth weight, body mass index (BMI), and placental weight were analyzed. RESULTS: Serum adiponectin and resistin levels were significantly decreased in macrosomic mothers compared with those in control women. The levels of adiponectin and resistin were diminished in macrosomic babies in comparison with control newborns. Umbilical serum adiponectin levels were inversely correlated with birth weight, newborn BMI, and placental weight, but not with maternal serum adiponectin levels. Umbilical serum resistin levels had a positive correlation with maternal serum resistin and a negative correlation with birth weight, newborn BMI, and placental weight. In addition, maternal serum resistin levels were inversely correlated with newborn birth weight. CONCLUSION: It is suggested that adiponectin and resistin play important roles in controlling body weight and may be related to the occurrence of fetal macrosomia.

[Relationship of adiponectin and visfatin with fetus intrauterine growth].

OBJECTIVE: To explore the correlation between adipocyte factors (adiponectin and visfatin) and fetus intrauterine growth. METHODS: Enzyme immunoassay was used to measure the adiponectin and visfatin levels in maternal and umbilical serum from 14 women with fetal growth restriction (FGR group), 14 women with macrosomia (macrosomia group) and 14 normal pregnant women (control group). The correlations of cord serum adiponectin and visfatin with maternal serum adiponectin and visfatin were analyzed. RESULTS: (1) Serum visfatin levels in FGR mothers [(41.4 +/- 5.5)] microg/L were significantly higher than that in control women [(34.7 +/- 4.9) microg/L] and macrosomia mothers [(37.3 +/- 4.4) microg/L; P < 0.01, P < 0.05]. Serum adiponectin levels in macrosomia mothers [(4.1 +/- 1.3) mg/L] were significantly lower than that in control women [(6.6 +/- 1.5) mg/L] and FGR mothers [(6.4 +/- 1.3) mg/L; P < 0.01]. (2) Serum visfatin levels in FGR babies [(58.1 +/- 7.6) microg/L] were significantly increased than that in control newborns [(42.6 +/- 7.8) microg/L] and macrosomia babies [(48.5 +/- 9.1) microg/L; P < 0.01, P < 0.05]. Serum adiponectin levels in macrosomia babies [(6.5 +/- 1.3) mg/L] were significantly decreased than that in control newborns [(7.7 +/- 1.5) mg/L] and FGR babies [(7.7 +/- 1.0) mg/L; P < 0.05, P < 0.05]. (3) Maternal serum visfatin levels were positively correlated with umbilical serum visfatin levels (r = 0.720, P < 0.01). Umbilical serum adiponectin levels were higher than that in maternal serum, but there were no relationship between them (r = 0.301, P > 0.05). CONCLUSION: The changes of visfatin and adiponectin levels may be related to the occurrence of FGR and fetal macrosomia.

[Changes of maternal plasma and umbilical cord plasma inhibin and epidermal growth factor in patients with hypertensive disorder complicating pregnancy].

OBJECTIVE: To study the levels of inhibin (INH) and epidermal growth factor (EGF) in maternal plasma and umbilical cord plasma of patients with hypertensive disorder complicating pregnancy, and to explore their influence on the disease and fetal growth. METHODS: Enzyme linked immunosorbent assay (ELISA) was used to detect maternal and umbilical cord plasma INH and EGF levels in 65 patients with hypertensive disorder complicating pregnancy (test groups) and 21 normal pregnant women (control group). RESULTS: Plasma level of INH in test groups (499 +/- 52) ng/L was significantly higher than that (421 +/- 36) ng/L in control group (P < 0.01); however, the umbilical cord plasma level of INH had no significant difference (P > 0.05). Plasma level of EGF in test groups (408 +/- 60) ng/L was significantly lower than that (463 +/- 87) ng/L in control group (P < 0.05), also there was significant difference in umbilical cord plasma level of two groups (232 +/- 99) ng/L vs (380 +/- 97) ng/L (P < 0.01). The level of EGF in umbilical cord blood was positively correlated with newborn's body weight and placental weight. CONCLUSIONS: Plasma levels of INH and EGF in pregnancy women are related with hypertensive disorder complicating pregnancy. EGF level of umbilical cord blood affects the growth of fetus and placenta.

[Relationship between changes of insulin like growth factor-1 and insulin like growth factor binding protein-1 in maternal serum and placenta and pathogenesis of hypertensive disorder complicating pregnancy].

OBJECTIVE: To investigate the role of insulin like growth factor-1 (IGF-1) and insulin like growth factor binding protein-1 (IGFBP-1) in the pathogenesis of hypertensive disorder complicating pregnancy. METHODS: The levels of IGF-1 and IGFBP-1 in serum and placenta were detected from 60 patients with hypertensive disorder complicating pregnancy (hypertensive disorder complicating pregnancy group) and 18 normal pregnant women (control group) by enzyme linked immunosorbent assay (ELISA) and immunohistochemistry. RESULTS: (1) Serum level of IGF-1 (229 +/- 100) microg/L in hypertensive disorder complicating pregnancy group was significantly lower than that in control group (336 +/- 120) microg/L, (P < 0.01). There were significant differences among gestational hypertension (303 +/- 80) microg/L, mild preeclampsia (233 +/- 77) microg/L and severe preeclampsia groups (155 +/- 73) microg/L, (P < 0.05). (2) The expression of IGF-1 in the placenta of hypertensive disorder complicating pregnancy group (48%, 29/60) was significantly reduced than that in control group (83%, 15/18; P < 0.01). Its expressions in mild and severe preeclampsia patients were lower than that in control group (P < 0.05, P < 0.01). (3) Serum IGFBP-1 from hypertensive disorder complicating pregnancy group (161 +/- 90) microg/L was significantly higher than that in control group (98 +/- 75) microg/L, (P < 0.01). There were significant differences among gestational hypertension (97 +/- 73) microg/L, mild preeclampsia (157 +/- 69) microg/L and severe preeclampsia groups (225 +/- 81) microg/L (P < 0.05). (4) The expression of IGFBP-1 in hypertensive disorder complicating pregnancy group (77%, 46/60) was higher than that in control group (39%, 5/18), (P < 0.01). Its expression in mild and severe preeclampsia patients were higher than that in control group (P < 0.05). (5) The levels of IGF-1 in serum and placenta had a significant negative relationship with that of IGFBP-1 in hypertensive disorder complicating pregnancy group (r = -0.269, P < 0.05; r = -0.369, P < 0.01). Levels of IGFBP-1 in maternal serum were positively related with that of placenta (P < 0.01). CONCLUSION: The changes of levels of IGF-1 and IGFBP-1 are related to the occurrence and development of hypertensive disorder complicating pregnancy.