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This study aimed to identify which element of body composition measurements taken before 17th week gestation was the strongest risk factor for gestational diabetes mellitus (GDM) in Chinese pregnant women. A retrospective study was performed using data retrieved from the Electronic Medical Record database of Chongqing Health Center for Women and Children (China) from January 2014 to December 2015. A total of 22,223 women were included with singleton pregnancies and no preexisting diabetes who underwent bioelectrical impedance analysis (BIA) before 17 gestational weeks and 75-g OGTT at 24–28 gestational weeks. The prevalence of GDM from 2014 to 2015 was 27.13% (IADPSG). All indicators of BIA (total body water, fat mass, fat-free mass, percent body fat, muscle mass, visceral fat levels, proteins, bone minerals, basal metabolic rate, lean trunk mass), age, weight and body mass index (BMI) were risk factors that significantly increased the occurrence of GDM (p <.001 for all). Women older than 30 years or with a BMI more than 23, had a significantly higher GDM prevalence (34.89% and 34.77%). After adjusted covariates, visceral fat levels at the third quartile, the ORs of GDM were 1.142 (95% CI 1.032–1.263) in model I and 1.419 (95% CI 1.274–1.581) in model II used the first quartile as reference (p <.05 for both); bone minerals at the third quartile, the ORs of GDM were 1.124 (95% CI 1.020–1.238) in model I and 1.311 (95% CI 1.192–1.442) in model II (p <.05 for both). After adjusted for age, visceral fat levels and bone minerals, OR of GDM for percent body fat more than 28.77% at the third quartile was 1.334 (95% CI 1.201–1.482) in model II (p <.05 for both). Visceral fat levels, bone minerals and percent body fat were significantly associated with an increased risk of GDM, providing the reference ranges of visceral fat levels, bone minerals and percent body fat as predictive factors for Chinese women to estimate the risk of GDM by BIA during pregnancy. [ABSTRACT FROM AUTHOR]

Abstract Background Progesterone supplementation after in vitro fertilisation/intracytoplasmic sperm injection (IVF/ICSI) can improve the rates of clinical pregnancy and live birth, but the optimal duration of treatment remains controversial. The objective of this meta-analysis was to investigate the effects of early progesterone cessation on pregnancy outcomes in women undergoing IVF/ICSI. Methods We searched MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL), the Chinese biomedicine (CBM) literature database, and the Wanfang database. The final search was performed in July 2012. All available randomised trials that compared the effects of early progesterone cessation with progesterone continuation during early pregnancy after IVF/ICSI were included. The main outcome measures were live birth rate, miscarriage rate and ongoing pregnancy rate. Fixed or random-effects models were chosen to calculate the risk ratio (RR). Results Six eligible studies with a total of 1,201 randomised participants were included in the final analysis. No statistically significant differences were detected between patients who underwent early progesterone cessation and those who received progesterone continuation for luteal phase support in terms of live birth rate (RR: 0.95, 95% CI: 0.86–1.05), miscarriage rate (RR: 1.01, 95% CI: 0.74–1.38) or ongoing pregnancy rate (RR: 0.97, 95% CI: 0.90–1.05). These results did not change after a sensitivity analysis. Conclusions The currently available evidence suggests that progesterone supplementation beyond the first positive hCG test after IVF/ICSI might generally be unnecessary, although large-scale randomised controlled trials are needed to strengthen this conclusion.

Objective: To study the changes in the expression of nicotinamide adenine dinucleotide phosphate (NADPH), a glucose metabolism-derived antioxidant, in late-onset preeclampsia (LOPE) placenta tissue and the correlation with oxidative stress., Methods: A total of 13 normal pregnant women and 13 pregnant women with LOPE who were hospitalized in the Obstetrics Department, the First Affiliated Hospital of Chongqing Medical University and who underwent elective cesarean section between November 2020 and October 2021 were included in the study. Placenta tissues were collected from the subjects. Dichloro-dihydro-fluorescein diacetate (DCFH-DA) assay was done to determine the ROS levels in the placenta tissues of the LOPE group and the normal control group. Spectrophotometric analysis was conducted to determine the levels of NADPH, glutathione (GSH), and glucose, and the expressions and activities of glucose-6-phosphate dehydrogenase (G6PD) and phospho-gluconate dehydrogenase (PGD), key rate-limiting enzymes of the pentose phosphate pathway (PPP), in the placenta tissues of the LOPE group and the normal control group. Western blot was done to determine changes in the protein expressions of phosphofructokinase 1 (PFK1), a key rate-limiting enzyme of the glycolytic pathway, G6PD, and PGD in the placenta tissues from the two groups., Results: ROS levels in the placenta tissue of the LOPE group were significantly higher than those of the control group ( P <0.05). The levels of NADPH and GSH, two antioxidants, and glucose in the LOPE placenta were significantly higher than those of the control group ( P <0.05). The expression of PFK1 was significantly elevated in the LOPE group ( P <0.05). However, there were no significant differences in the activities and protein expression of G6PD and PGD between the two groups., Conclusion: Glucose metabolism reprogramming takes place in LOPE placenta tissue, which may be one of the causes of the abnormal elevation of NADPH and GSH., (Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).)

Objective: To evaluate the expression of Krüppel-like factor 8 (KLF-8) and matrix metalloproteinase 9 (MMP-9) in placentas and their relationship with the pathogenesis of preeclampsia (PE)., Methods: Twenty-two women with PE(mild PE:4 cases; severe PE:18 cases) who received cesarean sections in the First Affiliated Hospital of Chongqing Medical University from September 2011 to March 2012 were recruited as the PE group (n = 22). And twenty women who received elective term cesarean section without perinatal complications were chosen as the control group (n = 20). Placentas were collected and immunohistochemical SP method were employed to detect the localization of KLF-8 protein.KLF-8 mRNA level was determined by quantitative real-time PCR technique and western blot analysis was used to quantify KLF-8 and MMP-9 protein levels., Results: (1) There was no difference of KLF-8 protein distribution in placentas of the PE group and the control group.It was mainly located in the nuclear and cytoplasm of syncytiotrophoblasts.KLF-8 immunostaining was apparently decreased in the placentas of preeclamptic women when compared with the control group.(2)The KLF-8 mRNA levels were significantly decreased in placentas of the PE group (0.69 ± 0.08) compared to those of the control group (1.14 ± 0.09, P < 0.01). (3) KLF-8 and MMP-9 protein levels significantly decreased in the PE placentas (0.68 ± 0.05 and 0.21 ± 0.03) when compared to the control group (0.94 ± 0.06 and 0.34 ± 0.03, respectively, P < 0.01).(4) There was a positive correlation between the expression of KLF-8 and MMP-9 protein in the placentas from PE and normal pregnancies (r = 0.64, P < 0.01)., Conclusions: KLF-8 mRNA and protein levels were decreased in placentas of PE patients compared to those of normotensive women.KLF-8 protein was primarily located in the invasion-related trophoblast cells and its expression had a positive correlation with MMP-9 levels.KLF-8 might have an important role in the pathogenesis of PE by regulation of trophoblast invasion.

Objective: To analyze the clinical characteristics and perinatal outcome of early-onset intrahepatic cholestasis of pregnancy (ICP)., Methods: A total of 305 ICP cases were collected in the First Affiliated Hospital of Chongqing Medical University between June 2006 and May 2012. According to the onset time of ICP, patients were divided into early-onset ICP group (onset time < 28 gestational weeks) and late-onset ICP group (onset time ≥ 28 gestational weeks). The late-onset ICP group was further divided into 28 - 31(+6) gestational weeks and ≥ 32 gestational weeks according to the onset time. The biochemical indices and perinatal outcome of each group were assessed., Results: (1) When the diagnosis was made for the first time, the maternal serum concentrations of total bile acid (TBA) and total bilirubin (TBIL) in early-onset ICP group were (41 ± 9) and (32 ± 9) µmol/L, respectively; while TBA and TBIL in late-onset ICP group were (32 ± 6) and (22 ± 9) µmol/L, and the difference between the two groups was statistically significant (P < 0.05). (2) There was no significant difference in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) between early-onset ICP group and late-onset ICP group (P > 0.05). The ALT of early-onset ICP group and late-onset ICP group were (159 ± 50) and (145 ± 52) U/L, respectively; and AST were (151 ± 49) and (138 ± 44) U/L, respectively. (3) The early-onset ICP group had significant higher (P < 0.05) incidence of meconium staining (18.8% vs. 7.4%), fetal distress (22.9% vs. 8.9%), newborn asphyxia (14.6% vs. 5.4%), premature delivery (33.3% vs. 15.6%), developing into severe ICP (41.7% vs. 25.3%) and cesarean section (91.7% vs. 78.6%) when compared to the late-onset ICP group. No significant difference in the incidence of premature delivery, developing into severe ICP and cesarean section was found between the two types of late-onset ICP. (4) There was significant differences in average birth weight and gestational weeks at delivery between the two groups [early-onset ICP group: (3113 ± 443) g and (36.3 ± 2.6) weeks]; late-onset ICP group: [(3513 ± 450) g and (37.7 ± 1.6) weeks]., Conclusion: The early-onset ICP patients presented worse clinical manifestations than late-onset ICP patients, and early-onset ICP is more likely to lead to premature delivery and fetal distress.

Objective: To explore the expression of pentraxin-3 (PTX3) in placentas from patients with severe preeclampsia and the relationship between PTX3 and the pathogenesis of severe preeclampsia., Methods: Fifty-three pregnant women who delivered from October 2010 to March 2011 in the First Affiliated Hospital of Chongqing Medical University were included in the study. Twenty-three women with severe preeclampsia were chosen as the preeclampsia group, and thirty healthy pregnant women were identified as the control group. All the women received cesarean section. The location of PTX3 protein in placentas was studied by immunohistochemical SP method. Quantitative real-time PCR technique and western blot analysis were employed to assay the levels of PTX3 mRNA and protein in placentas, respectively., Results: (1) The location of PTX3 protein in placentas: PTX3 protein was expressed in placentas from both groups, and there was no difference of PTX3 distribution between normal and preeclamptic placentas. PTX3 was mainly located in perivascular stroma, decidual cells and terminal villi. Neutrophilic infiltration was observed in the preeclamptic placentas. (2) The expression of PTX3 mRNA and protein in placentas:the level of PTX3 mRNA in placentas from the preeclampsia group was higher than that in the control group (1.98 ± 0.54 vs. 0.87 ± 0.27, P < 0.05). Compared with the control group, the level of PTX3 protein was significantly elevated in the preeclampsia group (1.42 ± 0.29 vs. 0.56 ± 0.25, P < 0.01)., Conclusion: The high expression of PTX3 in placentas from the preeclamptic patients suggests that PTX3 may be involved in the pathologic process of preeclampsia.

Aim: To investigate the occurrence law of autophagy in trophoblast cells from severe preeclampsia and its possible mechanisms of wrecking cells., Methods: 23 cases of placenta tissues were collected from women suffer from severe preeclampsia and normal pregnant women respectively. Surface villous of placental was observed by scanning electron microscope, and ultrastructure and autophagosome of trophoblast cells were observed by transmission electron microscopic. The expressions of Beclin-1 and LC3II in placenta tissues were detected by Immunohistochemical technique, then its relevance whit weight of fetus and placental was analyzed., Results: Compared with the control group, villous were decrease in placenta tissue from patients suffer from severe preeclampsia, and its arrangement was disordered; typical autophagosomes of trophoblast cells were observed by transmission electron microscope. The expression of Beclin-1, LC3IIwere significantly up-regulated in placenta tissue from patients suffer from severe preeclampsia.The correlation coefficient of Beclin-1, LC3II and placental weight, fetal weight respectively were -0.977, -0.930, -0.812, -0.849., Conclusion: Autophagy were significantly up-regulated in trophoblast cells from patients suffer from severe preeclampsia by increasing expression of Beclin-1, LC3II protein, and its expression was negatively related to weight of fetus and placental.

Aim: To investigate the effects and possible molecular mechanisms of inhibiting FOXM1 expression on SKOV3 cells by lentiviral vector targeting FOXM1 shRNA., Methods: SKOV3 cells were infected by lentiviral vector targeting FOXM1 shRNA with a multiplicity of infection (MOI) of 20, then growth curve of SKOV3 cells was determined by MTT assay, cell cycle was analysed by flow cytometry(FCM), and the expression of mRNA and protein of FOXM1, Cyclin D1, PLK1 by Real time PCR and Western blot., Results: Lentiviral vector targeting FOXM1 shRNA with a multiplicity of infection (MOI) of 20 could significantly inhibit the growth of SKOV3 cells. After infected by lentiviral vector targeting FOXM1 shRNA, the G(0);/G(1); phase cells increased and the S-phase cells decreased, and the expression of mRNA and protein of FOXM1, Cyclin D1, PLK1 of SKOV3 cells were significantly down-regulated., Conclusion: Inhibiting FOXM1 expression has a significantly effect of inhibiting proliferation on SKOV3 cells. Blocking SKOV3 cells in the G(0);/G(1); phase by down-regulating the expression of Cyclin D1, PLK1 protein may be its mechanism.

Objective: To study expression and activation of p38 mitogen activated protein kinase (MAPK) in vascular endothelial cells dysfunction in preeclampsia., Methods: From Sept. 2009 to Mar. 2010, 54 pregnant women underwent deliveries in the First Affiliated Hospital of Chongqing Medical University were enrolled in this study, including 20 patients in mild preeclampsia group, 16 patients in severe preeclampsia group and 18 women with term cesarean section without perinatal complications as control group. Placental endothelial cells were labeled by CD₃₄ to assay microvessel density (MVD) of each group. Immunohistochemical SP and western blot were used to detect localization and expression of p-p38 MAPK protein, respectively. The levels of sera soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng) were measured by ELISA., Results: (1) The MVD of placenta were 103 ± 3 in control group, 81 ± 5 in mild preeclampsia group and 63 ± 4 in severe group, respectively, which showed statistical difference among each group (P < 0.05). (2) The expression of p38 MAPK protein were 0.84 ± 0.05 in control group, 0.90 ± 0.14 in mild group and 0.86 ± 0.18 in severe group, which did not reach remarkable difference among each group (P > 0.05). The expression of p-p38 MAPK protein were 0.13 ± 0.05 in control group, 0.59 ± 0.12 in mild group and 1.16 ± 0.18 in severe group, which show statistical difference among each group (P < 0.05). (3) The localization of p-p38 was in trophoblast, endothelial cells and a few stromal cells in placenta. (4) The level of sFlt-1 and sEng: (1) The concentration of sFlt-1 and sEng were (5.2 ± 0.3) and (10.9 ± 0.4) µg/L in control group, (12.5 ± 1.2) and (20.4 ± 5.3) µg/L in mild group and (19.3 ± 3.0) and (29.5 ± 3.7) µg/L in severe group. When drawing paired comparison in those groups, the differences showed statistical difference (P < 0.05). (2) There were positive correlations between p-p38 MAPK protein levels and the concentrations of serum sFlt-1, sEng in preeclampsia groups (r = 0.68, P < 0.05; r = 0.87, P < 0.05)., Conclusions: The remarkable activation of the p38 MAPK in the placenta of patients with preeclampsia induced the increased levels of sFlt-l and sEng in maternal serum, which confer the injury of vascular endothelial cells that caused the significant decline of MVD in placentas. p38 MAPK signaling might be one of the key pathways in vascular endothelial cell dysfunction in preeclampsia.

Objective: To evaluate the expression and location of the growth arrest and DNA damage 45 alpha (Gadd45α) gene in human placenta and explore the relationship between Gadd45α and preeclampsia (PE)., Methods: Thirty-six women with preeclampsia who delivered from September 2009 to March 2010 in the First Affiliated Hospital of Chongqing Medical University were chosen as the study objects. They were classified into mild group (n = 20), severe group (n = 16) and elective term cesarean sections group without previous onset of labor and perinatal complications (control group, n = 18). Placentas were collected after they delivered and immunohistochemical streptravidin-biotin peroxidase (SP) method and histoscore were employed to detect the expression and localization of Gadd45α protein.Gadd45α mRNA level was determined by reverse transcription polymerase chain reaction (RT-PCR) technique and western blot analysis was used to quantify Gadd45α protein expression level., Results: (1) Gadd45α protein was detectable in placenta tissues of the mild and severe groups, mostly located in cytoplasm and nuclei of trophoblast, plus nuclei of vascular endothelial cells and a few stromal cells; whereas placenta tissues of control group showed weak staining, and only detectable in trophoblast, undetectable in vascular endothelial cells. (2) The Gadd45α mRNA levels in placenta tissues of the severe and mild groups were 0.75 ± 0.07 and 0.44 ± 0.13, respectively, significantly higher than that in control group (0.18 ± 0.04, P < 0.05); compared with mild group, Gadd45α mRNA level was significantly higher in severe group (P < 0.05). (3) The Gadd45α protein levels in placenta tissues of the severe and mild groups was 1.34 ± 0.17 and 0.65 ± 0.15, respectively, compared with mild group, Gadd45α protein level was higher in severe group (P < 0.05); they were both significantly higher than that in control group (0.22 ± 0.11, P < 0.05)., Conclusions: Gadd45α mRNA and protein levels in placenta tissues of patients with preeclampsia are higher than that of normotensive women, and up-regulated with aggravation of preeclampsia; the Gadd45α protein is located in trophoblast cells, which are closely related to pathogenesis of preeclampsia. These results indicate that Gadd45α plays an important role in the pathogenesis and progression of preeclampsia.

Objective: To study the feasibility of using amniotic cells plus collagen I complex for fetal membrane healing., Methods: Human amnion mesenchymal cells were embedded in three-dimensional (3D) collagen I and epithelial cells placed on the top. The amniotic cells plus collagen I complex was created to mimic the architecture of native amnion. As judged by DAPI staining, the number of amniotic cells cultured in 3D collagen I was counted after incubation for 2 and 8 days. The tensile strength of collagen I with a varying number of amniotic mesenchymal cells was measured after a 15-day incubation., Results: At Days 2 and 8, the mean number of mesenchymal cells was (121 ± 5)/cm(2) and (124 ± 4)/cm(2) (P > 0.05). The size of collagen I matrix was reduced to 45%, 15%, 14% at Days 5, 10, 15 respectively. Mesenchymal cell was capable of remodeling collagen I (P < 0.01) and it could not be inhibited by GM6001 and/or aprotinin. The tensile strength of amniotic cells plus collagen I scaffold complex was strengthened with an increasing number of amnion mesenchymal cells (P < 0.01)., Conclusion: The amniotic cells plus collagen I complex may be useful for healing preterm premature rupture of the membrane (PPROM).

Objective: To investigate the influence of intrahepatic cholestasis of pregnancy (ICP) on the pulmonary morphologic changes of fetal rats., Methods: Twenty pregnant SD rats at 15 days of gestations were randomly divided into ICP and control group. Rats in the ICP group were subcutaneously injected with 17-alpha-ethinylestradiol and progesterone for 5 consecutive days to establish the rat ICP model, and those of the control group received subcutaneous injection of sirasimeyu also for 5 days. The levels of serum alanine aminotransferases (ALT), aspartate transamlnase (AST), and total bile salt (TBA) were measured before and after the treatment, respectively. Maternal rats were sacrificed on 21 days of gestations and hysterotomies were performed immediately. Histopathologic changes of maternal rats' livers and fetal lungs were observed under light and electron microscopes., Results: (1) The maternal serum levels of ALT, AST, and TBA showed no significant difference between the ICP and control group [ALT: (55+/-15) vs (49+/-12) U/L; AST: (146+/-16) vs (145+/-20) U/L; TBA: (13+/-4) vs (14+/-4) micromol/L, P>0.05, respectively] before the ICP models were established, but higher levels were shown in the ICP group after [ALT: (94+/-12) vs (59+/-17) U/L; AST: (245+/-26) vs (163+/-27) U/L; TBA: (44+/-16) vs (17+/-3) micromol/L, P<0.05, respectively]. (2) The livers of maternal rats' in the ICP group were gloomy with blurred margins, however those of the control group were normal. Microscopic observed swollen and degenerated hepatocytes with narrowed hepatic sinusoid, dilated bile duct and necrosis of hepatocytes occasionally in the ICP group, while the morphology of hepatocytes and structures of lobuli hepatis in the control group were normal. (3) The fetal pulmonary tissues in the ICP group were dark, and normal in the control group. Histopathologic examination showed matured fetal pulmonary tissues with dilated and congested interstitial lung capillaries, thickened alveolar septum, mild focal inflammatory exudation and focal hemorrhage in alveolus. Furthermore, reduced microvilli, mitochondrion vacuolization, cytoplasm disintegration and increased lamellar body evacuation were observed in type II pneumonocytes in ICP group under light and electron microscopes. While fetal pulmonary tissues of the control group did not show any significant lesions., Conclusions: Rat model of ICP can be established with the combination of estrogen and progestin. Hyperbileacidemia in ICP rat may lead to pathological changes in fetal pulmonary tissues.

Objective: To investigate the role of transcription factor Ets-1 involved in premature rupture of membranes(PROM)by detecting its expression and location in human fetal membranes., Methods: Between Feb. and Nov. 2007, 100 pregnant women who delivered in the First Affiliated Hospital, Chongqing Medical University were enrolled in this study. According to gestational weeks, rupture of amniochorionic membranes and delivery mode, those women were classified into preterm labor group, preterm premature rupture of membranes (PPROM) group, term labor group and term premature rupture of membranes (TPROM) group, matched with elective term cesarean sections women as control group. There were 20 pregnant women in every group. The expression and distribution of Ets-1 protein in fetal membranes were detected by immunohistochemical streptravidin-biotin peroxidase (SP) method and histoscore. In the mean time, 6 cases were chosen from each group randomly and reverse transcription-PCR was used to measure the Ets-1 mRNA expression., Results: (1) The expression of Ets-1 mRNA in fetal membranes were 0.342 ± 0.016 in preterm labor group, 0.603 ± 0.027 in PPROM group, 0.325 ± 0.013 in term labor group, 0.582 ± 0.075 in TPROM group, 0.139 ± 0.012 in control group, respectively. When compared with that in control group, Ets-1 mRNA expression were significantly increased in both PPROM and TPROM group (P < 0.05). However, it did not show remarkably difference between preterm group and term labor group, as well as between PPROM and TPROM group (P > 0.05). (2) Ets-1 was in stromal layers of amniochorionic membranes and in both cytoplasm and nuclei of trophoblast, which were shown with diffuse intracellular positive granularities (brown-yellow) clearly. No expression of Ets-1 was observed in amniotic epithelial cells. (3) The expression of Ets-1 protein was 0.552 ± 0.018 in preterm labor group, 2.853 ± 0.174 in PPROM group, 0.538 ± 0.042 in term labor group, 2.731 ± 0.090 in TPROM group and 0.214 ± 0.013 in control group, respectively. Ets-1 protein was significantly increased in the stroma of both PPROM and TPROM group than that in control group (P < 0.05). However, no remarkable different expression of Ets-1 was observed between preterm and term labor group, so was that between PPROM and TPROM group (P > 0.05)., Conclusion: Transcription factor Ets-1 is expressed in human amniochorionic membranes and it could be up-regulated in PROM.

Objective: To determine the relationship between the residue amniotic fluid volume after preterm premature rupture of membranes (PPROM) and maternal-fetal prognosis., Methods: One hundred and forty-five pregnant women with PPROM during 28 - 34 gestational weeks were studied, hospitalized in department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University from Jan. 2002 to Feb. 2009, and Chongqing Health Center For Women And Children from Jan. 2005 to Feb. 2009. All patients are willing to take part in these experiments. According to Amniotic fluid index (AFI) by ultrasound, patients were devided into three groups: (1) Group of oligohydramnios: AFI < 50 mm; (2) Group of borderline oligohydramnios: 50 mm 0.05)., Results: (1) Group of oligohydramnios had a shorter latent period (P < 0.05) compared with other two groups; (2) Group of oligohydramnios had a high rates of cesarean section (69%), Intra-amniotic infection (IAI, 36%), fetal distress (19%), neonatal asphyxia (28%), early-onset neonatal sepsis (28%) and hypoxic-ischemic myocardial injury (56%) than those in Group of normal amniotic fluid (39%, 9%, 3%, 8%, 9%, 13%; P < 0.01); (3) Logistic regression analysis showed that group of oligohydramnios was an independent risk factor of IAI and early-onset neonatal sepsis (P < 0.05)., Conclusions: Oligohydramnios after pprom is associated with the shorter latent period, as well as the increasing risks of pregnancy complications of cesarean section, IAI, fetal distress, neonatal asphyxia, early-onset neonatal sepsis and neonatal hypoxic-ischemic myocardial injury. So, the amniotic fluid volume might be an important prognostic indicator to assess the outcomes of maternal and neonatal when PPROM happened.

Objective: To investigate cardiac reserve function and pregnant results of preeclampsia., Methods: Pregnant women chosen by randomized table and hospitalized in the department of obstetrics of the first affiliated hospital of Chongqing Medical University were involved in this study from January to December, 2008. Sixty-nine cases of normal pregnant women were divided into 3 groups: normal group 1 (20 cases), normal group 2 (26 cases) and normal group 3 (23 cases). The normal group number 1 to number 3 were paired to gestational hypertension (20 cases), mild preeclampsia (26 cases) and severe preeclampsia (23 cases), respectively. The digital technique of heart sound signal processing was used to measure cardiac reserve function parameters including the heart rate (HR), the ratio of the amplitude of the first heart sound to the second heart sound (S1/S2) and the ratio of diastolic to systolic duration (D/S) of pregnant women. The pregnant results were also recorded., Results: (1) The ratio of S1/S2 in the group of severe preeclampsia 4.5 +/- 3.2 was significantly higher than the group of gestational hypertension 2.2 +/- 1.1 and normal group 3 2.2 +/- 1.1 (P < 0.01). The ratio of D/S of the group of severe preeclampsia 1.1 +/- 0.3 was significantly lower than the group of gestational hypertension 1.4 +/- 0.3 and normal group 3 1.4 +/- 0.2 (P < 0.01). (2) All cases of the normal group number 1 to number 3 and the group of gestational hypertension were found the ratio of D/S >/= 1.00, whereas 1 case (1/26, 4%) of the group of mild preeclampsia and 4 cases (4/23, 17%) of the group of severe preeclampsia were found the ratio of D/S < 1.00. (3) The two cases of the pregnant women (including one woman died of cardiac arrest) with S1/S2 > 5.00 and D/S < 1.00, who were in the group of severe preeclampsia, were sent to Intensive Care Unit after delivery. There were 4 cases (4/26, 15%) and 6 cases (6/23, 26%) of 1 minute Apgar score less than 7, 7 cases (7/26, 27%) and 6 cases (6/23, 26%) sent to neonatal Intensive Care Unit, 2 cases (2/26, 8%) and 4 cases (4/23, 17%) of neonatal death in the group of mild preeclampsia and in the group of severe preeclampsia, respectively. All newborns in the normal group number 1 to number 3 and the group of gestational hypertension were normal., Conclusions: The cardiac reserve function of a pregnant woman with preeclampsia is decreased with the severity of preeclampsia and the parturient and neonatal results get worse. The digital technique of heart sound signal processing is a safe, harmless, simple and effective tool to measure cardiac reserve function of preeclampsia, and is worthy of widely used clinically.

Objective: To study the relationship between bone morphogenetic protein-2 (BMP-2) and premature rupture of membranes (PROM)., Methods: Ninety gravidas giving birth at 4 hospitals in Chongqing from January 2006 to January 2007 were selected and divided into 5 groups (18 in each): term labor group ( with intact membranes), term PROM group, preterm labor group (with intact membranes), preterm PROM (PPROM) group and control group (term pregnancy not in labor). The expression of BMP-2 in the chorioamniotic membranes of each group were detected by streptavidin-peroxidase methods and its relationship with PROM plus histological chorioamnionitis were analyzed., Results: (1) BMP-2 was detected in the cytoplasm of epithelial and interstitial cells of membranes in each group. (2) BMP-2 expression in term labor group, term PROM group, preterm labor group and PPROM group were 0.0137 +/- 0.0094, 0.0269 +/- 0.0127, 0.0273 +/- 0.0145, 0.0456 +/- 0.0114, respectively, which higher than that of the control group 0.0060 +/- 0.0079 (P < 0.01). BMP-2 expression in the term PROM group was higher than that of the term labor group (P < 0.01), that in the PPROM was higher than in the preterm labor group and term PROM group (P < 0.01). (3) Pathological examination found that 17 out of the 90 women with histologic chorioamnionitis, of which 13 (36%) came from the term PROM and PPROM group with a higher level of BMP-2 expression than those without chorioamnionitis (0.0201 +/- 0.0107 vs 0.0105 +/- 0.0092, P < 0.05)., Conclusion: The expression of BMP-2 in chorioamniotic membranes is closely related to PROM.

Objective: To determine the expression of Aquaporin 8(AQP8) in the fetal membrane and placenta of idiopathic polyhydramnios., Methods: The amnion, chorion and placenta were collected from 12 term pregnancies with idiopathic polyhydramnios( polyhydramnios group) and 12 term pregnancies who were normal (control group). The expression of AQP8 mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). The expression of AQP8 protein was detected by immunohistochemistry., Results: The expression of AQP8 mRNA in amnion, chorion and placenta of polyhydramnios group was (0.78 +/- 0.13), (0.58 +/- 0.10), and (0.86 +/- 0.15) respectively, and that of control group was (0. 39 0.07), (0.45 +/- 0.09), and (0.34 +/- 0.09) respectively. The expression of AQP8 protein in amnion, chorion and placenta of polyhydramnios group was (0.195 +/- 0.024), (0.170 +/- 0.028), and (0.193 +/- 0.024) respectively, and that of control group was (0.151 +/- 0.018), (0.156 +/- 0.024), and (0.152 +/- 0.023) respectively. In all 3 types of tissues the expression of AQP8 mRNA of polyhydramnios group was higher than that of control group (P < 0.05). In amnion and placenta the expression of AQP8 protein of polyhydramnios group was also increased compared to that of control group (P < 0.05), but in chorion the difference in AQP8 protein expression between the two groups was not significant (P > 0.05)., Conclusion: The expression of AQP8 mRNA and protein is significantly increased in the amnion and placenta of polyhydramnios, suggesting that AQP8 may play an important role in the regulation of amniotic fluid volume.