Objective:To investigate whether placental tissues produce leptin and determine the relationship between expression levels of leptin-mRNA in placenta and fetal growth and development.Methods:52 neonates were divided into 3 subgroups:(1)birth weight large for gestational age (LGA)( n =14),(2)birth weight appropriate for gestational age (AGA)( n =21),(3)birth weight small for gestational age (SGA)( n =17).Reverse transcription-polymerase chain reaction(RT-PCR) technique was used to detect human leptin-mRNA derived from placental-RNA.The expression levels of leptin-mRNA were quantitated using fluorescence intensity analysis.The correlations of expression level of placental leptin-mRNA with placental weight,birth weight,newborn Ponderal index(PI),maternal weight,maternal body mass index(BMI) and gender were studied.Results:The expression levels of placental leptin-mRNA in LGA infants(119.7?13.0) and SGA infants(76.8?15.1) were significantly higher and lower respectively than those in the AGA infants(94.4?17.4)( P

Evidence-based medicine (EBM) is a newly-developed model in medicine science.EBM demands that decision-making in clinical practice should be founded on objective evidences of study and emphasizes the combination of the clinical evidence with doctor's experience.At present,EBM has been applied in clinical teaching.This paper describes the significances and methods of EBM education in obstetrics teaching.

Objective:To investigate the relationship between serum creatine kinase level and histopathological observation of tubal ectopic pregnancy.Methods:Serum creatine kinase was determined by N-acetyl cysteine(NAC) assay in 22 patients with ruptured tubal pregnancies and 35 patients with unruptured tubal pregnancies.Fallopian tube tissues were examined by histopathology.Results:The mean levels of serum creatine kinase in patients with ruptured tubal pregnancies were significantly higher than that in those with unruptured tubal pregnancies(154.2?63.7 IU/L vs 107.8?51.3 IU/L, P

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 anmion 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 anmion and placenta of polyhydramnios, suggesting that AQP8 may play an important role in the regulation of amniotic fluid volume.

Objective To study the effect of cyclic adenosine monophosphate on aquaporin 8 (AQP8) expression and distribution in human amnion-derived WISH cells.Methods Human amnionderived WISH ceils were cultured.The cells were divided into control group and study group at random.The study group was established by exposure to various concentrations of 8-Br-cAMP.Western analysis was used to quantify AQP8 expression levels. RT-PCR was used to quantify AQP8 mRNA expression levels.Immunofluorescence was used to determine the localization of AQP8 in WISH cells.Results With increase of cAMP,AQP8 mRNA and protein expressions significantly increased in WISH cells in vitro.When the concentration of cAMP reached 200 μmol/L,AQP8 mRNA and protein expressions were highest.Incubation with cAMP (200 μmol/L) for 2 hours resulted in a 2-fold increase in AQP8 mRNA level,and incubation for 8 hours resulted in a peak.After incubation for 16 hours AQP8 mRNA level began to descend,and after 24 hours it decreased to baseline.Incubation with cAMP for 8 hours AQP8 protein level began to increase.Incubation for 24 hours resulted in a peak in AQP8 protein level,and after incubation for 48 hours it began to decline.By immunofluorescence microscopy after incubation with cAMP (200 μmol/L) cells,AQP8 labeling in plasma membrane was enhanced and intracellular AQP8 labeling was decreased.Conclusion The cAMP triggers translocation of AQP8 from cytosel to the plasma membrane via vesicle-transporting related protein instead of AQP8 itself,cAMP may upregulate the transcription of target gene protein kinase A.The cAMP may be the critical regulatory medium of AQP8 in WISH cells.

Objective To investigate the alteration on the expression levels of protein and messenger RNA(mRNA)of aquaporin-8(AQP8)in the hepatocytes of pregnant rats with intrahepatic cholestasis induced by ethinylestradiol.Methods A total number of 20 15-day pregnant rats were randomly divided into two groups:control group，intrahepatic cholestasis of pregnancy(ICP)group.In ICP group，rats were subcutaneously injected with ethinylestradiol(2.5 mg·kg-1·d-1)for 5 days to make the model of ICP.In control group，rats received subcutaneous injection of appropriate volume of propylene glycol for 5 days.The protein expression and subcellular localization of AQP8 in the hepatocytes of pregnant rats were detected using immunohistochemical methods.The mRNA expression of AQP8 in the hepatocytes was assayed by RT-PCR method.Results The model of ICP of pregnant ats was made successfully.Expressions of AQP8 protein and mRNA were detected in two groups.AQP8 protein level in ICP group was 10.8±2.4，significantly decreased than in control group 17.1±2.2(P＜0.05).AQP8 mRNA level in ICP group was 1.07±0.11，significantly higher than in control group 0.80±0.11(P＜0.05).Conclusion Down-regulated AQP8 protein expression and up-regulated AQP8 mRNA expression in the hepatocytes of pregnant rats with intrahepatic cholestasis may contribute to the pathogenesis of ICP.

Objective To investigate the pulmonary morphologic changes and pulmonary surfactant protein A (SP-A) mRNA expression in fetal rats with maternal intrahepatic cholestasis of pregnancy (ICP).Methods Animal models of intrahepatic cholestasis of pregnancy were induced by 17-α-ethinylestradiol and progesterone.Histopathologic examination of the fetal lungs was performed under light and electronic microscopes.The expression of SP-A mRNA in the fetal lungs was measured by reverse transcription-polymerase chain reaction technique.Results (1) Compared with the control group,histopathologic examination showed that fetal pulmonary tissues had 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 alveolar epithelial cell II in ICP group under light and electronic microscopes.(2) Expression of SP-A mRNA in fetal lungs of ICP group (0.71 + 0.10) was significantly lower than that in control group (1.00±0.27),t=3.093,P＜0.05.Conclusions Hyperbileacidemia in ICP maternal rat might lead to pathological changes in fetal pulmonary tissues.Low expression of SP-A mRNA might contribute to lesions of fetal lung with ICP.

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 amuiochorionic 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.

anes is closely related to PROM.

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-α-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 mammal 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) μmol/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) μmol/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.