34 weeks. The clinical data were evaluated. The relations between the pattern of end organ damage and maternal outcomes and perinatal mortality and morbidities were analyzed. Results 71. 70% of all 191 S-PE cases were involved in single organ systemic damage, and the rate was higher than those involved in two or more end organ damage. In those women with single end organ damage, placenta (55. 26%) and liver(15. 79%) were the two main organs concerned in early onset group; while in late onset group they were placental(18. 42% , compared with the early onset group P

Objective To investigate the effect of clinical risk factors including maternal underlying medical conditions on the development of preeclampsia (PE) in order to improve and strengthen the early assessment of high clinical risk population of PE.Methods Clinical.observational data of patients with PE in Peking University Third Hospital from November 2008 to January 2011 were analyzed.Comparative analysis was made among medical conditions with PE (M-PE) sub-group and isolated PE (I-PE) sub-group and non-PE pregnancy with or without medical conditions (control group).Results Totally 159 cases,43.09％ (159/369) of total cases of PE had high clinical risk factors (multiple pregnancy and medical conditions) and 32.3％ (97/300) of singleton PE accompanied with medical conditions.The incidence of PE in singleton pregnancies with medical conditions was significantly higher than those without medical conditions [ 15.0％ (97/646) versus 4.45％ (210/4719),P ＜ 0.05 ].In M-PE sub-group,the average age [ ( 31.7 ± 4.5 ) versus ( 29.3 ± 5.2) year-old] and body mass index (BMI) in first trimester [ (26.0 ±5.6) versus (23.3 ± 3.7) kg/m2],the proportion with previous preeclampsia [ 11％ (11/97) versus 4.9％ (10/203) ] and pregnancy loss in third trimester [ 11％ ( 11/97 ) versus 3.0％ ( 6/203 ) ],were higher than those of I-PE sub-group ( all P ＜ 0.05 ).The onset of preeclampsia in M-PE sub-group was earlier than I-PE ( 32.9 versus 34.4 gestation weeks,P ＜ 0.05 ).The proportion serious cases of PE occurring before 32 gestational weeks were higher in M-PE than that of I-PE sub-group [ 45％ (44/97)versus 34.0％ (69/203),P ＜0.05].Multivariate regression analysis showed that previous history of late pregnancy loss and irregular prenatal care were clinical risk factors for early-onset PE whether early-onset was defined as ＜ 34 or ＜ 32 gestational weeks respectively (all P ＜ 0.05) ; medical conditions were risk factors for PE if early-onset was defined as ＜ 32 gestational weeks ( OR =1.718,95％ CI:1.005 - 2.937,P =0.048).Conclusions Multiple pregnancies and pregnancies with medical conditions exceed one-third of total subjects of PE.The onset of PE in subjects with maternal underlying medical conditions was earlier which is the subgroup should not be ignored.The difference of early pregnancy BMI may show the maternal heterogeneity in early onset and late onset of preeclampsia.Assessment of clinical risk factors including the underlying medical disorders for preeclampsia in early trimester should be strengthened.

Objective To identify the early warning signs of severe preeclampsia (SPE). Methods A case-control (1: 2) observational study was conducted. Forty-seven pregnant women with SPE, who attended the prenatal clinics of Peking University Third Hospital regularly from Jan. 2002 to Dec. 2007, were selected as the study group, including 12 early onset and 35 late onset ones. The control group consisted of 94 healthy singleton pregnant women at the same period. Clinical data were collected and analyzed. Results (1) The basal body mass index (BMI) showed no difference between the study and control group [(23.27±4.31)kg/m2 vs (21.52±3.09)kg/m2, P>0.05]. (2) The net increase of BMI in the study group before the onset of SPE was higher than that in the control [(5.60±2.17)kg/m2 vs (4.85±1.52)kg/m2, P<0.05] and the increase of BMI per week was also higher [(0.74±0.41)kg/(m2*w)-1 vs (0.23±0.18)kg/(m2*w)-1, P<0.01]. The sensitivity and specificity of BMI increase per week in predicting SPE was 84% and 81% at a cut-off value of 0.39 kg/(m2*w)-1, respectively, and 79% and 91% at 0.41 kg/(m2*w)-1 correspondingly. (3) During the third trimester and before the onset of SPE, the weight gain per week in the study group was higher than that of the control [(0.93±0.70)kg vs (0.63±0.20)kg, P<0.01]. Significant difference was also found in the net weight gain between the two groups (P<0.01), but not in the percentage of women with excessive weight gain (>0.50 kg/w) [60%(25/42) in the study group vs 63%(53/84) in the control group, P>0.05]. (4) Higher percentage of women experienced pre-hypertension in the study group than in the controls [17%(8/47) vs 5%(5/94), P<0.01]. (5) In the study group, 53%(25/47) of the women had edema before SPE onset, but the figure dropped to 18% (17/94) in the controls(P<0.01). (6) Eight women in the study group and one in the control group suffered from hypoproteinemia before SPE onset with the average level of plasma albumin of (32.6±1.6)g/L and(38.4±2.1)g/L(P<0.01), respectively. (7) Proteinuria was reported in 10 cases (21%)in the study group and 4(4%) in the controls (P<0.01). (8) Logistic regression analysis showed that the risk factors for SPE included edema (OR=6.16,95%CI:2.29-16.57),pre-hypertension (OR=6.21,95%CI:1.56-24.77),proteinuria (OR=9.68,95%CI:1.86-50.30), and weight gain >0.85 kg/w during the third trimester (OR=11.60,95%CI:3.54-37.97). Conclusions Edema, excessive weight gain,pre-hypertension and hypoproteinemia are early warning signs of SPE. Pregnant women with the above signs required close monitoring during prenatal care.

Objective To investigate the effects of expression of mitochondria long-chain fatty acid oxidative enzyme (long-chain 3 hyroxyacyl CoA dehydrogenase,LCHAD) and p38 mitogen activated proteinkinase (p38MAPK) signal transduction pathway in severe preeclampsia.Methods Serum-free trophoblast cells cultured in vitro were stimulated by early onset severe preeclampsia serum (E-PE group),late onset severe preeclampsia serum (L-PE group),HELLP syndrome serum (HELLP group),and normal pregnancy serum (NP group) respectively; each group was added DMEM/F12 medium,reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor (NADPH-Ⅰ) and p38 MAPK inhibitor (p38-Ⅰ)to stimulate cells.Expression of mRNA and protein of LCHAD in trophoblast cells were detected by real-time PCR and western blot.Results (1) The expression of mRNA of LCHAD:the level of mRNA of LCHAD in NP+DMEM,E-PE + DMEM,E-PE + NADPH-Ⅰ,E-PE + p38-Ⅰ,L-PE + DMEM,L-PE + NADPH-Ⅰ,L-PE + p38-Ⅰ and HELLP + DMEM,HELLP + NADPH-Ⅰ,HELLP + p38-Ⅰ groups were 1.00 ± 0.03,0.14 ±0.08,0.95 ±0.20,1.43±1.02,0.37 ±0.18,1.51 ±0.36,1.60 ±0.31,0.10 ±0.04,0.49 ±0.10,0.44 ± 0.21,respectively.The relative expressions of mRNA of LCHAD were significantly reduced in E-PE + DMEM,L-PE + DMEM and HELLP + DMEM groups compared with the NP + DMEM group (P ＜0.05).Compared with the NP groups,the relative expressions of mRNA of LCHAD were significantly increased in L-PE + NADPH-Ⅰ and L-PE + p38-Ⅰ group (P ＜ 0.05),while reduced in HELLP groups (P ＜0.05).(2) The expression of protein of LCHAD:the relative expressions of protein of LCHAD in NP +DMEM,E-PE + DMEM,E-PE + NADPH-Ⅰ,E-PE + p38-Ⅰ,L-PE + DMEM,L-PE + NADPH-Ⅰ,L-PE +p38-Ⅰ and HELLP + DMEM,HELLP + NADPH-Ⅰ,HELLP + p38-Ⅰ groups were 19.4 ± 2.2,10.7 ± 1.1,17.9±3.3,19.1 ±2.9,16.4 ±2.3,20.3 ±2.3,20.9 ±4.3,12.4 ±2.3,17.6 ±2.6,17.7 ±2.0 respectively.Compared with the NP groups,the protein expressions of LCHAD were significantly remarkably reduced in E-PE + DMEM,L-PE + DMEM and HELLP groups (P ＜ 0.05).Compared with the DMEM groups,the protein expressions of LCHAD were significantly increased in NADPH-Ⅰ and p38-Ⅰ groups of E-PE,L-PE and HELLP groups (P ＜ 0.05).Conclusions These studies demonstrate that long chain fatty acid oxidation was involved in the pathogenesis and development of preeclampsia.The expressions of gene and protein of LCHAD were remarkably affected by early onset severe preeclampsia and HELLP syndrome.NADPH-Ⅰ and p38-Ⅰ may allay the disorder of fatty acid oxidation.p38MAPK signal transduction pathway may contributed in this process.

Objective Severe preeclampsia, and hemolysis, elevated liver enzymes, and low platelet syndrome (HELLP) are serious complications of pregnancy, and evidence suggests a genetic basis for these conditions. A G1528C mutation in the alpha-subunit of the mitochondrial trifunctional protein (MTP) gene has been identified in association with these conditions. The aim of this study is to explore the carrier rate of the G1528C mutation in the MTP gene in pregnant women with severe preeclampsia, HELLP syndrome and in their newborns, as well as in a normal pregnant population, so as to determine its association with maternal liver disease among women in Beijing. Methods A multicenter, prospective, case control study was carried out. Polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) was used to screen the G1528C mutations in the MTP gene. One hundred and forty cord blood samples from cases with severe preeclampsia (n=130) and HELLP syndrome (n=10) were collected. Ninety maternal peripheral blood samples among them (84 from severe preeclampsia and 6 from HELLP syndrome) were also collected for screening the common disease-causing mutation in Caucasians. Five hundred and sixty cord blood samples and 90 maternal peripheral blood samples obtained from normal pregnant women served as controls. Results The G1528C mutations in the MTP gene were not found in samples from women with severe preeclampsia and their newborns, from women with HELLP syndrome and their new borns, as well as in samples from the normal pregnant women and their new borns. Conclusions The common disease-causing mutation of G1528C in MTP gene in Caucasians is probably not a common mutation in Chinese Han people in Beijing. Further study is needed to expand the sample size among HELLP syndrome and maternal liver diseases in Chinese population.

Objective To investigate the clinical effect of therapeutic cervical cerclage on short cervix syndrome for anti-premature birth in the second trimester. Methods Totally 44 singleton pregnant patients were diagnosed as short cervix syndrome, which was cervical length ≤2.5 cm without cervical dilatation,and received treatment from January 2008 and July 2015 in Peking University Third Hospital were collected. Among them, 30 patients who received therapeutic cervical cerclage were defined as cerclage group and another 14 cases who received conservative treatment were defined as un-cerclage group. The days of conservative treatment, delivery rate of different gestational weeks, birth weight of newborns, neonatal survival rate within 7 days of birth were analyzed between the two groups. Results There were no significant differences between the two groups in days of pregnancy conservative treatment [103(84-141)vs 105(85-114)days], delivery weeks [38.0(35.5-39.4)vs 38.5(37.3-39.5)weeks], birth weight of newborns [3120(2750-3400)vs 3130(2760-3545)g], and survival rate of newborns [100％(30/30)vs 13/14]. The fetuses of both groups were all delivered after 28 weeks. There was no significant difference in accumulated delivery rate between the two groups after 32 weeks, 34 weeks, and 37 weeks, respectively(all P>0.05). Conclusions The treatment of cervical cerclage is not superior to conservative means in single pregnancy of cervical length ≤2.5 cm without cervical dilatation. For such patients with short cervix syndrome, the treatment of cervical cerclage may not be necessary, but dynamic monitoring and search for the causing factors and prompt treatment are more important.

Objective To investigate the incidence and relevant information of preterm birth and the outcomes of preterm infants delivered at various gestational weeks and for different causes. Methods Totally 955 women, who ended their pregnancies before term, and 1066 neonates of the previous mothers were enrolled in this survey, among 15 197 deliveries at Peking University First Hospital, Beijing Gynecological and Obstetric Hospital, Women's and Children's Hospital of Haidian District and Peking University Third Hospital, respectively, from December 1~(st), 2006 to May 31~(st), 2007. Results (1)Incidence of preterm birth: The overall incidence of preterm birth of the 4 hospitals was 6. 3% (955/15 197), and it was 8.1% (125/1549) in Peking University First Hospital, 13.1% (150/1142), which was the highest (P<0.01), in Peking University Third Hospital, 5.5% (369/6656) in Beijing Gynecological and Obstetric Hospital and 34.0% (311/5850) in Women's and Children's Hospital of Haidian District.The preterm birth rate at the two comprehensive hospitals was significantly higher than that of the two specialized hospitals [10.2% (275/2691) vs 5.4% (680/12 506), P <0.01]. (2) Gestational weeks at delivery: The incidence of preterm birth before 34 weeks was 28.5% (272/954) and the number changed to 71.5% (682/954)for those preterm deliveries after 34 weeks. However, this number varied among the 4 hospitals. Peking University First Hospital had the highest incidence of preterm birth before 34 weeks(P< 0.05), and the lowest was found in Women's and Children's Hospital of Haidian District(P<0.01), but no difference was found between Peking University Third Hospital and Beijing Gynecological and Obstetric Hospital. (3) Etiology of preterm birth: Preterm premature rupture of membranes (PPROM) accounted for the most proportion of all preterm birth cases, followed by iatrogenic preterm birth and spontaneous preterm birth. But the causes of preterm birth in the 4 hospitals were different. Peking University Third Hospital had a higher incidence of iatrogenic preterm birth than the others (P<0.01), and Peking University First Hospital had a higher incidence of preterm birth caused by PPROM and lower incidence of spontaneous preterm birth. The first four reasons of iatrogenic preterm birth were preeclampsia (143, 42.0%), fetal distress (58, 17.1%), placenta previa (43, 12.6%) and placenta abruption (33,9.7%). (4) Neonatal outcomes in different hospitals: The neonatal outcomes were quite different among the 4 hospitals due to different causes and different delivery weeks. The highest neonatal mortality rate was found in Beijing Gynecological and Obstetric Hospital (5.4%, 22/408) compared to that in Women's and Children's Hospital of Haidian District (1.3%,4/320) and Peking University Third Hospital (0. 6%, 1/170) (P< 0.01), but without any difference when compared to that in Peking University First Hospital (2.4%, 3/ 124) (P>0.05). (5) Neonatal outcomes at different gostational age: The recovery rate of preterm infants delivered at <32 weeks was lower than those delivered ≥32 weeks (P<0.01), and this number rose to 99. 6% in those delivered ≥34 weeks. More infants delivered <32 weeks were given up for treatment or died during the perinatal period than those delivered ≥32 weeks, with the neonatal mortality rate of 22.1% for those delivered at <32 weeks and only 0.3% for those delivered at ≥ 34 weeks (P<0.01). (6) Neonatal outcomes for various causes: The premature neonatal mortality rate for iatrogenic preterm births was higher than that of PPROM (4.9% vs 1.6%, P<0.05). But the neonatal recovery rates were similar among the PPROM, spontaneous and iatrogenic preterm birth group (P>0.05). Conclusions Preterm birth is associated with high perinatal mortality rate, especially for those delivered before 32 weeks which would be highlighted in prevention. Reduction of the iatrogenic preterm birth, combined with proper prevention of PPROM, is an important issue in decreasing the prevalence of preterm birth.

Gut microbiota plays a very important role in human metabolism and immunity.If intestinal dysbiosis occurs,the intestinal mucosal barrier will be destroyed and the immunoregulation will also be interrupted,resulting in systemic inflammatory response,excessive oxidative stress and unbalanced immtme tolerance.All of these may play an important role in the pathogenesis ofpreeclampsia.Therefore,the correlation between gut microbiota and preeclampsia has attracted increasing attention and is expected to provide new sights for revealing the pathogenesis ofpreeclampsia.