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简介：Traumatictricuspidvalveinsufficiency(TTVI)isarelativelyuncommondisease.

简介：AbstractServing as the interface between the fetal and maternal environments during gestation, the placenta plays critical roles in the protection of the developing fetus and the maintenance of maternal health. The placenta is primarily derived from the embryonic trophectoderm which differentiates into various subtypes of trophoblast cells through villous and extravillous pathways. The interactions among trophoblasts and multiple decidual cells and immune cells at the maternal-fetal interface fundamentally form the functional units of the placenta, which are responsible for blood perfusion and maternal-fetal material exchange, immune tolerance, and the regulation of pregnancy adaptation. Defects in placental development and functional maintenance are in tight association with adverse pregnancy outcomes such as preeclampsia. In this article, we review recent advances on human trophoblast cell differentiation and the construction of placental functional units and discuss the placental and maternal factors that may contribute to the occurrence of preeclampsia.

简介：客观：调查创伤的有三个尖头的不足的外科的治疗的最佳的时间和过程。方法：从1984年5月到2004年9月，八个病人为创伤的有三个尖头的阀门不足经历了操作。所有病人，男性，从7～67年变老[中部：38年，意味着：（38。5±18。1)年]。在损伤和操作之间的间隔从1个月到20年[中部：19个月，意味着：(52.5±80.3)月)]。Inseven病人，有三个尖头的不足被归因在三个病人包括车辆事故弄钝胸损伤，另外的病人是一处stab创伤。诊断是证实的byechocardiography。在病人的外科手术前的心脏的功能作为纽约HeartAssociation(NYHA)班Ⅱ-Ⅳ被分类。在手术期间，有三个尖头的阀门的前面的传单完全或部分在所有病人由于索的破裂被乱摆。氏族的传单的索的破裂在一个病人被发现。前面的传单在二个病人被穿孔。Septalleaflet被缩回并且支持者到在二个病人的室的中隔。阀门修理为所有病人被打算。最后，阀门修理在3个病人成功地被执行，有三个尖头的代替在5个病人被执行。结果：没有早或迟了的死亡发生了。与follow-upthrough为7-129月的临床的表明和回响心动描记法[中部：39个月，平均数:(53.4±42.8)月]，所有病人作为NYHA班Ⅰ被分类，没有任何changes.Conclusions：创伤的有三个尖头的不足的令人满意的治疗能被外科的治疗获得。更早的外科可以增加有三个尖头的阀门修理的可行性并且阻止恰好室的功能的恶化。

简介：AbstractObjective:To investigate the effects of vitrification on the expression of the imprinted gene Snrpn in neonatal placental tissue.Methods:Neonatal placental tissue was collected from women with natural pregnancy (control group) and from women in assisted reproductive technology (ART) pregnancy group, following fresh and vitrified embryo transfer (fresh group and vitrified group, respectively). Snrpn mRNA expression and SNRPN protein levels in placental tissue from these three groups were assessed by real-time reverse transcription polymerase chain reaction and Western blot, respectively. DNA methylation in the Snrpn promoter region was analyzed by bisulfite-pyrosequencing.Results:The expression of Snrpn mRNA and SNRPN protein was found to be higher in placental tissue from the fresh and vitrified ART groups, compared to the control group. There was no significant difference in SNRPN gene or protein expression between the fresh and vitrified groups. DNA methylation at the Snrpn promoter region was not significantly different between these three groups.Conclusions:Human ART may alter the transcriptional expression and protein levels of the imprinted gene Snrpn. However, compared to other ART methods, vitrification may not aggravate or reduce this effect. Moreover, the altered expression of Snrpn is likely not directly related to DNA methylation of the Snrpn promoter region.

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简介：BackgroundTherequisitetechniquesforsafefetalcardiacarrestduringcardiacinterventionsneedtobefurtherdeveloped.Furthermore,littleisknownaboutthepathophysiologiceffectofcardiopulmonarybypass(CPB)atdifferentlevelsoftemperaturewithcardioplegicarrestonthedevelopingfetus.MethodsTwelvepregnantgoatswererandomlydividedintohypothermicCPBgroup(Hgroup):cardiopulmonarybypasswithperfusionat30-32℃(n=6)andnormothermicCPBgroup(Ngroup):cardiopulmonarybypasswithperfusionat36℃-38℃(n=6).Fetalcardiopulmonarybypasswasmaintainedincluding30minutesofcardiacarrest.Fetalmeanarterialbloodpressure(MAP)andheartrate(HR)weremonitored.Fetalarterialbloodsampleswereanalyzed.Thepulseindex(PI)andresistanceindex(RI)ofthefetalumbilicalarterywererecorded.ResultsThematernalweight,fetalweightandpumpflowhadnosignificantdifferencebetweenthe2groups.Afterclampremoval,twofetalheartsdidnotauto-beatinHgroup.ThefetalHRandMAPbweresignificantlydifferent(P<0.05)etweenthe2groups.Therewasremarkabledecreasinginpost-CPBfetalHRandMAPinHgroup.AstabledecreaseinpartialpressureofoxygenwithaconcomitantstableincreaseofcarbondioxidepartialpressureinHgroupwasnoted.ThelacticacidinHgroupwassignificantlyhigherthanthatintheNgroup(P<0.05).ThePIandRIinHgroupweresignificantlyelevated1hourafteroffCPBandfurthermarkedlyincreased2hoursafteroffbypass.ConclusionsFetalCPBcouldbeperformedunderbothhypothermicandnormothermicconditions.However,normothermicbypassmayprovidebetterdeliveryofoxygentofetaltissue.

简介：AbstractUterus didelphys occurs in ~0.4% of females and is found in ~11%-20% of all uterus defects. It is a risk factor for cervical insufficiency, consequently contributing to late miscarriage or preterm birth. Thus far, only two prior cases of uterus didelphys accompanied by cervical insufficiency treated through laparoscopic cervical cerclage have been reported; however, livebirth only occurred in one hemiuterus. Herein, we report a case of uterus didelphys in a patient diagnosed with cervical insufficiency. Following the placement of a modified laparoscopic cervical cerclage, the patient had two successful livebirths through both hemiuteruses, respectively, with longer gestation age (ie, >36 weeks). The aim of this case report was to provide useful information for clinical practitioners to make better decisions on the management of cervical insufficiency in patients with uterus didelphys, and identify obstetric complications that clinicians should pay attention to during pregnancy.

简介：AbstractObjective:Structural abnormalities and dysfunction of the placenta contribute to pregnancy-related complications, such as preeclampsia. Syncytin-A (synA) has been reported to be expressed in the placenta. The contribution of synA to developmental abnormalities and dysfunction of the placenta remains elusive. In this study, we aimed to explore the role of synA in placental development and functions.Methods:SynA-knockout mice were generated using the CRISPR-Cas9 method, and the phenotypes of the placenta and fetus of synA-knockout mice were observed. Real-time quantitative polymerase chain reaction (PCR) and routine PCR were employed to detect the genotypes of the offspring. CD31 immunohistochemistry was used to evaluate the vessel density of the placenta, and the protein levels of key molecules were measured by western blotting.Results:SynA knockout caused fetal death. Furthermore, synA-knockout mice showed placental developmental abnormalities, indicated by a thinner labyrinth layer, thicker spongiotrophoblast layer, lower blood vessel density, and significantly higher numbers of apoptotic trophoblasts, when compared with wild-type littermates. Mechanistically, synA ablation induced apoptosis-inducing factor (AIF) cleavage and nuclear localization and promoted placental trophoblast apoptosis. In addition, synA knockout increased the calpain1 protein levels. The calpain1 inhibitor calpeptin blocked synA knockout-induced AIF cleavage, partially restoring the placental structural abnormalities of synA-knockout mice.Conclusions:SynA knockout leads to placental developmental abnormalities by inducing trophoblastic apoptosis via the calpain1-AIF pathway.

简介：AbstractObjective:This study was aimed to determine the changes in CXCR2 expression in preeclampsia placenta and its correlation with clinical parameters.Methods:Sixty-four gravidas ranging in age from 25 to 42 years referred to the obstetrics unit of the West China Second University Hospital from April 2012 to October 2012 were recruited in this case-control study; women were diagnosed and divided into early-onset preeclampsia group (n= 22), late-onset preeclampsia group (n= 22), and healthy pregnancy group (n= 20). After immunolocalized in human placenta, the levels of CXCR2 protein and messenger ribonucleic acid (mRNA) were detected by enzyme-linked immunosorbent assay and real-time quantitative polymerase chain reaction. Correlations between placental CXCR2 protein expression with systolic blood pressure and lactate dehydrogenase (LDH) in early-onset preeclampsia were examined using Pearson or Spearman’s correlation coefficients.Results:Placental CXCR2 protein and mRNA expression in early-onset preeclampsia was significantly lower than it was in placentas from healthy pregnancy pregnancies and late-onset preeclampsia (P < 0.05). The placental CXCR2 protein expression correlated negatively with systolic blood pressure and LDH in early-onset preeclampsia (r= -0.51, P < 0.05; r=-0.43, P < 0.05).Conclusion:Significant abnormal placental CXCR2 expression in early-onset preeclampsia, and its correlations with some clinical parameters (systolic blood pressure and LDH) were discovered, suggesting that CXCR2 may play a role in the pathogenesis of early-onset preeclampsia.

简介：AbstractObjective:This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods:Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group (n= 6), EE-sham group (n = 6), control-IR group (n= 6) and control-sham group (n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test.Results:Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats.Conclusion:Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.