胎盘内微生物组的研究进展

在很长一段时间内,人们都认为胎儿与母体进行物质交换的器官——胎盘是无菌的。但最新研究颠覆了人们的传统观念,研究者发现胎盘内确实存在一些微生物菌群,这引发了研究者对胎盘内微生物组的作用和来源的探索。本文主要针对胎盘内微生物组的发现、微生物组内菌群种类、来源、及其对婴幼儿生长发育和胎儿分娩的影响进行综述。     

胎盘微生物菌群的发现与研究进展

长期以来,孕妇胎盘被公认为是无菌环境,但最新一项研究结果却颠覆了这一传统认知。科学家们证实胎盘中可能存在一个小型但多元化的微生物群落。经分析发现胎盘的微生物群落组成与口腔的微生物群落最为相似。通过比较正常分娩的胎儿及早产胎儿的胎盘菌群组成,发现胎盘菌群可能与胎儿早产有一定的关系。本研究就现今国内外对胎盘中微生物菌群的新发现及其与早产的相关研究进展进行综述。     

过期妊娠并发羊水过少70例分析

目的 探讨过期妊娠合并羊水对围产儿的影响。方法 将２３３例过期妊娠的孕妇分为羊水过少组７０例及不适量组１５３例,动态观察两 组４０￣４３孕周１２ｈ尿Ｅ／Ｃ值、Ｂ超检测羊水量,产后胎盘检查,胎儿宫内窘迫,新生儿窒息剖宫产及围产儿死亡发生率,两组进行分析比较。结果 不过少组４０￣４１孕周即开始出现不量减少及胎盘功能下降,产时胎儿窘迫,羊水杂,Ａｐｇａｒ评分以及剖宫产率均地羊水适量组（Ｐ〈０．０５,Ｐ〈     

彩色多普勒超声对晚孕期羊水过少胎儿肾动脉血流的研究

目的:应用彩色多普勒血流显像(CDFI)观察晚孕期羊水过少胎儿肾动脉(RA)血流阻力参数的变化,为临床预测羊水过少时胎儿宫内缺氧及评价胎盘功能提供相关信息。方法:应用CDFI检测100例晚孕期孕妇(孕36～40周)RA的搏动指数(PI)、阻力指数(RI)及收缩期峰值流速与舒张末期流速比值(S/D)。其中羊水过少A组(5cm<羊水指数AFI≤8cm)40例,羊水过少B组(AFI≤5 cm)20例,正常对照C组(8cm相似文献   

早产或与胎盘中微生物有关

<正>美国一个研究小组说,孕妇胎盘并不像人们此前认为的那样是一个无菌环境,而是生存着一个小型但多元的微生物群落。这些微生物直接影响胎儿的健康,甚至可能与胎儿是否早产有关。微生物群落是细菌、病毒与真菌等的总称。休斯敦贝勒医学院副教授谢斯蒂·奥高及同事在美国《科学—转化医学》杂志上报告说,新研究表明,孕妇胎盘中的微生物可能来自口腔,说明孕妇口腔健康对胎儿健康至关重要。此外,早产胎儿与足月产胎儿的胎盘微生物群落组成存在明显不同,说明胎盘微生物群落与早产     

胎膜早破后羊水残余量与宫内感染和新生儿发病率的相关性分析

目的：探讨胎膜早破后残余羊水量与宫内感染和新生儿发病率的相关性。方法：根据产妇胎膜早破后残余羊水指数（Amnitic Fluid Index,AFI）的监测结果,将本组120例产妇分为三组：羊水量正常组82例;羊水量较少组20例;羊水量过少组18例。所有产妇入院后行胎膜早破常规处理,回顾分析并统计三组产妇宫内感染率,胎儿窘迫率和新生儿发病率。结果：在宫内感染发生率上,三组比较,差异具有显著性,羊水量较少组、羊水量过少组宫内感染的发生率明显高于羊水量正常组（P〈0．01）。在胎儿窘迫发生率上,三组比较,差异无统计学意义（P〉0．05）。在新生儿发病率上,三组比较,差异具有显著性,羊水量较少组、羊水量过少组新生儿的发病率明显高于正常纽（P〈0．01）。Logistic回归分析发现羊水量、产妇基础性疾病和分娩孕周为孕产妇宫内感染和新生儿发病的关键影响因素。结论：胎膜早破后残余羊水量过少与宫内感染和新生儿发病=翠的升高密切相关,产妇于胎膜早破后应加强残余羊水量的监测,以采取有效措施降低宫内感染和新生儿发病的发生率。     

静脉补液加饮水疗法治疗妊娠晚期羊水过少的临床疗效评价

目的观察静脉补液联合饮水疗法治疗妊娠晚期羊水过少的临床疗效。方法选择我院2015年4月~2016年4月收治的妊娠晚期羊水过少孕妇138例为观察组,给予静脉补液加饮水治疗,同期选择120例孕妇作为对照组仅行常规胎儿监护。监测两组羊水指数(AFI)变化情况,观察比较两组剖宫产率、胎儿宫内窘迫、羊水粪染率、新生儿窒息率等指标。结果两组干预前AFI比较无统计学意义(P0.05);干预后,观察组AFI值升高明显优于对照组,差异有统计学意义(P0.05)。观察组的剖宫产率、胎儿宫内窘迫、羊水粪染率、新生儿窒息等不良妊娠结局发生率明显低于对照组,差异均具有统计学意义(P0.05)。结论静脉补液加饮水疗法是治疗妊娠晚期羊水过少的可行、有效措施之一,能有效增加羊水量,降低剖宫产率,对改善母婴结局具有积极意义。     

胎儿肠道微生物的来源及其对胎儿发育的影响

肠道微生物组在调节人体新陈代谢、免疫功能和行为方面至关重要，并且在胎儿时期就已开始建立。母体各部位的微生物及其代谢物通过血液及阴道上行传播至胎儿组织，并影响胎儿的神经系统发育以及免疫系统的建立和启动。胎儿时期微生物的存在、发展及变化等过程对胎儿发育以及胎儿分娩后的健康状态具有深刻意义。本文着重介绍了胎儿时期肠道微生物的初始定植期、来源途径及其对胎儿发育产生的影响，以此更好地理解胎儿时期微生物与胎儿之间的相互作用及其与长期健康的关联，为改善婴儿短期和长期健康的相关研究提供参考。     

双胎输血综合征治疗进展

双胎输血综合征治疗方法有羊水减量术、胎儿镜下激光凝结胎盘血管交通支术、羊膜中隔打孔术和选择性减胎术。本文就TTTS的治疗做一综述。     

肠道菌群在肿瘤发生发展及免疫治疗中作用的研究进展北大核心CSCD

肠道菌群是一个与人体共生的复杂微生物区系,近年来被越来越多的研究者所关注。研究发现,肠道菌群不仅在维持人体正常生理功能中起到重要作用,在肿瘤发生、发展、诊断及治疗中也有不可忽视的作用。本文在对肠道菌群与肿瘤关系进行概述的基础上,重点介绍了肠道菌群促进肿瘤发生、发展的主要机制,以及肠道菌群对抗肿瘤免疫治疗尤其是免疫检查点抑制疗法的影响。此外,文中还总结了目前可行的调节肠道菌群以提高肿瘤治疗疗效的方法,并提出了其中可能存在的困难和挑战。     

Fetal-maternal transfer of [H3]-6 beta-hydroxycortisol in the pregnant ewe

Distribution and fetomaternal transfer of 6 beta-hydroxycortisol (6 beta-OHF) was studied using serial sampling following injection of tritium labelled 6 beta-OHF into various fluid compartments in the chronically cannulated unaesthesized pregnant ewe. There was a rapid transfer of 6 beta-OHF from the fetal circulation into amniotic fluid and maternal blood. In contrast, the maternal----fetal transfer of this steroid metabolite was considerably less. The sequence of appearance of 6 beta-OHF in fetal blood and amniotic fluid following injection into maternal blood suggests that this steroid is first transferred across the placenta to fetal blood before gaining entry into the amniotic fluid space. The half-lives of 6 beta-OHF after initial equilibration in maternal plasma, fetal plasma and amniotic fluid were 2.0 h, 5.1 h and 8.9 h respectively. The amniotic sac appears to contain a relatively static pool of 6 beta-OHF and may act as a "trap" for 6 beta-OHF in the ovine conceptus.     

Maternal cell contamination in amniotic fluid samples as a consequence of the sampling technique

Maternal cell contamination in amniotic fluid samples is easily detected by in situ hybridization if the karyotype of the fetus differs from the karyotype of the mother. One out of two amniotic fluid samples appears to contain more than 20% maternal cells. Bloody samples often contain even more than 50% maternal cells. Maternal cells can also be identified on the basis of their nuclear morphology. Maternal cell contamination is regularly observed in pregnancies with an anterior placenta, whereas it is rare in posterior placenta pregnancies. The maternal cells are therefore thought to be artificially introduced into the amniotic fluid sample, as a result of placental bleeding during amniocentesis. The implications of maternal cell contamination for prenatal diagnosis using uncultured amniotic fluid samples are discussed.     

Cholinesterases and arylesterase in the umbilical cord, the placenta, and the amniotic membrane, in the female at term]

Cholinesterasic activity of umbilical cord (tissue), completely bloodless, is exclusively due to pseudocholinesterase. Cholinesterase is more active in placenta than in cord; it is an acetylcholinesterase at 80 per cent. Both forms coexist, about equally, in amniotic membrane. A considerable arylesterasic activity is proved in cord, placenta and membrane, the greatest activity being in placenta. Comparing the greater activity in maternal plasma and cord blood's plasma to the very weak activity in amniotic fluid, it is possible to think that cork, membrane, placenta and also amniotic fluid pseudocholinesterase and arylesterase, come from plasma. On the contrary, placental acetylcholinesterase seems original and probably is the source of this enzyme activity in amniotic fluid.     

Chemical Analysis and Transplacental Transfer of Oseltamivir and Oseltamivir Carboxylic Acid in Pregnant Rats

In view of the limited information on the pharmacokinetics of oseltamivir (OSE) during pregnancy, this study aims to evaluate the placental transportation of OSE and its active metabolite oseltamivir carboxylic acid (OCA) in rats. A validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) system coupled to an in vivo transplacental model has been developed to determine OSE and OCA in the placenta, amniotic fluids and fetus of 13-day pregnant Sprague-Dawley rats. Concentrations of OSE and OCA in plasma, amniotic fluids, placenta, and fetus were measured by the validated LC-MS/MS after OSE administration (10 mg/kg, iv). The pharmacokinetic data of both analytes were examined by non-compartmental modeling. The area under the concentration-time curve (AUC) of OCA in maternal plasma was found to be 3.6 times larger than that of OSE. The AUCs of OCA in both amniotic fluid and fetus were significantly decreased, in comparison with that in maternal plasma (reduced by 76.7 and 98.1%, respectively). We found that both OSE and OCA can penetrate the placenta, amniotic fluids and fetus in rats during pregnancy; however, the penetration of OCA was much lower than that of OSE. The mother-to-fetus transfer ratio was defined as AUC_fetus/AUC_mother. The data demonstrated that the mother-to-fetus transfer ratio of OSE and OCA were 1.64 and 0.019, respectively, suggesting that OSE, but not OCA, penetrated through the placenta. Moreover, OCA might not be easily metabolized in the fetus due to the lack of carboxylase in the fetus.     

Pemphigoid gestationis autoantigen, transmembrane collagen XVII, promotes the migration of cytotrophoblastic cells of placenta and is a structural component of fetal membranes.

In pemphigoid gestationis (PG), autoantibodies target collagen XVII, a hemidesmosomal transmembrane protein, which is an important element in cutaneous epithelial adhesion and signalling. We report that collagen XVII is expressed in the first trimester and term syncytial and cytotrophoblastic cells of normal placenta and in epithelial cells of amniotic membrane. Immunoelectron microscopy confirmed the localization of collagen XVII to the hemidesmosomes of amniotic epithelium. Examination of three PG placentas showed mild villitis, but there were no differences between collagen XVII expression levels or immunostaining signals as compared to normal placenta. Collagen XVII expression was also detected in cultured extravillous trophoblast HTR-8/SVneo cells, where collagen XVII expression was upregulated by PMA and TGF-beta1. Interestingly, the presence of Col15, the cell migration domain of collagen XVII, induced the migration of HTR-8/SVneo cells in transmigration assay. Analysis of amniotic fluid samples at different gestational weeks revealed that a large quantity of collagen XVII ectodomain was shed into amniotic fluid throughout pregnancy. Biochemical and immunoblotting analysis indicated that the ectodomain in amniotic fluid is structurally very similar to the ectodomain produced by cultured keratinocytes. Cultured cells from amniotic fluid samples also expressed collagen XVII. Our results suggest that collagen XVII may contribute to the invasion of extravillous trophoblasts during placental development and is also required for the integrity of amniotic basement membrane. Although the exact pathomechanism of PG is still largely unknown, the clinical symptoms of PG are initiated after the expression of collagen XVII in placenta during the first trimester of pregnancy.     

Involvement of matrix metalloproteinases 2 and 9, tissue inhibitor of metalloproteinases and apoptosis in tissue remodelling in the sheep placenta

Placental growth and development is crucial for successful pregnancy. The aim of this study was to characterize the activity and localization of the matrix metalloproteinase 2 (MMP-2) and MMP-9, which are capable of degrading basement membrane collagen (predominantly collagen type IV), and their endogenous tissue inhibitor of matrix metalloproteinases (TIMPs), in amniotic fluid and in the developing ovine placenta. Cell deletion by apoptosis during placental development was also examined. Zymography with gelatin as substrate indicated that MMP-2 (72 kDa gelatinase A; predominantly latent form) was present in increasing amounts in amniotic fluid from day 70 of gestation to labour (days 140-145), and MMP-9 (92 kDa gelatinase B; predominantly latent form) was detectable from day 125 to labour; there was no increase in MMP-2 or -9 in labour. A broad range of TIMPs was detected in amniotic fluid; the molecular masses corresponded to TIMP-1, -2 and -3. Immunohistochemical techniques localized MMP-2, MMP-9 and TIMP-3 in the sheep placenta, predominantly in the trophoblast layer in uninucleate, but not binucleate, cells. However, MMP-2 and -9 activated proteins in placental homogenates were low throughout pregnancy. Apoptosis was identified by morphological criteria and also by TdT-mediated dUTP nick end labelling. Apoptosis was present in discrete regions in the placenta, predominantly in trophoblast cells near the tips and the basal regions of the fetomaternal interdigitations. During pregnancy the sheep placenta becomes more complex and the area of the fetomaternal interface increases. MMP-2 and -9 are likely to be involved in breaking down basement membranes to allow cell migration during this process. It is suggested that digestion of supporting extracellular matrix may trigger apoptosis and in some way increase the branching pattern in the villi.     

Do Maternal Microbes Shape Newborn Oral Microbes?

Strong evidence suggests that the early composition of the oral microbiota of neonates plays an important role for the postnatal development of the oral health or immune system. However, the relationship between the maternal microbiome and the initial neonatal microbiome remains unclear. In this study, 25 pregnant women and their neonates were recruited, and the samples were collected from the maternal oral cavity, amniotic fluid, placenta and neonatal oral cavity. High-throughput sequencing of 16S rRNA was performed using the Illumina MiSeq platform to analyze the correlation with microbial community structure between the maternal and the neonatal oral cavity. The results indicated that the number of shared OTUs was up to 635 in four groups. The PCoA showed that there were certain similarities in the microbial community structure of the four groups. The dominant bacterial genera of the shared OTUs were consistent with human oral microbes, including Streptococcus, Fusobacterium and Prevotella. The results showed that there might be a correlation between the maternal and neonatal oral microbiome, through the amniotic fluid and placenta.Electronic supplementary materialThe online version of this article (10.1007/s12088-020-00901-7) contains supplementary material, which is available to authorized users.     

Temperature responses following ventilation of the fetal sheep in utero

The mammalian fetus produces significant quantities of heat. This passes to the mother principally through the placenta and to a lesser extent via a pathway comprising the skin, amniotic fluid, and uterine wall. To assess the importance of the lesser pathway, temperature responses were recorded in 7 near-term fetal sheep after intrauterine ventilation with oxygen, after snaring the umbilical cord to block the placental route, and following fetal death. Four distinguishing characteristics of responses were observed: fetal temperature rose 0.10 +/- 0.03 (SEM) degrees C after oxygenation; it rose progressively an additional 0.9 +/- 0.1 degrees C during the 90-min interval after cord snaring; amniotic fluid temperature rose slowly until it was about midway between fetal and maternal temperature; and after fetal death, fetal amniotic fluid temperatures fell slowly. In a simple mathematical model with constant parameters these results could not be explained fully. It was necessary to assume that heat production rose with increased oxygenation and elevated body temperature and that ventilation increased heat transfer through the amniotic fluid, as would occur if chest wall movement were stirring the fluid. Using the model, the value for heat conductance from fetal skin to amniotic fluid was estimated to be 10.5 watts degrees C-1 under basal conditions.     

Expression of the corticotropin-releasing hormone (CRH) gene in human placenta and amniotic membrane

Immunoreactive corticotropin-releasing hormone (IR-CRH) in maternal plasma increases progressively during pregnancy and decreases rapidly after delivery, suggesting that IR-CRH is produced in the placenta. We studied the expression of the CRH gene in developing human chorionic tissue, the amniotic membrane, the uterine myometrium and a fresh surgical specimen of hydatidiform mole by Northern blot analysis. Our results were as follows: (1) CRH mRNA was demonstrated in the placenta in the third trimester and at term, but under detectable level in the first and second trimesters. (2) CRH mRNA expression was observed in the amniotic membrane, but its expression in the myometrium in normal pregnancy was under detectable level at term. (3) CRH mRNA was also under detectable level in trophoblasts of a hydatidiform mole. These results suggest that the sources of the increased level of IR-CRH in human plasma and amniotic fluid during pregnancy are the placenta and amniotic membrane, and that gene expression of placental CRH increases during pregnancy.     

Lactate dehydrogenase and its isoenzymes in human umbilical cord tissue]

Study on umbilical cord tissue, completely bloodless, for determination of lactate deshydrogenase activity and its distribution among the five iso-enzymes. Comparison with placenta, amniotic fluid, serums of blood of cord and of mother. Cord tissue is very active (about 360 muKatals, in average) and it is a similar result in placenta (as it is possibly bloodless). Blood serum of cord is more active than amniotic fluid, which is more active than maternal serum, but they are 80 to 200 times less active than cord tissue. After electrophoresis, a very large predominance of the slow iso-enzymes L.D.H. 4--5 is found in cord tissue (72%), amniotic fluid (67%) and placenta (56%), whereas the fast iso-enzymes L.D.H. 1--2 are predominant in the serums of cord blood and of mother. These data indicate an intense metabolic activity in the cord tissue, which has also an high level of lactate, and this seems related to the foetal metabolism for anaerobic glycolysis in oxygen weakly provided tissues.