胎盘部位过度反应及胎盘部位结节的临床病理分析

目的探讨胎盘部位过度反应及胎盘部位结节的临床病理学特征以及免疫组织化学染色在鉴别诊断中的意义。方法对15例胎盘部位过度反应及4例胎盘部位结节的临床及病理表现进行回顾性研究,并应用人绒毛膜促性腺激素(hCG)、人胎盘催乳素(hPL)、细胞角蛋白(CK)18、胎盘碱性磷酸酶(PLAP)、α-抑制素(inhibin),进行免疫组织化学染色。结果15例胎盘部位过度反应患者的年龄为25～40岁(平均31．5岁),4例胎盘部位结节患者年龄为26～39岁(平均34．3岁)。15例胎盘部位过度反应的组织学特征为：在子宫内膜、子宫肌层及螺旋动脉中有索条状及片状种植部位中间滋养细胞浸润,子宫内膜及肌层的结构没有破坏。4例胎盘部位结节在子宫内膜组织及变性坏死的绒毛间有多个以致密的嗜酸性玻璃样物质为背景的结节性病变,结节内为绒毛膜型中间滋养细胞。15例胎盘部位过度反应对hPL及CK18均呈阳性反应;4例胎盘部位结节均对CK18、α-抑制素及PLAP均呈阳性反应。所有15例胎盘部位过度反应Ki-67增生指数均≤5％。4例胎盘部位结节Ki-67增生指数均为0。结论胎盘部位过度反应及胎盘部位结节的临床及病理形态学特征不同于滋养细胞肿瘤。免疫组织化学染色对鉴别诊断有帮助。     

内皮型一氧化氮合酶运输介导物在子痫前期患者胎盘组织中的定位及定量研究

目的探讨内皮型一氧化氮合酶运输介导物(endothelial n itric oxide synthase traffic inducer,NOSTR IN)在子痫前期(pre-ec lampsia,PE)患者胎盘血管内皮细胞中表达的变化及其在子痫前期发病过程中的作用。方法HE染色后镜下观察胎盘组织及血管的病理变化,免疫组织化学方法及W estern b lot检测子痫前期患者胎盘组织中NOSTR IN的表达。结果HE染色显示子痫前期患者胎盘绒毛血管变细,数目减少,血管合体膜增厚,纤维素样坏死明显多于正常妊娠;免疫组织化学显示正常妊娠和子痫前期患者胎盘血管内皮细胞中都有NOSTR IN的表达,但子痫前期患者胎盘血管内皮细胞胞浆染色较正常妊娠明显增强;W estern b lot显示子痫前期患者胎盘组织中NOSTR IN的表达显著高于正常妊娠(P<0.01)。结论胎盘组织中NOSTR IN表达增加可能是子痫前期发病机制的重要环节之一。     

妊高征患者胎盘血循环中血管舒、缩物质水平的改变及意义

目的　通过测定胎盘部位子宫静脉血中一氧化氮 (nitricoxide,NO)及内皮素 (endothelin ,ET)的浓度 ,并与外周血中同类物质的对比 ,了解妊高征时胎盘血管的病变程度及其与外周血中血管活性物质浓度改变的关系。方法　分别于剖宫产手术前及手术中抽取胎盘部位子宫静脉血和外周静脉血 ,应用硝酸根还原酶与Griess反应相结合的方法测定NO ;应用放射免疫分析法测定ET。结果　妊高征组胎盘部位子宫静脉血中NO2 -/NO3 -为 (70 2 6± 12 6 0 ) μmol/l,外周血清NO-2 /NO-3 为 (6 5 5 2± 14 88) μmol/l,二者之间无显著差异。妊高征组外周血浆ET水平为 (5 3 72± 15 2 8)ng/L ,胎盘部位子宫静脉血浆ET水平为 (5 2 80± 14 19)ng/L ,两者之间无显著性差异 (P >0 .0 1)。与正常晚孕组比较 ,妊高征组血中ET、NO-2 /NO-3 水平均显著增高 (P <0 .0 1)。结论　妊高征患者的子宫、胎盘循环系统血管舒、缩物质平衡失调 ,血管内皮系统的功能亦遭到破坏 ;妊高征患者胎盘血循环ET、NO水平升高 ,但与外周血中ET、NO水平的升高无关。     

子痫前期胎盘、脐血管中神经激肽B表达及组织病理变化的研究

目的研究子痫前期患者胎盘、脐血管中神经激肽B（neurok in in B,NKB）的表达及组织的病理变化情况。方法采用SP法对轻、重度子痫前期组共40例和正常妊娠组20例的胎盘和脐血管组织进行NKB的免疫组化染色,观察各组NKB的定位、分布和表达量的差异。同时常规HE染色观察各组胎盘、脐血管的病理变化。结果NKB在各组胎盘合体滋养细胞、毛细血管内皮细胞、脐静脉内皮细胞中均有不同程度的表达。轻、重度子痫前期胎盘组织中,其NKB含量明显高于正常组（P〈0.05,P〈0.01）,HE染色可见子痫前期组细胞滋养细胞增生,合体细胞结节、纤维素样坏死显著增多等病理变化,与正常组相比有显著性差异。结论胎盘可能是NKB的重要产生释放部位。且NKB可能通过某些直接或间接的途径,参与了子痫前期损伤和代偿并存的复杂变化,在子痫前期的发生发展中起着重要作用。     

Toll样受体在母胎界面的表达与早产的关系

早产严重危及围生儿的生命及预后,宫内感染是导致早产的重要原因之一。Toll样受体（TLRs）是固有免疫系统中重要的病原模式识别受体,可调控适应性免疫应答,在母胎界面有广泛表达。TLRs参与母胎界面的炎症反应应答,保护胎儿免受外源性病原微生物感染,同时介导母儿间的免疫耐受。近来众多研究发现,感染导致的TLRs表达失调与早产的发生有一定的相关性。综述TLRs在胎盘、羊膜、蜕膜上的表达及其在早产中可能的作用机制。     

107例胎盘前置状态中期妊娠终止方法探讨

目的:探讨胎盘前置状态中期妊娠的最佳终止方法。方法:回顾性分析107例中期妊娠合并胎盘前置状态终止妊娠病例,按胎盘位置分为边缘型组(A组)、中央型组(B组),每组再按孕周大小分为<16周组、≥16周组,比较各组引产结局。结果:①采用依沙吖啶、天花粉及米非司酮配伍米索前列醇(药物)引产成功率A组分别为100%,80%,88.9%;B组分别为93.3%,100%,66.7%;孕周≥16周组分别为100%,94.1%,75%;孕周<16周组分别为90.9%,88.9%,92.4%。②采用天花粉引产时各组的出血量及总出血量均最少,引产与住院时间均最长(P<0.05)。③引产出血≥300 ml者共10例,分别为A组4例(药物组1例,依沙吖啶组3例);B组6例药物组1例,依沙吖啶组3例,天花粉组1例,小型剖宫产1例);引产失败6例,分别为A组4例(天花粉2例,药物组2例)及B组2例(依沙吖啶1例,药物组1例)。④依沙吖啶注射及药物引产2种引产方法的急诊手术(钳胎盘术及清宫术)率分别为27.1%和28.6%,天花粉组急诊手术率最低(3.8%)。结论:①终止边缘型胎盘前置状态中孕患者<16孕周可首选药物引产,≥16孕周可首选依沙丫啶引产;②部分及完全型胎盘前置状态中孕患者可首选天花粉引产;③钳刮术是引产失败及急诊处理出血的最佳方式之一,宫腔纱条填塞能有效止血;④宫颈条件差、孕周偏大(孕周>20周)的完全型胎盘前置状态患者可选用小型剖宫产术。     

Does oxygen concentration affect shedding of trophoblastic debris or production of inflammatory mediators from first trimester human placenta?

Preeclampsia is a major cause of pregnancy morbidity and mortality. It is hypothesised that necrotic syncytial knots and/or inflammatory factors released from the placenta into the maternal circulation are responsible for inducing the widespread endothelial cell activation that is seen in preeclampsia. Poor placental perfusion has been associated with preeclampsia, this had led to the hypothesis that placental hypoxia has an important role in the pathogenesis of preeclampsia. In this study, using a placental explant model, we investigated whether different oxygen environments induced abnormal shedding of trophoblastic debris or secretion of cytokines from the placenta. There was no significant difference in the numbers of trophoblasts shed from explants cultured in 1% or 8% oxygen containing environments. There was also no difference in the levels of activated caspases in trophoblasts shed from explants cultured in these two oxygen environments nor was there a significant difference in the endothelial cell responses to trophoblasts shed from explants cultured in 1% or 8% oxygen. Similarly, there was no significant change in the secretion of nine cytokines into the conditioned medium from explants cultured in 1% or 8% oxygen. This study supports the growing evidence that levels of oxygen in the placental environment during the first trimester of pregnancy may not in itself be the essential component contributing to the pathogenesis of preeclampsia.     

Autophagy in term normal human placentas

Autophagy is an inducible catabolic process that responds to environment and is essential for cell survival during stress, starvation and hypoxia. Its function in the human placenta it is not yet understood. We collected 14 placentas: 7 at vaginal delivery and 7 at elective caesarean section after uneventful term pregnancies. The presence of autophagy was assessed in different placental areas by immunoblotting, immunohistochemistry and electron microscopy. We found that autophagy is significantly higher in placentas obtained from cesarean section than in those from vaginal delivery. Moreover there is a significant inverse relationship between autophagy and umbilical arterial glucose concentration.     

Characterization and role of NUMB in the human extravillous trophopblast

NUMB is a multifunctional protein involved in asymmetric cell differentiation, proliferation and maintenance. Four mammalian NUMB isoforms have been identified, which utilize the phosphotyrosine binding (PTB) domain and the proline rich region (PRR) domain to regulate cell growth and differentiation in the developing nervous system. The observation that a decrease in spongiotrophoblast number and thickness of placentae of null (Numb^−/−) mouse embryos, which died at E10.5, suggests NUMB may play a role in placental development. In this study, we demonstrated for the first time, that NUMB isoforms 1, 2, 3, and 4 are present in the human placenta and the human extravillous trophoblast (EVT) cell line HTR8/SVneo. We report three novel isoforms, NUMB 7, 8, and 9, identified by cloning of RT-PCR products and sequencing. Corresponding sequences of novel isoforms were submitted to genebank (accession numbers for each new isoform: NUMB 7- EU265736, NUMB 8- EU265737 and NUMB 9-EU265738). Western blot analysis confirmed the presence of all NUMB isofoms in human placental samples in all trimesters and in EVT cells. NUMB immunosignals were extensively localized in human extravillous trophoblasts and decidual cells at the maternal-fetal interface. NUMB 8 appeared to be the predominant isoform in placental villi. Furthermore, cell migration studies revealed NUMB isoform 1 to be involved in EVT cell migration and NUMB isoforms 2 and 4 to induce EVT apoptosis.