血管内皮生长因子在妊高征胎盘中的表达研究

目的观察血管内皮生长因子(VEGF)在妊高征(PIH)胎盘中的表达情况.方法用免疫组织化学法,检测30例正常晚孕胎盘(对照组)和34例妊高征胎盘(妊高征组)中的VEGF表达水平,并作计算机图像分析,测定各组标本的阳性染色光度值.结果VEGF在正常晚孕胎盘和妊高征胎盘中均有表达,其分布基本一致,主要在滋养细胞、血管内皮及绒毛间质.计算机图像分析结果示,对照组VEGF阳性染色光度为0.23780±0.00434,妊高征组VEGF阳性染色光度为0.20688±0.01530,其中轻度0.22603±0.00828,中度0.20364±0.00365,重度0.19151±0.00441,妊高征组中VEGF表达明显低于对照组P＜0.01.且随妊高征病情的加重,VEGFF表达水平呈下降趋势.结论妊高征胎盘中VEGF表达水平降低可能与胎盘血管生成减少及胎盘滋养细胞侵入异常有关,在妊高征的发病中起重要作用.     

胎盘滞留96例临床分析

目的 积极预防和正确处理胎盘滞留,减少产后出血及产褥感染。方法 产后胎盘滞留时间较短的可以行人工剥离胎盘术。如用手剥离过程中发现宫壁与胎盘之间没有分界线或有草根样条索状连接时,可能有胎盘植入,需停止剥离,根据情况决策保守治疗或行子宫切除术。若产后胎盘滞留时间较长,有明显感染,再行清宫术。结果 96例产后胎盘滞留患,均痊愈出院。结论 落实好避孕措施,减少流产次数;提高引产,流产技术操作水平;正确处理第三产程等可有效预防胎盘滞留的发生。对于胎盘滞留,应根据不同情况给予相应的处理,可减少产后出血及产褥感染。     

剖宫产术中大出血的原因分析与治疗

目的探讨剖宫产术中大出血的原因及治疗.方法回顾性分析39例剖宫产术中出血≥1000ml作为研究组,出血＜1 000ml,且＞500ml者作为对照组1,出血≤500ml者600例作为对照组2.结果研究组中出血首位原因主要为前置胎盘和低置胎盘,占53.85%(21/39),显著高于对照组1中的10.67%(27/253),P＜0.01.在药物控制出血失败后,11例子宫动脉结扎中8例治疗成功、29例宫腔填塞纱条中28例治疗成功,得以保留子宫,2例行子宫切除术.结论前置胎盘和低置胎盘是剖宫产术中大出血的主要原因,宫腔填塞纱条治疗剖宫产术中大出血有良好效果.     

Placental leptin correlates with intrauterine fetal growth and development

目的　探讨胎盘肥胖基因及其蛋白表达水平与脐血瘦素和胎儿宫内生长发育的关系。方法　在 4 0例产妇分娩时采集胎盘与脐血 ,采用逆转录聚合酶链反应 (RT PCR)检测胎盘肥胖基因mRNA相对表达水平 ,采用Western Blot检测胎盘肥胖基因蛋白 (瘦素leptin)表达水平 ,采用免疫组化观察胎盘肥胖基因蛋白表达位点 ,采用放射免疫法 (RIA)检测脐血瘦素水平 ,采用Ponderal指数 [PI=10 0×体重 (g) /身长 (cm) 3]估测新生儿营养状态。结果　胎盘组织肥胖基因呈现高效表达 ,在胎盘滋养层细胞浆内肥胖基因蛋白阳性表达。胎盘肥胖基因及其蛋白表达水平与胎儿宫内生长发育状态显著相关 ,13例小于胎龄儿胎盘组织leptin mRNA及其蛋白表达水平显著低于 15例适于胎龄儿 (P =0 .0 0 3和 0 .0 0 8) ,12例大于胎龄儿胎盘组织leptin mRNA及其蛋白表达水平显著高于适于胎龄儿 (P =0 .0 4和 0 .0 2 )。胎盘肥胖基因mRNA及其蛋白表达水平与脐血瘦素水平显著相关 (r =0 .39和0 .4 3,P <0 .0 5) ,与新生儿Ponderal指数 (PI)显著相关 (r=0 .66和 0 .69,P <0 .0 1)。结论　胎盘是脐血瘦素重要来源 ,胎盘瘦素可能对胎儿宫内生长发育有促进作用。     

检测孕妇血浆中的urocortin

目的：研究ｕｒｏｃｏｒｔｉｎ（促肾上腺皮质激素释放激素肽类家族新成员）是否存在于孕妇血循环中及其含量,以证实ｕｒｏｃｏｒｔｉｎ是否能在妊娠中产生并由此调节子宫－胎盘的血管张力。方法：用放射免疫测定法从受孕１６周起检测孕妇血浆中是否含有ｕｒｏｃｏｒｔｉｎ,并用凝胶层析法检测从孕妇血浆中提取的ｕｒｏｃｏｒｔｉｎ是否与人工合成的ｕｒｏｃｏｒｔｉｎ标准品一致。结果：从受孕１６周起孕妇的血浆中即可测得ｕｒｏ     

Placenta growth factor: potential role in pregnancy

PROBLEM: In spite of the known requirement for adequate vascularity during placentation, little is known regarding the regulation of angiogenic growth factor production by trophoblast. Placenta growth factor (PIGF) is a recently discovered angiogenic growth factor whose expression is relatively limited to trophoblast. METHOD OF STUDY: Current literature of PIGF was reviewed, with emphasis on its expression, regulation, role in angiogenesis, and potential function(s) at the maternal-fetal interface. RESULTS: PIGF is abundantly expressed by trophoblast, which implies that it could act in a paracrine manner to modulate vascular development, stability, and/or function within the decidua and placental villi. In addition, expression of the PIGF receptor, fms-like tyrosine kinase (flt-1) receptor, on trophoblast raises the potential for an autocrine role of PIGF in regulating trophoblast growth and/or function. CONCLUSIONS: The potential for PIGF to influence both vascular endothelial cells and trophoblast suggests that aberrant trophoblast production of PIGF could compromise cellular function during gestation and contribute to the vascular and placental pathologies noted in many obstetric complications.     

Immunopathology of the implantation site utilizing monoclonal antibodies to natural killer cells in women with recurrent pregnancy losses

PROBLEM: Placental lesions of 71 women with documented recurrent spontaneous abortions of unknown etiology were evaluated using immunohistochemical staining. METHOD OF STUDY: Placental tissue blocks (less than 12 weeks gestation) from prior pregnancy losses were obtained, recut, and analyzed utilizing monoclonal antibody to identify the trophoblast (cytokeratin 8/18) and natural killer (NK) cells (CD57) at the implantation site. The following features were evaluated: trophoblast invasion pattern; syncytium formation; vasculitis and thromboembolism of decidual vessels; decidual inflammation; decidual necrosis; fibrin deposition at the decidual necrosis site; mononuclear-cell infiltration in villi and intervillous space; perivillous fibrin deposition; trophoblast morphology; and quantitation of CD57+ NK cells within the decidual tissue near the implantation site. Controls consisted of 20 healthy women with no history of recurrent pregnancy losses, who had their pregnancies electively terminated. RESULTS: Of the women studied, 29.6% demonstrated elevated CD57+ NK cells at the implantation site (P = 0.030), 54.1% had inadequate cytotrophoblast invasion depth (P = 0.000), 44.1% demonstrated inadequate syncytium formation (P = 0.004), and 33.9% presented thromboembolism in decidual vessels (P = 0.025). CONCLUSION: Some women with recurrent spontaneous abortions demonstrate abnormal placental lesions at the implantation site. Immunopathologic evaluation of the placental implantation site that terminated in a spontaneous abortion may reveal the immunopathogenesis of previous pregnancy losses.     

铁路危险品货运站空气污染物的致遗传毒性作用研究

采用ＳＯＳ／ｕｍｕ 试验和ＳＯＳ 原位试验,对铁路危险品货运站（ 以下简称危货站） 空气污染物的致遗传毒性进行了研究。结果表明：在不加Ｓ９ 活化系统的条件下,危货站空气污染颗粒提取物具有致遗传毒性作用,可使ＴＡ１５３５／ＰＳＫ１００２ 菌株产生β半乳糖苷酶的量增加,并存在剂量—反应关系;加入Ｓ９ 活化系统后,则ＳＯＳ／ｕｍｕ 试验阴性。同时,应用ＳＯＳ 原位法,对危货站空气污染的综合致遗传毒性进行了现场监测。结果显示,随采样体积的增加,β半乳糖苷酶的量也增加,采样体积与酶诱导率之间,存在剂量—反应关系。     

安替比林的体外人胎盘灌流

以安替比林为参照物,建立体外人胎盘灌流技术,采用局部胎盘小叶的开放及封闭灌流方法。开放灌充安替比林消除率与时间、母体循环中的浓度无显著相关性,只随流速比的增大而增大,二者之间有显著相关性（ｒ＝０９０６）。封闭灌流两个方向的灌流,供体面安替比林浓度逐渐降低,且都符合指数函数Ｃ（ｔ）＝Ｃｏ×ｅ－ｋｔ,受体面浓度逐渐升高。两个方面的清除率分别为０４１ｍｌ／ｍｉｎ,０５２ｍｌ／ｍｉｎ,两者间无显著差异,提取效率母体面到胎儿面方向略低（Ｐ＜００５）,分别是６８３％,２８９％。以上结果与相关资料一致,说明本室体外人胎盘灌流设备、技术均已完备,结果可靠。