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1.
目的探讨超常胎盘部位(EPS)反应的临床病理特点及其鉴别诊断要点。方法对5例经病理诊断为EPS的患者,采用免疫组化标记法及光镜,进行临床病理研究与分析。结果EPS组织学特征为以中间型为主的滋养细胞(IT)向蜕膜及平滑肌浸润,不破坏原有组织结构,同时保持部分胎盘的结构特点。免疫组化表现为胎盘泌乳素(HPL)、上皮膜抗原(EMA)呈阳性或强阳性,人绒毛膜促性腺素(ECG)阴性或弱阳性,波形蛋白(Vim)阴性。结论EPS反应为绒毛外中间型滋养细胞的良性非肿瘤性病变,是妊娠状态下中间型滋养细胞在胎盘部位的过度反应。鉴别诊断应结合光镜、免疫组织化学及临床表现综合判断。  相似文献   

2.
了解各孕期胎盘组织中胰岛素样生长因子-Ⅰ(IGF-Ⅰ)的细胞定位,评估IGF-Ⅰ在胎儿、胎盘生长发育中的作用,采用免疫组化法对早、中、晚期妊娠胎盘组织中IGF-Ⅰ阳性细胞定位.结果显示:三个时期胎盘组织中IGF-Ⅰ主要位于绒毛小叶的合作细胞滋养层及细胞滋养层胞浆中。此外,中、晚期妊娠的Hoffbauer细胞及胎膜平滑绒毛层亦存在,但染色较以上两种细胞明显减弱,胎膜的羊膜细胞及蜕膜细胞偶尔可见阳性,胎盘蜕膜细胞则未见阳性着色.说明胎盘组织中IGF-Ⅰ主要由胎盘小叶的合体滋养层细胞、细胞滋养层细胞、Hoffbauer细胞及胎腹中的平滑绒毛膜细胞合成和分泌后作用于胎儿、胎盘组织,从而促进胎儿生长发育。  相似文献   

3.
胎盘部位结节是少见的良性滋养细胞疾病,目前对该病的认识尚少。其中病理诊断为金标准,但是现在对病理表现为非典型性的胎盘部位结节的认识也不足。现报道 1 例子宫非典型胎盘部位结节,旨在提高对此疾病的认识。  相似文献   

4.
妊娠滋养细胞疾病(gestational trophoblastic disease, GTD)包括一组不同的疾病, 其共同特征为滋养层异常, 是一组以滋养细胞异常增生为特征的异质性疾病 [1 ]。包括葡萄胎、侵袭性葡萄胎、绒毛膜癌和胎盘部位滋养细胞肿瘤。这些病变在形态学及临床生物学行为上有着明显的不同。细胞遗传学和免疫组织化学染色的研究提出GTD的不同类型与正常受精卵的发育和胎盘形成的特殊病理差异有关。患者血清及尿液中人类绒毛膜促性腺激素(human chorionic gonadotropin,HCG)的含量皆比正常妊娠高,检测患者HCG水平,可作为这组疾病的临床辅助诊断及治…  相似文献   

5.
万贵平  俞淑 《江苏医药》1998,24(11):799-800
了解各孕期胎盘组织中胰岛素生长因子-I(IGF-I)的细胞定位,评估IGF-1在胎儿,胎盘生长发育中的作用,采用免疫组化法对早,中,晚期妊娠胎盘组织中的IGF-I阳性细胞定位,结果显示:三个时期胎盘组织中IGF-I主要位于绒毛小叶的合体细胞滋养层及细胞滋养层胞浆中,此外,中,晚期妊娠的Hoffbauer细胞及胎膜平滑绒毛亦存在,但当染色较以上两种细胞明显减弱,胎膜的羊膜细胞及蜕膜细胞偶尔可见阳性,  相似文献   

6.
孔燕 《中国实用医药》2012,7(11):182-183
胎盘部位滋养细胞瘤(Placental Site Trcphobastlc Tumor,PSTT)是一种妊娠性滋养层细胞肿瘤,1895年 Marshand首次报道此病[1].PSTT曾称为异型绒毛膜瘤、合体细胞瘤,绒毛上皮增殖、滋养细胞假瘤等多种名称[2].我院近来遇1例孕32周的子宫破裂-胎盘原位滋养细胞瘤(PSTT),行次全子宫切除术.术后病理诊断为胎盘部位滋养细胞瘤.现报告如下.  相似文献   

7.
祝林玉 《现代医药卫生》2006,22(20):3117-3118
目的:观察妊娠高血压综合征(妊高征)患者子宫胎盘床及胎盘血管的免疫病理变化,探讨妊高征的发病机制.方法:对重度妊高征孕妇(妊高征组)24例及正常妊娠产妇25例(对照组)进行子宫胎盘床螺旋动脉和胎盘绒毛血管病变进行观察,应用免疫组化技术进行IgA、IgG、IgM和C3的检测.结果:妊高征组与对照组在妊娠生理性改变、管壁纤维素样坏死以及急性动脉粥样硬化病变等差异均有显著性(P<0.01),子宫胎盘血管免疫组化标记,妊高征组阳性表达率平均为77.05%,对照组均阴性表达.结论:妊高征的发生可能与免疫因素关系密切.  相似文献   

8.
孙丽洲  彭韬 《江苏医药》2003,29(12):946-946
妊娠高血压综合征(妊高征)是一种常见的严重危害母亲与胎儿健康的妊娠并发症,其病因与发病机制至今尚未完全阐明。近来研究表明,胎盘滋养层细胞显凋亡,导致绒毛植入宫壁过浅,使胎盘无法从母体获得丰富血供,可能是构成妊高征的病因。分析妊高征胎盘滋养层细胞的凋亡及其特征,探讨其与妊高征的病因及发病机制的关系,将为  相似文献   

9.
目的探讨胎盘部位过度反应的临床病理特征,提高对其诊断水平。方法运用组织病理学对6例胎盘部位过度反应标本常规石蜡切片,做HE染色及免疫组织化学染色并复习文献加以分析。结果胎盘部位过度反应的病理学特征为在胎盘种植部位的子宫内膜和其下浅肌层及血管壁中有广泛的中间滋养细胞浸润,除单核中间滋养细胞外,也可见到合体滋养细胞性巨细胞,但子宫内膜和肌层的整体结构未扭曲、未破坏。免疫组化染色结果为:细胞角蛋白(CK18),胎盘碱性磷酸酶(pLAP),人胎盘催乳素(hpL),绒毛膜促性腺激素(β-hCG)均呈局限性阳性反应,上皮生长因子受体(EGFR)呈阴性反应,K i-67增生指数均为0。结论胎盘部位过度反应有其独特的临床及病理特征,免疫组化染色有助于诊断及鉴别诊断。  相似文献   

10.
胶体金早早孕试纸在临床的应用   总被引:1,自引:0,他引:1  
人绒毛膜促性腺激素(HCG)是胎柱绒毛膜滋养层细胞产生生的一种多肽类激素。凡妊娠及胎盘滋养层细胞肿痛如葡萄胎、绒毛膜上皮癌、胎盘床滋养层细胞假瘤(PSTT)及男性睾丸畸胎瘤均分泌HCG,使尿HCG呈阳性反映。  相似文献   

11.
Previous investigations in this laboratory have indicated that arachidonic acid stimulates a rapid, dose-dependent, and reversible increase in human placental lactogen (hPL) release which is not dependent on cyclooxygenase or lipoxygenase metabolism. To investigate further the mechanism by which arachidonic acid stimulates the release of hPL, the effects of arachidonic acid on phosphoinositide hydrolysis were examined in an enriched cell culture population of term human syncytiotrophoblast. Phosphoinositide hydrolysis was assayed by three methods: the release of 3H from perfused cells prelabeled with [3H]myoinositol, the measurement of inositol phosphate accumulation, and the distribution of radioactivity in phospholipids separated by two-dimensional thin layer chromatography after exposure of 32P-labeled placental cells to arachidonic acid. Arachidonic acid stimulated a concentration-dependent, rapid, and reversible increase in the release of both [3H]myoinositol and hPL from perfused placental cells. This effect was not inhibited by prior incubation of cells with indomethacin (20 microM). In contrast, palmitic acid and oleic acid stimulated phosphoinositide hydrolysis only at a high concentration (100 microM). Arachidonic acid also stimulated the rapid appearance of inositol monophosphate in placental cells. The effect of arachidonic acid was specific for hydrolysis of phosphoinositides and phosphatidylserine and did not involve other phospholipids. Since phosphoinositide hydrolysis is associated with hormone release in a variety of secretory systems, these results suggest that the stimulation of hPL release by arachidonic acid may be mediated, at least in part, by the activation of phospholipase C.  相似文献   

12.
Purpose We investigated whether the pregnancy-related hormones, estriol (E3), testosterone, human placental lactogen (hPL), human prolactin (hPRL), and human chorionic gonadotropin (hCG) affect BCRP expression in human placental BeWo cells. Materials and Methods The effects of these hormones on BCRP protein and mRNA expression in BeWo cells were determined by immunoblotting and quantitative real-time RT-PCR, respectively. The effects of these hormones on membrane localization of BCRP in BeWo cells were examined by immunofluorescent confocal microscopy. Results E3, hPL, and hPRL significantly increased BCRP protein and mRNA approximately two to threefold at physiological concentrations. Induction of BCRP by E3 was abrogated by the estrogen receptor (ER) antagonist ICI-182,780. However, knock-down of ERα by RNA interference did not abolish the inductive effect of E3. Testosterone by itself did not affect BCRP expression at physiological concentrations. However, testosterone together with 17β-estradiol (E2) increased BCRP protein and mRNA approximately twofold, and this induction was abolished by ICI-182,780 or the testosterone receptor (TR) antagonist flutamide or knock-down of ERα expression. Further analysis revealed that E2 increased TR mRNA approximately 5.9-fold, suggesting that testosterone in combination with E2 increases BCRP expression, possibly through E2-mediated up-regulation of TR. hCG at physiological concentrations had no effect on BCRP expression. Conclusions E3, hPL, hPRL, and testosterone in combination with E2 may up-regulate BCRP expression in the placenta during pregnancy.  相似文献   

13.
卡介菌多糖核酸治疗充血性心力衰竭   总被引:1,自引:0,他引:1  
目的 :研究卡介菌多糖核酸 (BCG PSN)对慢性充血性心力衰竭 (心衰 )病人免疫机能、心衰治疗周期及住院医疗费用的影响。方法 :5 9例心衰病人 ,常规抗感染、强心、利尿、扩血管等治疗 ,分BCG PSN组与常规组。BCG PSN组在常规治疗基础上给BCG PSN 1mg ,im ,qod× 2 6d。观察 2组T淋巴细胞CD4 /CD8,IgG ,IgA ,IgM及C3,住院费用及心衰缓解时间。另有 36例健康人作为对照。结果 :心衰病人IgG及C3升高 ,T细胞亚群CD4 /CD8下降 ;BCG PSN组较常规组治疗后IgG[(14 .2± 2 .4 ) g·L- 1vs (16 .3± 2 .4 ) g·L- 1,P <0 .0 5 ]和CD8[(30±5 ) %vs (38± 6 ) % ,P <0 .0 1]降低更明显 ,IgM[(3.0± 0 .6 ) g·L- 1vs (2 .1± 0 .5 ) g·L- 1,P <0 .0 1]及CD4 [(46± 6 ) %vs(38± 5 ) % ,P <0 .0 1]升高更明显 ;BCG PSN组较常规组心衰改善所需时间缩短 [(6± 3)dvs (8.4± 2 .6 )d ,P <0 .0 1],住院总药费有所降低。结论 :BCG PSN可提高心衰病人的免疫功能 ,加快心衰改善 ,住院费用降低  相似文献   

14.
1. Pre-eclampsia is a human disease of pregnancy characterized by high blood pressure, proteinuria and end-organ damage, if severe. Pre-eclampsia is thought to be related to changes in early placental development, with the formation of a shallower than normal placental bed. 2. Transforming growth factor (TGF)-beta1 is a multifunctional fibrogenic growth factor involved in immune regulation that is elevated in some populations with a high risk of hypertensive end-organ disease related to increases in endothelin release. Transforming growth factor-beta1 is also an important factor in placental implantation. Alterations in TGF-beta1 may be related to abnormal placental development in early pregnancy and, thus, are a candidate for the development of hypertension in pre-eclampsia. 3. The aim of the present study was to examine the placental distribution and serum concentration of TGF-beta1 in patients with pre-eclampsia compared with normal pregnancy. 4. Patients with pre-eclampsia (n = 12) were compared with patients with normal pregnancy (n = 14). Transforming growth factor-beta1 was determined by TGF-beta1 Max ELISA (Promega, Madsion, WI, USA) after serum dilution (1/150) and acid activation. Placental distribution was determined by immunostaining with TGF-beta1 (Santa Cruz, Santa Cruz, CA, USA; 20 ng/mL) and the villi and decidual trophoblast were scored for intensity and extent of staining. 5. Patients with pre-eclampsia had a mean gestational age of 36 weeks, whereas those with a normal pregnancy had a mean gestational age of 39.0 +/- 0.4 weeks. There was no difference in TGF-beta1 concentration between the two groups (mean (+/-SEM) 27.1 +/- 1.0 vs 26.4 +/- 0.7 pg/mL for normal pregnancy and pre-eclampsia, respectively; P = 0.73, Mann-Whitney U-test). There was no correlation between systolic or diastolic blood pressure and TGF-beta1 concentration (regression analysis P = 0.4 and 0.2). Immunostaining was absent in the villous trophoblast cells and endovascular and extravillous trophoblast of term placentas. 6. Although TGF-beta1 is present in trophoblast cells in early pregnancy during placental development, TGF-beta1 concentrations were not increased in the placenta at term in pre-eclampsia and there was no correlation between blood pressure and serum TGF-beta1, suggesting that TGF-beta1 does not play a role in the development of late gestation pre-eclampsia and hypertension.  相似文献   

15.
目的探讨STOX1在子痫前期发病中的作用及临床意义。方法免疫组化检测正常妊娠及子痫前期胎盘组织中STOX1蛋白的表达情况;Western blot检测胎盘组织中STOX1蛋白的表达水平。结果 STOX1蛋白主要表达于绒毛的合体滋养细胞和细胞滋养细胞,与正常妊娠组相比,子痫前期胎盘组织中STOX1蛋白的表达水平明显升高(P<0.05),重度子痫前期组胎盘组织中STOX1蛋白的表达明显高于轻度子痫前期组(P<0.05),轻度子痫前期组胎盘组织中STOX1蛋白的表达明显高于正常妊娠组(P<0.05)。结论 STOX1与子痫前期的发病密切相关,在子痫前期的发生、发展中可能起到重要作用。  相似文献   

16.
The presence of moderate amounts of histamine in the human placenta was confirmed (0.72 +/- 0.10 microgram/g wet weight), and the hitherto unknown storage site of this biogenic amine was elucidated. Mast cells were identified by their characteristic morphology, staining reactions and secretory activity measured in terms of histamine release. Human placental tissue contains 7.6 x 10(5) mast cells/g wet weight, identified by staining with toluidine blue or alcian blue, and these cells were positive for chloro-acetate-esterase. Light microscope studies of placental tissue stained with HRP-conjugated anti-human IgE demonstrated cells with a typical 'halo' effect indicating cell-bound IgE, and electron microscopy revealed cells containing membrane-bound electron dense granules. A single mast cell was calculated to contain approximately 1 pg of histamine. Enzymatic digestion of placental tissue with collagenase (1.5 mg/ml) yielded viable cell suspension. containing mast cells in a purity of 0.6% which exhibited a low spontaneous output of histamine (12%). Placental mast cells released histamine in a concentration dependent manner upon challenge with anti-human IgE and the calcium ionophore A23187. Also, unlike other human mast cells so far studied. with the exception of skin, those dispersed from human placenta were responsive to the polybasic secretagogue compound 48/80. These findings represent a novel source of human mast cells and, since placentas are readily available in quantity, such tissue is proposed as an ideal source of mast cells for biochemical and pharmacological use.  相似文献   

17.
Using JEG-3 and BeWo cells, we examined the effect of “real life” mixtures of polycyclic aromatic hydrocarbons (PAHs), at doses reported in maternal blood (Mix I) and in placental tissue (Mix II), on human chorionic gonadotropin (hCG), placental lactogen (hPL) and placental growth factor (hPLGF) secretion, protein expression and immunolocalization. Additionally, the action of PAH mixtures on basal and hormone-stimulated matrix metalloproteinase-2 (MMP-2), MMP-9 and vascular endothelial growth factor (VEGF) protein expression was evaluated. Under basal conditions, the PAH mixtures increased hCG and decreased hPLGF levels in both cell lines, while hPL expression was stimulated in JEG-3 and inhibited in BeWo. There was no effect on the MMP-2/MMP-9 ratio or VEGF expression. In hormone-stimulated cells, PAH mixtures changed the MMP-2/MMP-9 ratio in JEG-3 cells in favor of MMP-9, while in BeWo MMP-2 was favored. The effect on VEGF expression was cell specific and dependent on the mixture. In hCG-treated cells, only Mix II inhibited VEGF expression in JEG-3 cells. Neither PAH mixtures affected this protein in BeWo cells. In hPL-treated cells, Mix I had a stimulatory effect in JEG-3 cells, while Mix II exerted an inhibitory effect in BeWo cells. In hPLGF-treated cells, Mix II decreased in JEG-3 cells, but in BeWo cells, both mixtures increased VEGF expression. Considering that the evaluated protein hormones play crucial roles in angiogenesis and neovascularization in the placenta, “real life” PAH mixtures by disrupting protein hormones levels, the MMP-2/MMP-9 ratio and VEGF expression can lead to insufficiency and many pregnancy-related disorders.  相似文献   

18.
王东杰  吴香  吴晓梅 《天津医药》2016,44(2):217-220
目的 评估输卵管壶腹部妊娠患者滋养细胞浸润输卵管壁深度与血管内皮生长因子 (VEGF) 及β-人绒毛膜促性腺激素(β-HCG)血清浓度之间的关联性。方法 选择输卵管壶腹部妊娠且已行患侧输卵管切除术患者 80 例。手术当天检测血清 VEGF 和β-HCG 浓度。血清 VEGF 含量的测定采用 ELISA 法。留取切除的患侧输卵管及妊娠组织, 输卵管肌纤维用 Masson 染色, 滋养细胞用人胎盘催乳素 (HPL) 免疫组织化学染色。依据术后病理结果中滋养细胞浸入输卵管壁的深度, 将 80 例患者分为Ⅰ~Ⅲ期。血清β-HCG 采用双抗体夹心光化学测定法。结果 Ⅰ 期血清 VEGF 和β-HCG 浓度的平均值明显低于Ⅱ期, 而Ⅱ期明显低于Ⅲ期 (P<0.05)。Ⅰ期和Ⅱ期临界值 VEGF 浓度为 308.6 ng/L, 敏感度 100.0%, 特异度 92.6%, Ⅱ期和Ⅲ期临界值 VEGF 浓度为 431.9 ng/L, 敏感度 79.3%, 特异度 79.2%; Ⅰ期和Ⅱ期临界值β-HCG 浓度为 2 509.6 IU/L, 敏感度 91.7%, 特异度 81.5%, Ⅱ期和Ⅲ期临界值β-HCG 浓度为 13 142.6 IU/L, 敏感度 72.4%, 特异度 95.8%。结论 输卵管妊娠患者血清中的 VEGF 和β-HCG 浓度与滋养细胞浸润输卵管壁深度有关, 可作为妊娠滋养细胞浸润输卵管管壁深度组织学分期的评估指标。  相似文献   

19.
CK(AE1/AE3)在喉鳞癌淋巴结微转移诊断中的应用   总被引:1,自引:0,他引:1  
目的 研究细胞角蛋白广谱抗体CK(AE1/AE3)作为免疫标志物在喉鳞癌淋巴结微转移诊断中的应用与临床病理意义.方法 对50例喉鳞癌患者喉标本及其常规病理报告为阳性的140个淋巴结和阴性的756个淋巴结重新切片,以CK(AE1/AE3)作为免疫标志物,采用免疫组化PV9000两步法检测.结果 在50例喉鳞癌原发灶和病理检查阳性淋巴结中,CK AE1/AE3全部表达,和临床T分期、病理分级无明显相关(P>0.05),756个阴性淋巴结标本中,有9例(18.0%)16个淋巴结(2.1%)发现了微转移灶.结论 CK(AE1/AE3)免疫组化法是检测喉鳞癌淋巴结转移的敏感而便捷的方法,特别对筛选组织学检查淋巴结阴性但存在微转移的患者有一定实用价值.  相似文献   

20.
《Environmental toxicology》2018,33(4):436-445
Butyl paraben (BP) has antimicrobial effects and is widely used as a preservative in cosmetics, foods, and pharmaceuticals. It is also absorbed into various tissues of the human body. It is known that BP is measurable in maternal and fetal tissues during pregnancy, but the effects of BP on placental development, essential for maintaining normal pregnancy, are unclear. Therefore, we investigated the effect of BP on the proliferation, apoptosis, and invasiveness of human trophoblast cells, using an HTR8/SVneo cell line. BP inhibited cell proliferation and induced both apoptosis and endoplasmic reticulum stress. In addition, BP promoted the production of intracellular reactive oxygen species, increased Ca2+ concentration in HTR8/SVneo cells, and induced mitochondrial membrane depolarization. BP also inhibited the activation of PI3K/AKT pathways including AKT, ribosomal protein S6, P70 S6 kinase, and glycogen synthase kinase 3β. Furthermore, pretreatment of cells with LY294002 (an AKT inhibitor) and U0126 (ERK1/2 inhibitor) revealed that ERK1/2 activity is also involved in BP‐mediated signal transduction in HTR8/SVneo cells. We therefore suggest that exposing human trophoblast cells to BP diminishes normal physiological activity, leading to apoptosis and problems with early placental development.  相似文献   

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