抗乙肝胎盘转移因子的特异免疫活性观察

本研究由ＨＢＶＭ－Ａｂ阳性胎盘提取的抗乙肝胎盘转移因子（ＰＳＴＦ）的特异免疫活性证明，经注射，小鼠外周血淋巴细胞明显增多，胸腺重量和指数亦显著增加，酯酶染色证明７５％属Ｔ－样淋巴细胞，２５％属Ｔｈｙ－样淋巴细胞，人白细胞或小鼠白细胞体外转移ＰＳＴＦ特异免疫活性、或豚鼠和小鼠体内转移ＰＳＴＦ特异免疫活性，再取其白细胞作白细胞粘附抑制、白细胞移动抑制、特异淋巴细胞转化、小鼠足掌注射和诱生γ－干扰素试验     

人胎盘提取组织凝血活酶及其质量评价

利用人胎盘抽提得组织凝血活酶，并对其质量进行了评价，同时初步应用于临床。结果显示：用含表面活性剂的抽提剂粉碎抽提的效果较好，所得组织凝血活酶重复性、灵敏度、稳定性均令人满意；与上海荣盛生物制品厂生产的ＰＴ试剂盒比较相关性好：Ｙ＝２．７５＋０．９０５ｘ，ｒ＝０．９２５３，经相关系数ｔ检验，ｔ＝２６．５４６９，Ｐ＜０．００１，呈直线正相关。临床初步应用显示：肝病及抗凝治疗等病人ＰＴ时间明显延长，９３例正常人ｘ＝１１．３秒，ｓ＝０．９６秒，正常范围９．４２－１３．１８秒。     

人胎盘组织液抗炎药效学研究

目的研究人胎盘组织液的主要药效作用。方法建立二甲苯所致小鼠耳肿胀及大鼠棉球肉芽肿的药理模型，观察人胎盘组织液对炎症模型动物的抗炎作用。结果与模型对照组相比，连续7d肌肉注射0．1mL/kg剂量的人胎盘组织液对二甲苯所致小鼠耳肿胀起到明显抑制作用，且差异显著（P〈0．01）；连续6d肌肉注射0．1mL／kg剂量的人胎盘组织液对大鼠棉球肉芽组织增生起到明显抑制作用，且差异显著（P〈0．01）。结论人胎盘组织液具有明显的抗炎作用。     

人胎盘脂多糖辅助治疗支气管哮喘临床疗效观察

目的观察人胎盘脂多糖辅助治疗儿童支气管哮喘的临床疗效。方法将我院91例支气管哮喘患儿随机分成2组,治疗组46例,采用综合疗法,发作期应用沙丁胺醇、普米克令舒、氨茶碱治疗,缓解期肌内注射人胎盘脂多糖、气雾吸入倍氯米松;对照组45例,发作期用沙丁胺醇、普米克令舒、氨茶碱治疗,缓解期气雾吸入倍氯米松。结果治疗2周后治疗组、对照组对改善喘息、咳嗽症状比较,差异有显著性意义(P<0.05)。随访1年,治疗组复发率与对照组比较,差异有显著性意义(P<0.05)。结论人胎盘脂多糖辅助治疗支气管哮喘疗效确切,复发率低,值得临床推广应用。     

牛胎盘中肝细胞生长因子的纯化

用高速离心、分段盐析、亲和层析、超滤和阴离子交换层析法，从牛胎盘中分离纯化出一种肝细胞生长因子。结果表明，此因子的最终得率为０．００５ｍｇ／ｇ牛胎盘，其分子量约为９９０００ｕ，它能强烈刺激原代培养大鼠肝细胞的ＤＮＡ合成。提示利用自制的亲和层析凝胶，通过此提纯流程可以得到一种肝细胞生长因子。     

黄芪丹参复方成分对一氧化氮合成阻滞孕鼠模型血浆IL-1、IL-10变化的影响

目的探讨黄芪丹参复方成分提高胎盘血供的分子机制，为临床有效防治胎盘血供不足所致妊娠并发症提供思路。方法提取分离黄芪、丹参复方成分，运用NOS（一氧化氮合酶）阻滞剂L－精氨酸甲酯（L—NAME）建立一氧化氮合成阻滞大鼠模型，ELISA法检测妊娠18d大鼠血浆IL－1、IL－10水平。以及胎盘超微形态学变化，大鼠血压、尿蛋白变化，以及仔鼠重、肝重、脑重、胎盘重等。结果一氧化氮合成阻滞模型组IL－1含量明显高于空白组（P〈0．01），经黄芪丹参注射液治疗后，血浆IL－1水平比模型组降低（P〈0．05）；模型组IL－10含量较空白组低（P〈0．01），中药组血浆IL－10水平高于模型组（P〈0．05）；胎盘形态学、血压、尿蛋白以及仔重、仔肝重、脑重等均有显著差异（P〈0．05，P〈0．01）。结论黄芪丹参复方成分可能对妊娠早期母－胎界面免疫平衡具有调控作用，通过促进局部生理抑制性免疫反应增强和杀伤、排斥免疫反应减弱，从而有利于母胎循环构建，维持胎盘血液供应。     

THE PHYSIOLOGY OF PRE-ECLAMPSIA

1. Pre-eclampsia is a multisystem disorder of human pregnancy with a genetic predisposition. It occurs more commonly in first pregnancies and primarily affects maternal renal, cerebral, hepatic and clotting functions while elevating blood pressure. The foetus is affected through placental insufficiency arising from abnormal ‘placentation’, that is, failure of adequate trophoblast invasion of maternal vasculature, and possibly from abnormal autacoid production. 2. Pre-eclampsia is caused by the placenta; delivery of the placenta is the only known cure. Its manifestations are considered secondary to organ hypoperfusion which arises as a result of vasoconstriction, intravascular coagulation and reduced maternal blood volume. 3. Current hypotheses propose that pre-eclampsia is due to widespread maternal endothelial cell damage, perhaps secondary to a cytotoxic factor released by the placenta. This hypothesis has gained wide acceptance, but scientific evidence is lacking. 4. Defining the abnormal balance of vasoactive factors in pre-eclampsia has proved a difficult task. There is enhanced pressor reactivity to infused angiotensin 11 (AII) despite reduced plasma concentrations of AII, renin and aldosterone. Prostacylclin production appears reduced, and the balance of thromboxane/prostacyclin favours vasoconstriction and platelet aggregation. There is no convincing evidence for enhanced endothelin or reduced nitric oxide production. Plasma concentrations of atrial natriuretic peptide are paradoxically elevated in the face of plasma volume contraction. An intriguing observation, which remains unexplained, is why some vascular beds are affected predominantly in one patient (eg. hepatic ischaemia) while another has a similar degree of hypertension but involvement of a different organ system (eg. renal insufficiency yet normal liver function). 5. Volume homeostasis is disturbed with redistribution of intravascular volume to the interstitial fluid space due to increased capillary permeability and in some cases reduced plasma oncotic pressure. This redistribution is not always clinically apparent as peripheral oedema. Whether this change in volume is compensated for by venoconstriction and maintenance of adequate cardiac output is undetermined. 6. Improved understanding of the pathophysiology of pre-eclampsia is necessary to allow better clinical management of this serious disorder.     

Increased apoptosis in third-trimester placental tissue from gestations complicated by PIH

Objective: To investigate a possible role of apoptosis in the pathophysiologic mechanisms of PIH ( pregnancy-induced hypertension syndrome). Methods: In this study, placental samples were obtained from 16 uncomplicated third-trimester pregnancies and from 16 cases of PIH. We used light microscopy, electron microscopy to identify apoptosis. Light microscopy was used to quantify their incidence of apoptosis. Electron microscopy was used to confirm the occurrence of apoptosis. Results: Apoptosis has been conclusively demonstrated within human third-trimester placental tissue. Medians and interquartile ranges of normal placenta (n = 16) was 0. 12% (0. 08% -0. 19% ) ; Medians and interquartile ranges of PIH group (n = 16) was 0. 37% (0. 15% -0.49% ). Compared to normal placentas, the incidence of apoptosis was higher in placentas from gestations complicated by PIH ( P < 0. 05 , T'-test). Conclusion: Placental apoptosis increases significantly in PIH, and it may play a role in the pathophysiologic mechanisms     

中西医结合治疗慢性盆腔炎100例疗效观察

目的:采用中西医结合治疗慢性盆腔炎,减少复发,提高治愈率。方法:对我院门诊患者100例采用胎盘组织液肌注,金钢藤胶囊口服,并用我院自制中药妇炎肠疗液灌肠。结果:临床显效40例,有效56例,无效4例,总有效率96％。结论:中西医结合治疗慢性盆腔炎疗效满意,是目前治疗慢性盆腔炎的最好方法。     

一氧化氮与胚胎异常发育的相关性研究

为了解开一氧化氮（ＮＯ）是否与畸胎发生有关这一谜团和进一步阐明砷致畸作用机理，本实验应用诱生型ＮＯ合成酶（ｉＮＯＳ）组织化学、扫描电镜（ＳＥＭ）及体内致畸试验等方法研究了砷对小鼠卵黄囊胎盘（ＹＳＰ）和胚胎发育的影响。结果表明ＹＳＰ细胞ｉＮＯＳ表达与砷浓度之间存在明显的剂量—反应关系（Ｐ＜０．０５）；ＳＥＭ观察可见ＹＳＰ内皮层和间皮层细胞受损；光镜下可见ＹＳＰ变小、萎缩和微血管分化不良；随着染毒剂量的升高，畸胎率和死胎率亦逐步增加，最高分别达到５６．８％和２４．７％；畸胎的主要表现是神经管未闭，心包积液和体位异常等。研究结果率先提示过量ＮＯ与畸胎发生及致畸机理关系密切；推荐在致畸研究中ｉＮＯＳ可作为一种有效的生物标志物。