子痫前期与宫内死胎的相关性研究进展

子痫前期(preeclampsia,PE)是一种动态进展的妊娠相关性疾病,病因具有异质性,是导致孕产妇和胎儿死亡的主要原因之一.正常胎盘的形成是维持胎儿正常生长发育的关键.不正常的胎盘植入被认为是子痫前期的主要发病机制,以胎盘浅着床为中心环节.宫内死胎是一种由多因素导致的严重的妊娠期并发症,60％的宫内死胎与胎盘有关,...     

毒物的胎盘转运

近年来,毒物经胎盘转运对发育中胚胎的毒理学作用日益引起人们的兴趣。外源性化学物质通过胎盘转运对胎儿的影响大致可有两种情况:一是影响胎盘本身的结构和功能,间接导致对胎儿的毒性影响;另一方面是母体血浆中未结合的化学物质以其原型透过胎盘,造成胎儿宫内直接暴露。后一过程称之为胎盘转运。毒物经胎盘转运造成宫内暴露,是一可供参考的指标。对女工妊娠中期及后期的劳动保护具有重要意义。     

2,3,7,8-四氯二苯并二恶英对体内氧化应激反应的研究进展

二恶英是一种毒性极大的环境污染物,通过活性氧和氧化应激反应损伤多种靶器官。本文综述了近年来该毒物的研究进展,着重介绍二恶英对氧化应激和抗氧化系统的影响及TCDD的作用机制。     

胎盘滋养层细胞模型的建立及其应用

滋养层细胞是胎盘结构中体现其屏障作用最重要的细胞,与多种妊娠疾病的发生、发展有关.另外,大多数病毒可导致胎盘感染并波及胎儿,因此滋养层细胞与宫内传播也有关.为了阐明多种妊娠相关疾病的发病机制及病毒宫内传播的机制,目前众多研究者通过在体外建立滋养层细胞模型进行了大量有价值的研究,此文对相关的研究进展进行综述.     

二恶英污染对人体健康的影响

二恶英是一类氯化芳香族化合物,主要来源于有氯供体存在时的燃烧过程和有氯处理工艺的化学工业过程。近年来的研究资料显著：二恶英是环境中毒性最大的物质之一。它们具有致癌性、致畸性、免疫毒性、生殖毒性、内分泌毒性等。随着工业化的发展,二恶英污染有加重的趋势,这对人类健康构成了严重威胁。本文主要对二恶英的分子结构、理化性质、污染来源、环境归宿及对体健康的影响作一介绍。     

环状RNA与子痫前期发病机制的研究进展

子痫前期(preeclampsia,PE)是妊娠期常见且特有的并发症,发生率为3%~5%。主要临床表现为妊娠20周后,出现高血压、蛋白尿及全身器官功能损害。常引起胎儿宫内缺氧和生长受限,是导致孕产妇和围产儿死亡的重要原因[1-2]。子痫前期的发病机制至今仍不明确,一般认为与胎盘血管功能障碍和胎盘异常形成有关[1]。     

乙型肝炎病毒宫内感染中母胎外周血单核细胞的转运机制

研究宫内感染的机制对降低我国HBsAg慢性携带率具有非常重要的意义.妊娠过程中母体血液中的血小板和白细胞可通过胎盘屏障,而胎盘细胞凋亡与胎盘屏障通透性增加又存在不可分割的内在联系,PBMC是HBV肝外感染的主要细胞,在HBV复制、感染及迁延中起着重要作用,可以作为HBV的载体.这些证据提示PBMC母胎转运在HBV宫内感...     

低出生体重对肾脏发育和血压的影响

众所周知,由于孕期母体营养不良、子宫．胎盘供血不足或营养物质通过胎盘受限等原因引起胎儿宫内生长受限（fetalgrowthrestriction,FGR）或宫内发育迟缓（intrauterinegrowthrestriction,IUGR）,导致患儿低出生体重（10wbirhweight,LBW）,LBW成为围产儿发病和死亡的主要危险因素之一。     

先兆子痫与大于胎令儿的关联

先兆子痫仍然是孕产妇和围生儿发病与死亡的一个重要原因。虽然过去 5 0年中已经进行了大量相关的基础、临床以及流行病学研究 ,但对其病因和发病机制仍不十分清楚。对先兆子痫的发病机制比较公认的一个假说是胎盘血流灌注减少 ,从而导致胎儿宫内生长发育迟缓和低出生体重。虽然有许多的研究支持该假说 ,但是否这是先兆子痫的唯一发病机制尚存在争议。而且 ,实验研究认为先兆子痫孕妇的心输出量增加 ,血流量也增大 ,相应地子宫胎盘的血流灌注也增加。流行病学研究也没有发现先兆子痫与胎儿生长发育不良有决定性关系。虽然先兆子痫孕妇的胎儿…     

CDFI对胎儿脐带缠绕时宫内缺氧的研究

脐带是连接胎儿与胎盘循环的纽带,胎儿脐带缠绕过紧可造成脐血流受阻,导致宫内缺氧危及胎儿生命,对胎儿预后和分娩方式均有很大的影响.本研究应用彩色多普勒超声,在产前了解宫内情况,明确有无脐带缠绕及脐带血流受阻时预测胎儿宫内缺氧,对提高围产医学质量有重要的意义.     

Dioxin: exposure-response analyses and risk assessment

Low-levels of dioxin cause cancer in animals. In 1997 dioxin was found to be a human carcinogen by the International Agency for Research on Cancer, based largely on four studies of industrial workers exposed to high levels. Recently there has been interest in estimating human cancer risk at low level environmental exposures. Here we review quantitative exposure-response analyses and risk assessment for low environmental levels based on the largest existing cohort of workers exposed to dioxin (the U.S. NIOSH cohort). We estimate that doubling background levels of exposure, which may occur for example by eating a lot of fish which have accumulated dioxin, will increase lifetime risk of cancer death by 0.1 to 1.0%. In the US the background risk of cancer death by age 75 is 12%, so doubling background levels of dioxin exposure would increase this lifetime risk to somewhere between 12.1 and 13.0%. Our results agree broadly with results from a German cohort, which is the only other cohort for which a quantitative risk assessment has been conducted.     

Environmental dioxin compounds as the cause of endometriosis and other diseases

There has been much debate of late about whether or not dioxin, an industrial toxin, could be a causative agent in the onset of endometriosis, a gynaecological disease associated with infertility and pain. Studies found either no difference in serum dioxin concentrations when cases were compared to controls or a non-significant increase, or reached low statistical power. The introductory results on Rhesus monkey contradict with the observations on mice fed with dioxin and oestrogen simultaneously. Genetic comparison shows that human belongs to the dioxin resistant races so dioxin concentrations measured in the population could not cause disease especially not an oestrogen dependent one, like endometriosis.     

维生素与胎儿发育的关系

胎儿在母体宫内需要经过配种、胚胎、胎儿三个阶段,任何影响母胎健康的病因都可以会影响宫内受精卵、胚胎、胎儿发育,严重者甚至胚胎停育、胎死宫内。研究表明各种维生素的缺乏容易诱发人体各种各样的疾病,孕期母体维生素的需要量增加,如果孕期母体维生素摄入不足、补充不够、未得到及时增加或增加过量都会给宫内的胎儿带来害处,影响胎儿器官功能的正常发育,导致胎儿发育不良;有些严重的胎儿畸形是致死性的,孕期要注意筛查及时处理。孕期加强母胎保健,重视优生优育,改善孕妇和儿童营养状况,合理调配膳食和进食并适当补充维生素,了解各种维生素的功效和胎儿发育相关性,对于降低胎儿出生缺陷、防治妇女儿童营养缺乏病、提高人口素质均具有重要实际意义。     

急性胎儿宫内窘迫1273例临床分析

目的:探讨急性胎儿宫内窘迫与新生儿预后的关系。方法:对诊断为急性胎儿宫内窘迫的1 273例临床病例作回顾性分析。结果:胎儿宫内窘迫是宫内胎儿缺氧的危急状态,处理及时是关键。结论:急性胎儿宫内窘迫是新生儿围产期死亡及新生儿神经后遗症的常见原因,及时正确处理,新生儿预后良好。     

Accuracy of fetal death reports: comparison with data from an independent stillbirth assessment program

We evaluated the completeness and accuracy of reporting on Wisconsin fetal death report forms (FDF) through case by case comparison with data from the Wisconsin Stillbirth Service Project (WiSSP), which uses extensive protocols for etiologic investigation of stillborns. Fetal deaths are underreported: no FDF was submitted for 17.8 per cent of fetal deaths evaluated through the WiSSP. For those for whom FDF were submitted, fetal anomalies were often unrecognized or unreported: only 60 per cent of stillborns identified by the WiSSP as having fetal anomalies had any indication of the presence of such anomalies on FDF. When causes of death were classified into fetal, placental/cord, maternal/environmental, and unknown, comparison of reported underlying cause of death revealed marked inaccuracies on FDF. Placental/cord causes reported on FDF often could not be documented subsequently while, in contrast, fetal causes of death were underreported. Few accurate fetal diagnoses were present on FDF. Even among common lethal malformations misdiagnosis occurred frequently.     

Use of multiple-cause mortality data in epidemiologic analyses: US rate and proportion files developed by the National Institute for Occupational Safety and Health and the National Cancer Institute.

The authors have created US mortality rates (age, sex, race, and calendar-time specific) and proportions, using multiple cause-of-death data, for the years 1960-1989. Multiple cause-of-death data include the usual underlying cause of death from the death certificate as well as contributory causes and other significant conditions. US multiple-cause rates and proportions enable the user to calculate the expected occurrences of disease on the death certificates of a cohort under study. There is an average of 2.66 causes and/or contributory conditions listed on US death certificates, increasing over time from 2.54 in the 1960s to 2.76 in the 1980s. The ratio of multiple-cause listings to underlying cause listings varies by disease, from low ratios for cancers to high ratios for diseases such as diabetes, arthritis, prostate disease, hypertension, pneumoconiosis, and renal disease. Use of these data is illustrated with two cohorts. Multiple-cause analysis (but not underlying cause analysis) revealed twofold significant excesses of renal disease and arthritis among granite cutters. For workers exposed to dioxin, neither multiple-cause nor underlying cause analysis indicated any excess of diabetes, an outcome of a priori interest. Good candidates for multiple-cause analysis are diseases that are of long duration, not necessarily fatal, yet serious enough to be listed on the death certificate.     

Reproductive outcomes of mothers with potential exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Animal laboratory studies have demonstrated that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has fetotoxic and teratogenic effects at low doses. TCDD contamination of soil in nine residential areas of eastern Missouri began in 1971 when several horse arenas and dirt roads were sprayed for dust control with a mixture that contained waste oil and dioxin. The authors conducted an epidemiologic investigation to determine if adverse human reproductive outcomes are associated with exposure to soil contaminated with dioxin. The authors attempted to identify all births during the period of January 1, 1972 through December 31, 1982 that had potential exposure to dioxin, based on proximity of the maternal address to a location of known TCDD contamination. This group totaled 410 births. A matched set of 820 unexposed births was selected as a comparison group after being matched for maternal age and race, year of birth, hospital of birth, and plurality. The exposed group had increased risk ratios for infant, fetal, and perinatal death; low birth weight; and several subcategories of birth defects. None of these increased risk ratios for the exposed group were statistically significant. These results do not provide evidence that TCDD exposure has a substantial impact on the reproductive outcomes investigated. If TCDD does produce effects on reproductive health, a larger study and/or better measures of exposure may be needed to discover them.     

铝对小鼠宫内胚胎发育致畸作用的研究

为了了解铝的胚胎毒性，用实验畸胎学的方法，研究了孕期里经口摄入不同剂量铝对妊娠小鼠宫内胚胎发育的影响。结果发现，铝的过量摄入对小鼠胚胎发育具有明显的致畸作用和毒性。它可导致胚胎发生露脑畸形和骨发育不全，及胎儿宫内生长迟缓和小鼠胚胎死亡率升高，并表现出明显的剂量－效应关系。提示，铝的过量摄入可能是先天性神经管缺陷（ＮＴＤｓ）和胎儿宫内生长迟缓（ＩＵＧＲ）以及围产儿死亡的危险因素之一。     

Dioxin effects on neonatal and infant thyroid function: routes of perinatal exposure, mechanisms of action and evidence from epidemiology studies

Objectives: Animal experiments suggest that thyroid function alterations in newborns and infants may represent one of the most sensitive markers of toxicity from 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Dioxin can be transferred from the mother to the offspring either in utero or through lactation. It has been suggested that thyroid-hormone alterations produced by dioxin in utero or shortly after birth may underlie long-term effects, such as cognitive-ability and neurodevelopment impairment. In the present review article, we appraise available evidence on the effects of perinatal exposure to dioxin on fetal and infant thyroid function. Methods: We summarized the routes of perinatal dioxin exposure and research results on possible mechanisms of dioxin toxic effects on thyroid function. We performed a systematic review of epidemiology studies conducted on mother–child pairs exposed to background environmental levels to investigate dioxin effects on neonatal and infant thyroid function. Results: Toxicological and mechanistic data indicate that dioxin may impair thyroid function in exposed newborns and infants. Investigations on background-exposed children have not consistently demonstrated an association between perinatal TCDD exposure and thyroid function, although some of the studies suggest that sub-clinical hypothyroidism may be induced by perinatal dioxin exposure within 3 months from birth. Between studies inconsistencies may be related to lab method differences, mixed exposures, and small sample size of the populations evaluated. Conclusion: Epidemiology studies have as yet failed to demonstrate an association between perinatal TCDD exposure and thyroid function alterations in human subjects, although suggestive evidence from animal and in-vitro experimental data is available.     

The coding of underlying cause of death from fetal death certificates: issues and policy considerations.

Recently, plans to implement nationwide coding of underlying cause of fetal death have been promulgated. To examine the validity and potential utility of nationwide coding, this paper presents data from a five-state (Wisconsin, Arkansas, Maine, North Carolina, California) analysis of underlying causes of fetal death from vital records for 1985 through 1987. Nosological coding rules varied somewhat from state to state. Underlying causes were grouped into categories; distributions were similar for each state. Many deaths (20.3% to 32.9%) were coded as unspecified conditions. Congenital anomalies accounted for only 6.9% to 10.3% of fetal deaths, including implausible and nonspecific causes. In total, 29.5% to 42.8% of the reports were not valid or useful. To obtain better data, researchers must focus on improving fetal death reporting, which will entail the promotion of comprehensive autopsy, placental and laboratory evaluation, systematic vital records query procedures, and implementation of multiple-cause-of-fetal-death coding.