Prenatal diagnosis of congenital cystic adenomatoid lung malformation: A report of seven cases

Six cases of macrocystic and one case of microcystic congenital adenomatoid lung malformation were diagnosed by ultrasound between 20 and 31 weeks of gestation. Combined polyhydramnios and fetal hydrops was present in three cases, polyhydramnios alone in one case, and isolated fetal hydrops also in one case. In the remaining two cases, both polyhydramnios and fetal hydrops were absent. Fetal outcome was poor, i.e., two terminations of pregnancy, three early neonatal deaths, and two survivors.     

上海市若干环境污染物的诱变性

用中国仓鼠肺成纤维细胞(V_(79)),进行次黄嘌呤—鸟嘌呤磷酸核糖转移酶位点(HGPRT Locus)试验,检测了上海市若干环境污染物的诱变性。结果发现,污染物量与诱变性之间呈剂量—反应关系。所有样品经代谢活化后(加S_9),其诱变性均有增高的趋势。卷烟焦油、油烟冷凝物的T/C值均>3,而不加S_9的黄浦江水和自来水样,则对V_(79)细胞可能具有间接的诱变作用(T/C值<3)。     

Prenatal detection of trisomy 21 in uncultured amniocytes by fluorescence in situ hybridization: A prospective study

A prospective study was undertaken to evaluate the use of fluorescence in situ hybridization (FISH) for the detection of trisomy 21 in interphase nuclei of uncultured amniotic fluid cells. Five hundred cases were analysed in situ and classified as normal or abnormal; the results were subsequently checked against the cytogenetic findings. Four hundred and ninety-three were correctly identified as normal with an 86·6 per cent average frequency of scored nuclei exhibiting two signals; six cases were correctly identified as trisomic for chromosome 21 with 81·7 per cent of scored nuclei exhibiting three signals; and one abnormal case involving an unbalanced chromosome 21·21 translocation was falsely scored as normal due to poor hybridization/detection efficiency. The method has been substantially improved and simplified so that it is suitable for the rapid detection of trisomy 21. As aneuploidy detection in interphase does not identify structural chromosome aberrations, it is not a substitute for fetal chromosome analysis.     

长江、嘉陵江(重庆段)源水有机提取物的类雌激素活性评价

为了解长江、嘉陵江(重庆段)源水有机提取物的类雌激素活性，分别于夏季和冬季采用GDX—120大孔树脂对位于城区上、中、下游5个断面长江、嘉陵江(重庆段)源水进行有机物的浓缩提取。用体外MCF—7细胞增殖试验检测有机提取物的类雌激素活性。结果显示，源水有机提取物均具有类雌激素活性。其类雌激素活性中、下游均高于上游，丰水期高于枯水期。     

纳米氧化锌颗粒物通过氧化应激和离子通道失调诱导大鼠气管上皮细胞凋亡的机理

纳米氧化锌具有广泛的工业用途,其生态安全性受到广泛关注,针对纳米氧化锌诱导的呼吸道细胞毒性及其作用机理研究尚不广泛.本研究分别采用不同浓度和粒径(30 nm和90 nm)的氧化锌颗粒物处理大鼠气管上皮细胞(rat tracheal epithelial cells,RTE cells),暴露时间为12 h,通过检测细胞内锌元素含量,细胞增殖抑制率,细胞凋亡率,凋亡相关caspsae 3基因与蛋白相对表达量,细胞内金属硫蛋白活性,ROS和MDA含量、细胞内Ca~(2+)-ATP酶和Na~+/K~+-ATP酶活性来分析纳米氧化锌诱导细胞毒效应机理.在90 nm纳米氧化锌高浓度暴露时,其细胞内锌元素浓度为0.845μg·L~(-1),约为低浓度暴露组的4.7倍,是30 nm低浓度暴露组的9倍;纳米颗粒物诱导的细胞增殖和凋亡毒效应具有剂量和尺寸依赖效应;30 nm处理组的pro-caspase 3和cleaved-caspase 3蛋白表达量均高于90 nm暴露组;暴露浓度为10 mg·L~(-1)的90 nm处理组的金属硫蛋白增加量为0.533μg·L~(-1),增幅达到46%;不同粒径氧化锌颗粒物处理后,细胞内ROS和MDA含量显著上升,且30 nm处理组结果均高于90 nm处理组;纳米氧化锌颗粒物暴露诱导细胞Ca~(2+)-ATP酶和Na~+/K~+-ATP酶活性显著下降,30 nm氧化锌颗粒物暴露组,其Na~+/K~+-ATP酶活性分别是对照组的1.8倍和3.5倍.纳米氧化锌颗粒物进入RTE细胞,通过干扰锌在细胞内代谢,诱导细胞内ROS和MDA水平升高,产生氧化应激,进而诱导细胞凋亡是导致纳米氧化锌产生细胞毒性的主要原因之一.纳米氧化锌会导致细胞内Ca~(2+)-ATPase和Na~+/K~+-ATPase活性下降,离子通道失调,破坏细胞内离子平衡,进一步造成细胞凋亡.     

经手口途径摄入室内含PAHs灰尘颗粒的致癌风险评价

为了探究经手口途径摄入被PAHs污染室内灰尘的致癌风险,构建了居民经手口途径摄入被污染室内灰尘颗粒的概率风险模型,运用蒙特卡罗模拟方法评价了中国上海地区居民由PAHs引起的致癌风险,分析了致癌风险的主要来源及手口途径中各参数的重要程度。结果表明:幼儿和儿童所承受的风险最大,婴儿和成年人次之,青少年和老年人较小;对于致癌风险,幼儿和儿童超过10-6的概率都为80%,但超过10-4的概率都小于5%,婴儿和成年人超过10-6的概率都为50%,但婴儿超过10-4的概率小于5%,成年人的小于0.1%,青少年和老年人超过10-6的概率分别为10%和15%,不会高于10-4;室内硬表面灰尘引起的致癌风险远大于软表面灰尘引起的致癌风险;与致癌风险相关性最大的因素为灰尘颗粒中PAHs的等效斜率、灰尘在室内软硬表面的浓度、手到口途径发生的频率和颗粒物从手掌皮肤表面到口腔的转移率。     

中国食管癌发病区环境地球化学及相关模型的研究进展

食管癌是一种常见的消化道疾病,在世界许多国家和地区均有发生,其中环境因素是引发地方病食管癌的重要因素。目前,模型被应用于食管癌的研究中,食管癌研究模型主要有食管癌发病率预测模型,食管癌预防模型及食管癌动物模型等。本文主要综述了前人对中国食管癌发病区的土壤、饮用水和食物等环境地球化学因素,以及与食管癌研究相关的土壤模型和食管癌模型的研究进展。     

典型电子垃圾拆解区居民多卤代芳烃的膳食暴露及其癌症风险评估

收集浙江典型电子垃圾拆解区和对照区的饮用水、蔬菜、豆类、米饭、鸡蛋、鱼、鸡肉和猪肉等8类食物样品共191个;采用GC/MS 5975B分析样品中23种PBBs,12种PBDEs和27种PCBs;评估当地居民的PHAHs膳食暴露现状及其癌症风险.结果表明,拆解区居民这三大类PHAHs的平均日摄入量是对照区的2~3倍,通过米饭摄入PHAHs的量占当地居民PHAHs总摄入量的48%以上.拆解区居民因食物摄入PHAHs的癌症风险(3.81×10-4)是对照区(1.50×10-4)的2倍多,其中二英类PCBs的风险值占总癌症风险的45%以上.通过米饭摄入PHAHs是主要的暴露途径,二英类PCBs是引起癌症风险的主要贡献因子,电子垃圾拆解释放出的PHAHs通过食物摄入进入居民体内引起的癌症风险要明显高于对照区.     

Mechanism of Deca-BDE-induced apoptosis in Neuro-2a cells: Role of death-receptor pathway and reactive oxygen species-mediated mitochondrial pathway

Decabromodiphenyl ether (BDE-209) is a prevalent polybrominated diphenyl ether (PBDE) congener known to have neurotoxicity. Effects of BDE-209 on Neuro-2a cells were performed in the present study and the possible apoptotic pathway was discussed. Results indicated that BDE-209 induced Neuro-2a cell apoptosis, increased the protein expression of Fas and Fas-associated death domain-containing protein (FADD) and activated the caspase-8 and -3 activities in a concentration-dependent manner, inferring the death-receptor pathway was involved in the apoptotic process. Meanwhile, BDE-209 exposure increased the Bax/Bcl-2 ratio and decreased the cellular mitochondrial membrane potential (MMP) which led to cytochrome C released to the cytoplasm. The intracellular caspase-9 was elevated simultaneously, which caused downstream caspase cascade and triggered cell apoptosis. Moreover, BDE-209 exposure increased cellular reactive oxygen species (ROS) level in a concentration-dependent manner and the addition of N-acetyl-l-cysteine (NAC), known as ROS scavengers, obviously reduced the apoptotic rate and a positive relationship was observed between the degree of apoptosis blocking and the loss of MMP and ROS production. We thus concluded that BDE-209 induced Neuro-2a cell apoptosis via the combination of the death-receptor signaling pathway and the mitochondrial signaling pathway. The elevated ROS production was considered to magnify the intracellular apoptosis signal and played a crucial role in apoptosis of Neuro-2a cells induced by BDE-209.