全氟化合物(PFCs)作为一类新型的有机污染物已被持续关注.本文以双台子河口为研究对象,采用固相萃取(SPE)前处理与高效液相色谱串联质谱联用(HPLC-MS/MS)相结合的方法分析水样中包含短链全氟丁酸(PFBA)、全氟丁基磺酸(PFBS)、全氟戊酸(PFPeA)在内的15种主要PFCs的含量水平,并对全氟辛烷磺酸(PFOS)与全氟辛酸(PFOA)的生态风险及人群健康风险进行评价.结果表明,双台子河口水体存在PFCs污染,∑PFCs介于43.40～ 157.71 ng·L-1之间,PFBA和PFPeA是水体中的主要污染物.此外,采用风险商法粗略评估得到PFOS与PFOA的风险值均远低于参考值,风险较小.

Perfluorooctane sulfonate (PFOS) is an ubiquitous persistent organic pollutant, which can be bioaccumulated and cause adverse effects on organisms. However, there is very limited information about the toxic effects of PFOS to marine organisms and its mechanisms. Therefore, in the present study, adult sea urchins Glyptocidaris crenularis were exposed to PFOS for 21 d, followed by a 7-d depuration period, in order to investigate the toxicity of PFOS to sea urchin and its potential epigenetic mechanisms. Sea urchins dropped spines, and lowered down the motor ability and feeding ability after the PFOS exposure. Superoxide dismutase activities in supernatant of coelomic fluid of sea urchin increased firstly and then dropped down, while the change of the catalase activity took an opposite trend during the exposure period. They both approached to the corresponding activity of the control after the depuration period. The DNA methylation polymorphism, methylation rate and demethylation rate in sea urchin gonad all increased following the prolonged exposure time, and then decreased after the depuration period. The demethylation rates were lower than the corresponding methylation rates, therefore methylation events were dominant during the whole experimental period. This might suggest that sea urchin have strong self-protection mechanisms and can survive from the PFOS exposure presented in this study. Further efforts are needed to more precisely investigate the DNA methylation effects of PFOS and the self-protection mechanism of sea urchin.

Many investigations have reported the successful mapping of quantitative trait loci (QTLs) for gene expression phenotypes (eQTLs). Especially local eQTLs, where expression phenotypes map to the genes themselves, are of great interest, because they are direct candidates for previously mapped physiological QTLs. Here we show that many mapped local eQTLs in genetical genomics experiments do not reflect actual expression differences caused by sequence polymorphisms in cis -acting factors changing mRNA levels. Instead they indicate hybridization differences caused by sequence polymorphisms in the mRNA region that is targeted by the microarray probes. Many such polymorphisms can be detected by a sensitive and novel statistical approach that takes the individual probe signals into account. Applying this approach to recent mouse and human eQTL