曙光油田节能减排现状调查及对策研究

曙光采油厂随着超稠油的不断开发,生产能耗也随之增加,通过开展节能减排及节能挖潜工作,全厂能耗增长状态得到了良好的控制,能耗总量由2005年的58.21×10~4t标煤下降到2008年的47.75×10~4t标煤;原油(气)液生产单位综合能耗为52.02 kg标煤/t,同期对比减少0.38 kg标煤/t;生产系统运行效率不断提高。文章详细介绍了曙光油田从机采系统、热注系统、集输系统等方面推广应用节能新技术、新产品,达到其投资和运行费用最少,经济性较好,对油田减排挖潜进行了探讨。     

膜蒸馏技术在石化废水处理领域的应用进展

综述了一种新型分离技术——膜蒸馏技术在石化废水处理领域的应用现状,重点介绍了在高盐度废水处理和挥发性有机物废水处理两个方面的进展;指出膜蒸馏应用过程中存在的主要问题是膜污染;预测了膜蒸馏及其集成技术在废水处理领域的发展前景。     

蒽醌染料中间体溴氨酸降解酶的特性

从污染地分离筛选出的菌株BX26对蒽醌染料中间体溴氨酸有显著的降解脱色作用,降解过程受降解酶的控制,试验结果表明,降解酶为溴氨酸诱导的胞外酶,该酶在温度高于50℃处理后失活,盐度对该酶失活有影响,盐度高于1%会显著降低该酶活力,酶对溴氨酸的催化脱色要有氧参加,氮气气氛中酶活受抑制。     

A mini review of fluoride-induced apoptotic pathways

Fluorine or fluoride can have toxic effects on bone tissue and soft tissue at high concentrations. These negative effects include but not limited to cytotoxicity, immunotoxicity, blood toxicity, and oxidative damage. Apoptosis plays an important role in fluoride-induced toxicity of kidney, liver, spleen, thymus, bursa of Fabricius, cecal tonsil, and cultured cells. Here, apoptosis activated by high level of fluoride has been systematically reviewed, focusing on three pathways: mitochondrion-mediated, endoplasmic reticulum (ER) stress-mediated, and death receptor-mediated pathways. However, very limited reports are focused on the death receptor-mediated apoptosis pathways in the fluoride-induced apoptosis. Therefore, understanding and discovery of more pathways and molecular mechanisms of fluoride-induced apoptosis may contribute to designing measures for preventing fluoride toxicity.     

O／W型乳化液的处理

采用药剂破乳－电解破乳工艺处理Ｏ／Ｗ型乳化液，药剂破乳选用聚合硫酸铁为破乳剂，破乳时最佳ＰＨ为８，聚合硫酸铁的最佳投量为１５００ｍｇ／Ｌ，电解破乳选用铁作阳极，铝作阴极，电流密度０．８６Ａ／ｄｍ＾２，极距２５ｍｍ，电解时间３ｈ。在上述条件下，破乳效果良好，出水清澈透明，ＣＯＤ总去除率可达到９６－９７％。     

Effect of acute exposure to PFOA on mouse liver cells in vivo and in vitro

Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction. In serological tests, PFOA-exposed mice showed increased treads of liver functional enzymes in alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin (T-BIL), trypsinase, low density lipoprotein-cholesterol (LDL-C), and insulin, while blood glucose, high density lipoprotein-cholesterol (HDL-C), and glucagon levels were reduced. In histocytological observations, PFOA-exposed liver showed visible cytoplasmic vesicles, and intact pancreatic islets were observed in PFOA-exposed pancreas. Additionally, increased insulin-positive cells and reduced glucagon-positive cells were detected in PFOA-exposed islets. As shown in immunoassays, PFOA-exposed liver resulted in elevations of cluster of differentiation 36 (CD36)-labeled cells and CD36 protein. In mouse liver cell study, PFOA-exposed cells showed increased cell apoptotic count, and increased phosphorylated levels of Bcl-2 and Bad in the cells. Furthermore, PFOA-exposed liver cells exhibited elevations of CD36-labeled cells and CD36 protein. Taken together, the present data demonstrate that acute exposure to PFOA-impaired liver function is associated with inducting CD36 expression and apoptosis, as well as disrupting key hormones in the pancreas.     

Urinary metabolomic profiling in rats exposed to dietary di(2-ethylhexyl) phthalate (DEHP) using ultra-performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS)

Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental chemical with widespread nonoccupational human exposure through multiple ways. Although considerable efforts have been invested to investigate mechanisms of DEHP toxicity, the key metabolic biomarkers of DEHP toxicity remain to be identified. The aim of this study was to assess the urinary metabonomics of dietary DEHP in rats using the technique of ultra-performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS). Fourteen female Wistar rats were divided into two groups and given increasing dietary doses of DEHP for 30 consecutive days. The urinary metabolite profile was studied using ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry. Principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) enabled clusters to be clearly separated. Eleven principal urinary metabolites were identified as contributing to the clusters. The clusters in the positive electrospray ionization (ESI) mode were xanthurenic acid, kynurenic acid, nonate, N6-methyladenosine, and L-isoleucyl-L-proline. The clusters in the negative ESI mode were hippuric acid, tetrahydrocortisol, citric acid, phenylpropionylglycine, cPA(18:2(9Z, 12Z)/0:0), and LysoPC(14:1(9Z)). The urinary metabonomic changes indicated that exposure to dietary DEHP can affect energy-related metabolism, liver and renal function, fatty acid metabolism, and cause DNA damage in rats. The findings of this study on the urinary metabolites and metabolic pathways of DEHP may form the basis for future studies on the mechanisms of toxicity of this commonly found environmental chemical.     

Genetic diversity and population structure of the invasive plant <Emphasis Type="Italic">Solanum rostratum</Emphasis> in China

The level of genetic diversity of 13 Chinese populations of S. rostratum was investigated using nine microsatellite loci. The genetic diversity of the Weisanlu population in Hebei province was the highest and the Hohhot population was the lowest. The genetic differentiation among the populations was highly significant (P < 0.001). A total of 68.54% of the total genetic variation of population was within populations, and the genetic variation between populations accounted for 31.46%. The long-distance dispersal of its seeds by human transport mainly resulted in the rapid dispersal of S. rostratum in China.     

文思湖底泥COD释放规律模拟研究

采用室内模拟实验方法,研究环境因子（温度、pH、扰动强度、供气量）对底泥释放COD的影响。结果表明,水温升高能加速底泥中有机质的释放;上覆水在弱酸至中性条件下底泥释放有机质最低;扰动上覆水体会加快有机质的释放。