过敏与非过敏儿童室内PM2.5的细胞毒性比较研究

流行病学研究表明,空气细颗粒污染物(PM_(2.5))的暴露与过敏性疾病有一定的联系;然而,PM_(2.5)暴露与过敏性疾病之间的关系尚未完全阐明,特别是室内环境中PM_(2.5)涉及到过敏或非过敏的作用不详.为了比较研究过敏与非过敏儿童室内PM_(2.5)的细胞毒性,在武汉市洪山区10户家庭室内进行了为期3个月的采样,分别收集过敏与非过敏儿童的室内PM_(2.5).采用有机/元素碳测定仪对二者PM_(2.5)成分中的含碳组分进行了分析,并通过检测昆明小鼠巨噬细胞的形态及吞噬功能影响、细胞活力、乳酸脱氢酶(LDH)漏出率等指标,来检测PM_(2.5)暴露所致的细胞毒性.结果表明,高剂量(200μg·mL~(-1))PM_(2.5)暴露对小鼠巨噬细胞的形态及吞噬功能会产生不利的影响;与非过敏儿童的室内PM_(2.5)暴露组相比,过敏儿童的室内PM_(2.5)暴露组诱导巨噬细胞产生的毒性作用更明显.细胞体外测试结果提示:在相同PM_(2.5)暴露剂量下,引起儿童过敏症的室内PM_(2.5)成分具有重要影响.     

Soil selenium concentration and Kashin-Beck disease prevalence in Tibet, China

In order to investigate the correlation between the prevalence of Kashin-Back disease (KBD) and Se concentrations, natural soil samples and cultivated soil samples were collected from southeastern Tibet, China; and the soil Se concentrations were measured by atomic fluorescent spectrophotometer. It was found that the mean Se concentrations of natural soil samples in KBD areas, from the first layer to the third layer, were 0.17 mg/kg, 0.11 mg/kg, and 0.10 mg/kg, respectively, and in nondisease areas were 0.21 mg/kg, 0.24 mg/kg, and 0.13mg/kg, respectively. The mean Se concentrations of cultivated soil samples were 0.10 mg/kg in KBD areas and 0.23 mg/kg in non-disease areas, respectively. Soil Se concentrations in KBD areas were lower than that in non-disease areas, and the mean concentrations of soil Se in Tibet were lower than the average of China (0.29 mg/kg). Therefore, there is a close relationship between soil Se concentrations and KBD in Tibet. More studies should be concentrated on the impacts of Se deficiency in soils and its relationship with Se concentrations in food-grain and the human body in Tibet areas.     

疾病预防控制中心废水处理技术工程实例

疾病预防控制机构废水具有重金属种类繁多、含病原体数量大、间断性排放等特点,通过运用混凝沉淀＋曝气生物滤池（BIOFOR）＋ClO2消毒工艺对其废水进行处理,处理后废水达到《医疗机构水污染物排放标准（》GB18466-2005）排放标准。     

Exploring the association between working memory and driving performance in Parkinson's disease

Objective: The aim of this study was to explore whether varying levels of operational and tactical driving task demand differentially affect drivers with Parkinson's disease (PD) and control drivers in their sign recall.

Methods: Study participants aged between 50 and 70 years included a group of drivers with PD (n = 10) and a group of age- and sex-matched control drivers (n = 10). Their performance in a sign recall task was measured using a driving simulator.

Results: Drivers in the control group performed better than drivers with PD in a sign recall task, but this trend was not statistically significant (P =.43). In addition, regardless of group membership, subjects' performance differed according to varying levels of task demand. Performance in the sign recall task was more likely to drop with increasing task demand (P =.03). This difference was significant when the variation in task demand was associated with a cognitive task; that is, when drivers were required to apply the instructions from working memory.

Conclusions: Although the conclusions drawn from this study are tentative, the evidence presented here is encouraging with regard to the use of a driving simulator to examine isolated cognitive functions underlying driving performance in PD. With an understanding of its limitations, such driving simulation in combination with functional assessment batteries measuring physical, visual, and cognitive abilities could comprise one component of a multitiered system to evaluate medical fitness to drive.     

影响人体硒低的环境因素——陕西渭北高塬大骨节病区的调查

对陕西渭北高塬的调查研究证明,大骨节病发病率不同的相邻村庄内,居民发中的9种重要生命元素,唯硒的含量与各村居民患病率呈极显著的负相关。同时,该病流行地点的人发中各元素含量唯硒低于国内外健康人的发硒水平.通过对病区内不同地貌环境的土壤及饮水类型分布等项研究,阐明了重、中、轻病村交错分布的人体硒低的原因,这对大骨节病的产生与环境通过食物链导致人体硒低有关又再次提出一些新的依据。     

皖江流域及其以南地区的血吸虫病害度区划

皖江流域及其以南地区是安徽省血吸虫病害的主要区域。本文通过对血吸虫病害的孕灾环境,致灾因子和承灾体的分析,探讨了血吸虫病害的区划指标,并进行了病害度分区。     

Effect of ambient polycyclic aromatic hydrocarbons and nicotine on the structure of Aβ42 protein

● B[a]P, nicotine and phenanthrene molecules altered the secondary structure of Aβ₄₂. ● β-content of the peptide was significantly enhanced in the presence of the PAHs. ● Nicotine made stable cluster with Aβ₄₂ peptide via hydrogen bonds. ● Phenanthrene due to its small size, interfered with the Aβ₄₂ monomer more strongly. Recent studies have correlated the chronic impact of ambient environmental pollutants like polycyclic aromatic hydrocarbons (PAHs) with the progression of neurodegenerative disorders, either by using statistical data from various cities, or via tracking biomarkers during in-vivo experiments. Among different neurodegenerative disorders, PAHs are known to cause increased risk for Alzheimer’s disease, related to the development of amyloid beta (Aβ) peptide oligomers. However, the complex molecular interactions between peptide monomers and organic pollutants remains obscured. In this work, we performed an atomistic molecular dynamics study via GROMACS to investigate the structure of Aβ₄₂ peptide monomer in the presence of benzo[a]pyrene, nicotine, and phenanthrene. Interestingly the results revealed strong hydrophobic, and hydrogen-bond based interactions between Aβ peptides and these environmental pollutants that resulted in the formation of stable intermolecular clusters. The strong interactions affected the secondary structure of the Aβ₄₂ peptide in the presence of the organic pollutants, with almost 50 % decrease in the α-helix and 2 %–10 % increase in the β-sheets of the peptide. Overall, the undergoing changes in the secondary structure of the peptide monomer in the presence of the pollutants under the study indicates an enhanced formation of Aβ peptide oligomers, and consequent progression of Alzheimer’s disease.     

Arsenic species in the well water and sediments of the blackfoot disease area in Taiwan

The blackfoot disease (BFD) observed in southwestern Taiwan is due to drinking high arsenic concentrations in well water. This paper presents some results concerning the distributions of arsenic species in water and sediments collected in the BFD (well, river and coastal) area and the background (lake and ocean) area for comparison. The results show that the concentrations of arsenate (870 ± 26 ug/L) and arsenite (70.2 ± 2.6 ug/ L) in well waters, and the contents of arsenic (1640 ug/g) with high percentage of easily reducible (Fe and Mn oxides, 91.7%) and exchangeable and carbonate (4.6%) phases in well sediments were much higher than those in river, lake and coastal samples. Low arsenic (3.46–31.8 ug/g) with high percentages (73.8–97.3%) of detritus and minerals phase with low percentages (0.4–9.8%) of total carbonate and exchangeable phases were found in the river and coastal samples in the BFD area as well as the lake and ocean samples in background area. It might suggest that the higher concentrations of toxic As(III) in well water and arsenic with higher values of easily reducible, carbonate and exchangeable phases in the well sediments, combined with the higher values of dissolved organic carbon, humic and fulvic acids and aromatic carbon as well as the higher fluorescence indensity in the well water are the key factors to cause the BFD in Taiwan.     

Reduced effect of Tasmanian devil facial tumor disease at the disease front

Pathogen-driven declines in animal populations are increasingly regarded as a major conservation issue. The Tasmanian devil (Sarcophilus harrisii) is threatened with extinction by devil facial tumor disease, a unique transmissible cancer. The disease is transmitted through direct transfer of tumor cells, which is possible because the genetic diversity of Tasmanian devils is low, particularly in the major histocompatibility complex genes of the immune system. The far northwest of Tasmania now holds the last remaining disease-free wild devil populations. The recent discovery of unique major histocompatibility complex genotypes in the northwestern region of Tasmania has raised the possibility that some animals may be resilient to the disease. We examined the differences in the epidemiology and population effects of devil facial tumor disease at 3 well-studied affected sites in eastern Tasmania and 1 in western Tasmania (West Pencil Pine). In contrast to the 3 eastern sites, there has been no rapid increase in disease prevalence or evidence of population decline at West Pencil Pine. Moreover, this is the only onsite at which the population age structure has remained unaltered 4 years after the first detection of disease. The most plausible explanations for the substantial differences in population effects and epidemiology of the disease between eastern and western sites are geographic differences in genotypes or phenotypes of devils and functional differences between tumor strains in the 2 regions. We suggest that conservation efforts focus on identifying whether either or both these explanations are correct and then, if resistance alleles exist, to attempt to spread the resistant alleles into affected populations. Such assisted selection has rarely been attempted for the management of wildlife diseases, but it may be widely applicable.