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Xu H.,Guangdong Poison Control Center | Wang L.,CAS Changchun Northeast Institute of Geography and Agroecology | Liu G.,Guangdong University of Technology | Zheng L.,Henan Normal University
2010 4th International Conference on Bioinformatics and Biomedical Engineering, iCBBE 2010 | Year: 2010

The joint acute toxicity of chlorpyrifos and batacypermethrin on freshwater protozoan community was examined with the polyurethane foam unit method. Forty-eight-hour LC50 values were 8.72 mg/L for chlorpyrifos and 1.92mg/L for batacypermethrin in individual acute toxicity test. Our data indicated that the extent of toxic interactions of two insecticides showed synergism in 48h exposure. Additive Index (AI) was 2.2 associated to the joint acute toxicity test. In addition, the structure of protozoan community was simplified and the functional-trophic groups changed with the increasing concentration of insecticides. The species and population of Algivores(A) and Predators Raptors (P) reduced but Bactivoresdetrivores(B) became predominant relatively. © 2010 IEEE.

Shuga J.,University of California at Berkeley | Zeng Y.,University of California at Berkeley | Zeng Y.,University of Kansas | Novak R.,University of California at San Francisco | And 10 more authors.
Nucleic Acids Research | Year: 2013

Cancers are heterogeneous and genetically unstable. New methods are needed that provide the sensitivity and specificity to query single cells at the genetic loci that drive cancer progression, thereby enabling researchers to study the progression of individual tumors. Here, we report the development and application of a bead-based hemi-nested microfluidic droplet digital PCR (dPCR) technology to achieve 'quantitative' measurement and single-molecule sequencing of somatically acquired carcinogenic translocations at extremely low levels (<10-6) in healthy subjects. We use this technique in our healthy study population to determine the overall concentration of the t(14;18) translocation, which is strongly associated with follicular lymphoma. The nested dPCR approach improves the detection limit to 1 × 10-7 or lower while maintaining the analysis efficiency and specificity. Further, the bead-based dPCR enabled us to isolate and quantify the relative amounts of the various clonal forms of t(14;18) translocation in these subjects, and the single-molecule sensitivity and resolution of dPCR led to the discovery of new clonal forms of t(14;18) that were otherwise masked by the conventional quantitative PCR measurements. In this manner, we created a quantitative map for this carcinogenic mutation in this healthy population and identified the positions on chromosomes 14 and 18 where the vast majority of these t(14;18) events occur. © 2013 The Author(s).

Hosgood H.D.,U.S. National Cancer Institute | Zhang L.,University of California at Berkeley | Tang X.,Guangdong Poison Control Center | Vermeulen R.,University Utrecht | And 23 more authors.
American Journal of Industrial Medicine | Year: 2013

Background: Formaldehyde is used in many occupational settings, most notably in manufacturing, health care, and embalming. Formaldehyde has been classified as a human carcinogen, but its mechanism of action remains uncertain. Methods: We carried out a cross-sectional study of 43 formaldehyde-exposed workers and 51 unexposed age and sex-matched controls in Guangdong, China to study formaldehyde's early biologic effects. To follow up our previous report that the total lymphocyte count was decreased in formaldehyde-exposed workers compared with controls, we evaluated each major lymphocyte subset (i.e., CD4+ T cells, CD8+ T cells, natural killer [NK] cells, and B cells) and T cell lymphocyte subset (CD4+ naïve and memory T cells, CD8+ naïve and memory T cells, and regulatory T cells). Linear regression of each subset was used to test for differences between exposed workers and controls, adjusting for potential confounders. Results: Total NK cell and T cell counts were about 24% (P=0.037) and 16% (P=0.0042) lower, respectively, among exposed workers. Among certain T cell subsets, decreased counts among exposed workers were observed for CD8+ T cells (P=0.026), CD8+ effector memory T cells (P=0.018), and regulatory T cells (CD4+FoxP3+: P=0.04; CD25+FoxP3+: P=0.008). Conclusions: Formaldehyde-exposed workers experienced decreased counts of NK cells, regulatory T cells, and CD8+ effector memory T cells; however, due to the small sample size; these findings need to be confirmed in larger studies. © 2012 Wiley Periodicals, Inc.

Bassig B.A.,U.S. National Cancer Institute | Zhang L.,University of California at Berkeley | Vermeulen R.,University Utrecht | Tang X.,Guangdong Poison Control Center | And 23 more authors.
Carcinogenesis | Year: 2016

Benzene, formaldehyde (FA) and trichloroethylene (TCE) are ubiquitous chemicals in workplaces and the general environment. Benzene is an established myeloid leukemogen and probable lymphomagen. FA is classified as a myeloid leukemogen but has not been associated with non-Hodgkin lymphoma (NHL), whereas TCE has been associated with NHL but not myeloid leukemia. Epidemiologic associations between FA and myeloid leukemia, and between benzene, TCE and NHL are, however, still debated. Previously, we showed that these chemicals are associated with hematotoxicity in cross-sectional studies of factory workers in China, which included extensive personal monitoring and biological sample collection. Here, we compare and contrast patterns of hematotoxicity, monosomy 7 in myeloid progenitor cells (MPCs), and B-cell activation biomarkers across these studies to further evaluate possible mechanisms of action and consistency of effects with observed hematologic cancer risks. Workers exposed to benzene or FA, but not TCE, showed declines in cell types derived from MPCs, including granulocytes and platelets. Alterations in lymphoid cell types, including B cells and CD4+ T cells, and B-cell activation markers were apparent in workers exposed to benzene or TCE. Given that alterations in myeloid and lymphoid cell types are associated with hematological malignancies, our data provide biologic insight into the epidemiological evidence linking benzene and FA exposure with myeloid leukemia risk, and TCE and benzene exposure with NHL risk. © The Author 2016. Published by Oxford University Press 2016.

Vermeulen R.,University Utrecht | Zhang L.,University of California at Berkeley | Spierenburg A.,University Utrecht | Tang X.,Guangdong Poison Control Center | And 21 more authors.
Carcinogenesis | Year: 2012

Epidemiological studies suggest that trichloroethylene (TCE) exposure may be associated with renal cancer. The biological mechanisms involved are not exactly known although nephrotoxicity is believed to play a role. Studies on TCE nephrotoxicity among humans, however, have been largely inconsistent. We studied kidney toxicity in Chinese factory workers exposed to TCE using novel sensitive nephrotoxicity markers. Eighty healthy workers exposed to TCE and 45 comparable unexposed controls were included in the present analyses. Personal TCE exposure measurements were taken over a 2-week period before urine collection. Ninety-six percent of workers were exposed to TCE below the current US Occupational Safety and Health Administration permissible exposure limit (100 ppm 8h TWA), with a mean (SD) of 22.2 (35.9) ppm. Kidney injury molecule-1 (KIM-1) and Pi-glutathione S transferase (GST) alpha were elevated among the exposed subjects as compared with the unexposed controls with a strong exposure-response association between individual estimates of TCE exposure and KIM-1 (P < 0.0001). This is the first report to use a set of sensitive nephrotoxicity markers to study the possible effects of TCE on the kidneys. The findings suggest that at relatively low occupational exposure levels a toxic effect on the kidneys can be observed. This finding supports the biological plausibility of linking TCE exposure and renal cancer. Abbreviations: GSTglutathione-S-transferase. KIM-1kidney injury molecule-1. NAGN-acetyl-beta-(d)-glucosaminidaseOVMorganic vapour monitoring. TCEtrichloroethylene. VEGFvascular endothelial growth factor. © The Author 2012. Published by Oxford University Press. All rights reserved.

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