摘要：
The impacts of ambient PM2.5 on public health have become great concerns worldwide, especially in the developing countries. Epidemiological and toxicological studies have shown that PM2.5 does not only induce cardiopulmonary disorders and/or impairments, but also contributes to a variety of other adverse health effects, such as driving the initiation and progression of diabetes mellitus and eliciting adverse birth outcomes. Of note, recent findings have demonstrated that PM2.5 may still pose a hazard to public health even at very low levels (far below national standards) of exposure. The proposed underlying mechanisms whereby PM2.5 causes adverse effects to public health include inducing intracellular oxidative stress, mutagenicity/genotoxicity and inflammatory responses. The present review aims to provide an brief overview of new insights into the molecular mechanisms linking ambient PM2.5 exposure and health effects, which were explored with new technologies in recent years. (C) 2016 Elsevier Inc. All rights reserved.
期刊：
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer,2013年1836(2):197-210 ISSN：0304-419X
通讯作者：
Feng, Shaolong
作者机构：
[Feng, Shaolong] Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.;[Cao, Zhaohui] Univ South China, Sch Pharm & Life Sci, Hengyang 421001, Peoples R China.;[Wang, Xinming] Chinese Acad Sci, Guangzhou Inst Geochem, State Key Lab Organ Geochem, Guangzhou 510640, Guangdong, Peoples R China.
通讯机构：
[Feng, Shaolong] Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.
关键词：
Aryl hydrocarbon receptor (AHR);Cancer
摘要：
Aryl hydrocarbon receptor (AHR), a cytosolic ligand-activated transcription factor, belongs to the member of bHLH/PAS family of heterodimeric transcriptional regulators and is widely expressed in a variety of animal species and humans. Recent animal and human data suggested that AHR is involved in various signaling pathways critical to cell normal homeostasis, which covers multiple aspects of physiology, such as cell proliferation and differentiation, gene regulation, cell motility and migration, inflammation and others. Dysregulation of these physiological processes is known to contribute to events such as tumor initiation, promotion, and progression. Increasing epidemiological and experimental animal data provided substantial support for an association between abnormal AHR function and cancer, implicating AHR may be a novel drug-interfering target for cancers. The proposed underlying mechanisms of its actions in cancer involved multiple aspects, (a) inhibiting the functional expression of the key anti-oncogenes (such as p53 and BRCA1), (b) promoting stem cells transforming and angiogenesis, (c) altering cell survival, proliferation and differentiation by influencing the physiologic processes of cell-cycle, apoptosis, cell contact-inhibition, metabolism and remodel of extracellular matrix, and cell-matrix interaction, (d) cross-talking with the signaling pathways of estrogen receptor and inflammation. This review aims to provide a brief overview of recent investigations into the role of AHR and the underlying mechanisms of its actions in cancer, which were explored by the new technologies emerging in recent years. (C) 2013 Elsevier B.V. All rights reserved.
期刊：
Journal of Nanoscience and Nanotechnology,2010年10(8):4868-4874 ISSN：1533-4880
通讯作者：
Yuan, Yali
作者机构：
[Yuan, Yali; Deng, Jian] Univ S China, Sch Chem & Chem Engn, Hengyang 421001, Peoples R China.;[Ding, Jianqiang] Zhenhai Ctr Dis Control & Prevent, Ningbo 315200, Peoples R China.;[Xu, Jinsheng] Hengyang Normal Univ, Dept Chem & Mat Sci, Hengyang 421008, Peoples R China.;[Guo, Jianbo] Univ S China, Sch Publ Hlth, Hengyang 421001, Peoples R China.
通讯机构：
[Yuan, Yali] Univ S China, Sch Chem & Chem Engn, Hengyang 421001, Peoples R China.
会议主办单位：
(1) School of Chemistry and Chemical Engineering, University of South China, Hengyang 421001, China; (2) Zhenhai Center for Disease Control and Prevention, Ningbo 315200, China; (3) Department of Chemistry and Materials Science, Hengyang Normal University, Hengyang 421008, China; (4) School of Public Health, University of South China, Hengyang 421001, China
作者机构：
[Rang, Wei-Qing; Huang, Bo; Tu, Wen-Zhi; Tang, Yan; Zhou, Ping-Kun] Univ South China, Coll Publ Hlth, Inst Environm Med & Radiat Hyg, Hengyang 421000, Hunan, Peoples R China.;[Wang, Yu; Guan, Hua; Zhang, Shi-Meng; Tu, Wen-Zhi; Liu, Xiao-Dan; Zhou, Ping-Kun; Li, Bing] Beijing Inst Radiat Med, Dept Radiat Toxicol & Oncol, Beijing 100850, Peoples R China.;[Rang, Wei-Qing] Univ South China, Coll Publ Hlth, Inst Environm Med & Radiat Hyg, 28 Changsheng West Rd, Hengyang 421000, Hunan, Peoples R China.
通讯机构：
[Rang, Wei-Qing] Univ South China, Coll Publ Hlth, Inst Environm Med & Radiat Hyg, 28 Changsheng West Rd, Hengyang 421000, Hunan, Peoples R China.
关键词：
γH2AX;CHK2;DNA-PKcs;DNA damage;Mitosis
摘要：
Phosphorylated H2AX is considered to be a biomarker for DNA double-strand breaks (DSB), but recent evidence suggests that gamma H2AX does not always indicate the presence of DSB. Here we demonstrate the bimodal dynamic of H2AX phosphorylation induced by ionizing radiation, with the second peak appearing when G2/M arrest is induced. An increased level of gamma H2AX occurred in mitotic cells, and this increase was attenuated by DNA-PKcs inactivation or Chk2 depletion, but not by ATM inhibition. The phosphorylation-mimic CHK2-T68D abrogated the attenuation of mitotic gamma H2AX induced by DNA-PKcs inactivation. Thus, the DNA-PKcs/CHK2 pathway mediates the mitotic phosphorylation of H2AX in the absence of DNA damage. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
作者：
Ling, H. -y.;Hu, B.;Hu, X. -b.;Zhong, J.;Feng, S. -d.;Qin, L.;Liu, G.;Wen, G. -b.;Liao, D. -f.*
期刊：
Experimental and Clinical Endocrinology & Diabetes,2012年120(9):553-559 ISSN：0947-7349
通讯作者：
Liao, D. -f.
作者机构：
[Ling, H. -y.; Hu, B.] Univ S China, Sch Med, Dept Physiol, Hengyang, Peoples R China.;[Liao, D. -f.] Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hu, Div Stem Cell Regulat & Applicat, Changsha 410208, Hunan, Peoples R China.;[Ling, H. -y.] Univ S China, Ctr Basic Med Postdoctoral Studies, Hengyang, Peoples R China.;[Hu, X. -b.] Univ S China, Sch Life Sci & Technol, Dept Biochem & Mol Biol, Hengyang, Peoples R China.;[Wen, G. -b.; Zhong, J.] Univ S China, Affiliated Hosp 1, Inst Clin Res, Hengyang, Peoples R China.
通讯机构：
[Liao, D. -f.] Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hu, Div Stem Cell Regulat & Applicat, Changsha 410208, Hunan, Peoples R China.
摘要：
Silver nanoparticles (AgNPs) attract considerable public attention both for their antimicrobial properties and their potential adverse effects. In the present study, endoplasmic reticulum (ER) stress was used as a sensitive and early biomarker to evaluate the toxic potential of AgNPs in three different human cell lines in vitro and in vivo in mice. In 16HBE cells, the activation of ER stress signaling pathway was observed by upregulated expression including xbp-1s, chop/DDIT3, TRIB3, ADM2, BIP, Caspase-12, ASNS and HERP at either the mRNA and/or protein levels. However, these changes were not observed in HUVECs or HepG2 cells. Furthermore, mice experiments showed that different tissues had various sensitivities to AgNPs following intratracheal instillation exposure. The lung, liver and kidney showed significant ER stress responses, however, only the lung and kidney exhibited apoptosis by TUNEL assay. The artery and tracheal tissues had lower ER stress and apoptosis after exposure. The lowest observable effect concentrations (LOEC) were proposed based on evaluation of AgNP induced ER stress response in cell and mouse models. In summary, preliminary evaluation of AgNP toxicity by monitoring the ER stress signaling pathway provides new insights toward the understanding the biological impacts of AgNPs. The adverse effects of exposure to AgNPs may be avoided by rational use within the safe dose. (C) 2015 Elsevier Ltd. All rights reserved.
摘要：
A novel sensitive method has been developed for the detection of adenosine (AD) in human urine by using enhanced resonance light scattering (RLS). This method is based on the specific recognition and signal amplification of adenosine aptamer (Apt) coupled with gold nanoparticles (GNPs) via G-quartet-induced nanoparticle assembly, which was fabricated by triggering a structure switching of the 3' terminus G-rich sequence and aptamer duplex. RLS signal linearly correlated with the concentration of adenosine over the range of 6-115 nM. The limit of detection (LOD) for adenosine is 1.8 nM with relative standard deviations (RSD) of 2.90-4.80% (n = 6). The present method has been successfully applied to determination of adenosine in real human urine, and the obtained results were in good agreement with those obtained by the HPLC method. Our investigation shows that the combination of the excellent selectivity of aptamer with the high sensitivity of the RLS technique could provide a promising potential for aptamer-based small molecule detection, and be beneficial in extending the application of RLS. (C) 2009 Elsevier Inc. All rights reserved.
摘要：
A novel signal enhanced liquid crystal biosensor based on using AuNPs for highly sensitive DNA detection has been developed. This biosensor not only significantly decreases the detection limit, but also offers a simple detection process and shows a good selectivity to distinguish perfectly matched target DNA from two-base mismatched DNA.
摘要：
BACKGROUND: Small non-coding RNAs (sRNAs) facilitate host-microbe interactions. They have a central function in the post-transcriptional regulation during pathogenic lifestyles. Hfq, an RNA-binding protein that many sRNAs act in conjunction with, is required for Y. pestis pathogenesis. However, information on how Yersinia pestis modulates the expression of sRNAs during infection is largely unknown. METHODOLOGY AND PRINCIPAL FINDINGS: We used RNA-seq technology to identify the sRNA candidates expressed from Y. pestis grown in vitro and in the infected lungs of mice. A total of 104 sRNAs were found, including 26 previously annotated sRNAs, by searching against the Rfam database with 78 novel sRNA candidates. Approximately 89% (93/104) of these sRNAs from Y. pestis are shared with its ancestor Y. pseudotuberculosis. Ninety-seven percent of these sRNAs (101/104) are shared among more than 80 sequenced genomes of 135 Y. pestis strains. These 78 novel sRNAs include 62 intergenic and 16 antisense sRNAs. Fourteen sRNAs were selected for verification by independent Northern blot analysis. Results showed that nine selected sRNA transcripts were Hfq-dependent. Interestingly, three novel sRNAs were identified as new members of the transcription factor CRP regulon. Semi-quantitative analysis revealed that Y. pestis from the infected lungs induced the expressions of six sRNAs including RyhB1, RyhB2, CyaR/RyeE, 6S RNA, RybB and sR039 and repressed the expressions of four sRNAs, including CsrB, CsrC, 4.5S RNA and sR027. CONCLUSIONS AND SIGNIFICANCE: This study is the first attempt to subject RNA from Y. pestis-infected samples to direct high-throughput sequencing. Many novel sRNAs were identified and the expression patterns of relevant sRNAs in Y. pestis during in vitro growth and in vivo infection were revealed. The annotated sRNAs accounted for the most abundant sRNAs either expressed in bacteria grown in vitro or differentially expressed in the infected lungs. These findings suggested these sRNAs may have important functions in Y. pestis physiology or pathogenesis.
摘要：
Numerous studies have indicated the neurotoxicity of perfluorooctane sulfonate (PFOS), a persistent and bioaccumulative compound, particularly during developmental stages of higher organisms. To explore the pro-inflammatory effect in the developmental neurotoxicity, effects of prenatal exposure to PFOS on glial activation in hippocampus and cortex were examined in offspring rats. Dams received 0.1, 0.6 and 2.0 mg/kg bw PFOS by gavage from gestational day 2 (GD2) to GD21. Astrocyte activation markers, glial fibrillary acidic protein (GFAP) and 5100 calcium binding protein B (s-100 beta) in hippocampus and cortex were both upregulated on postnatal day 0 (PNDO) or PND21. In addition, the astrocyte activation was accompanied with the elevation of pro-inflammatory cytokines interleukin (IL-1 beta) and tumor necrosis factor (TNF)-alpha. The mRNA levels of pro-inflammatory transcription factors, including activation protein-1 (AP-1), nuclear factor-kappa B (NF-kappa B), and cAMP response element-binding protein (CREB) were also increased, at least in the 2.0 mg/kg group. In addition to the inflammatory response, two synaptic proteins, synapsin 1 (Syn1) and synaptophysin (Syp) were reduced in cortex on PNDO and PND21. In hippocampus, the Syn1 were also reduced, while the Syp were increased in cortex on either PNDO or PND21. Obtained results indicated chronic glial activation with coexisting inflammatory and synapse injury features as a new mechanism of PFOS developmental neurotoxicity, and enhanced expression of AP-1, NF-kappa B and CREB may contributed to the adverse effect. (C) 2010 Elsevier Inc. All rights reserved.
摘要：
Flood is one of the most common and severe forms of natural disasters. Posttraumatic stress disorder (PTSD) is a common disorder among victims of various disasters including flood. Early prediction for PTSD could benefit the prevention and treatment of PTSD. This study aimed to establish a prediction model for the occurrence of PTSD among adults in flood districts. A cross-sectional survey was carried out in 2000 among individuals who were affected by the 1998 floods in Hunan, China. Multi-stage sampling was used to select subjects from the flood-affected areas. Data was collected through face-to-face interviews using a questionnaire. PTSD was diagnosed according to DSM-IV criteria. Study subjects were randomly divided into two groups: group 1 was used to establish the prediction model and group 2 was used to validate the model. We first used the logistic regression analysis to select predictive variables and then established a risk score predictive model. The validity of model was evaluated by using the model in group 2 and in all subjects. The area under the receiver operation characteristic (ROC) curve was calculated to evaluate the accuracy of the prediction model. A total of 2336 (9.2%) subjects were diagnosed as probable PTSD-positive individuals among a total of 25,478 study subjects. Seven independent predictive factors (age, gender, education, type of flood, severity of flood, flood experience, and the mental status before flood) were identified as key variables in a risk score model. The area under the ROC curve for the model was 0.853 in the validation data. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of this risk score model were 84.0%, 72.2%, 23.4%, and 97.8%, respectively, at a cut-off value of 67.5 in the validation data. A simple risk score model can be used to predict PTSD among victims of flood.
期刊：
Research in Microbiology,2012年163(6-7):413-418 ISSN：0923-2508
通讯作者：
Yang, Ruifu
作者机构：
[Zhang, Yiquan; Zhao, Xiangna; Deng, Zhongliang; Liu, Zizhong; Han, Yanping; Ji, Xiaolan; Meng, Xiangrong; Su, Shanchun; Yang, Ruifu; Wang, Xiaoyi] Beijing Inst Microbiol & Epidemiol, State Key Lab Pathogen & Biosecur, Beijing 100071, Peoples R China.;[Deng, Zhongliang; Yang, Ruifu] So Med Univ, Guangzhou 510450, Guangdong, Peoples R China.;[Deng, Zhongliang] Univ S China, Sch Publ Hlth, Dept Sanit Inspect, Changsha 421001, Hunan, Peoples R China.;[Ji, Xiaolan; Meng, Xiangrong] Jiangsu Univ, Dept Biochem & Mol Biol, Zhenjiang 212013, Jiangsu, Peoples R China.;[Su, Shanchun] Sichuan Agr Univ, Microbiol Lab, Chengdu 625014, Sichuan, Peoples R China.
通讯机构：
[Yang, Ruifu] Beijing Inst Microbiol & Epidemiol, State Key Lab Pathogen & Biosecur, Beijing 100071, Peoples R China.
关键词：
Yersinia pestis;RyhB;Hfq-dependent stability
摘要：
Small non-coding RNAs (sRNAs) have been shown to modulate gene expression at the post-transcriptional level. RyhB, an iron-responsive sRNA, is conserved in Escherichia coli and other Enterobacteriae, indicating the downregulation of numerous genes during iron depletion. This sRNA is tightly regulated by the ferric uptake regulator (Fur) and interacts with the RNA binding protein Hfq. Hfq is generally purported to be essential for stabilizing sRNAs and promoting sRNA-mRNA duplex formation. Maintenance of iron homeostasis is an essential step in the lifecycle of Yersinia pestis. Y. pestis encodes two RyhB homologs, RyhB1 and RyhB2. In this study, we found that as in the case of E. colt, both RyhB homologs in Y. pestis are negatively regulated by Fur and have a half-life of >30 min. In the absence of Hfq, RyhB1 is rapidly degraded, while RyhB2 retains its stability. RyhB I stabilization is mediated by Hfq, but RyhB2 does not require Hfq for stability. Additionally, both RyhBs are upregulated in lungs infected with Y. pestis, while the ryhB mutant shows no visible effects on virulence in mice upon either subcutaneous or intranasal inoculation. Collectively, our results indicate that the two RyhB homologs have common regulatory features in Y. pestis-infected lungs and in vitro, but that stability of RyhB1 and RyhB2 is differentially dependent on Hfq. (c) 2012 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
