Detection of RASSF1A promoter hypermethylation in serum from gastric and colorectal adenocarcinoma patients

AIM：To evaluate the diagnostic role of serum RASSF1A promoter hypermethylation in gastric and colorectal adenocarcinoma. METHODS：Methylation-specific polymerase chain reaction （MSPCR） was used to examine the promoter methylation status of the serum RASSF1A gene in 47 gastric adenocarcinoma patients, 45 colorectal adenocarcinoma patients, 60 patients with benign gastrointestinal disease （30 with benign gastric disease and 30 with benign colorectal disease）, and 30 healthy donor controls. Apaired study of RASSF1A promoter methylation status in primary tumor, adjacent normal tissue, and postopertive serum were conducted in 25 gastric and colorectal adenocarcinoma patients who later were underwent surgical therapy. RESULTS：The frequencies of detection of serum RASSF1A promoter hypermethylation in gastric （34.0%） and colorectal （28.9%） adenocarcinoma patients were significantly higher than those in patients with benign gastric （3.3%） or colorectal （6.7%） disease or in healthy donors （0%） （P 〈 0.01）. The methylation status of RASSF1A promoter in serum samples was consistent with that in paired primary tumors, and the MSPCR results for RASSF1A promoter methylation status in paired preoperative samples were consistent with those in postoperative serum samples. The serum RASSF1A promoter hypermethylation did not correlate with patient sex, age, tumor differentiation grade, surgical therapy, or serum carcinoembryonic antigen level. Although the serum RASSF1A promoter hypermethylation frequency tended to be higher in patients with distant metastases, there was no correlation between methylation status and metastasis. CONCLUSION：Aberrant CpG island methylation within the promoter region of RASSF1A is a promising biomarker for gastric and colorectal cancer.

Hepatitis B virus x gene and cyanobacterial toxins promote aflatoxin B_1-induced hepatotumorigenesis in mice

AIM： To assess the combinative role of aflatoxin B1 （AFB1）, cyanobacterial toxins （cyanotoxins）, and hepatitis B virus （HBV） x gene in hepatotumorigenicity. METHODS： One-week-old animals carrying HBV x gene and their wild-type littermates were intraperitoneally （ip） injected with either single-dose AFB1 [6 mg/kg body weight （bw）], repeated-dose cyanotoxins （microcystin- LR or nodularin, 10 μg/kg bw once a week for 15 wk）, DMSO （vehicle control） alone, or AFB1 followed by cyanotoxins a week later, and were sacrificed at 24 and 52 wk post-treatment. RESULTS： AFB1 induced liver tumors in 13 of 29 （44.8%） transcjenic mice at 52 wk post-treatment, significantly more frequent than in wild-type mice （13.3%）. This significant difference was not shown in the 24-wk study. Compared with AFB1 exposure alone, MC-LR and nodularin yielded approximately 3-fold and 6-fold increases in the incidence of AFB1-induced liver tumors in wild-type animals at 24 wk, respectively. HBV x gene did not further elevate the risk associated with coexposure to AFB1 and cyanotoxins. With the exception of an MC-LR-dosed wild-type mouse, no liver tumor was observed in mice treated with cyanotoxins alone at 24 wk. Neither DMSO-treated transgenic mice nor their wild-type littermates had pathologic alterations relevant to hepatotumorigenesis in even up to 52 wk. CONCLUSION： HBV x gene and nodularin promote the development of AFB1-induced liver tumors. Co-exposure to AFB1 and MC-LR tends to elevate the risk of liver tumors at 24 wk relative to exposure to one of them. The combinative effect of AFB1, cyanotoxins and HBVx on hepatotumorigenesis is weak at 24 wk.

Contribution of Soil Lead to Blood Lead in Children: A Study from New Orleans, LA

In recent years, a significant number of environmental studies have been conducted in New Orleans, LA and surrounding Gulf Coast areas due in part to the occurrence of hurricanes Katrina and Rita. Data collected from studies in the New Orleans area indicate that inorganic contaminants including arsenic (As), iron (Fe), lead (Pb), and vanadium (V);high concentration of bioaerosols, particularly Cladosporium and Aspergillus, and several organic pollutants (PAHs, pesticides, and volatiles) may pose a risk to human health in New Orleans. While many of these results resemble historical data, a current quantitative exposure assessment has not been conducted. We engaged in one such assessment for lead (Pb) contamination in surface soils. We used Pb concentrations in surface soils ( μg/day to 102 μg/day for our study area within urbanNew Orleans. These data are concerning because children exposed to >33.5 μg/d Pb may cause their blood-Pb levels to exceed the Centers for Disease Control and Prevention (CDC) threshold for blood-Pb of 10 μg/dL. It has generally been accepted that a more protective blood Pb concentration threshold of 6 - μg/dL is warranted. Using the 6-μg/dL threshold puts children exposed to as little as 20.2 μg/day Pb at risk.

Health implications of engineered nanoparticles in infants and children

Background:The nanotechnology boom and the ability to manufacture novel nanomaterials have led to increased production and use of engineered nanoparticles(ENPs).However,the increased use of various ENPs inevitably results in their release in or the contamination of the environment,which poses significant threats to human health.In recent years,extraordinary economic and societal benefits of nanoproducts as well as their potential risks have been observed and widely debated.To estimate whether ENPs are safe from the onset of their manufacturing to their disposal,evaluation of the toxicological effects of ENPs on human exposure,especially on more sensitive and vulnerable sectors of the population(infants and children)is essential.Data sources:Papers were obtained from PubMed,Web of Science,and Google Scholar.Literature search words included:"nanoparticles","infants","children","exposure","toxicity",and all relevant cross-references.Results:A brief overview was conducted to 1)characterize potential exposure routes of ENPs for infants and children;2)describe the vulnerability and particular needs of infants and children about ENPs exposure;3)investigate the current knowledge about the potential health hazards of ENPs;and 4)provide suggestions for future research and regulations in ENP applications.Conclusions:As the manufacturing and use of ENPs become more widespread,directed and focused studies are necessary to measure actual exposure levels and to determine adverse health consequences in infants and children.

食管癌危险因素的病例对照研究

目的:探讨食管癌高发区——淮安市楚州区居民的食管癌危险因素。方法:采用以人群为基础的1?2匹配的病例对照研究方法,用专门设计的调查表对207例食管癌病例及414例正常对照者进行1对1的询问调查,采用条件logistic回归分析法对所获得的调查资料进行统计学分析。结果:人均月收入低、体质指数(body mass index,BMI)偏低、既往食管病变、不按时就餐、10年前喜食辣食、10年前喜食烫食、喜食肥肉、不食大蒜和肿瘤家族史等可能是食管癌的危险因素。结论:饮食习惯、人均月收入、既往食管病变等因素可影响食管癌的发生,应针对相关危险因素采取相应的预防措施。

市售花生、玉米中黄曲霉毒素与伏马菌素污染水平调查

[目的]了解南京市市售花生、玉米及其制品的黄曲霉毒素(aflatoxin,AFT)和伏马菌素B(FumonisinB,FB)的污染水平,就两者的联合污染水平进行探讨。[方法]收集南京市超市和农贸市场的部分花生、玉米及其制品,采用ELISA法测定FB与黄曲霉毒素B(1AFB1)的含量。[结果]超市所采集的19份样品AFB1的检出率为68%,平均含量为0.53μg/kg,FB的检出率为21%,平均含量为0.56mg/kg。农贸市场所采集的49份样品AFB1的检出率为59%,平均含量为6.98μg/kg,FB的检出率为76%,平均含量为9.89mg/kg。所有玉米及其制品样品AFB1和FB的联合污染率为33%,其中超市样品的联合污染率为21%,农贸市场样品的联合污染率为38%。[结论]南京市市售花生、玉米及其制品中存在AFB1和FB的污染,且玉米及其制品存在联合污染问题。

淮安楚州居民饮食、行为因素与食管癌关系的病例-对照研究

目的探讨淮安市楚州区居民的饮食、行为因素与食管癌高发的关系。方法进行1∶1配对病例-对照研究,对107例食管癌病例及对照进行问卷调查,采用条件Logistic回归对所获资料进行统计分析。结果进食速度快、喜食咸辣、腌制品、十年前粮食霉变可能是食管癌的危险因素;而饮茶和摄入豆制品则具有保护作用。结论食管癌是多种环境因素对具有不同遗传素质的个体长期反复作用的结果,宜采取综合性防治措施。

青海省兴海县大骨节病病户主食中T-2毒素的检测

为了解大骨节病重病区唐乃亥乡上鹿圈村、下鹿圈村病户主食中T 2毒素的污染状况 ,在两村分别选择病户 19名 ,每户收集小麦及面粉样品各 1份 ,用ELISA法检测样品中T 2毒素的含量。上鹿圈村面粉、小麦中T 2毒素阳性率均为 89 5 % (17 19) ,平均含量分别为 70 7μg kg(8～2 0 1μg kg)、2 37 1μg kg(5～ 5 43μg kg) ;下鹿圈村面粉、小麦中T 2毒素阳性率均为 6 8 4 % (13 19) ,平均含量分别为 13 0 μg kg(9～ 197μg kg)、4 0 0 μg kg(19～ 333μg kg)。其中 2个采样点T 2毒素的阳性率和含量差异均存在显著性 ,2种样品T 2毒素的含量差异也存在显著性 (P <0 0 5 )。小麦中T 2毒素的污染情况比面粉严重 ,上鹿圈村主食中T 2毒素的污染情况比下鹿圈村严重 ,具体原因有待进一步研究。

时间序列分析法在香港结核病预测中的应用

目的阐述ARIMA模型拟合时间序列的方法和步骤,并将其应用于结核病的预测,为传染病预警系统提供决策依据。方法利用SPSS统计软件对香港1997年到2008年结核病数据进行基本趋势分析并检验数据的平稳性,对平稳处理后的时间序列构建ARIMA模型,并对所建立的模型进行相关性检验,预测出未来一年的数据。结果通过对结核病的预测,相对误差在3%左右,预测效果较为可靠。结论在结核病的近期预测中引入时间序列的ARIMA模型分析方法 ,能够对结核病的预测产生积极的指导意义。

空气燃烧排放提取物小鼠致肺癌作用(英文)

目的 评价 6种具有致突变作用的空气燃烧排放提取物的致肺癌作用。方法 用CD 1小鼠肺瘤生物测试方法 ,在小鼠断奶前处理受试物 3次 ,6个月后观察肿瘤的发生率和病理组织学改变。并以苯并芘作为阳性对照。结果 6种具有突变作用的空气燃烧排放提取物均具有致肺癌作用 ,并呈剂量 效应关系 。

Role of cellular reprogramming and epigenetic dysregulation in acquired chemoresistance in breast cancer

Acquired resistance to chemotherapy is a major limitation in clinical treatment for breast cancer.Accumulating evidence from in vitro,in vivo and clinical studies suggest that acquired chemoresistance is progressive,multifactorial and involve genetic and epigenetic aberrations.Among various mechanisms that contribute to chemoresistance,cellular reprogramming has extensively been implicated in breast cancer resistance lately.Cellular reprogramming events such as acquisition of epithelial to mesenchymal transition(EMT)and cancer stemness(CSCs)not only provide cancer cells with reversible phenotypic plasticity and survival advantage against cytotoxicity but also leads to aggressiveness,metastasis,clinical resistance,tumor recurrence and poor survival.The transient and reversible nature of cellular reprogramming processes and their controlled interaction with epigenetic regulatory complexes strongly support the involvement of dynamic epigenetic regulatory network in governing the cellular reprogramming and associated acquired chemoresistance.Further,epigenetic modulations are also gaining interest as promising interventions addressing the cancer cell reprogramming machinery to overcome acquired chemoresistance.This review discusses the previous reports and our recent findings that lead to current understanding of epigenetic dysregulation dictating the cellular reprogramming processes such as acquisition of EMT and CSCs phenotype and how they co-ordinate to establish acquired drug resistance in breast cancer.

Evolutionary responses to climate change and contaminants： Evidence and experimental approaches

A fundamental objective within ecotoxicology lies in understanding and predicting effects of contaminants. This ob- jective is made more challenging when global climate change is considered as an environmental stress that co-occurs with con- taminant exposure. In this multi-stressor context, evolutionary processes are particularly important. In this paper, we consider several non-＂omic＂ approaches wherein evolutionary responses to stress have been studied and discuss those amenable to a mul- tiple stressor context. Specifically, we discuss common-garden designs, artificial and quasi-natural selection, and the estimation of adaptive potential using quantitative genetics as methods for studying evolutionary responses to contaminants and climate change in the absence of expensive molecular tools. While all approaches shed light on potential evolutionary impacts of stressor exposure, they also have limitations. These include logistical constraints, difficulty extrapolating to real systems, and responses tied strongly to specific taxa, populations, and/or testing conditions. The most effective way to lessen these inherent limitations is likely through inclusion of complementary physiological and molecular tools, when available. We believe that an evolutionary context to the study of contaminants and global climate change is a high priority in ecotoxicology and we outline methods that can be implemented by almost any researcher but will also provide valuable insights [Current Zoology 61 （4）： 690-701, 2015].

The dynamics of murine mammary stem/progenitor cells

The stem/progenitor cells in the murine mammary gland are a highly dynamic population of cells that are responsible for ductal elongation in puberty, homeostasis maintenance in adult, and lobulo-alveolar genesis during pregnancy. In recent years understanding the epithelial cell hierarchy within the mammary gland is becoming particularly important as these different stem/progenitor cells were perceived to be the cells of origin for various subtypes of breast cancer. Although significant advances have been made in enrichment and isolation of stem/progenitor cells by combinations of antibodies against cell surface proteins together with flow cytometry, and in identification of stem/progenitor cells with multi-lineage differentiation and self-renewal using mammary fat pad reconstitution assay and in vivo genetic labeling technique, a clear understanding of how these different stem/progenitors are orchestrated in the mammary gland is still lacking. Here we discuss the different in vivo and in vitro methods currently available for stem/progenitor identification, their associated caveats, and a possible new hierarchy model to reconcile various putative stem/progenitor cell populations identified by different research groups.

汽车座垫革样品测试长度对所测拉伸性能的影响

断裂点最大负荷与断裂伸长率是皮革最重要的两个机械力学性能，直接影响皮革的性能和最终的应用。我们采用汽车座垫革，沿着动物背脊线的平行方向和垂直方向取样，分别对矩形样品和哑铃形样品，研究了测试样品的长度对断裂最大负荷值与断裂伸长率的影响。结果显示，随着测试样品长度的增加，断裂点最大负荷和断裂伸长率均有下降的趋势。从基础研究和实际应用角度来看，研究测试样品的长度对断裂点最大负荷和断裂伸长率的影响是非常重要的。更重要的是，它可以完善皮革工业上的测试方法，有助于加强皮革生产的质量控制和管理。