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Objective To estimate the mortality and years of life lost among youth aged 18-44 in Chongqing from 2011 to
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<p><b>OBJECTIVE</b>To analyze the changes in endogenous small molecule metabolites after benzo[a]pyrene (B[a]P) exposure in rat cerebral cortex and explore the mechanism of B[a]P neurotoxicity.</p><p><b>METHODS</b>Five-day-old SD rats were subjected to gavage administration of 2 mg/kg B[a]P for 7 consecutive weeks. After the exposure, the rats were assessed for spatial learning ability using Morris water maze test, ultrastructural changes of the cortical neurons under electron microscope, and metabolite profiles of the cortex using GC/MS. The differential metabolites between the exposed and control rats were identified with partial least squares discriminant analysis (PLS-DA) and the metabolic pathways related with the differential metabolites were analyzed using Cytoscape software.</p><p><b>RESULTS</b>Compared with the control group, the rats exposed to B[a]P showed significantly increased escape latency (P<0.05) and decreased time spent in the target area (P<0.05). The exposed rats exhibited widened synaptic cleft, thickened endplate membrane and swollen cytoplasm compared with the control rats. Eighteen differential metabolites (VIP>1, P<0.05) in the cortex were identified between the two groups, and 9 pathways associated with B[a]P neurotoxicity were identified involving amino acid metabolism, tricarboxylic acid cycle and Vitamin B3 (niacin and nicotinamide) metabolism.</p><p><b>CONCLUSION</b>B[a]P can cause disturbance in normal metabolisms and its neurotoxicity is possibly related with disorders in amino acid metabolism, tricarboxylic acid cycle and vitamin metabolism.</p>
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<p><b>OBJECTIVE</b>To investigate the effect of air pollution on respiratory health in school-aged children in the main urban area of Chongqing, China.</p><p><b>METHODS</b>The main urban area of Chongqing was divided into polluted area and clean area according to the air pollution data shown on the Environmental Protection Agency Website of Chongqing between 2010 and 2015. A cluster sampling method was used to select 695 third- or fourth-grade children from 2 primary schools in the clean or polluted area as study subjects, with 313 children from the clean area and 382 children from the polluted area. Pulmonary function was examined for all children and a standard American epidemiological questionnaire (ATS-DLD-78-C) was used to investigate the prevalence of respiratory diseases and symptoms.</p><p><b>RESULTS</b>Compared with the clean area, the polluted area had significantly higher concentrations of inhalable particles (PM), fine particulate matter (PM), and nitric oxide (NO) (P<0.05). The multivariate logistic regression analysis was performed after adjustment for confounding factors, and the results showed that compared with those in the clean area, the children in the polluted area had significantly higher risks of cough (OR=1.644), cough during cold (OR=1.596), expectoration during cold (OR=2.196), persistent expectoration (OR=1.802), and wheezing (OR=2.415). The boys and girls in the clean area had significantly higher forced vital capacity and forced expiratory volume in one second than those in the polluted area (P<0.05).</p><p><b>CONCLUSIONS</b>Air pollution in the main urban area of Chongqing is associated with the increased prevalence of respiratory symptoms in school-aged children and has certain effect on children's pulmonary function.</p>
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Child , Female , Humans , Male , Air Pollution , Forced Expiratory Volume , Logistic Models , Respiratory Tract Diseases , Vital CapacityABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of exposure to vehicle exhaust in pregnant mice on the reproductive function and DNA methylation in male offspring mice.</p><p><b>METHODS</b>Twenty pregnant mice were randomized into control group and vehicle exhaust exposure group (n=10) and exposed to routine laboratory condition and to vehicle exhaust for 10 consecutive days (8 h per day) in a tunnel with a heavy traffic, where the concentrations of TSP, PM10, PM2.5, SO2 and NOX and the decibel of noise were measured. The offspring mice were raised till reaching maturity, and the epididymides of the male mice were collected to test the weight coefficients, DNA methylation level, and mRNA levels of Aldh7a1 and Rpe.</p><p><b>RESULTS</b>The body weight and the weight coefficients of the epididymides and testes differed significantly between the exposure group and the control group (P>0.05). The concentrations of TSP, PM2.5, PM10 and NOx and the decibel of noise were significantly higher in the traffic environment and the control environment (P<0.05). Reduced representation bisulphite sequencing (RRBS) and Gene ontology (GO) showed that 58 genes had significantly different methylation levels between the two groups, mostly relating to the process of spermatogenesis (P<0.05). Compared with the control group, Aldh7a1 and Rpe mRNA expressions in the testes were down-regulated significantly in the exposure group (P<0.05).</p><p><b>CONCLUSION</b>Exposure of pregnant mice to vehicle exhaust causes damages of the reproductive function in the male offspring mice.</p>
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<p><b>OBJECTIVE</b>To observe the effect of chronic arsenic exposure on cerebral cortex and serum metabolics of mice and explore the mechanism of arsenic neurotoxicity.</p><p><b>METHODS</b>Twelve 3-week-old male C57BL/6J mice were randomly assigned into exposure group and control group and exposed to sodium arsenite (50 mg/L) via drinking water and deionized water for 12 weeks, respectively. After the exposure, arsenic level in the cerebrum was determined by hydride generation-atomic fluorescence spectrometry. The metabolites in the cerebral cortex and serum were determined using gas chromatography-mass spectrometry (GC/MS) analysis. Principal component analysis (PCA) was used to analyze the difference of the metabolites between the exposure and the control groups. Online tools for analyzing metabolic pathways were used to identify the related metabolites pathways.</p><p><b>RESULTS</b>Arsenic content in the brain of exposure group was significantly higher than that in the control group (P<0.05). The mice exposed to arsenic had a higher level of citric acid, phenylalanine, tyrosine, histidine and lysine in the cerebral cortex (P<0.05). Serum levels of serine, glycine, proline, aspartate and glutamate were significantly higher while α-ketoglutaric acid level was significantly lower in the exposure group than in the control group (P<0.05). PCA analysis showed a significant difference in cerebral cortex and serum metabolites between the two groups.</p><p><b>CONCLUSION</b>Chronic arsenic exposure may affect the function of the central nervous system by interfering with amino acid metabolism and tricarboxylic acid cycle, which may be one of the mechanisms of arsenic neurotoxicity.</p>
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Objective To investigate the distribution of ghitathione-S-transferase M1 (GSTM1) and T1 (GSTT1) genes polymorphisms in Chinese population and smear-positive pulmonary tuberculosis cases of Jilin province. Methods Articles about GSTM1 and GSTT1 genes polymorphisms published before 2009 in China were searched. The study population was obtained from fourteen counties (or districts) of Jilin province, which included all cases from November, 2007 to May, 2008, totally 1120. The genotypes of GSTM1 and GSTT1 were detected by multiplex PCR technique. Results The frequencies of GSTM1 and GSTT1 'null' genotypes and combination M1-T1 'null' genotype acquired from systematic review were 54.2%, 46.8% and 26.2%, respectively, in Chinese Hans they were 53.4%, 44.9% and 25.5%, and in our research they are 57.2%, 20.4% and 13.7%, respectively. No significant differences between the frequencies of males and females as well as among that of different age groups were observed(P>0.05). The frequency of GSTM1 'null' genotype in our research is slightly higher than that in systematic review (P=0.016) , and the frequencies of GSTT1 'null' genotype and combination M1-T1 'null' genotype and are significantly lower than those in systematic review (both P<0.001). Conclusion The frequencies of GSTM1 and GSTTI 'null' genotypes were different among ethnics. The statistical difference between systematic review and our research may due to our large sample size and mostly Soutbern people in previous studies.
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<p><b>OBJECTIVE</b>To evaluate effect of NaFeEDTA on serum ferritin level in iron deficient epidemic population.</p><p><b>METHODS</b>A comprehensive literature retrieval was performed via searching electronic databases, hand searching bibliographies of books and relevant journals, collecting grey literatures, looking into conference abstracts, contacting fields experts and reviewing references and citations. Criteria from Cochrane EPOC review group were used to assess the quality of the included studies. Generic inverse variance method was used to undertake Meta-analysis.</p><p><b>RESULTS</b>The pooled estimate for serum ferritin level (weighted mean difference) was 1.58 microg/L (95% CI 1.20-2.09; P < 0.001).</p><p><b>CONCLUSION</b>This systematic review indicates that NaFeEDTA might improve serum ferritin concentration significantly in iron deficient epidemic population.</p>
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Humans , Anemia, Iron-Deficiency , Drug Therapy , Edetic Acid , Therapeutic Uses , Ferric Compounds , Therapeutic Uses , Ferritins , Blood , Iron, Dietary , Randomized Controlled Trials as TopicABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effect of NaFeEDTA on hemoglobin level in iron deficient population.</p><p><b>METHODS</b>Comprehensive literature retrieval was performed via searching electronic databases, hand searching bibliographies of books and relevant journals, collecting grey literatures, looking into conference abstracts, contacting fields experts and reviewing references and citations. Criteria from Cochrane EPOC review group were used to assess the quality of included studies. Generic inverse variance method was used to undertake meta-analysis.</p><p><b>RESULTS</b>The pooled estimate for hemoglobin level (weighted mean difference) was 12.14 g/L (95% CI: 5.60-18.69; P < 0.001). Subgroup analysis indicated that lower baseline hemoglobin level and higher dose for intervention were associated to greater increase in hemoglobin level.</p><p><b>CONCLUSION</b>This systematic review indicated that NaFeEDTA improved hemoglobin significantly in iron deficient population.</p>
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Humans , Anemia, Iron-Deficiency , Blood , Drug Therapy , Metabolism , Edetic Acid , Therapeutic Uses , Ferric Compounds , Therapeutic Uses , Hemoglobins , Metabolism , Iron Chelating Agents , Therapeutic UsesABSTRACT
<p><b>OBJECTIVE</b>To explore the effects of nonylphenol on brain gene expression profiles in F1 generation rats by microarray technique.</p><p><b>METHODS</b>mRNA was extracted from the brain of 2-day old F1 generation male rats whose F0 female generation was either exposed to nonylphenol or free from nonylphenol exposure, and then it was reversely transcribed to cDNA labeled with cy5 and cy3 fluorescence. Subsequently, cDNA probes were hybridized to two BiostarR-40S cDNA gene chips and fluorescent signals of cy5 and cy3 were scanned and analyzed. Results Two genes were differentially down-regulated.</p><p><b>CONCLUSION</b>Nonylphenol may disturb the neuroendocrine function of male rats when administered perinatally.</p>