• Environmental Engineering Research
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• v.20 no.3
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• pp.260-267
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• 2015

The $PM_{10}$, $SO_2$ and $NO_2$ mass concentrations were obtained over five years from monitoring stations across Nanchong, a southwest city in China. Changes in urban air quality over time, as well as the factors influencing that change, were evaluated based on air pollutant concentrations, the Air Pollution Index (API), and the Comprehensive Pollution Index (P). The results showed that the total annual mean $PM_{10}$, $SO_2$ and $NO_2$ concentrations over the five years studied were $61.1{\pm}1.1$, $45.0{\pm}3.9$ and $34.9{\pm}4.9{\mu}g{\cdot}m^{-3}$, respectively. The annual mean concentrations displayed a generally decreasing trend; lower than the annual mean second-level air quality limit. Meanwhile, the annual mean API values were in a small range of 52-53, the air quality levels were grade II, and P values were 1.06-1.21 less than the slight level ($P{\leq}1.31$). Total monthly mean $PM_{10}$, $SO_2$, $NO_2$ concentrations, and API and P values were consistently higher in winter and spring than during autumn and summer. The results of a correlation analysis showed that temperature and pressure were the major meteorological factors influencing pollution levels. Pollution sources included industrial coal and straw burning, automobiles exhaust and road dust, fireworks, and dust storms.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5897-5901
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• 2012

The aim of the study was to clarify the role of gastrokine 1 in the process of formation and development of gastric cancer. The expression of gastrokine 1 in gastric cancer and corresponding non-cancerous gastric tissues of 52 gastric cancer patients was assessed with the real-time fluorescence quantitative polymerase chain reaction (RT-PCR) and immunohistochemistry. We also analyzed the relationship between the expression level and clinicopathological characteristics. Gastrokine 1 gene and protein expression in gastric cancer tissues was in both cases significantly lower than in corresponding non-cancerous gastric tissues (both P<0.01), but no significant relationship was found with clinicopathological parameters including tumor location, depth of invasion, differentiation, lymph node metastasis, stage, gender, age and carcinoembryonic antigen (CEA), and carbohydrate antigen 19-9 (CA19-9) level in peripheral blood preoperation of patients (P>0.05, respectively). Furthermore, gastrokine 1 gene expression was markedly lower in gastric cancer tissues of Helicobacter pylori (HP)-positive patients than negative ones (P<0.05). The result of the study showed that gastrokine 1 might play a significant role in the process of formation and development of gastric cancer as an anti-oncogene. Its effect might be weakened by HP infection.

• Biomolecules & Therapeutics
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• v.25 no.5
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• pp.490-496
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• 2017

Imatinib resistance has become a major clinical problem for chronic myeloid leukemia. The aim of the present study was to investigate the involvement of MEG3, a lncRNA, in imatinib resistance and demonstrate its underlying mechanisms. RNAs were extracted from CML patients' peripheral blood cells and human leukemic K562 cells, and the expression of MEG3 was measured by RT-qPCR. Cell proliferation and cell apoptosis were evaluated. Western blotting was used to measure the protein expression of several multidrug resistant transporters. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.12
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• pp.4977-4982
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• 2014

Background: Cytochrome P450 2E1 (CYP2E1) might be involved in the development of bladder cancer. However, previous studies of any association between CYP2E1 RsaI/PstI polymorphism and bladder cancer risk have yielded conflicting results. In this study, we performed a more precise estimation of the relationship by a meta-analysis based on the currently available evidence from the literature. Method: To assess the effect of CYP2E1 RsaI/PstI polymorphism on bladder cancer susceptibility, a meta-analysis of 6 available studies with 1,510 cases and 1,560 controls were performed through Feb 2014. Summary odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were used to estimate the strength of association for CYP2E1 RsaI/PstI polymorphism under different genetic models. Results: When available studies were pooled into the meta-analysis, we found that the C1C2 and C2C2 genotypes of CYP2E1 RsaI/PstI polymorphism significantly decreased bladder cancer risk under different genetic models (heterozygote: OR=0.766, 95%CI=0.613-0.957, $P_{OR}$=0.019; homozygote: OR=0.51, 95%CI=0.303-0.858, $P_{OR}$=0.011; dominant: OR=0.733, 95%CI=0.593-0.905, $P_{OR}$=0.004; recessive: OR=0.565, 95%CI=0.337-0.947, $P_{OR}$=0.030). Subgroup analysis indicated that C2C2 genotype was significantly associated with decreased bladder cancer risk under the homozygote genetic model in Caucasians. There was no evidence of heterogeneity or publication bias. Conclusions: The current meta-analysis suggested that the CYP2E1 RsaI/PstI polymorphism might be associated with bladder cancer susceptibility, especially in Caucasians. Further studies are needed to validate the above conclusion.