Emission and distribution of PCDD/Fs and CBzs from two co-processing RDF cement plants in China.

An analysis of the emission and distribution characteristics of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and chlorobenzenes (CBzs) from two cement kilns (CK1 and CK2) is done. Six measurements in CK1 showed an increase of PCDD/F emission from 76 to 97 pg I-TEQ/Nm(3) after feeding 10 ton/h RDF (refuse derived fuel). For CK2, the effect of increasing the RDF substitution rates from 0 to 21 t/h on the emission of PCDD/Fs was investigated. The correlation analysis indicated that replacing parts of the conventional fuel with RDF could not increase the emission of PCDD/Fs. Furthermore, the gas/particle partitions of PCDD/Fs and CBzs in stack gas were investigated, indicating that PCDD/Fs and CBzs were more associated in gas phase, especially for the lower chlorinated ones. Moreover, the bag filter fly ash was characterized by its particle distribution, XRD- and EDS-analysis. Additionally, the level of PCDD/Fs in outflowing fly ash escalates for smaller particle size. In order to evaluate the environmental effect on inhabitants, the levels of PCDD/Fs were also determined in samples of ambient air collected in the vicinity of CK2 (~200 m).

Angiogenesis in a rat model following myocardial infarction induced by hypoxic regulation of VEGF165 gene-transfected EPCs.

Hypoxia-response elements (HREs) regulate the expression of the vascular endothelial growth factor 165 (VEGF165) gene and enhance the safety and efficacy of therapeutic angiogenesis. However, the role of hypoxic regulation of VEGF165 gene-modified stem cells in promoting angiogenesis in the ischemic myocardium remains unclear. In this study, the effects of the hypoxic regulation of genetically modified endothelial progenitor cells (EPCs) on angiogenesis in the ischemic myocardium and on changes in cardiac function following acute myocardial infarction (AMI) were investigated through the transplantation of hypoxia-regulated VEGF165 gene-modified EPCs into the ischemic myocardium. Rat bone marrow-derived EPCs transfected with plasmid p6HRE-CMV­VEGF165 (6HRE-VEGF165-E), and plasmid pCMV-VEGF165 (VEGF165-E) were injected into rats with a successfully established model of AMI. The levels of VEGF165 mRNA and protein expression in the EPCs and ischemic myocardium were determined using reverse transcription-polymerase chain reaction and western blot assay, respectively, and the capillary density in the ischemic myocardium and the cardiac function of the rats were detected using immunohistochemistry and echocardiography, respectively. We found that the hypoxia promoter 6HRE-CMV effectively regulated the expression of the VEGF165 gene in the EPCs and the ischemic myocardium. In rats of the 6HRE-VEGF165-E-transplanted group, the levels of VEGF165 gene expression and capillary density in the ischemic myocardium were significantly higher than those in the other experimental groups. Moreover, cardiac function was also improved compared with that in other groups. VEGF165 gene-modified EPCs are able to significantly promote angiogenesis in the ischemic myocardium and markedly ameliorate the cardiac function of rats following AMI, especially under 6HRE regulation.

Clinical analysis of the risk factors of slow coronary flow.

Slow coronary flow (SCF) phenomenon is a coronary microvascular disorder characterized by the delayed passage of contrast in the absence of obstructive epicardial coronary disease, and is an important clinical entity because it may be the cause of precordial pain when the body is at rest and/or during exercise. Although clinical and pathological features of SCF have been previously described, its etiopathogenesis remains unclear. The present study aims to investigate the risk factors of slow coronary flow, in order to provide the foundation for further exploration of potential mechanisms of SCF. A total of 47 consecutive patients with documented slow coronary flow, and 33 patients with normal coronary flow--as defined by TIMI frame count (TFC)--were recruited for this study. Clinical information was collected, and biochemical indicators including high-sensitivity C-reactive protein (hs-CRP), and a marker of systemic inflammation were detected. Logistic regression analysis was performed for statistical analysis. SCF patients had a higher level of serum uric acid (323.2 ± 79.3 vs. 282.8 ± 82.4 µmol/l, p = 0.03), 2-h postprandial blood glucose (8.6 ± 2.7 vs. 7.5 ± 1.8 mmol/l, p = 0.04), platelet count (165.9 ± 51.6 × 10(3) vs. 127.0 ± 32.0 × 10(3) cells/µl, p = 0.0003) and hs-CRP (3.4 ± 0.8 vs. 2.0 ± 0.9 mg/l, p < 0.0001) than those of patients in the control group. No marked differences in other variables were observed between the two groups. Logistic regression showed serum uric acid level (χ(2) = 3.84, ß = 0.007, p = 0.049), 2-h postprandial blood glucose (χ(2) = 5.02, ß = 0.277, p = 0.025) and blood platelet count (χ(2) = 12.16, ß = 0.026, p = 0.001) were independent predictors of SCF. When hs-CRP was included in the multivariate model, hs-CRP (χ(2) = 21.19, ß = 1.90, p < 0.0001) was the only independent predictor of SCF. These findings suggested that an elevation of serum uric acid level, 2-h postprandial blood glucose, and blood platelet count might be the causes of SCF, and inflammation was likely to be implicated in the causal pathway leading to SCF.

[Study on the relationship between the polymorphism of p53 gene intron 7 and non-small cell lung cancer (NSCLC) and p53 mutation in NSCLC tissues].

OBJECTIVE: To investigate the relationship between p53 gene intron 7 polymorphism and non-small cell lung cancer (NSCLC). METHODS: One hundred and five patients with NSCLC and 100 controls were selected with case-control analysis. Polymerase chain reaction (PCR), Apa I restriction enzyme digestion and agarose gel electrophoretic separation were used to identify genotypes of p53 intron 7 in peripheral blood. Then, NSCLC biopsy tissues (n=64) and NSCLC paraffin-embedded tissues (n=40) were selected for mutation analysis. PCR products of p53 exons 5-8 were sequenced on an automated sequencer following the identification of intron 7 genotypes as previously described. RESULTS: In NSCLC patients, the homozygote positive for ApaI site in p53 intron 7 was 23.8%, the homozygote negative was 12.34%, and the heterozygote was 63.8%. Whereas in control group, the homozygote positive, the homozygote negative and the heterozygote were 44.0%, 11.0% and 45.0%, respectively (P<0.01). In the second part, mutation rate of p53 exons 5-8 was 20.0%, 50.0% and 52.9% in samples with ApaI positive, negative and heterozygotes, respectively (P<0.05). CONCLUSION: p53 intron 7 ApaI polymorphism may be associated with human NSCLC.

[p53 gene intron 7 polymorphism and its association with oral neoplasms].

OBJECTIVE: To investigate the association between oral neoplasm genetic susceptibility and genetic polymorphism of p53 intron 7. METHODS: The intron 7 ApaI polymorphism of p53 was analyzed in 95 oral neoplasm patients and 105 healthy individuals by utilizing polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genotyping assay technique, and direct sequencing was performed in 30 cases which were selected from the patients and controls by random sampling. RESULTS: In oral neoplasms cases, haplotype combinations were T-G 43.2%, C-T 56.8%, and frequencies of genotype were T-G/T-G 15.8%, C-T/T-G 54.7%, C-T/C-T 29.5%, while in controls they were T-G 30.9%, C-T 69.1% and T-G/T-G 10.5%, C-T/T-G 41.0%, C-T/C-T 48.5%. There was a significant difference in the allelic frequency and the genotypical distributions between the oral neoplasm patients and the controls. The individuals with the T-G allele had a slight increasing neoplasm risk than individuals with C-T allele; the OR for T-G versus C-T was 1.69 (95% CI, 1.12 - 2.51). The risk of suffering from oral neoplasms was higher in the individuals of T-G/T-G genotype and of T-G/C-T genotype than in individuals of C-T/CT genotype with odds ratio of 2.48 versus 2.20. CONCLUSIONS: There are two polymorphic points in the 7th intron of human p53 gene, which could be associated with genetic susceptibility of oral neoplasms. T-G allele may be the risk factor of oral neoplasms.