Objective To investigate the effects of human umbilical cord mesenchymal stem cells (UC-MSCs) on vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6) expression in acute myocardium infarction (AMI) rats. Methods The human UC-MSCs were cultured to the 4th generation for experiment. Sixty male Sprague-Dawley (SD) rats were randomly divided into sham group, AMI model group and UC-MSCs group, with 20 in each group. AMI animal model was produced by ligation of anterior descending coronary artery; in the sham group, the threading vein was gone below without ligation. In UC-MSCs group 2×106 UC-MSCs were infused through the caudal vein at 24 hours after successful model production. The animals were sacrificed after 7 days; the myocardial tissue and coronary artery below the ligation line were harvested. The mRNA and protein expressions of IL-6 in myocardium were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot. The positive expression of VEGF in coronary artery was observed by immunohistochemisty. Results Compared with the sham group, the mRNA and protein expressions of IL-6 in myocardium in AMI model group were increased significantly (gray value: 0.732±0.131 vs. 0.321±0.080, 0.678±0.191 vs. 0.286±0.061, both P < 0.05). Compared with the AMI model group, the mRNA and protein expressions of IL-6 in myocardium in UC-MSCs group were decreased significantly (gray value: 0.300±0.104 vs. 0.732±0.131, 0.312±0.101 vs. 0.678±0.191, both P < 0.05). Observation under light microscope, the VEGF positive cells in AMI model group was increased significantly compared with the sham group (cells/HP: 21.1±2.2 vs. 7.6±1.3, P < 0.05), the VEGF positive cells in UC-MSCs group were increased significantly compared with the AMI model group (cells/HP: 41.5±3.1 vs. 21.1±2.2, P < 0.05). Conclusion Human UC-MSCs could promote angiogenesis by the improvement of VEGF in coronary artery and inhibit the inflammation by the reduction of IL-6 in rats with AMI.

Objectives To observe the frequencies of mutations at glycophorin A(GPA)of erythro-cytes in patients with high arsenic coal poisoning(HACP)in comparison with normal controls.Methods The peripheral erythrocytes were isolated and immunolabelled,and were detected by flow cytometry in40patients and18normal adults.Results The mutation frequencies(MF)were(21.23?13.97)?10 -6 for type NN,(33.13?25.72)?10 -6 for type NO,(110.90?63.58)?10 -6 for type MM,and(20.35?21.26)?10 -6 for type MO of erythrocytes in patients with HACP,which were significantly higher than those in normal controls.The mutation frequencies were(31.50?16.13)?10 -6 for type NN,(54.50?38.13)?10 -6 for type NO,(159.33?66.22)?10 -6 for type MM,and(45.16?12.69)?10 -6 for type MO of erythrocytes in tumor group of HACP patients,which were significantly higher than those of non-tumor group of the patients.Conclusions Arsenic poisoning may induce the mutation at the glycophorin-A locus of erythrocytes,sug-gesting that arsenic may be one of potential mutagens.GPA-MF may serve as a parameter for the detection of patients with HACP.