Objective To investigate the methylation situation of let‐7a‐3 promoter in patients with chronic myeloid leukemia (CML) and its clinical significance .Methods The methylation level of let‐7a‐3 promoter in the bone marrow mononuclear cells of 52 CML patients and 25 controls was detected by using the real‐time quantitative methylation‐specific PCR (RQ‐PCR) .Results The non-hypomethylation of let‐7a‐3 promoter was positive in 31 cases(59 .6% ) of 52 CML patients ,while only 1 case(4% ,1/25) in the control group ,the difference between the two groups were statistically significant (P< 0 .01) .The ROC curve analysis showed that the non -hypomethylation of let‐7a‐3 has better specificity for the auxiliary diagnosis of CML .The significantly posi‐tive correlation was found between the non -methylation level of let‐7a‐3 promoter and the BCR/ABL transcription level (r=0 .641 ,P=0 .001) .In contrast ,there was no obvious correlation between the non -methylation level of let‐7a‐3 promoter and the WBC count ,platelet count and hemoglobin levels(P>0 .05) .The non-hypomethylation level of let‐7a‐3 in chronic phase and accel‐erate phase was significantly higher than that in blastic crisis of CML .Conclusion The hypomethylation level of let‐7a‐3 promoter is decreased with disease progression .

Background and Objectives: Chronic obstructive pulmonary disease (COPD) is a common, frequently-occurring disease and poses a major health concern. Unfortunately, there is current no effective treatment for COPD, particularly emphysema. Recently, experimental treatment of COPD using mesenchymal stem cells (MSCs) mainly focused on bone marrow-derived MSCs (BM-MSCs). Human umbilical cord-derived MSCs (hUC-MSCs) have more advantages compared to BM-MSCs. However, studies on the role of hUC-MSCs in management of COPD are limited. This study sought to explore the role of hUC-MSCs and its action mechanisms in a rat model of VEGF receptor blocker SU5416-injured emphysema. Methods: and Results: hUC-MSCs were characterized by immunophenotype and differentiation analysis. Rats were div-ided into four groups: Control, Control＋MSC, SU5416 and SU5416＋MSC. Rats in model group were administered with SU5416 for three weeks. At the end of the second week after SU5416 administration, model group were infused with 3×106 hUC-MSCs through tail vein. After 14 days from hUC-MSCs transplantation, rats were euthanized and data were analyzed. HE staining and mean linear intercepts showed that SU5416-treated rats exhibited typical emphysema while emphysematous changes in model rats after hUC-MSCs transplantation disappeared completely and were restored to normal phenotype. Furthermore, hUC-MSCs inhibited apoptosis as shown by TUNEL and Western blotting.ELISA and Western blotting showed hUC-MSCs rescued VEGF-VEGFR2-AKT pathway in emphysematous lungs. Conclusions The findings show that hUC-MSCs effectively repair the emphysema injury. This study provides the first evidence that hUC-MSCs inhibit apoptosis via rescuing VEGF- VEGFR2-AKT pathway in a rat model of emphysema.