Objective To observe the clinical characteristic and prognosis of primary lung cancer patients with venous thromboembolism (VTE).Methods 589 primary lung cancer patients were selected and divided into VTE group(n =49) and non VTE group(n =540).49 cases with VTE were divided into pulmonary thromboembolism (PTE) group(n =15),including single PTE and PTE combined with deep venous thrombosis(DVT) and DVT group (n =34).Single factor and multiple logistic regression analysis were performed to determine the factors influencing primary lung cancer patients with VTE.Clinical manifestation,time of onset and prognosis of patients with VTE were analyzed.Results 49 patients with VTE included 10 patients(20.4％) with single PTE,34 patients(69.4％) with single DVT and 5 PTE patients combined with DVT(10.2％).D-dimer(OR =1.560,95％ CI =1.018 ～ 2.392,x2 =4.161,P =0.041),interleukin-1 (IL-1,OR =1.846,95％ CI =1.054-3.234,x2 =4.594,P =0.033),tumor necrosis factor (TNF OR =1.486,95％ CI =1.014-2.178,x2 =4.126,P =0.042),adenocarcinoma (OR =2.854,95％CI=1.217-6.695,x2 =5.812,P=0.016) and phase Ⅲ-Ⅳ(OR =2.198,95％CI=1.122-4.305,x2 =5.272,P =0.022) were the factors influencing primary lung cancer patients with VTE.Chest tightness,coughing,accelerated heart rate,swelling and pain in lower limb were common clinical manifestations of primary lung cancer patients with VTE.Most patients with VTE occurred within 3 months after a diagnosis of primary lung cancer.There was no significant difference in the time of onset between PTE group and DVT group(P ＞0.05).As of July 2014,31 cases (63.2％) died,12 cases (24.5 ％) survived,and 6 cases (12.2％) lost in 49 patients with VTE.The median survival time of 49 patients with VTE was 9.5 months.The median survival time of PTE group was 5.8 months,while DVT group was 15.2 months,but no significant difference between them (P ＞ 0.05).Conclusion Increased D-dimer,increased IL-1,increased TNF,adenocarcinoma and phase Ⅲ-Ⅳ could increase the risk of primary lung cancer patients with VTE.There were little typical.clinical symptoms in most patients with VTE,which occurred with in 3 months after a diagnosis of primary lung cancer.They had high mortality and needed to take early diagnosis and treatment through auxiliary examination.

Objective To study if 5-Aza-2’-deoxycytidine along or together with 4-phenylbutyric acid could affect miR-196b expression levels in chronic myeloid leukemia cells .Methods K562 cells were treated with DNA methylation inhibitor 5-Aza-2’-deoxycytidine, histone deacetylase inhibitors 4-phenylbutyric acid separately and the combined treatment with both of them, then expression levels of miR-196b were detected using Real-time PCR.Results The half inhibition concentration of 4-phenylbutyric acid was 1.58mmol/L.Comparing with the expression level of miR-196b in normal human bone marrow cells, the expression levels of miR-196b were significantly lower in Aza group , PBA group and negative control cells and nearly consistent among three groups , and as high as normal cells in combined treatment group . Conclusion The expression level of miR-196b in K562 cells could not return to normal treated with 5-Aza-2 ’-deoxycytidine or 4-phenylbutyric acid separately , while could restore normal when treated with both agents , indicating that miR-196b expression level in K562 cells is related with both DNA methylation and histone acetylation .

Objective To study the application of Cell Counting Kit-8(CCK-8) in detecting the growth inhibiting effect of 5-Aza-2’-deoxycytidine on chronic myeloid leukemia cell .Methods The proliferation of K562 cells was detected by CCK-8 with different concentrations of 5-Aza-2 ’-deoxycytidine and the cell cycle and apoptosis of K 562 cells were detected after K562 treated by 50% inhibitory concentration of 5-Aza-2 ’-deoxycytidine .Results The 50% inhibitory concentration of 5-Aza-2’-deoxycytidine was 15.55nmol/L, after treated with this concentration , K562 cells showed that G2 phase arrest occurred , proliferation inhibited and apoptosis peaks appeared .Conclusion Inhibition of proliferation of K562 cells with different concentrations of 5-Aza-2’-deoxycytidine varied in a dose-dependent relationship , and 5-Aza-2’-deoxycytidine could promote apoptosis of K 562 cells.CCK-8 can be used in detecting the effect of 5-Aza-2’-deoxycytidine on chronic myeloid leukemia cells .