Aim: To investigate the expression and the regulation of Bim protein in leukemic cell of patient with chronic myelognous leukemia(CML). Methods: The primary leukemic cells from the peripheral blood or bone marrow of patients with CML were isolated and cultured. The expression of Bim in the present or absence of ima-tinib(BCR/ABL inhibitor) was detected by the Western blotting, immunohistochemical analysis and real-time quantitative PCR. Results: Bim was consecutively expressed in normal bone marrow, but significantly decreased in the bone marrow of patients with CML( P < 0. 05). Imatinib significantly enhanced Bim mRNA transcription and expression in the manner of time- and dose-dependence. Moreover, there was reverse correlation between Bim protein level and the percent of leukemic cell in bone marrow( r =0. 849 1, P <0. 05). Conclusion: Bim is the Bcl-2 family pro-apoptitic factor. The decreased expression of Bim could be vital in the CML, Bim protein up-expression following the suppression of BCR/ABL might be of importance in investigation of the Bim-induced ap-optosis for potential clinical therapy.

ObjectiveTo analyze the effect and possible mechanism of the synergistic treatment with Qingjin Huazhuo Formula （清金化浊方， QHF） on the occurrence of thrombotic events in hospitalized patients with acute exacerbation of chronic obstructive pulmonary disease （AECOPD） and phlegm heat stasis obstructing in the lung syndrome. MethodsIn a retrospective cohort study， 305 AECOPD inpatients with the syndrome of phlegm heat stasis obstructing in the lung were included. According to whether using QHF （the course of treatment ≥ 7 days）， they were divided into the exposure group （193 cases） and the non-exposure group （112 cases）. Totally， 109 pairs of cases were obtained by 1∶1 propensity score matching （PSM）. After matching， the occurrence of thrombotic events during hospitalization， the remission of main symptoms or signs （including cough， expectoration， wheezing， cyanosis） after 10 days （±3 days） of treatment， and the difference of the indicators including D-dimer， percentage of neutrophils （NEUT%）， C-reactive protein （CRP）， arterial partial pressure of oxygen （PaO₂）， and arterial partial pressure of carbon dioxide （PaCO₂） before treatment and after 10 days （±3 days） of treatment during the first auxiliary examination. ResultsAfter matching， the incidence of thrombotic events during hospitalization in the exposure group （5 cases， 4.59%） were lower than that of the non-exposure group （15 cases， 13.76%， P＜0.05）. The exposure factor that taking QHF for 7 days or above was a protective factor for thrombotic events in AECOPD hospitalized patients with phlegm heat stasis obstructing in the lung syndrome （RR = 0.333， 95% CI 0.126 to 0.885）. The remission rates of cough （100/109， 91.74%）， expectoration （103/109， 94.50%）， wheezing （102/109， 93.58%）， and cyanosis （97/109， 88.99%） in the exposure group were significantly higher than those in the non-exposure group （90/109， 82.57%； 94/109， 86.24%； 89/109， 81.65%； 86/109， 78.90%） after treatment （P＜0.05）. After treatment， the levels of D-dimer， NEUT%， CRP and PaCO₂ in both groups significantly decreased （all P＜0.05）， and the level of PaO₂ significantly increased （P＜0.05）. The difference of the levels of D-dimer， NEUT% and PaO₂ in the exposure group before and after treatment were larger than those in the non-exposure group （P＜0.05）， while the pre-post difference of CRP and PaCO₂ were not significantly different between the two groups （P＞0.05）. ConclusionThe synergistic treatment with QHF can effectively reduce the occurrence of thrombotic events， alleviate the clinical symptoms or signs such as cough， expectoration， wheezing， and cyanosis， and can improve lung function in hospita-lized patients with AECOPD and phlegm heat stasis obstructing in the lung syndrome. Its mechanism may be related to improving blood coagulation and inflammatory status.