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Chinese Circulation Journal ; (12): 1056-1059, 2017.
Article in Chinese | WPRIM | ID: wpr-667328


Objective: To compare the clinical features between very late stent thrombosis (VLST) and very late in-stent restenosis, to discuss the potential risk factors for VLST occurrence. Methods: Our research included in 2 groups: VLST group, 21 ACS patients with coronary angiography (CAG) confirmed VLST admitted in our hospital and Control group, 38 ACS patients with CAG confirmed very late in-stent restenosis at same period of time. Basic clinical data, laboratory tests and relevant examinations were compared between 2 groups; potential risk factors for VLST occurrence were studied by Logistic regression analysis. Results: ① There were 8 (38.1%) patients discontinued anti-platelet therapy in a month by themselves in VLST group and 5 (13.2%) in Control group, P=0.03. ② 13 (61.9%) patients presented as ST-segment elevation myocardial infarction (STEMI) in VLST group, while all (100%) patients presented as Non-ST-segment elevation ACS (NST-ACS) in Control group, P<0.001. ③ The age, gender, previous histories of hypertension, diabetes, MI, smoking and interventional therapy were similar between 2 groups, P>0.05. ④ Compared with Control group, VLST group had decreased LVEF, P=0.001, increased peak values of TnI and NT-pro BNP, elevated WBC and hs-CRP, all P<0.001. ⑤ The index of echocardiography, blood lipid profiles, glucose and creatinine were similar between 2 groups, P>0.05. ⑥ Logistic regression analysis showed that discontinued anti-platelet therapy, elevated NT-pro BNP and hs-CRP were the independent risk factors for VLST occurrence, P<0.05. Conclusion: VLST may have life-threatening clinical features, insisted anti-platelet therapy and improved cardiac function could reduce VLST occurrence.

Journal of Experimental Hematology ; (6): 1157-1161, 2013.
Article in Chinese | WPRIM | ID: wpr-283962


The purpose of this study was to investigate the effects of Celecoxib on the proliferation of the FLT3-ITD positive and negative acute myeloid leukemia cells and its mechanism. The proliferation inhibition effect of Celecoxib with different doses on the FLT3-ITD positive cells MV4-11 and the FLT3-ITD negative K562 cells was detected by CCK-8 method, the cell apoptosis was determined by flow cytometry, and the MEK, Mcl-1, pAKT expression was tested by Western blot. The results showed that Celecoxib inhibited the proliferation of both MV4-11 and K562 cells, but the IC50 for MV4-11 was (29.14 ± 2.4) µmol/L, which was significantly lower than that of K562 cells (39.84 ± 1.0) µmol/L (P < 0.05); The induced apoptosis rate of Celecoxib at 20-80 µmol/L on MV4-11 was not observed, but there was apparent influence on K562 at the same concentration. Western blot showed that Celecoxib down-regulated the expression of MEK and Mcl-1 but did not change the expression of pAKT obviously on MV4-11 cells, while the expression of Mcl-1 was reduced a little, but no obvious change were found in the expression of MEK and pAKT on K562 cells. It is concluded that the Celecoxib can inhibit the proliferation of FLT3-ITD positive AML cells distinctly, and the potential mechanism may be related to the inhibition of the MEK/Mcl-1 signaling pathway.

Apoptosis , Celecoxib , Cell Proliferation , Cyclooxygenase 2 Inhibitors , Pharmacology , Gene Expression Regulation, Leukemic , Humans , K562 Cells , Leukemia, Myeloid, Acute , Drug Therapy , Metabolism , Pathology , MAP Kinase Kinase 1 , Genetics , Myeloid Cell Leukemia Sequence 1 Protein , Genetics , Proto-Oncogene Proteins c-akt , Genetics , Pyrazoles , Pharmacology , Signal Transduction , Sulfonamides , Pharmacology , fms-Like Tyrosine Kinase 3 , Genetics