Objective To investigate the effects of taxol on QBC939 and its mechanism. Methods The cell proliferation was assessed by MTT assays; cell cycle kinetics and apoptosis were analyzed by flow cytometry and microscopic examination. Results Taxol inhibited the cell growth in concentration and time-dependent manners. The cell showed S and G2/M arrest and apoptosis. Conclusion Taxol suppresses the growth of QBC939 cells in vitro by causing cell-cycle arrest, and apoptosis of the cells.The mechanisms of taxol will provide theoretical guidance for clinical treatment.

Objective:To investigate the influence of chronic kidney disease(CKD),including slight renal damages,on prognosis of coronary artery disease(CAD).Methods: A retrospective study was performed in 732 patients who visited our Cardiology Department and Cardiothoracic Surgery Department in 2000-2004.All patients suspected of CAD underwent a selective coronary angiography.Five hundred and seventy-nine patients with established diagnosis of CAD were followed up and their cardiovascular events(angina pectoris,myocardial infarction,recurrent myocardial infarction,heart failure,stroke,death,etc.) were recorded.Patients with CAD were divided into normal,slight,moderate,and severe groups according to the degree of renal function damages.The influences of different degrees of renal damages on the prognosis of CAD were compared.Results: There were obvious differences in the morbidities of angina pectoris,myocardial infarction,recurrent myocardial infarction,heart failure,stroke,etc.in CAD patients with different degrees of renal function damages.The worse the renal function,the higher the incidences of angina pectoris,myocardial infarction,recurrent myocardial infarction,heart failure and stroke,etc((P

Objective To explore the surgical methods and clinical application effects of repairing hand soft tissue defect with free vascularized flaps based on the distal perforator of ulnar artery.Methods From March, 2001 to December, 2012 in our hospital, 90 patients with hand soft tissue defects were repaired by free vascularized flaps based on the distal perforator of ulnar artery, including 74 patients cases were repaired by Phase Ⅰ emergency surgery, 16 patients cases with scar contracture were repaired by Phase Ⅱ surgery.There were 34 cases were rebuild the sensory by repaired the continuity between the dorsal branch of the ulnar nerve and dorsal digital nerve or palmar digital nerve.The free vascularized flaps that used the emerging point of perforator of the ulnar artery as center of the flap was designed, which based on the distal perforator to repairing the hand soft tissue defect.Results All 89 patients postoperative flaps were survived.Necrosis was seen in 1 flap which was repaired by skin grafting.Follow-up ranged from 3 to 36 months with an average of 12 months.The appearance of flap was not clumsy, the quality was good.The sensation was S3-S3+ in 34 cases after nerve reconstruction surgery.The active and passive activity of 16 cases with scar contracture were improved significantly.The incision in 72 cases for direct suture were healed without scar contracture, 18 cases of skin grafts were all survived without contracture.Conclusion The free vascularized flaps based on the distal perforator of ulnar artery has constant perforating point, which can carry sensory nerves and leads to little donor site damage without major vascular injury.The flap serves as a simple approach to repair hand defects, and get satisfied skin flap appearance and texture, the fingers feel and function recovered well.

BACKGROUND:Embryonic stem cells (ESCs) serve as a major cell source for smooth muscle cells,but the heterogeneity of cells derived from ESCs result in difficulty to obtain high purity smooth muscle cells.OBJECTIVE:To construct a double expression vector of puromycin resistance (pac) gene and enhanced green fluorescence protein (EGFP) gene driven by smooth muscle specific SM22α promoter (pSM22α-PAC-IRES2-EGFP),in addition,to detect its availability and specificity in ESCs.DESIGN,TIME AND SETTING:The observational experiment of gene level was performed at the Cardiovascular Institute,General Hospital of Shenyang Military Region from April 2007 to September 2008.MATERIALS:ESCs line R1 with number SCRC-1011TM was purchased from American ATCC Company.The pSM22α-EGFP vector was constructed by our laboratory.And the pIRES2-EGFP,pSM2C and pSuper.basic vectors were purchased from Invitrogen Company.METHODS:SM22α promoter was cloned from pSM22α-EGFP by polymerase chain reaction.CMV promoter of pIRES2-EGFP vector was replaced by SM22 promoter to establish pSM22α-IRES2-EGFP.Pac gene,excised from pSM2C by HindⅢ/Clal digestion,was sub-cloned into pSuper.basic to establish pSuper-PAC.After BgⅢ/Accl enzyme digestion of pSuper-PAC,pac gene fragment was obtained,which was further sub-cloned into pSM22α-IRES2-EGFP to produce pSM22α-PAC-IRES2-EGFP.ESCs were transfected with pSM22α-PAC-IRES2-EGFP using lipofectamine.Positive clones were selected by G418 and induced to differentiate and further identified by amplification of pac gene by RT-PCR.Differentiated cells were immunostained by SM α-actin,and expression of SM α-actin and EGFP was observed simultaneously under fluorescence microscope.MAIN OUTCOME MEASURES:Sequencing result of pSM22α-PAC-IRES2-EGFP;Amplification of pac gene;EGFP expression;as well as SM α-actin immunostaining.RESULTS:Three segments of 261 bp,664 bp,and 5000 bp were obtained by HindⅢ/Clal digestion,which was coincident with expectation,and the sequencing results showed that pSM22α-PAC-IRES2-EGFP vector was successfully constructed.Amplification of pac gene identified 4 ESCs clones successfully transfected.After induction of differentiation,partial portion of differentiated cells expressed EGFP,accompanied by positively stained by SM α-actin antibody.CONCLUSION:pSM22α-PAC-IRES2-EGFP vector was successfully constructed.ESCs clones transfected with this vector expressed pac gene and EGFP gene,and the expression of EGFP is smooth muscle specific.