OBJECTIVE:To compare the efficacy and safety of dabigatran and warfarin respectively used in atrial fibrillation patients after radiofrequency ablation(RFCA). METHODS:Data of 141 nonvalvular atrial fibrillation patients,who scheduled for RFCA,were retrospectively analyzed and divided into warfarin group(71 cases)and dabigatran group(70 cases)by different med-ication. Patients in warfarin group should stop warfarin if they took before,then changed to Low molecular weight heparin calcium injection 100 U/kg,subcutaneous injection,taking RFCA when INR was lower than 1.5,stopping low molecular weight heparin 12 h before surgery;Low molecular weight heparin calcium injection 100 U/kg was intravenously injected when surgery;orally tak-ing Warfarin sodium tablet 4.5 mg after 4-6 h,once a day,meanwhile bridged overlapping treated at least 3-5 d with low molecu-lar weight heparin;monitoring once INR every 3 d after surgery,maintaining INR 2.0-3.0,taking warfalin at least 3 months. Pa-tients in dabigatran group stopped taking the anticoagulant drugs when admission,then changed to Dabigatran etexilate capsule 110 mg(age≥70 years old or body mass<60 kg)or 150 mg(age<70 years old or body mass≥60 mg),twice a day;stopping dabig-atran 24 h before surgery,the same medication as warfalin group when surgery;orally taking dabigatran after 6 h,taking at least 3 months. The total mortality rate,incidence of stroke(transient cerebral ischemia,ischemic encephalopathy),peripheral thrombosis rate and incidence of bleeding after 1 and 3 month(s)in 2 groups were observed. RESULTS:There were no significant differences in the total mortality rate,incidence of stroke,peripheral thrombosis rate and incidence of bleeding after 1 and 3 month(s) in 2 groups(P>0.05). CONCLUSIONS:Dabigatran has similar anticoagulant efficacy and safety with warfarin in atrial fibrillation pa-tients after RFCA.

Chemotherapy is the preferred therapeutic approach for advanced ovarian cancer, but a successful long-term treatment is prevented by the development of drug resistance. Recent works have underlined the involvement of non-coding RNAs, microRNAs (miRNAs) in cancer development, with several conjectures regarding their possible involvement in the evolution of drug resistance. This study is to investigate the promoting effects and mechanism of miR-125b involved in the development of chemoresistance in ovarian cancer. The different expression of miR-125b in cisplatin-sensitive ovarian cancer cell line (OV2008) and its resistant variant (C13*) was identified by real-time PCR. An in vitro cytotoxicity assay and apoptosis assay using CCK-8 assay and flow cytometry, were carried out to detect the effect of miR-125b and Bak1 on cisplatin resistance of cells. Real-time PCR, Western blotting and luciferase reporter assay were used to detect whether Bak1 is a target of miR-125b. As compared with OV2008 cells, the expression levels of miR-125b in C13* cells were increased. It was found that the up-regulation of microRNA-125b caused a marked inhibition of cisplatin-induced cytotoxicity and apoptosis and a subsequent increase in the resistance to cisplatin in OV2008 and C13* cells. Moreover, Bak1 was a direct target of miR-125b, and down-regulation of Bak1 suppressed cisplatin-induced apoptosis and led to an increased resistance to cisplatin. Our study indicates that miR-125b has a significantly promoting effect on chemoresistance of C13* cells and up-regulation of miR-125b expression contributes to cisplatin resistance through suppression of Bak1 expression. This finding has important implications in the development of targeted therapeutics for overcoming cisplatin resistance in ovarian cancer.

Objective To explore the sensitivity and the molecular mechanism of cisplatinresistance ovarian cancer cell line C13 to proteasome inhibitors and the combination with cisplatin. Methods After different treatments, methyl thiazolyl tetrazolium (MTT) assay was applied to examine the cell viability, annexin-V/propidium iodide(PI) apoptosis detection kit was used to determine the apoptosis rate of different groups, western blot assay was introduced to evaluate the expression levels of Fas-associated death domain-like interleukin-1 beta converting enzyme inhibitory protein (cFLIPs), and the activity of caspase-8 was examined. Results MTT assay shown that the cell viability ratios of combination group at serial time points from 12, 24, 36, 48, 60, 72 hours were ( 56.0 ± 8.4 ) %, (44.7 ± 7.3 ) %, ( 33.7 ±11.2) %, (27.6 ± 8.0) %, (27. 6 ± 7.6) % and (28.1 ± 2.4) %, which were much lower than those of cisplatin group (P <0.05). After treated for 24 hours, apoptosis rates of cisplatin group, bortezomib group and combination group were ( 16.7 ± 1.7) %, (23.4 ± 2.1 ) % and (26.9 ± 1.6) %, respectively. The rate of combination group was much higher than that of non-treated group and that of cisplatin group or bortezomib group ( P < 0.05 ). Western blot assay showed the changes of expression levels of cFLIPs, which were downregulated seriously after cisplatin, bortezomib or combination treatment [ (43.2 ± 2.3 )% vs( 75.7 ± 3.0)%vs (67.9 ± 2.1 ) %, P < 0.05 ]. The caspase-8 activity of combination group was (5.6 ± 1.6) folds than that of non-treated group, which was higher than those of other two groups [ ( 2.3 ± 1.0) and (4.2 ± 0.9 ) folds,P < 0.05 ]. Conclusions The tumor cell lethal effect of cisplatin could be increase significantly by the combination application of proteasome inhibitors, bortezomib. And the cFLIPs/caspase-8 signaling pathway may be play an important role in the molecular mechanism of the combination treatment.

OBJECTIVETo search an effective method to correct the secondary nasal deformity.

METHODSThe "spilth" tissue asymmetry to the another side on the cleft side alar is formed as a flap, which is used to drive up or reconstruct the nostril base (sill), readjust nostril size and shape. The cleft side alar cartilage lateral foot is disassociated, replaced and fixed into the normal place.

RESULTSNineteen patients were received this operation, their nasal alar, nostril, sill, on the two sides are symmetry, and the result is good.

CONCLUSIONSThe cleft side alar flap and alar cartilage sling procedure is effective to correct secondary cleft lip nasal deformity.

Abnormalities, Multiple ; surgery ; Adolescent ; Adult ; Cartilage ; transplantation ; Child ; Cleft Lip ; surgery ; Female ; Follow-Up Studies ; Humans ; Male ; Nose ; abnormalities ; surgery ; Reconstructive Surgical Procedures ; methods ; Rhinoplasty ; methods ; Surgical Flaps

Chemotherapy is the preferred therapeutic approach for advanced ovarian cancer,but a suceessful long-term treatment is prevented by the development of drug resistance.Recent works have underlined the involvement of non-coding RNAs,microRNAs (miRNAs) in cancer development,with several conjectures regarding their possible involvement in the evolution of drug resistance.This study is to investigate the promoting effects and mechanism of miR-125b involved in the development of chemoresistance in ovarian cancer.The different expression of miR-125b in cisplatin-sensitive ovarian cancer cell line (OV2008) and its resistant variant (C13*) was identified by real-time PCR.An in vitro cytotoxicity assay and apoptosis assay using CCK-8 assay and flow cytometry,were carried out to detect the effect of miR-125b and Bak1 on cisplatin resistance of cells.Real-time PCR,Western blotting and luciferase reporter assay were used to detect whether Bak1 is a target of miR-125b.As compared with OV2008 cells,the expression levels of miR-125b in C13* cells were increased.It was found that the up-regulation of microRNA-125b caused a marked inhibition of cisplatin-induced cytotoxicity and apoptosis and a subsequent increase in the resistance to cisplatin in OV2008 and C13* cells.Moreover,Bakl was a direct target of miR-125b,and down-regulation of Bak1 suppressed cisplatin-induced apoptosis and led to an increased resistance to cisplatin.Our study indicates that miR-125b has a significantly promoting effect on chemoresistance of C13* cells and up-regulation of miR-125b expression contributes to cisplatin resistance through suppression of Bakl expression.This finding has important implications in the development of targeted therapeutics for overcoming cisplatin resistance in ovarian cancer.