Objective To evaluate the effectiveness of color doppler ultrasound(CDU)in combination of computed tomographie angiography(CTA)in diagnosis of the arteriosclerosis occlusion.Methods:43 patients with arteriosclerosis occlusion were assessed by color doppler ultrasound,CTA and digital subtraction angiography(DSA).By using DSA as the reference standard,the results were compared.Results The sensitivity.specificity,positive and negative predictive values for CDU were 82.96%,95.2%,94.92%,83.8% respectively.Those for CTA were 88.89%,96.75%,96.77%,88.81% respectively,and for the two combination,were 94.81%,99.17%,99.22%,94.44% respectively.Conclusion The color doppler ultrasound combined with CTA is an effective way in diagnosing arteriosclerosis occlusion.

Objective:To study the early application of color duplex ultrasound in the evaluation of the arteriosclerosis occlusion after operation.Methods:we retrospectively divided the patients with atherosclerotic occlusion after open crossover surgery and endovascular treatment into groups 1( 12 patients ) and group 2( 13 patients ) respectively.In group 1,we assessed the relationship between the separated results of MG and the volume flow measurement in out-flow arteries before and after operation.In group 2,we assessed the relationship between the volume flow measurement in out-flow arter ies and the result of the DSA examination and all the data of group 2 is after treatment.Results:In group 1,the correlation of the separated results of MG and the increased amplitude of volume flow measurement in out-flow arteries was negative(P=0.0138,r=-0.6859).In group 2,the correlation of the volume flow measurement in out-flow arteries and the result of the DSA examination was negative(P=0.0316,r=-0.6198).In the patients after open crossover surgery and endovascular treatment,the MG and the volume of out-flow arteries were the significant hemodynamics index respectively.Conclusion:The color duplex ultrasonic early application is a perfect method in the follow-up of arteriosclerosis occlusion after operation.

OBJECTIVETo investigate the effect of 2-deoxy-D-glucose (2-DG) in enhancing the sensitivity of oral cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis.

METHODSThe oral cancer cell line KB was incubated in the presence of different concentrations (0, 0.625, 1.25, 2.5, 5, and 10 mmol/L) of 2-DG with or without TRAIL (200 ng/ml). The cell viability was measured using MTT assay and cell apoptosis was detected using flow cytometry with propidium iodide (PI) staining. KB cells treated with 5 mmol/L 2-DG with or without TRAIL for 0, 6, 16, or 24 h were examined with Western blotting for protein expressions of death receptor 5 (DR5) and caspase-3.

RESULTSTreatment of the cells with 5 mmol/L 2-DG for 24, 48 and 72 h resulted in a cell viability of 25.25%, 69.06%, and 59.19%, respectively. Combined treatment with 5 mmol/L 2-DG with TRAIL for 24 significantly enhanced the cell apoptotic rate (72.5%) as compared to the rate induced by TRAIL alone (45.3%) and by 2-DG (15.9%) alone. 2-DG treatment markedly up-regulated DR5 and caspase-3 expression and enhanced the inhibitory effect of TRAIL on cell colony formation.

CONCLUSION2-DG sensitizes oral cancer cells to TRAIL- induced apoptosis by up-regulating DR5 and caspase-3 expressions.

Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Deoxyglucose ; pharmacology ; Drug Synergism ; Gene Expression Regulation, Neoplastic ; Humans ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; metabolism ; TNF-Related Apoptosis-Inducing Ligand ; pharmacology

OBJECTIVETo investigate the effect of small interfering RNA-mediated glucose-regulated protein 78 (GRP78) knockdown on the chemosensitivity of breast cancer cells to cisplatin.

METHODSHuman breast cancer cell line MDA-MB-231 was exposed to different doses of cisplatin (0, 1, 2, 4, 8, and 16 µmol/L), and the changes in cell viability were detected using MTT assay. PI/Annexin V staining was used to observe the apoptosis of the cells in response to transfection with a small interfering RNA targeting GRP78 (pSH1Si-GRP78). Western blotting was employed to detect GRP78 expression in pSH1Si- GRP78-transfected cells after exposure to 8 µmol/L cisplatin for 24, 48 and 72 h.

RESULTSExposure of the cells to 8 µmol/L cisplatin for 24, 48 and 72 h resulted in a cell survival rate of 83.13%, 54.22% and 35.79%, respectively, but the cell apoptosis rate was only 10.8% at 24 h. Transfection of MDA-MB-231 cells with pSH1Si-GRP78 caused a cell apoptosis rate of 24.6%, which increased to 48.9% in cells with both pSH1Si-GRP78 transfection and cisplatin exposure. Cisplatin exposure caused an initial up-regulation followed then by a down-regulation of GRP78 expression in MDA-MB-231 cells, while pSH1Si-GRP78 transfection produced an obvious down-regulation of GRP78 expression.

CONCLUSIONSInhibition of GRP78 expression increases the apoptosis and enhance cisplatin chemosensitivity of breast cancer cells in vitro, suggesting the value of GRP78 as a potential therapeutic target in the clinical treatment of breast cancer.

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Survival ; Cisplatin ; pharmacology ; Female ; Gene Knockdown Techniques ; Heat-Shock Proteins ; metabolism ; Humans ; RNA, Small Interfering ; Transfection

OBJECTIVETo investigate the effect of small interfering RNA-mediated receptor-interacting protein kinase 1 (RIP1) knockdown on the sensitivity of human oral squamous carcinoma cells to to oxaliplatin (L-OHP)-induced apoptosis and explore a new target for clinical treatment of oral squamous carcinoma.

METHODSThe viability of human oral squamous carcinoma cell line KB exposed to different concentrations (0, 0.25, 0.5, 1, 2, 4 µmol/L) of L-OHP were detected by MTT assay. PI/Annexin V staining was used to observe cell apoptosis in naive KB cells, cell and transfected with pSH1Si-RIP1 or with the empty plasmid. Western blotting was used to detect RIP1 expression in KB cells exposed to L-OHP and in cells transfected with pSH1Si-RIP1.

RESULTSExposure to L-OHP (1µmol/L) for 24, 48, 72 h resulted in KB cell survival rates of 67.66%, 55.17%, and 41.34%, respectively, but the cell apoptosis rate was only 9.6% following a 24-h exposure. KB cells transfected with pSH1Si-RIP1 showed an apoptotic rate of 9.4%, which increased to 29.1% following L-OHP exposure. RIP1 expression was first up-regulated and then down-regulated in KB cells treated with L-OHP, and was significantly reduced after cell transfection with pSH1Si-RIP1.

CONCLUSIONSuppression of RIP1 expression increases the apoptotic rate of human oral squamous carcinoma cells, suggesting the potential of RIP1 as a new candidate target for clinical treatment of oral squamous carcinoma.

Apoptosis ; drug effects ; Carcinoma, Squamous Cell ; genetics ; pathology ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Mouth Neoplasms ; genetics ; pathology ; Organoplatinum Compounds ; pharmacology ; RNA Interference ; RNA, Small Interfering ; genetics ; Receptor-Interacting Protein Serine-Threonine Kinases ; genetics ; Transfection

Objective: To investigate the mechanism of lncRNA XIST (XIST) on modulating gastric cancer progression via regulating miR-337-3p/HOXC8 axis. Methods: A total of 58 cases of gastric cancer tissues and corresponding para-cancerous tissues resected from March 2013 to January 2018 in Department of General Surgery, Kailuan General Hospital of Tangshan City were collected for this study; in addition, human gastric cancer cell lines (AGS, MGC803, HGC27) and human gastric mucosal GES-1 cells were also collected. qPCR was used to detect the expressions of XIST and miR-337-3p in above mentioned gastric tissues and cell lines. XIST-knockdown vectors, miR-337-3p mimics, miR-337-3p inhibitor and HOXC8-overexpression vectors were transfected into AGS cells. The proliferation and invasion of AGS cells were detected by CCK-8 and Transwell experiments respectively, and the expression levels of HOXC8, E-cadherin, N-cadherin and vimentin were detected by WB. The targeting relationships between XIST, miR337-3p and HOXC8 were verified by dual-luciferase reporter gene assay. Results: XIST was up-regulated in gastric cancer tissues and cell lines (all P<0.01). XIST knockdown significantly inhibited proliferation, invasion and EMT of AGS cells (P<0.05 or P<0.01). Moreover, XIST directly interacted with miR-337-3p and down-regulated its expression, while HOXC8 was the target gene of miR-3373p. Furthermore, XIST knockdown suppressed proliferation, invasion and EMT ofAGS cells through up-regulating the inhibitory effect of miR-337-3p on HOXC8 (P<0.05 or P<0.01). Conclusion: XIST knockdown can suppress the proliferation, invasion and EMT of AGS cells, which may be related with down-regulation of HOXC8 by targeting miR-337-3p.