Objective To investigate the relationship between serum cystatin C and coronary artery disease in type 2 diabetes mellitus (T2DM) patients with normal uric protein.Methods According to the coronary artery lesion diagnosed by 320-dynamic volume CT,the 126 T2DM patients with normal uric protein were divided into three groups:no coronary stenosis group (group A,32 cases),coronary atherosclerosis group(group B,38 cases),coronary heart disease group (group C,56 cases).Then the serum cystatin C etc were compared among the three groups.Results The levels of serum cystatin C in group A,B,C were (0.89 ± 0.27),(1.31 ± 0.53),(1.54 ± 0.62) mg/L.With the increase of coronary artery lesions,it gradually increased,there was significant difference among the three groups (P ＜ 0.05).The patients were divided into three groups according to the level of serum cystatin C quartile.The incidence of coronary artery lesion in creased with the increased levels of serum cystatin C.The level of serum cystatin C increased from 75th percentile to 100th percentile,the incidence of coronary heart disease increased significantly (OR =8.32,P ＜0.05).The result of multiple Logistic regression analysis showed that history of hypertension (regression coefficient 4.135,P =0.000),glycosylated hemoglobin (regression coefficient 1.257,P =0.002),low density lipoprotein-cholesterol (regression coefficient 3.381,P =0.015),cystatin C (regression coefficient 2.046,P =0.030) were the independent risks of coronary heart disease in patients with T2DM.Conclusion The level of serum cystatin C may be a predictor for coronary heart disease in T2DM patients with normal uric protein.

Objective To observe the inhibitory effect of Tirofiban on different shear-induced platelet aggregation, and to provide medication suggestions for the treatment of thrombosis in different hemodynamic environment. Methods Polydimethylsiloxane ( PDMS)-glass microchannel chips were fabricated by soft lithography. The whole blood of healthy volunteers anticoagulated with sodium citrate was collected and incubated with different concentrations of Tirofiban in vitro. The blood flowed through the straight microchannel or channel with 80% narrow for 150 seconds at the speed of 11 μL/ min and 52 μL/ min, respectively. The wall shear stress rates in straight channel at 11 μL/ min and 52 μL/ min were 300 s-1 and 1 500 s-1, respectively. The maximum wall shear rates in the channel with 80% occlusion at 11 μL/ min and 52 μL/ min were 1 600 s-1 and 7 500 s-1, respectively. The adhesion and aggregation images of fluorescent labeled platelets on glass surface were photographed with the microscope, and the fluorescent images were analyzed with Image J. The platelet surface coverage ratio was used as a quantitative index of platelet aggregation behavior, and the IC50 of Tirofiban for platelet inhibition was calculated under different shear rates. Flow cytometry was used to detect the platelet activation index (CD62P, PAC-1) in the whole blood at 52 μL/ min in channel with 80% occlusion. Results Tirofiban inhibited platelet aggregation in a dose-dependent manner, and the inhibitory effect was related to the shear rate. Under the shear rates of 11 μL/ min and 52 μL/ min, the aggregation was almost completely inhibited when the concentration in straight channel reached 100 nmol / L. When the concentration in channels with 80% occlusion reached 1 μmol / L, the aggregation was almost completely inhibited. IC50 values at 11 μL/ min and 52 μL/ min in straight channel were 2. 3 nmol / L and 0. 5 nmol / L, respectively. IC50 values at 11 μL/ min and 52 μL/ min in channels with 80% occlusion were 20. 73 nmol / L and 4. 5 nmol / L. Pathologically high shearforce induced an increase in platelet activation, which could be inhibited by Tirofiban. Conclusions Tirofiban can effectively inhibit shear-induced platelet aggregation, and different concentrations of Tirofiban should be given according to the thrombus formed in different shear force environment in clinic practice