0.05) during follow-up angiography. Conclusion Pullback atherectomy is an effective method of plaque removal for coronary artery disease with optimal short-term angiographic results, and large cutter and eccentric lesion seem to come with good immediate and follow-up angiographic results.

Objective To study the relationship of secretory type Ⅱ phospholipase A2(sPLA2),coronary artery score and atherogenic index in patients with coronary artery disease.Methods One hundred and seventy nine patients confirmed by angiography were enrolled in the coronary heart disease(CHD)group and another 89 non-CHD patients were enrolled in the control group.Serum levels of sPLA2 were measured by ELISA in all subjects.The severity of coronary artery lesions was analysed in terms of coronary artery score by quantitive computer system(QCA).The atherogenic index(AI)was also evaluated in the 2 groups.Results Compared with the control group,serum level of sPLA2 was higher in the CHD group(55.18?11.75 u/mL vs 68.15?16.70 u/mL,P

Objective To evaluate the effect of Beijing' s separation of clinic from pharmacy reform.Methods Use difference-in-difference method based on dataset on patients having Urban Worker Medical Insurance from twelve state-owned hospitals.Results The reform incurs a decrease in the outpatient and inpatient expenditure on medicine per visit (30％ and 21％,respectively),a decline in hospital's pharmaceutical ratio (9 percentages and 4 percentages,respectively); reduces the outpatient and inpatient expenditure per visit (19 ％ and 8 ％,respectively),with a decrease in the out-of-pocket part (23％ and 3％,respectively),and a slight increase in the Medical Insurance's part (2％); raises hospital's turnover (11％),outpatient's visits (22％),and inpatient visits (43％).Conclusion The reform encourages physicians to prescribe more scientifically,and hence reduces patient 's expenditure on medicine and hospital's pharmaceutical ratio; leads to a decrease in patience' s expenditure per visit;raises hospital's turnover; and doesn't cause a significant increase in the expenditure from social medical insurance.

Objective To build finite-element models of cerebral hemorrhage on which a simulation study of electrical impedance tomography(EIT) is based.Method With a kind of four-layer concentric circle model of head,finite-element method and dynamic NOSER algorithm are performed to reconstruct the images.Result As to the single-focus model of the cerebral hemorrhage,the focus can be clearly imaged,while to the several-focus model,the focuses can be imaged with vaguely adjacent boundaries.Conclusion The dynamic NOSER algorithm is an effective method to image cerebral hemorrhage in EIT.

the two drugs than using one alone.

AIM:To investigate the effect of resveratrol on the apoptosis of endothelial progenitor cells (EPC) induced by tert-butyl hydroperoxide (tBHP) and the underlying mechanisms.METHODS:Total mononuclear cells were isolated from peripheral blood by density gradient centrifugation, and the cells were cultured on fibronectin-coated culture dishes.After 4 d of culture, attached cells were divided into control group, tBHP group, and resveratrol plus tBHP group (pretreated with resveratrol for 24 h and then cultured with 100 μmol/L tBHP for 6 h).The proliferation and migration abilities of the EPC were assessed by MTT assay, BrdU incorporation assay and modified Boyden chamber assay.The proportion of apoptotic EPC was determined by flow cytometry after staining with fluorescein isothiocyanate-conjugated Annexin V and propodium iodide.The level of reactive oxygen species (ROS) was determined by H2DCF-DA method.Caspase-3 activity was assay using a caspase-3 colorimetric assay kit.The protein levels of cleaved caspase-3, Bcl-2 and Bax were determined by Western blot.RESULTS:Resveratrol decreased EPC apoptosis induced by tBHP in a dose-dependent manner.Moreover, resveratrol increased the proliferation and migration abilities of the EPC.Resveratrol decreased intracellular ROS level, caspase-3 activity and the protein level of cleaved caspase-3.Resveratrol also decreased protein expression of Bax and increased protein expression of Bcl-2.CONCLUSION:Resveratrol attenuates EPC apoptosis induced by oxidative stress, and its mechanisms may be related to protecting the mitochondrial function.

Objective To investigate the relationship between HBV polymerase gene mutations and HBV genotypes in chronic hepatitis B (CHB) patients resistant to adefovir dipivoxil (ADV).Methods Blood samples were collected from 114 ADV-resistant CHB patients during February 2010 and May 2012.The HBV polymerase regions from serum samples were amplified with real-time PCR,and the PCR products were sequenced.Normal distribution data were presented as x ± s,and non-normal distribution data were presented as M (P25-P75) ; for homogeneous data analysis of variance and LSD-t test were performed.Results There were 8 types of HBV polymerase gene mutations in 114 CHB patients; single point mutation was detected in 102 patients (89.47％) and double or triple points mutations were detected in 12 patients (10.53％).rtA181V/T/S (57.89％),rtN236T (14.91％) and rtA181V/T/S + N236T (9.65％) were the predominant mutations.For 21 patients (18.42％) with HBV genotype B,rtN236T mutation was prevalent (47.62％,10/21) ; while for those with HBV genotype C (93,81.58％),rtA181V/T/S mutation was the predominant (65.59％,61/93).The differences of rtA181V/T/S (x2 =12.269,P ＜0.01) and rtN236T (x2 =18.658,P ＜0.01) mutation rates between B and C genotypes were statistically significant.Conclusion rtA181V/T/S,rtN236T and rtA181V/T/S + rtN236T are the major HBV polymerase gene mutation types in ADV resistant CHB patients,and mutation types are related with HBV genotypes.

AIM: To clarify the protective effect of long-term administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on ventricular remodeling after myocardial infarction (MI) in rats and its mechanisms. METHODS: Myocardial infarction were established by ligated left coronary anterior artery in SD rats, 24 hours after the operation, the survival rats were treated by gavage fluvastatin (20 mg?kg~(-1)?d~(-1)) or distilled water for 8 weeks. Doppler echocardiography, homodynamic and cardiac histomorphometry were used to assess the ventricular remodeling and cardiac function. The plasma levels of total cholesterol (Tch), creatinine (Cr), glutamic-oxal (o) acetic transaminase (AST), lipid peroxidation (LPO), glutathione perioxidase (GSH-PX), nitrogen monoxide (NO_2~-/NO_3~-) were detected. RESULTS: The Tch, Cr and AST were not significant difference in groups. Left ventricular end-diastole pressure, right relative weight, left ventricular posterior wall thickness, collagen volume fraction and the lung weight were decreased in AMI+fluvastatin group compared to AMI group (P

0.05)). The Val/Leu genotype and Leu allele frequencies in subjects without MI were significantly higher than that in subjects with MI (P

AIM: To examine the relation between serum concentrations of interleukin-18, interleukin-10, interleukin-6 and acute coronary syndrome (ACS). METHODS: Serum concentrations of IL-18, IL-10, IL-6 were measured in 17 patients with acute myocardial infarction (AMI), 30 patients with unstable angina pectoris (UAP), 15 patients with stable angina pectoris (SAP) and 20 controls by enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA).The relation between IL-18, IL-6 and IL-10 was compared. RESULTS: Serum concentrations of IL-18, IL-6 were significantly increased in the AMI and UAP groups in comparison with the SAP and control groups. Conversely, serum concentrations of IL-10 were significantly decreased in the AMI and UAP groups in comparison with the SAP and control groups. The correlation of concentrations of IL-18 and IL-6 had no significance; but the levels of IL-18 and IL-6 were negatively correlated with IL-10. CONCLUSION: Serum IL-18, IL-6 concentrations increase while serum IL-10 concentration decreases in patients with acute coronary syndromes. The inflammatory imbalance between IL-18, IL-6 and IL-10 may play an important role in the instability of atherosclerotic plaque.