Objective To explore the value of 64-slice multi-detector computed tomography coronary angiography (64SCTA) in detecting the coronary artery plaque and to analyze the risk factors for unstable plaque. Methods A total of 112 inpatients who had been diagnosed as coronary artery disease by 64SCTA received catheter coronary angiography (CAG). The levels of serum endothelin-1 (ET-1), matrix metalloproteinase-9 (MMP-9), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) were measured. The effect of 64SCTA in detecting the coronary artery plaque was evaluated as compared with CAG. The patients were divided into the soft plaque group (n=51) and non-soft plaque group (n=61) according to the CT value of correctly detected plaque. The differences in the above detection indexes between two groups and the risk factors for soft plaque forming were analyzed. Results The 64SCTA had 87.4% sensitivity and 87.1% specificity in detecting coronary artery plaque, the positive predictive value was 82.2% and the negative predictive value was 91.0%. There were significant differences between soft plaque group and non-soft plaque group in the levels of MMP-9, IL-6, hs-CRP, the number of coronary lesions and the composition ratios of gender, diagnosis and diabetes. Logistic regression analysis showed that MMP-9>5.231 ng/L (P=0.0215, OR=2.33, 95%CI 1.13-4.79), hs-CRP>3.583 mg/L (P=0.0008, OR=4.32, 95%CI 1.84-10.15) and unstable angina pectoris (P=0. 0339, OR=4.33, 95% CI 1.12-16.77) were the risk factors for soft plaque formation. Conclusions 64SCTA has highervalue in detecting the coronary artery plaque, and is one of most reliable means in non-invasive methods. MMP-9, hs-CRP and unstable angina pectoris are independent risk factors of plaque instability.

Objective To investigate the effects of sevoflurane on inhibition of growth of human lung adenocarcinoma A549 cells by cisplatin and γ ray.Methods The human lung adenocarcinoma cell line A549 was seeded in culture plate.After being cultured for 24 h,the cells were randomly divided into 6 groups (n =6each):control group (group C),sevoflurane group (group S),cisplatin group (group D),cisplatin + sevoflurane group (group DS),γ ray group (group R) and γ ray + sevoflurane group (group RS).A549 cells were exposed to 2.5% sevoflurane for 4 h in group S.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then incubated for 4 h in group D.Cisplatin with the final concentration of 3 mg/L was added to the culture medium and the cells were then exposed to 2.5 % sevoflurane for 4 h in group DS.A549 cells were exposed to γ irradiation (2 Gy) for 4 h in group R.A549 cells were exposed to γ irradiation (2Gy) and to 2.5% sevoflurane for 4 h in group RS.The cells were cultured for another 24 h after the end of treatment,the colony formation was detected and the rate of colony formation was calculated by colony formation assay.Proliferation of A549 cells was measured by plate colony formation and MTF assay and the rate of proliferation inhibition was calculated.Cell apoptosis was detected with flow cytometer.The expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-3 was detected by Western blot.Results Compared with group C,the rate of colony formation was significantly decreased,the rate of proliferation inhibition and percentage of apoptotic cells were increased,XIAP expression was down-regulated and caspase-3 expression was up-regulated in groups S,D,DS,R and RS (P ＜ 0.05).The rate of colony formation was significantly lower,the rate of proliferation inhibition and percentage of apoptotic cells were higher,XIAP expression was lower and caspase-3 expression was higher in group DS than in groups S and D,and in group RS than in groups S and R (P ＜ 0.05).Conclusion Sevoflurane can enhance cisplatin and γ ray-induced inhibition of growth of human lung adenocarcinoma A549 cells,and downregulation of XIAP expression and up-regulation of caspase-3 expression may be involved in the mechanism.

Early diagnosis of esophageal cancer is essential for improving both the effectiveness of esophageal cancer treatment and the prognosis of patients.As a new technology for esophageal cancer early diagnosis,narrow-band imaging (NBI) enables surgeon to clearly observe the mucosa and submucosal blood vessels changes in early esophageal cancer.It has initially shown excellent application value in the early diagnosis.In particular it has obvious advantages to the ordinary white light endoscopy which is currently used in esophageal cancer early diagnosis.If combined with Lugol iodine staining,magnifying endoscopy and other diagnostic methods in clinical,NBI will have a better value in early diagnosis of esophageal.

Objective To preliminarily evaluate the role of Ras homolog gene (Rho)/Rho-associated coiled coil-forming protein kinase (ROCK) signaling pathway in propofol-induced inhibition of metastasis of human gastric cancer cells.Methods Human gastric cancer MKN-45 cells cultured in vitro,with the concentration of 1.0× 106 cells/ml,were seeded in culture plates,and incubated for 24 h.The plates were then randomly divided into 4 groups using a random number table:control group (group C),propofol group (group P),lysophosphatidic acid group (group L) and propofol + lysophosphatidic acid group (group PL).Group C received no administration.In group P,propofol at the final concentration of 16 μg/ml was given.In group L,lysophosphatidic acid at the final concentration of 1 μmol/L was administered.In group PL,propofol and lysophosphatidic acid were given with the final concentration of 16 μg/ml and 1 μmol/L,respectively.All the cells were then incubated for another 24 h.The migration of cells was determined by wound healing assay,and cell migration rates were calculated.The invasion of cells was determined by Transwell assay,and the invaded cells were counted.The expression of matrix metalloproteinases-2 (MMP-2),MMP-9,RhoA,and ROCK1 in cells was detected by Western blot.Results Compared with group C,cell migration rates and the number of invaded cells were significantly increased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was up-regulated in group L,and cell migration rates and the number of invaded cells were decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group P.Compared with group L,cell migration rates and the number of invaded cells were significantly decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group PL.Conclusion Inhibition of RhoA/ROCK1 signaling pathway is involved in the mechanism by which propofol decreases metastasis of human gastric cancer cells.

Objective To evaluate the effect of propofol on invasiveness of human gastric cancer MKN-45 cells.Methods Human gastric cancer cell line MKN-45 were seeded in culture plates.After being cultured for 24 h,the cells were randomly divided into 5 groups(n =12 each):control group (group C),intralipid group (group Ⅰ),4 μg/ml propofol group (group P1),8 μg/ml propofol group (group P2) and 16μg/ml propofol group (group P3).The cells were treated with 10％ intralipid and 4,8 and 16 μg/ml propofol for 24 h in I and P1-3 groups,respectively.The cells were then cultured for another 24 h.The migration of cells was determined by cell scratch test.The invasion of cells was determined by Transwell invasion assay.The expression of RhoA and ROCK1 was detected by Western blot.Results Compared with group C,the cell migration and invasion were significantly decreased,and the expression of RhoA and ROCK1 was down-regulated in P1-3 groups,and no significant changes were found in the parameters mentioned above in group Ⅰ.With the increasing concentrations of propofol,the cell migration and invasion were gradually decreased,and the expression of RhoA and ROCK1 was gradually down-regulated in P1-3 groups.Conclusion Propofol can inhibit the invasiveness of human gastric cancer MKN-45 cells cultured in vitro dose-dependently and inhibition of RhoA/ROCK1 signaling pathway may be involved in the mechanism.

Objective To evaluate the effect of percutaneous coronary intervention (PCI) on left ventricular function in patients with different types of myocardial infarction and to explore the correlation factors for the left ventricular function.Methods A total of 43 patients diagnosed as acute myocardial iffarction were enrolled in this study.The perfusion and delayed enhancement magnetic resonance imaging (DE-MRI) was applied to observe the following parameters before the PCI and at month 6 after the procedure:infarct mass,left ventricular ejection fraction (LVEF) and abnormal wall motion score.The subjects were divided into the following three groups by the transmural extent of myocardial infarction manifested in the DE-MRI:the transmural enhancement group,the nontransmural group and the mixed group.Laboratory test was done to detect the level of endothelin (ET),matrix metal enzyme 9 (MMP-9) and high sensitive C reactive protein (hsCRP) before PCI and at month 6 after the procedure.The t test was used to compare the differences among the groups and the multiple regression analysis was taken to explore the correlation factors for the left ventricular function.Results Compared with the parameters before PCI,the infarct mass after PCI significantly decreased in the nontransmural group and the mixed group [(4.0 ± 2.9) g/cm3 vs (9.8 ±5.6) g/cm3 and (6.0 ±3.5) g/cm3 vs (11.8 ±6.2) g/cm3,all P ＜0.05],while LVEF was significantly improved after PCI in both groups [(52.6 ± 15.4) ％ vs (41.9 ± 16.3) ％,(45.6 ± 15.4)％ vs (38.9 ± 16.3)％,all P ＜0.05].The infarct mass was an independent correlation factor for LVEF before PCI (RR =0.318,P ＜0.05) and LVEF after PCI(RR =0.293,P ＜0.05).LVEF before PCI was independently correlated with the level of hsCRP (RR =0.318,P ＜ 0.05).Conclusion The effect of PCI on the improvement of left ventricular function differs in patients with different extent of myocardial infarction,which is correlated with the amount of survival myocardium and the inflammatory factors.

Objective To detect and type herpes simplex virus (HSV) in genital lesions of the patients attending STD clinic. Methods Clinical data were collected and analyzed from patients with anogenital non-herpetic lesions including induration or furuncle, fissure, folliculitis, single ulcer and so on. HSV was detected and typed by culture and PCR with specimens taken from these lesions. Results One hundred and five cases were recruited in this study. Among them, 18 cases presented induration (furuncle), 15 fissure, 16 folliculitis, 7 abrasion, 12 single ulcer, 25 nonspecific erythema and 12 balanoposthitis with edema and exudation. HSV was found in 33.3%(6/18), 20%(3/15), 37.5%(6/16), 28.6%(2/7), 33.3%(4/12), 20%(5/25) and 50%(6/12) of these lesions, repectively, by PCR, while in 22.2%(4/18), 13.3%(2/15), 25%(4/16), 14.3%(1/7), 33.3%(4/12), 8%(2/25) and 41.7%(5/12), repectively, by viral culture. The positive rates of HSV from all these non-herpetic lesions were 30.5% (32/105) and 21% (22/105), respectively (? = 0.095, P = 0.114), by PCR and viral culture. The results of HSV typing were consistent between PCR and immunofluorescence with type-specific monoclonal antibodies. Among those with HSV infections, HSV-1 infection acounted for 9.4% (3/32), and HSV-2 90.6% (29/32). Conclusions The clinical manifestations of genital HSV infections vary, and HSV could be isolated from lesions of induration (furuncle), fissure, folliculitis, abrasion, single ulcer, nonspecific erythema and balanoposthitis with edema and exudation. HSV-2 is the predominant type.

Objective To investigate the relationship between serum levels of alanine aminotransferase (ALT)or aspartate aminotransferase (AST)apportioned by the same hepatic parenchyma cell volume and liver histological necroinflammation grades in HBeAg-negative chronic hepatitis B (CHB)patients.Methods A total of 145 CHB patients were divided into four groups:Gl,G2,G3 and G4 based on the liver histological necroinflammation grade.The serum ALT and AST levels were determined by automatic biochemical instrument in these four groups.Furthermore,serum ALT and AST levels were then apportioned by the same hepatic parenchyma cell volume.The data were analyzed by ANOVA.Results Mean serum ALT levels in G1,G2,G3 and G4 groups were (35.3±29.1),(91.6±120.4),(111.6± 116.1)and (118.0±122.1)U/L,respectively,and the serum ALT levels apportioned by same hepatic parenchyma cell volume were ( 54.0 ± 45.1 ),( 144.2 ± 184.9 ),(191.3± 204.8)and (215.1 ± 226.5)U/L,respectively.The pairwise comparison between G1 and other three groups all showed statistically significant difference (P＜0.05).Meanwhile,AST levels in G1 to G4 groups were (35.5± 29.0),(64.9±71.7),(96.0±81.9)and (102.8±77.0)U/L,respectively and the serum AST levels apportioned by the same hepatic parenchyma cell volume were (54.3±44.6),(102.3± 107.9),(165.2±148.7)and (189.4±145.4)U/L,respectively.The pairwise comparison between G1 and G3,G1 and G4,G2 and G3,G2 and G4 all showed statistically significant difference (P＜0.05).Conclusion Both AST and ALT levels are sensitive indicators for liver inflammation grading in HBeAg-negative CHB patients during the natural history of the disease.

Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the up-regulation of expression of Cav3.2 T-type calcium channels in spinal cord in a rat model of neuropathic pain (NP).Methods Forty-eight male Sprague-Dawley rats,aged 3 months,weighing 220-250 g,were randomly divided into 6 groups (n =8 each)∶ sham operation group (group S),group NP,dimethyl sulfoxide group (group D) and different concentrations of a specific CaMK Ⅱ inhibitor KN93 groups (groups K1-3).NP was produced by chronic compression of dorsal root ganglion.The rats in groups D and K1-3 received a single intrathecal injection of dimethyl sulfoxide and KN93 15,30,60 nmol/L (10 μl),respectively,on 5th day after NP.Paw withdrawal threshold to von Frey filament stimulation (MWT) and paw withdrawal latency to thermal nociceptive stimulus (TWL) were measured before NP,before intrathecal injection on 5th day after NP,and at 30 and 60 min and 3,6 and 8 h after intrathecal injection on 5th day after NP (T1-7).The rats were sacrificed after the measurement of pain threshold at T7 and their lumbar enlargements were removed to detect the expression of Cav3.2 mRNA and protein using Western blot and RT-PCR.Results Compared with group S,MWT was significantly decreased,TWL was shortened and the expression of Cav3.2 mRNA and protein was up-regulated in NP,D and K1-3 groups (P ＜ 0.05).Compared with NP group,MWT was significantly increased,TWL was prolonged and the expression of Cav3.2 mRNA and protein was down-regulated in a concentration-dependent manner in K1-3 groups (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group D (P ＞ 0.05).Conclusion CaMK Ⅱ is involved in the development and maintenance of chronic NP by up-regulating the expression of Cav3.2 T-type calcium channels in rat spinal cord.

Objective:To evaluate the relationship between chemokine CXC-ligand 16 (CXCL16) and natural killer T cells during renal fibrosis in mice with acute kidney injury (AKI).Methods:Twenty-four healthy male C57BL/6 mice, aged 8-10 weeks, weighing 20-30 g, were divided into 4 groups ( n=6 each) using a random number table method: control group (group C), AKI group, control+ rCXCL16 group (group C-rCXCL16) and AKI+ rCXCL16 group.In AKI-rCXCL16 and AKI groups, folic acid 250 mg/kg was intraperitoneally injected to induce AKI in anesthetized mice, and rCXCL16 0.1 mg/kg and the equal volume of solution were intraperitoneally injected, respectively, at 3, 6, 9 and 12 days after injection of folic acid.The equal volume of solution and rCXCL16 were intraperitoneally injected at the corresponding time points in group C and group C-rCXCL16, respectively.The orbital blood samples were taken on day 14 after injection of folic acid for determination of the serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The renal tissues were obtained for measurement of the renal fibrosis size (using Sirius red staining and Masson staining), for determination of the expression of fibronectin (FN), collagen-Ⅲ (Col-Ⅲ) and α-smooth muscle actin (α-SMA) (by immunofluorescence) and expression of interleukin-4 (IL-4), mannose receptor (CD206) and arginase 1 (Arg-1) mRNA (by real-time polymerase chain reaction), and for evaluation of the ratio of CD1d Tetramer + -IL-4 + cells (by flow cytometry). Results:Compared with group C, the serum BUN and Cr concentrations were significantly increased, the renal fibrosis size was increased, the expression of IL-4, CD206, Arg-1 mRNA, FN, Col-Ⅲ and α-SMA was up-regulated, and the ratio of CD1d Tetramer + -IL-4 + cells was increased in AKI and AKI-rCXCL16 groups ( P<0.05), and no significant change was found in the parameters mentioned above in group C-rCXCL16 ( P>0.05). Compared with group AKI, the serum BUN and Cr concentrations were significantly increased, the renal fibrosis size was increased, the expression of IL-4, CD206, Arg-1 mRNA, FN, Col-Ⅲ and α-SMA was up-regulated, and the ratio of CD1d Tetramer + -IL-4 + cells was increased in group AKI-rCXCL16 ( P<0.05). Conclusion:The mechanism by which CXCL16 is involved in the process of renal fibrosis is related to the recruitment of natural killer T cells secreting IL-4 which regulates macrophage M2 polarization in mice with AKI.