Correlation between plasma zine-α2-glycoprotein and degree of coronary atherosclerosis lesion / 重庆医学

Objective To observe the correlation between zinc-a2-glycoprotein (ZAG) in human plasma and the degree of coronary atherosclerosis lesion.Methods A total of 242 research subjects were included.The clinical indexes were perfected and plasma ZAG level was detected.The coronary angiography was performed.The subjects were divided into the coronary atherosclerosis group (CAD group) and control group according to the examination results.The Gensini score was used to assess the degree of coronary artery lesion,different degree subgroups were divided according to the assessment results.The correlation between the ZAG level with the clinical indexes was analyzed by Spearman analysis.The ROC curve was used to evaluate the efficiency of ZAG in the diagnosis of coronary atherosclerosis and its sensitivity and specificity were analyzed.Results The plasma ZAG level in the CAD group was significantly lower than that in control group,the difference was statistically significant [(45.12±5.02)μg/mL vs.(53.93±2.96)μg/mL,P＜0.01].With the increase of Gensini score,plasma ZAG level showed the decreasing trend,the difference among the groups were statistically significant (P＜0.05).The Spearman correlation analysis showed that body mass index (BMI),waist circumference and waist to hip ratio(WHR) were negatively correlated with ZAG (P＜0.05),and positively correlated with high density lipoprotein cholesterol(HDL-C,P＜0.05).The sensitivity of plasma ZAG for evaluating coronary atherosclerosis was 89.8％ and its specificity was 91.2％.Conclusion Plasma ZAG is negatively correlated with the severity of coronary atherosclerosis lesion,and its level detection has a certain value in the screening of coronary atherosclerosis.

Effects of JAZF1 overexpression on proinflammatory cytokines in hepatocytes induced by palmitic acid / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the effects of JAZF1 overexpression on the pro-inflammatory cytokines in hepatic steatosis.</p><p><b>METHODS</b>The model of hepatic steatosis was established by incubating hepatocytes with palmitic acid (PA) at 0, 0.125, 0.25, 0.5 and 1 mM dose and for 0, 6, 12, 24 and 48 hours, after which recombinant adenovirus expressing JAZF1 (Ad-JAZF1) was introduced to up-regulate expression. Triglyceride level was measured by GOD. Cell viability was detected by CCK-8. The mRNA and protein expression of TNF-alpha, MCP-1, IL-8 and JAZF1 was examined by RT-PCR, ELISA, and western blotting.</p><p><b>RESULTS</b>The PA-treated hepatocytes showed dose-dependent significant increases in TNF-alpha, MCP-1 and IL-8 mRNA expression for doses up to 0.25 mM; there were no significant increases for the highest doses of 0.5 and 1 mM. The 0.25 mM PA-treated hepatocytes showed time-dependent significant increases in TNF-alpha, MCP-1 and IL-8 mRNA expressions (FTNF-alpha = 26.51, FMCP-1 = 57.20, FIL-8 = 353.85, P less than 0.01), with the maximum level reached at 12 h and followed by a gradual decrease with longer treatment times. JAZF1 mRNA and protein expression was markedly increased in hepatocytes infected with Ad-JAZF1 (P less than 0.01). However, the AP-treated hepatocytes with JAZF1 overexpression showed down-regulation of TNF-alpha, MCP-1 and IL-8 mRNA expression (decreased by 89.69%, 77.68%, and 83.21%, respectively) and secretion (37%, 37% and 41%, respectively, P less than 0.01).</p><p><b>CONCLUSION</b>Stimulation of hepatocytes by the PA fatty acid in vitro promotes mRNA expression of TNF-alpha, MCP-1 and IL-8, but overexpression of JAZF1 inhibits the PA-induced expression and secretion of these factors.</p>

Association of N-terminal pro-brain natriuretic peptide with the severity of coronary artery disease in patients with normal left ventricular ejection fraction / 中华医学杂志(英文版)

<p><b>UNLABELLED</b>Backround N-terminal pro-brain natriuretic peptide (NT-proBNP) is a reliable predictor in acute coronary artery disease (CAD). Little is known about patients with stable CAD, especially Chinese patients with CAD. The aim of the present study was to investigate the association of NT-proBNP levels with the severity of CAD in patients with normal left ventricular ejection fraction.</p><p><b>METHODS</b>A total of 658 consecutive patients were divided into two groups based on angiograms: CAD group (n = 484) and angiographic normal control group (n = 174). The severity of CAD was evaluated by modified Gensini score, and its relationship with NT-proBNP was analyzed.</p><p><b>RESULTS</b>The prevalence of risk factors such as age, male gender, diabetes mellitus (DM), dyslipidemia, smoking, and family history of CAD in the CAD group were higher than that in the control group. In multivariate regression model analysis, age, gender, and DM were determinants of the presence of CAD. NT-pro BNP was found to be an independent predictor for CAD (OR:1.66 (95% CI: 1.06-2.61), P < 0.05). In a receiver operating characteristic (ROC) curve analysis, an NT-proBNP value of 641.15 pmol/L was identified as a cut-off value in the diagnosis or exclusion of CAD (area under curve (AUC) = 0.56, 95% CI: 0.51-0.61). Furthermore, NT-proBNP was positively correlated with Gensini score (r = 0.14, P < 0.001) in patients with CAD.</p><p><b>CONCLUSION</b>NT-proBNP was an independent predictor for Chinese patients with CAD, suggesting that the NT-proBNP level might be associated with the presence and the severity of CAD.</p>

Serum interleukin-10 levels and adverse events in patients with acute coronary syndrome: a systematic review and meta-analysis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Several studies investigating the prognostic utility of interleukin-10 (IL-10) in patients with acute coronary syndrome (ACS) have provided conflicting findings. The aim of the study was to assess the existing evidence regarding association between serum IL-10 levels and adverse events.</p><p><b>METHODS</b>Literature search was performed in PubMed, EMBASE, and Cochrane Trials Register databases from their inception to September 30, 2012. In addition, reference lists of the included articles and their related citations in PubMed were also reviewed for additional pertinent studies.</p><p><b>RESULTS</b>A total of 12 eligible studies comprising a total of 5882 patients were identified. The pooled relative risks for both studies reporting the risk estimates by IL-10 categories and studies reporting the risk estimates by unit IL-10 indicated an association between high IL-10 levels and adverse events. Sensitivity and subgroup analysis indicated that the results obtained in IL-10 categories were not stable.</p><p><b>CONCLUSIONS</b>Data from our meta-analysis supported the existence of a relationship between high serum IL-10 levels and adverse events in patients with ACS. Large study with longer follow-up is needed to confirm the findings.</p>

Expression of human alpha-galactosidase and alpha1,2-fucosyltransferase genes modifies the cell surface Galalpha1,3Gal antigen and confers resistance to human serum-mediated cytolysis / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To explore the strategies which reduce the amount of xenoantigen Galalpha1,3Gal.</p><p><b>METHODS</b>Human alpha-galactosidase gene and alpha1,2-fucosyltransferase gene were transferred into cultured porcine vascular endothelial cells PEDSV.15 and human alpha-galactosidase transgenic mice were produced. The Galalpha1,3Gal on the cell surface and susceptibility of cells to human antibody-mediated lysis were analyzed.</p><p><b>RESULTS</b>Human alpha-galactosidase gene alone reduced 78% of Galalpha1,3Gal on PEDSV.15 cell surface while human alpha-galactosidase combined with alpha1,2-fucosyltransferase genes removed Galalpha1,3Gal completely. Decrease of Galalpha1,3Gal could reduce susceptibility of cells to human antibody-mediated lysis, especially during co-expression of alpha-galactosidase gene and alpha1,2-fucosyltransferase gene. RT-PCR indicated positive human alpha-galactosidase gene expression in all organs of positive human alpha-galactosidase transgenic F1 mice including heart, liver, kidney, lung, and spleen, the amount of Galalpha1,3Gal antigens on which was reduced largely. 58% of spleen cells from F1 mice were destroyed by complement-mediated lysis compared with 24% of those from normal mice.</p><p><b>CONCLUSIONS</b>Human alpha-galactosidase gene and alpha1,2-fucosyltransferase gene effectively reduce the expression of Galalpha1,3Gal antigens on endothelial cell surface and confers resistance to human serum-mediated cytolysis. The expression of human alpha-galactosidase in mice can also eliminate the Galalpha1,3Gal antigens in most tissues and decrease the susceptibility of spleen cells to human serum-mediated cytolysis.</p>

Induction of Specific CTLs and Their Tumor Suppressing Activity in BALB/c Mice by Peptide HER2/neu Immunization / 中国肿瘤生物治疗杂志

Objective: To study the cellular immune responses and the anti-tumor effects induced by peptides derived from onco-protein HER2/neu. Methods: Two HER2/neu peptides compatible with H-2Kd binding motif as tumor rejection antigens were synthesized. The ability of inducing peptide-specific CTLs and suppressing the tumor growth in BALB/c mice immunized by HER2/neu peptide was analyzed. Results: HER2/neu peptides could promote the proliferation of BALB/c lymphocytes both in vitro and in vivo. HER2/neu peptide-specific CTLs could be induced from peptide-immu-nized BALB/c mice, which showed specifically killing effects on HER2/neu positive SP2/OHER2 cells but not on HER2/neu negative SP2/O cells. Moreover, the growth of SP2/OHER2 tumor were significantly suppressed in BALB/c mice immunized with HER2/neu peptides. Conclusion: These results suggested that it was feasible to use MHC-I epitopes derived from tumor-specific antigens as vaccines for cancer immunotherapy.