Along with detection techniques develop continuously, sensitivity of cardiac troponin (cTn) detection becomes higher and higher.It improves diagnostic rate of patients with acute coronary syndrome,but accompanied by specificity reduction.Therefore, it's necessary to identify non-coronary heart disease that may lead to increase of cTn level.The present article made a review on manifestation of cTn in non-coronary heart disease.

Objective To investigate the effects and the mechanism of telmisartan and pyridoxamine on oxidative stress in spontaneously hypertensive rats(SHR).Methods SHRs(male,20 weeks of age) were randomly divided into four groups (n＝ 12 for each):hypertension control (HC) group (2 ml of distilled water),telmisartan group[T,6 mg/(kg · d)],pyridoxamine group[P,200 mg/(kg · d)]and combined group(TP,6 mg/kg telmisartan and 200 mg/kg pyridoxamine per day).Treatments were continued for 16 weeks.The normal control group included 13 WKY rats and received gastric lavage with distilled water.SBP of tail artery was measured during the intervention ervey 2 weeks.The levels of AGEs,SOD and MDA were measured by ELISA,xanthine oxidase and thiobarbituric acid methods after the intervention.Expressiones of NF-κBp65,ERK1 and ERK2 in renal tissue were detected by immunohistochemistry.Expression of RAGE in the renal cortex was investigated by Western blot.Results SOD activity was decreased in the HC group.The levels of AGEs,MDA,RAGE and the activations of NF-κBp65 and ERK1/2 were increased in the HC group (t＝4.53,5.52,2.93,al1 P＜0.05).After the 16 weeks' intervention,SOD activity was elevated in T,P and TP groups compared to that in HC group (P＜0.05).The positive expressiones of NF-κBp65,ERK1 and ERK2 were significantly reduced in T,P and TP groups compared to those in HC group (F＝20.13、148.82、18.70,all P＜0.05).All the positive expressiones of NF-κBp65,ERK 1and ERK2 were lowest in the TP group versus T and P groups (t ＝ 3.58、2.84,P ＜ 0.05).Conclusions Telmisartan and pyridoxamine can alleviate the oxidative stress in spontaneously hypertensive rats,which may result from the blocking effect of Ang Ⅱ,the reduction of AGEs-RAGE and inhibiting the signal pathways of ROS,NF-κBp65 and ROS-ERK1/2.

Objective:To explore influence of monotherapy or combined use of telmisartan and pyridoxamine on aor-tic remodeling in spontaneously hypertensive rats (SHR)and its possible mechanism.Methods:A total of 48 male SHE were randomly and equally divided into hypertension control group,telmisartan group,group,and telmisartan+ group (combined treatment group). Kyoto Wistar rats of the same age and gender were regarded as normal blood pressure control group (normal control group). Thoracic aortic section were examined by related staining af-ter 16 weeks intervention to calculate the ratio of aortic wall thickness to radius of lumen (Tw/Rl),the ratio of wall area to lumen area (W/L),and the area ratio of media elastic fiber/collagen fiber. Concentrations of related en-zymes and receptor etc. of abdominal aortic were measured.Results:Compared with hypertension control group, there was significant rise in ratio of media elastic fiber/collagen fiber area and significant reduction in media collagen fiber/media area ratio in telmisartan group,pyridoxamine monotherapy group and combined treatment group,and there were significant decrease in Tw/Rl [(0.17±0.02)vs. (0.12±0.01)]and W/L [(0.29±0.03)vs. (0.22± 0.02)]ratios in combined treatment group,P <0.05 or <0.01;immunohistochemistry indicated that there were significant reductions in thoracic aortic receptor of advanced glycation end products (RAGE) [(0.24±0.03)vs.(0.17±0.03)]and extracellular signal-regulated kinase 1/2 (p-ERK1/2 )expression [(0.63 ± 0.06)vs. (0.37± 0.04)]in combined treatment group,P <0.05,<0.01. Fluorescence quantitative PCR indicated that medication can significantly reduce nicotinamide adenine dinucleotide phosphate (NADPH)oxidase subunit p47phox mRNA ex-pression (P <0.01 all),especially in combined treatment group (P =0.001).Conclusion:Combined use of telmis-artan and pyridoxamine is superior to the single use of either drug on improving thoracic aortic remodeling in SHR, the mechanism may be related to it reduces local expression of RAGE and p-ERK1/2 ,and inhibits oxidase subunit p47 of NADPH.

[Summary] The basic data and serum targets of 3 349 residents were collected by multi stage stratified cluster random sampling and analyzed by correlation and regression analysis to access its association with cardiovascular risk factors. The result showed that morbidity of hyperuricemia was 18. 85% . The risk of hyperuricemia was raised in people with high triglycerides, high low-density lipoprotein-cholesterol ( LDL-C), low high-density lipoprotein-cholesterol(HDL-C), and low estimated glomerular filtration rate(eGFR). The people with hyperuricemia are usually accompanied with many cardiovascular risk factors.

Objective To explore the relationship of serum uric acid level with estimated glomerular filtration rate (eGFR) of elderly patients with hypertention based on a retrospective cohort study.Method The subjects included 465 cases who had a readmission after 3 years of follow-up in an original cohort of 1648 patients with diagnosis of essential hypertension in Fujian Provincial Hospital from August 2007 to September 2009.Multiple regression analysis was performed to examine the effect of serum uric acid level on renal function.Results Four hundred and sixty-five subjects were followed up for an average of 3.9 years.Mean patient age was 68.3 ± 9.7 years.There was no significant difference in uric acid between the baseline and 3 years later (P ＞ 0.05).Multiple regression analysis showed that after adjustment for age,gender,diabetes,body mass index,blood pressure etc,each 100 μmol/L-higher uric acid at baseline was associated with 4.40 ml· min-1· (1.73m2)-1 decrease in eGFR[95％ confidence interval (CI):-6.25--2.55,P ＜ 0.01].According to the alteration of the serum uric acid,all patients were divided into the group with decreased uric acid and the group with increase uric acid.The eGFR was lower in patients with increased uric acid than that in patients with decreased uric acid 3 years later [(70.63±21.54) ml· min-1 · (1.73m2)-1 vs (79.62±21.16) ml· min-1· (1.73 m2)-1,P ＜ 0.01] and there was no significant difference at baseline between the two groups (P ＞ 0.05).Multiple logistic regression analysis showed that after adjusting for aging,gender,diabetes,alteration of blood pressure etc,baseline uric acid was associated with a higher risk for eGFR decreasing more than 10 ml· min-1· (1.73 m2)-1 3 years later [hazard ratio (HR)=2.11,95％CI:1.24-3.59,P ＜ 0.01]; increased uric acid 3 years later resulted in a higher risk for renal function deterioration (HR=2.60,95％ CI:1.67-4.07,P ＜ 0.01).Conclusions Elderly hypertensive patients with baseline hyperuricemia have a lower eGFR,resulting an increased risk of chronic kidney disease.While the patients with declined uric acid had a lesser imparied renal function.It suggests that the improvement of uric acid may help to slow down the deterioration of renal function in elderly hypertensive patients.

AIM: To investigate the effects of adenovirus-mediated human tissue kallikerin (Ad-hKLK1) gene delivery on the proliferation, migration of VSMC_(SHR) induced by platelet derived growth factor-BB (PDGF-BB). METHODS: The VSMC_(SHR) proliferation induced by PDGF-BB was accessed by cell counting and methyl thiazolyl tetrazoliuin (MTT). The migration was assessed by modified Boyden chamber assay. Western blotting was used to determine the expressions of the cycle-independent kinase inhibitors p27~(Kip1) and p21~(Cip1).RESULTS: Proliferation of VSMC_(SHR) induced by PDGF-BB was inhibited after transfection of Ad-hKLK1 (20-100 MOI) in a MOI-dependent manner. The peak inhibition titer of Ad-hKLK1 fell on 100 MOI, with the peak inhibition rate of 39.3% (cell counting, n=3, P<0.01), 30.2% (MTT, n=3, P<0.01), peak stunning rate of cell-cycle in phase G0/G1 at 36.4%. The inhibitory effects of proliferation and cell-cycle caused by hKLK1 gene delivery were significantly abolished by Hoe140, a bradykinin B2 receptor antagonist. Migration of VSMC_(SHR) induced by PDGF-BB was inhibited after hKLK1 gene delivery, with the peak inhibitory rate of 34.6% (n=6, P<0.01). However the inhibitory effects of migration were not blocked by Hoe140. The protein expression of p27~(Kip1) and p21~(Cip1) increased significantly after the hKLK1 gene delivery, whereas Hoe140 nearly completely blocked these effects (n=3, P<0.01, respectively).CONCLUSION: The hKLK1 gene delivery may inhibit the proliferation and migration of VSMC_(SHR) induced by PDGF-BB. Bradykinin B2 receptor probably mediates the up-regulating expression of p27~(Kip1) and p21~(Cip1) that contributes to the inhibitory effects of proliferation of hKLK1. However, the inhibitory effects of migration by hKLK1 gene delivery may not be mediated by bradykinin B2 receptor.

ObjectiveTo investigate the effect of resveratrol on the expressions of E-selectin and monocyte chemoattractant protein-1 (MCP-1) in activated endothelial cells.Methods After being pretreated with resveratrol followed by tumor necrosis factor-α (TNF-α) stimulation, human umbilical vein endothelial cells (HUVEC) were randomly divided into three groups: TNF group,resveratrol+TNF-α group and control group. The expression of E-selectin molecule on the surface of HUVEC was detected by flow cytometric analysis and the mRNA expressions of E-selectin and MCP -1 were determined by semiquantitative RT-PCR. ResultsTNF-α induced the expression of E-selectin and MCP-I of HUVEC.Resveratrol (10 μmol/L) inhibited E-selectin expression.The positive cells of E-selectin in TNF group, resveratrol + TNF-α group and control group were(47.84±3.2)%, (15.3±1.7)% and (3.74±1.6)%, respectively, and the differences among the three groups were statistically significant (P<0.05). Conclusions Resveratrol may contribute to the anti-atherosclerotic effect by inhibiting the expression of E-seleetin and MCP-1 of HUVEC.

Objective To explore the effect of resveratrol on the expression of matrix metalloproteinases-9 (MMP-9) in soluble CD40 ligand (sCD40L)-activated macrophages. Methods Human monocytic cell line THP-1 cells under an inducing of phorbol ester differentiated into macrophages. Then the macrophages were sitimulated by sCD40L independently and after a preincubation with resveratrol. The mRNA expression of MMP-9 and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in macrophages were investigated by semiquantitative RT-PCR. The secretions of MMP-9 and TIMP-1 protein were measured by Western blot. The MMP-9 activity was analyzed by gelatin zymography technique. Results The expressions of MMP-9 gene(1.53±0.04 vs. 0.75±0.01,P＜0.05) and protein(244 930.8±31 268.6 vs. 192 976.8±20 223.1,P＜0.05)were higher in macrophages when stimulated by sCD40L. Resveratrol (10 μmol/L and 50 μmol/L)can inhibit the CD40L-induced gene expression and the protein secretion of MMP-9 (P＜0.01). The activity of MMP-9 was degraded by resveratrol (P＜0.05). Meanwhile resveratrol could increase the gene expression and protein secretion of TIMP-1 (P＜0.05). Conclusions Resveratrol can inhibit the CD40L-activated macrophage expression of MMP-9. It may be one of its mechanisms on antiatherosclerosis and stabilization of atheromatous plaques.

Objective To investigate the characteristics of plasma glucose, insulin secretion and changes of insulin resistance (IR) after a glucose load in obese children, and to predict islet β-cell function. Methods A total of 635 obese children were classified into normal glucose tolerance (NGT) group (n=483), impaired glucose regulation (IGR) group (n=112) and type 2 diabetes mellitus (DM) group (n=40) based on their glucose levels. Subjects were also divided into G1 group (23 kg/m2≤BMI<30 kg/m2, n=393) and G2 group (BMI≥30 kg/m2, n=242) based on their different BMI levels. Level of fast plasma glucose (FPG, 0.5 h-PG, 1 h-PG, 2 h-PG and 3 h-PG) and insulin (FINS, 0.5 h-INS, 1 h-INS, 2 h-INS and 3 h-INS) were measured 0 h, 0.5 h, 1 h, 2 h and 3 h after a glucose load. Insulin resistance index (HOMA-IR), whole body insulin sensitivity index (WBISI), function of pancreatic beta-cell (HOMA-β), first-phase insulin secretion index (ΔI30/ΔG30) and area under curve of insulin (AUCI) were calculated and compared between groups. Results The value of insulin at each time point was significantly higher in IGR group than that of NGT group. The values of insulin at 0.5 h, 1 h, and 2 h were significantly lower in DM group than those of IGR group, respectively (all P<0.05). Compared with NGT group, AUCI, HOMA-IR and HOMA-β increased, but WBISI and ΔI30/ΔG30 decreased in IGR group (all P<0.05). HOMA-IR increased but WBISI, HOMA-βandΔI30/ΔG30 decreased in DM group (all P<0.05). Compared with IGR group, AUCI, HOMA-βandΔI30/ΔG30 decreased in DM group (all P<0.05). Values of FINS, AUCI, HOMA-IR, 2h-PG and HOMA-βwere significantly higher in G2 group than those of G1 group, but WBISI decreased (all P<0.05). There were no significant differences in FPG and ΔI30/ΔG30 between these two groups. Conclusion From NGT, IGR to DM, the peak of insulin secretion is postponed, insulin resistance is getting heavier and the compensation of insulin secretion after a glucose load is increased first and then decreased.

Aim To investigate the effect of MAPK signal transduction pathway on the expression of TNF-? in AM(alveolar macrophage) of CB(chronic bronchitis) rats,meanwhile,to initially discuss the possible regulated target of TAL(triterpene acids of loquat.leaf),to explain the mechanism about anti-inflammatory action of TAL on CB rats.Methods The depurated AM was incubated with the special inhibitors of MAPK signal transduction pathway respectively(ERK,p38 or JNK) and the expression of TNF-? was observed by RT-PCR and Western blot.Using factorial design,TNF-? level in AM culture supernatant was detected by ELISA.Results The special inhibitors of ERK(PD98059) and p38(SB203580) could change the expression of TNF-? in AM of CB rats apparently.Factorial analysis shows there is statistical significance between TAL,PD98059/SB203580 and mixture of them.Conclusions TAL reducing the expression of TNF-? may be related with the inhibition of ERK and p38 signal transduction pathway.It may be one of the mechanisms by which TAL has the preventive and therapeutic effects on chronic bronchitis.