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.

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.

[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.

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.

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.

Objective To investigate the association of urinary albumin-to-creatinine ratio (UACR) and the diameter of retinal vessel in population with essential hypertension in Fujian coastal area.Methods Central retinal artery and vein equivalents (CRAE and CRVE) were measured from the avoiding mydriatic digitized photographs and semi-automatic fundus analysis software,as well as albumin and urine creatinine.Results There were significant differences in CRAE levels among the normal control group,normoalbuminuria with essential hypertension group and microalbuminuria with essential hypertension group [(135.68 ± 10.10) μm,(129.79 ± 10.48) μm,(125.29 ± 11.17) μm,all P values ＜0.01].The CRAE levels were significantly negative correlated with UACR (r =-0.29,P ＜ 0.01).Linear regression analysis showed CRAE was associated with UACR in the patients with hypertension(β =-5.0,P ＜ 0.01).Logistic regression analysis showed,systolic blood pressure (β =1.08,P =0.02) was risk factor for CRAE abnormality.The CRAE abnormality was increased in turn in the normal control group,normoalbuminuria with the essential hypertension group and microalbuminuria with essential hypertension group (P ＜ 0.01).Conclusion The reduction of central retinal artery diameter are associated with the hypertensive renal damage.UACR and CRAE could be used to evaluate the microvascular lesions and be used as an indicator to assess the target organs damage in essential hypertension patients.

Background Resveratrol has been unanimously recognized as an cardiovascular protective substance in red wine. It has been speculated that the anti-atherosclerosis effect of resveratrol is ascribed to its powerful anti-inflammatory effect. Objective To investigate the effects of resveratrol on injured human umbilical veno-endothelial cells (HUVEC) and the reactive oxygen species(ROS) production induced by TNF-? or soluble CD40L (sCD40L). Methods Cultured HUVEC were pre-incubated with resveratrol(1-50 ?mol/L) for 2 hours and then treated with TNF-?(10 ?g/L) or sCD40L?(10 ?g/L) for another 4 hours. MTT assay was used to detect proliterative activity of HUVEC. Immunofluorescence microscopy was used for determination of ROS expression. Results Both TNF-? and sCD40L impaired HUVEC proliferation (-32.7% and -26% vs control,P

Objective To study the effect of annexin A1 on cardiac function,tumor necrosis factorα(TNF?α),and interleukin 1β(IL?1β)in diabetic rats. Methods Twenty?four SD rats were randomly divided into normal control and diabetic groups. The type 2 diabetes model was in?duced with a high?glucose and high?fat diet and administration of low?dose streptozotocin.Left ventricular end?diastolic volume(LVEDV),left ven?tricular end?systolic volume(LVESV),peak velocity of early diastolic mitral?to?late diastolic peak velocity(e/a)ratio,left ventricular ejection frac?tion(LVEF),and stroke volume(SV)were measured by using color Doppler ultrasonography at the end of week 8. The expression levels of TNF?αand IL?1βin blood were measured by using enzyme?linked immunosorbent assay,and the expression level of annexin A1 in blood was measured at weeks 0,4,and 8 by using real?time polymerase chain reaction. Results Compared with the normal control group,the diabetic group had de?creased LVEDV,e/a,and SV(P<0.05).The annexin A1 expression level in the diabetic group decreased significantly after 8 weeks(P<0.01). The TNF?αand IL?1βlevels in the diabetic group were significantly higher than those in the normal control group(P<0.05)and increased signifi?cantly after 8 weeks(P<0.01). Annexin A1 level correlated with the TNF?αand IL?1βlevels in the diabetic group(P<0.01). Conclusion Annexin A1 expression shows an anti?inflammatory effect that improved the cardiac function of diabetic rats.