Objective To investigate angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in patients with hypertension in the elderly and it's relation with serum ACE level among Chinese population.Methods Polymorphism of ACE gene was categorized into three genotype:two deletion alleles (genotype DD),heterozygous alleles (genotype ID),and two insertion alleles (genotype II).Polymerase chain reaction(PCR) was used to examine ACE gene polymorphism.Compared the distribution of three ACE genotypes frequencies and D allele frequency in 56 patients with hypertension in the elderly and 40 healthy subjects,whose serum ACE levels were measured.Results The frequency of D allele was higher in the hypertension group (0.61) than in healthy subjects (0.46) (P<0.05).A significant difference in serum ACE level was observed between the hypertensives and healthy (31.0±11.1) U/L and (25.1±10.0) U/L respectively,P<0.05.The highest level of serum ACE activity was in genotype DD,and the lowest level in genotype II,and intermediate in genotype ID.A significant difference in serum ACE level was observed among the genotype DD and ID,and among the genotype DD and II.Conclusion ACE gene I/D polymorphism was associated with serum ACE level.D allele might be a genetic risk factor for hypertension in the elderly.

Objective To investigate the association between the insertion/deletion(I/D) polymorphism of angiotensin converting enzyme (ACE) gene and the myocardial infarction (MI) among Chinese population. Methods Polymerase chain reaction(PCR) was applied to the examination of ACE gene polymorphism. A comparison was performed between 50 patients with MI and another 50 healthy subjects.Results The frequencies of DD genotype (0.38) and D allele (0.58) were both higher among the MI group than that among the control group (0.16 and 0.41 respectively,P

Objective To investigate the role of nitric oxide synthase (NOS) in neurotoxic mechanisms of beta amyloid (A?) and the pathogenesis of Alzheimer′s disease (AD). Methods 35 adult rats were divided into 3 groups: normal control,saline injection,and A? 1 40 injection groups A? 1 40 was initially solubilized in saline (10?g/?l) and incubated for at least 1 week before use 1?l incubated A? 1 40 or saline were injected into dorsal blade of dentate gyrus in right hippocampus of rats Immunohistochemical assay of neuronal NOS (nNOS) and inducible NOS (iNOS) was performed at the 2 nd,10 th,and 30 th day after A? 1 40 or saline injection. Results The nNOS like immunoreactivity (nNOSLIR) neurons were found in different brain regions such as cortex,striatum and hippocampus of normal rats,and the number of neurons in dentate gyrus was 8 96?0 31 The number and configuration of nNOSLIR neurons were found without changes after saline injection (8 97?0 29) At 2,10,and 30 d after A? 1 40 injection,the number of nNOS neurons at the site around injection was significantly reduced (3 13?0 27,2 89?0 19 and 2 91?0 25 respectively),but there were no notable differences at these three experimental time points iNOS like immunoreactivity (iNOSLIR) cells were not found in any brain region of normal or saline injected rats After A? 1 40 injection,a large percentage of glia (mainly were astrocytes) had an activated morphological change and showed a strong iNOSLIR around the injection site The responded areas with these cells were 0 905?0 082,0 962?0 161 and 0 935?0 125 mm 2 respectively at 2,10 and 30 day after A? 1 40 injection,but there appeared no significant differences among them. Conclusions The results demonstrate that intrahippocampal injection of A? 1 40 may result in a significant loss of nNOS neurons and induce a considerable expression of iNOS in astrocytes,indicating that NOS may play an important role in neurotoxic mechanisms of A? and the pathogenesis of AD

Objective To evaluate the feasibility of detecting peripheral artery disease (PAD) using ankle-brachial index (ABI) determined by an electronic sphygmomanometer in patients with type 2 diabetes mellitus (DM). Method The brachial blood pressure and the ankle blood pressure were measured in each upper limbs and lower limbs by the Doppler ultrasound method and the electronic sphygmomanometer method in fifty-nine DM patients who were selected from Department of Geriatric Endocrinology of General Hospital of PLA. ABI was calculated with the formula of ABI = ankle systolic blood pressure/ brachial systolic blood pressure. The measurement data were expressed as x?s. Then the data of systolic pressure and ABI were analyzed by paired Student's t tests and correlations. The related diagnosis criteria of PAD, such as sensitivity, specificity, positive predictive value, negative predictive value, and the global accuracy were calculated. Furthermore, the correlation of brachial blood pressure as measured by the electronic sphygmomanometer and the mercury column sphygmomanometer was compared. Results There were no significant differences but good correlations between the data of systolic pressures and ABI obtained as measured by two methods. The correlation for systolic pressure was: right upper limbs 0.92, P

Objective To investigate the complex effect of soman and hypoxia on PC12 cell line as shown by the expression changes in IL-6/GP130, JAK1 and STAT1. Methods A cell model of intoxication by combining effect of hypoxia and soman was reproduced, and it was divided into four groups: control, soman intoxication, hypoxia combined with soman intoxication, and Genistein inhibition groups. PC12 cells were cultured in RPMI 1640 and were treated with NGF (50ng/ml) for seven days. The differentiated PC12 cells were then exposed to hypoxia in an incubator containing 5% CO2, 95% N2 and (or) incubated with soman (20?mol/L) for 2, 6, 12 or 24 hours. The expression levels of IL-6/GP130, JAK1, STAT1 mRNA and protein were assessed by RT-PCR and Western blot in PC12 cells. The products were sequenced by Sanger's double strand DNA sequence determination. Results In soman intoxicated group, the expression levels of IL-6/GP130, JAK1, STAT1 mRNA and protein were elevated in PC12 cell, reaching the peak level at 12 hours, and then lowered at 24 hours, but remaining higher than that of control group. In combined soman intoxicated and hypoxia group, the expression levels of IL-6/GP130, JAK1, STAT1 mRNA and protein reached the peak value at 6 hours, being higher than that of control group, soman intoxicated group and Genistein inhibition group. It was shown that the sequences of the products as amplified by RT-PCR were the same as that found in the GenBank. Conclusion Soman intoxication or (and) hypoxia up-regulate the expression of IL-6/GP130. Both hypoxic condition and soman treatment can up-regulate the expression of JAK1/STAT1 mRNA and protein in PC12 cells. JAK-STAT pathway may play a role in the mechanisms of brain injury resulted from hypoxia and soman poisoning.

Objective To analyze the characteristics of hypertension by cross-sectional study of the aged patients with metabolic syndrome (MS). Methods The data, collected from senile population who underwent medical examination in the General Hospital of PLA in 2005, were analyzed retrospectively in order to identify the clinical features of hypertension in aged patients with MS, and the significance of hypertension, as single or one of the components of MS, the prevalence of MS, including the prevalence of MS and its component ailments, prevalence of hypertension in MS population, the constituent ratio of MS and coronary heart disease, and cerebrovascular disease in patients with hypertension. Results The prevalence of MS was 32.19%, in which 8.16% patients were having all the four metabolic abnormalities. Hypertension was the most common metabolic abnormality with a prevalence of 61.78%, which tended to increase with increasing age. The most common combination in MS was abnormalities of blood pressure, glucose and BMI, with a prevalence of 24.67%. Among the population with hypertension, 46.67% of them could be diagnosed as MS, accounting for 89.57% of all MS patients. Patients with MS but without hypertension accounted for only 10.43%. Hypertension complicated with MS or another metabolic disorder showed a high risk of cardiovascular diseases, and the prevalence was 73.52% and 72.69%, respectively. No significant difference was found in the incidence of cerebrovascular disease. The prevalence of abnormal renal function was significantly increased in the group of MS with hypertension, by 1.69 and 1.65 folds of that in the group without MS and the group only with MS and without hypertension. Conclusions There was higher prevalence of MS in the elderly people, and in about 2/3 hypertensive patients it co-existed with one of the components of MS. Hypertension was the most common disorder in MS. Patients with MS and hypertension are having a higher risk of suffering from cardiovascular diseases and abnormal renal function.

Hyperglycemia has been identified as one of the important factors involved in the microvascular complications of diabetes, and has been related to increased cardiovascular mortality. Endothelial damage and dysfunction result from diabetes; therefore, the aim of this study was to determine the response of endothelial cells to stressful stimuli, modelled in normal and high glucose concentrations in vitro. Eahy 926 endothelial cells were cultured in 5 mmol/L or 30 mmol/L glucose conditions for a 24 hour period and oxidative stress was induced by exposure to hydrogen peroxide (H2O2) or tumour necrosis factor- α (TNF- α ), following which the protective effect of the glucocorticoid dexamethasone was assessed. Apoptosis, necrosis and cell viability were determined using an ELISA for DNA fragmentation, an enzymatic lactate dehydrogenase assay and an MTT assay, respectively. High glucose significantly increased the susceptibility of Eahy 926 cells to apoptosis in the presence of 500 μmol/L H2O2, above that induced in normal glucose (P<0.02). A reduction of H2O2- and TNF- α -induced apoptosis occurred in both high and low glucose after treatment with dexametha-sone (P<0.05). Conclusion high glucose is effective in significantly augmenting stress caused by H2O2, but not in causing stress alone. These findings suggest a mechanism by which short term hyperglycemia may facilitate and augment endothelial damage.

Coronary Artery Disease ; diagnosis ; etiology ; Graft Occlusion, Vascular ; diagnosis ; etiology ; Heart Transplantation ; adverse effects ; Humans

Animals ; Heart Function Tests ; Heme Oxygenase (Decyclizing) ; metabolism ; In Vitro Techniques ; Ischemic Preconditioning, Myocardial ; methods ; Male ; Malondialdehyde ; metabolism ; Rats ; Rats, Wistar

ObjectiveTo investigate the effect ofpinacidil hyperpolarizaed arrest on p38 mitogen-activited protein kinase (p38MAPK) during myocardial ischemia-reperfusion (I/R) in isolated rat hearts.MethodsFortyeight male SD rats weighting 250-300 g were randomly divided into 6 groups( n =8 each): natural arrest group (group A) ; St.Thomas group (group B) ; pinacidil hyperpolarization arrest group (group C) ;5-hydroxydecanoate (5-HD) group (group D);HMR-1098 group(group E) and 5-HD + HMR-1098 group(group F).Langendorff reperfusion model was established and K-H solution was retrogradely perfused for 15 min.In group A the hearts were arrested naturally afar perfusion was stopped; in group B St.Thomas solution was perfused; in group C pinacidil hyperpolarization solution was perfused; in the other three groups,K-H solution was perfused to isolated rat hearts for 10 min followed by 5 min 5-HD (group D) or HMR-1098(group E) or 5-HD and HMR-1098(group F) perfusion,then hyperpolarization arrest solution was given in each group.Each hearts suffered 60 min ischemia after arrest followed by 30 min K-H solution reperfusion.Coronary flow(CF),HR,left ventricular developed pressure( LVDP),left ventricular systolic pressure(LVSP) and the maximum rate of pressure rise (dp/dtmax) were measured at the end of 15 min K-H solution perfusion and at 20 min of reperfusion.Myocardial phosphatic and nonphosphatic p38MAPK expression was determined by Western blot at 30 min of reperfusion.ResultsCompared with group C,CF,HR,LVDP,LVSP and dp/dtmax were significantly decreased at 20 min of reperfusion and phosphatic p38MAPK expression was down-regulated,non-phosphatic p38MAPK expression was up-regulated at 30 min of reperfusion in groups A,B,D,E and F (P ＜ 0.05).Compared with group E,CF,HR,LVDP,LVSP and dp/ dtmax were significantly decreased at 20 min of reperfusion and phosphatic p38MAPK expression was down-regulated,non-phosphatic p38MAPK expression was up-regulated at 30 min of reperfusion in groups D and F ( P ＜0.05).ConclusionHyperpolarized arrest induced by pinacidil can improve cardiac function following myocardial I/R injury by up-regulating phosphatic p38MAPK expression,down-regulating non-phosphatic p38 MAPK expression and mitochondrial potassium channel is more important than membranous one during the regulation of phosphatic p38MAPK expression.