An anodic stripping voltammetric method for the determination of cardiac troponin I (cTnI) at a MCM-41 mesoporous material modified carbon paste electrode (MCM-MCPE) was investigated. The test was based on the dual monoclonal antibody “sandwich” principle using colloidal gold as a labeled substrate. Four main steps were carried out to obtain the analytical signal, i.e. electrode preparation, immunoreaction, silver enhancement, and anodic stripping voltammetric detection. The anodic stripping peak current increased linearly with the concentration of cTnI over the range of 0.8–5.0 ng/ml. A detection limit of 0.5 ng/ml was obtained. The established method was applied to detect cTnI in acute myocardial infarction (AMI) samples using routine enzyme-linked immunoadsorbent assay (ELISA) for comparison analysis, and good results were obtained.

The present study was designed to determine whether or not an increase in endothelial intracellular concentration of calcium ([Ca2+]i) evokes endotheliumdependent contractions in the aorta from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acetylcholine, adenosine triphosphate (ATP) and the calcium ionophore, A 23187, produced endothelium-dependent relaxations in isolated aortic rings of both WKY and SHR. These relaxations in response to the three agonists were significantly smaller in the SHR when compared with the WKY. Endothelium-dependent contractions to acetylcholine, ATP and A 23187 were observed only in the aorta isolated from the SHR. In the presence of NG-nitro-Larginine, an NO synthase inhibitor, the endothelium-dependent contractions in response to acetylcholine, ATP and A 23187 were potentiated significantly in the aorta SHR and were unmasked in that of WKY. However, the contractions were still significantly greater in SHR than in WKY. These contractions were abolished by indomethacin and valeryl salicylate (two cyclo-oxygenase inhibitors) as well as by S 18886 (a TP-receptor antagonist), indicating that the endothelium-dependent contraction produced by the three agonists share the same characteristics. The results of the present study indicate that the release/generation of endotheliumderived contracting factor, requires an increase in endothelial [Ca2+]i.

The cardiovascular pre-participation screening proposal for young competitive athletes has the potential to save young lives. This study aimed to identify individuals at risk for potentially lethal cardiovascular diseases in athletes before competition. Between June 2005 and July 2005, 351 (170 male and 181 female) elite Chinese athletes from 21 sports were profiled. The 12-lead electrocardiogram and echocardiography were employed to evaluate cardiovascular diseases. The vast majority had no definitive evidence of cardiovascular disease. However, abnormal ECGs were identified in 16 athletes (4.5%), including 4 with distinctly abnormal and 12 with mildly abnormal patterns. Only 13 athletes (3.7%) had echocardiographic evidence of relatively mild valve regurgitation that had not been previously suspected. In three athletes with relatively mild ventricular septal hypertrophy (13-14 mm), it was not possible to discern with absolute certainty whether the wall thickening was a manifestation of hypertrophic cardiomyopathy or secondary to athletic conditioning (‘‘athlete heart’’). This screening protocol identified no athletes with definite evidence of hypertrophic cardiomyopathy, Marfan’s syndrome or other cardiovascular diseases that convey a significant potential risk for sudden death or disease progression during athletic activity. This is largely due to the relative low prevalence of conditions resulting in sudden cardiac death in young athletes and high false positive/ negative rates in the tests used as part of the screening process (due to a large overlap between cardiovascular changes due to pathology and those due to intense training).

We have investigated the effects of insulin on the phosphorylation of glycogen phosphorylase in skeletal muscle. Rat epitrochlearis muscles were incubated in vitro with 32Ptio label cellular phosphoproteins, before being treated withho rmones. Phosphorylase, phosphorylase kinase, and glycogen synthase were immunoprecipitated under conditions that prevented changes in their phosphorylation states. Based on measurements of the activity ratio( -AMP/+AMP) and the 32P content of phosphorylase, 4-8% of the phosphorylase in untreated muscles appeared to be phosphorylated. Epinephrine promoted increases of approximately 4-fold in the32P content and activity ratio. Neither these effects nor the epinephrine-stimulated increases in phosphorylation of glycogen synthase andp hosphorylase kinase were attenuated by insulin. However, insulin at physiological concentrations rapidly decreased the 32P content of phosphorylase in muscles incubated without epinephrine. Results from peptide mapping experiments indicate that phosphorylase was phosphorylated at a single site in both control anhdo rmonetreated muscles. The maximum effect of insulin on phosphorylase represented a decrease in32Po f approximately 50%. By comparison, the 32P content of glycogen synthase and the

Three different kinds of molecular sieves (mesoporous materials SBA-15 and MCM-41, microporous zeolite Y) have been used as the modifiers to fabricate the modified carbon paste electrodes (MCPEs). Based on these MCPEs, a novel electrochemical immunoassay for cardiac troponin I (cTnI) combining the concepts of the dual monoclonal antibody ‘‘sandwich’’ principle, the silver enhancement on the nanogold particles, and the anodic stripping voltammetry is described. Four main steps were carried out to obtain the analytical signal, i.e. electrode preparation, immunoreaction, silver enhancement, and the anodic stripping voltammetric detection. Among the molecular sieves selected in this study, the performance of SBA-15 was the best probably due to its rather larger pore size. A linear relationship between the anodic stripping peak current and the concentration of cTnI from 0.5 to 5.0 ng/ml and a limit of detection of 0.2 ng/ml were obtained using SBA-15 modified CPE (SBA-MCPE). The established method was tested by determining cTnI in acute myocardial infarction (AMI) samples using enzyme-linked immunoadsorbent assay (ELISA) for comparison analysis, and good results were obtained. _ 2005 Elsevier Inc. All rights reserved.