This work presented a rapid, inexpensive, reliable, and flexible quantitative immunoassay for cardiac troponin I (cTnI). The assay was based on the concepts of one-step dual monoclonal antibody “sandwich” principle, the low density protein array, the nanogold probe, and the silver enhancement on the gold particles. The capture antibody (IgG1) coated supporting nitrocellulose membrane and the colloidal gold-labeled detection antibody (cAu-IgG2) were prepared before the detection. The detection procedure involved two steps, i.e., immunoreaction and silver amplification. The assay needs only small amounts of serum samples of patients. The whole detection procedure of the assay could be fulfilled within 40 min (much faster than the routine enzyme-linked immunosorbent assay (ELISA) that takes usually at least 3 hours for a turnaround test). The detection results could be easily imaged with a simple flatbed scanner or even observed with the naked eye. The assay showed good specific response to cTnI with very little cross-reactivity to the skeletal isoforms of troponin I (sTnI), cardiac troponin T (cTnT), and myoglobin (Mb). A cut-off value of 0.3 ng/ml was obtained from a reference control group (200 normal serum samples). 588 patients’ serum samples were assayed simultaneously by routine ELISA and this colloidal gold method to test the validity of the method. The data were analyzed using the statistical package SPSS version 11.0 (SPSS Inc.) There was no significant difference between these two assays (P = 0.66 > 0.05). The agreement between this method (≥ or < 0.3 ng/ml) and ELISA was 86%.

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.

Dysregulation of intracellular Ca2+ homeostasis plays an important role in mediating myocardial injury. We tested the hypothesis that treatment with trimetazidine (TMZ) would improve intracellular Ca2+ handling in myocardial injury of rats. The control group received saline only (10 ml kg-1 day-1, I.P.) for 7 days. In a second group, isoprenaline (ISO; 5 mg kg-1 day-1,S.C.) was administered to rats for 2 days to induce an acute injury of the myocardium. In a third group, treatment with TMZ (10 mg kg-1 day-1, I.P.) was initiated 1 day before ISO administration and continued for 7 days (n=7 rats in each group).Histopathological evaluation showed that TMZ prevented ISO-induced myocardial damage. TMZ preserved the ATP levels and decreased the maleic dialdehyde (MDA) content in the hearts compared with ISO-treated rats. The diastolic [Ca2+]I measured by loading with fura-2AM in isolated cardiomyocytes was increased significantly in ISO-treated rats compared to the control animals. TMZ prevented the rise of diastolic [Ca2+]I and the depression of caffeine-induced Ca2+ transients caused by ISO administration. The reduction in sarcoplasmic reticulum (SR) Ca2+ content in the heart cells and in cardiac SR Ca2+-ATPase activity in ISO-treated rats was abolished by TMZ, although there were no differences in SR Ca2+-ATPase protein levels between the control, ISO and ISO + 7 mz-treated rats. In addition, TMZ prevented the reduction in sarcolemmal L-type Ca2+ current density in the heart cells induced by ISO treatment. These results demonstrate that the treatment of rats with TMZ inhibited the increase of diastolic [Ca2+]I and prevented the decrease of SR Ca2+ content, SR Ca2+-ATPase activity and L-type Ca2+ current density in cardiomyocytes in ISO-mediatedmyocardial injury of rats. These changes inCa2+ handling could help to explain the favourable action of TMZ in myocardial injury.

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).