No association between thrombospondin-4 A387P polymorphism and acute coronary syndrome in Chinese Han population

Objective： The thrombospondin-4 （TSP-4） gene G29926C （A387P） polymorphism was recently reported to be associated with an increased risk of MI （myocardial infarction） in American population. However, several subsequent studies produced controversial findings. The aim of this study was to explore the possible association between TSP-4 A387P polymorphism and ACS （acute coronary syndrome） in Chinese Han population. Methods：A case-control study including 412 patients with ACS and 337 controls free from CAD （coronary artery disease） was conducted. TSP-4 A387P polymorphism was determined by PCR （polymerase chain reaction） and RFLP （restriction fragment length polymorphism） analysis. Results：Slightly decreased frequency of GC genotype was observed in patients with ACS, compared with controls（5.3% vs. 7.1%）, but the difference did not reach statistical significance （P = 0.31 ）. Similarly, the prevalence of C allele was 2.7% and 3.6% for ACS and control groups, respectively （P = 0.32）. None of homozygote was detected for C allele. Further analyses in subjects subgrouped according to sex and age also showed no association of TSP-4 A387P polymorphism with ACS. Furthermore, after adjustment for conventional risk factors by multiple logistic regression analysis, the carrier prevalence of C allele did not differ significantly between ACS and control groups （OR = 0.85; 95% CI：0.45-1.59; P = 0.60）. Conclusion：The present study suggested that the TSP-4 A387P variant showed a low prevalence compared with western populations and failed to associate with an altered risk of ACS in Chinese Han population. The findings further supplement experimental data for TSP-4 gene study of coronary disease.

Three-Biomarker Joint Strategy for Early and Accurate Diagnosis of Acute Myocardial Infarction via a Multiplex Electrochemiluminescence Immunoarray Coupled with Robust Machine Learning

Acute myocardial infarction(AMI)represents a leading cause of death globally.Key to AMI recovery is timely diagnosis and initiation of treatment,ideally within 3 h of symptom onset.Cardiac troponin T(cTnT)is the gold standard yet a low cTnT result cannot rule out AMI at early times.Here,we develop a three-biomarker joint strategy for early and accurate diagnosis of AMI via an electrochemiluminescence(ECL)immunoarray coupled with robust machine learning.The ECL immunoarray is based on an array microchip with a singleelectrode and chemiluminescent immuno-Gold(ciGold)nanoassemblies.The ciGold immunoarray was obtained by successively assembling nanocomposites of Cu^(2+)/cysteine complexes and N-(aminobutyl)-N-(ethylisoluminol)bifunctionalized gold nanoparticles combined with chitosan and antibody conjugated gold nanoparticles on the surface of a microchip.Three biomarkers,including cardiac troponin I,heart type fatty acid binding protein,and copeptin,were simultaneously detected in 260 serum samples from patients presenting with chest pain by an innovative multiplexed ECL immunoarray,and classified via the three-biomarker joint assessment model using support vector machines.The model achieved perfect discrimination(100%sensitivity and specificity)for AMI vs non-AMI patients,substantially higher than cTnT alone.Within 12 h of symptom onset,high-sensitivity cardiac troponin T(hs-cTnT)misclassified>20%of patients,while the joint biomarker assessment model retained perfect accuracy.As the time between symptom onset and testing became shorter,the degree to which the joint assessment model outperformed hs-cTnT increased.The proposed threebiomarker joint strategy is obviously superior to hs-cTnT for early and accurate diagnosis of AMI,hopefully reducing AMI mortality and saving limited medical resources.