Objective: To study the relationship between ABO blood type and spontaneous re-canalization (SR) in patients with acute myocardial infarction (AMI). Methods: A total of 1209 consecutive AMI patients were enrolled. Based on TIMI grade, the patients were divided into 2 groups: Non-SR group, the patients with TIMI grade 0-1,n=442 and SR group, the patients with TIMI grade 2-3,n=767. The relationship between ABO blood type and SR was investigated. Results: Compared with Non-SR group, SR group had more patients with blood type O (32.3% vs 24.7%) and less blood type A (31.7% vs 24.9%). Meanwhile, we found that a lower cholesterol level was related to patients with O blood type and SR occurrence, bothP<0.05. Multi regression analysis indicated that with adjusted age, gender, BMI, hypertension, diabetes, smoking, LDL-C and C-reactive protein, ESR, fibrinogen, D-dimmer, endothelial cardiac function, blood type O may independently predict SR occurrence in AMI patients (OR=1.49, 95% CI 1.10-2.05), while blood type A may have disadvantage for SR (OR=0.65, 95% CI 0.48-0.80). Conclusion: ABO blood type has been related to SR in AMI patients, blood type O is in favor of SR, while blood type A has disadvantage for SR occurrence.

[Abstract] Objective: To investigate the effect of lncRNA MAFG-AS1/ miR-11181-3p/GLG1 axis on cell migration, invasion and aerobic glycolysis of gastric cancer (GC) cells and its possible mechanism. Methods: AGS, a GC cell line with relatively high expression of MAFG-AS1, was selected as the study object. qPCR was used to detect RNA expression levels of MAFG-AS1, miR-11181-3p and GLG1. Transwell and glycolysis analysis were used to investigate cell migration, invasion and aerobic glycolysis. Bioinformatics analysis and Dual luciferase reporter gene assay were used to analyze the interaction among MAFG-AS1, miR-11181-3p and GLG1. Results: Knockdown of MAFG-AS1 significantly up-regulated miR-11181-3p and down-regulated GLG1 expression (both P<0.01), and significantly inhibited migration, invasion and aerobic glycolysis of GC cells (all P<0.01). Luciferase reporter gene assay confirmed that MAFG-AS1 competitively sponged miR-11181-3p (P<0.01). Inhibition of miR-11181-3p or overexpression of GLG1 partially reversed the inhibitory effect of MAFG-AS1 knockdown on GC cell migration, invasion, and aerobic glycolysis (all P<0.05 or P<0.01). Conclusion: MAFG-AS1 promotes cell migration, invasion and aerobic glycolysis of GC cells via miR-11181-3p/GLG1 axis, and may be a potential molecular target for GC diagnosis and therapy.