Objective To evaluate the early diagnostic value of circulating microRNA-1 (miR-1) on acute myocardial infarction (AMI). Methods A prospective cohort study was conducted. The patients with chest pain admitted to the Second People's Hospital of Wuxi from November 2012 to June 2015 were enrolled. According to AMI diagnostic criteria, the patients were divided into AMI group and non-AMI group, and healthy individuals during the same period were served as heath controls. The venous samples of the onset patients were collected within 3 hours after admission. The plasma miR-1 was determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR), and the levels of plasma cardiac troponin I (cTnI) and MB isoenzyme of creatine kinase (CK-MB) were measured by electrochemiluminescence. The correlation between plasma miR-1 and cTnI as well as CK-MB was performed by Spearman analysis. The early diagnostic performance of plasma miR-1, cTnI, and CK-MB for AMI was estimated by receiver operating characteristic (ROC) curve analysis. Results There were 127 patients in AMI group, and 107 in non-AMI group, including 82 patients with angina pectoris, 2 with pulmonary embolism, 3 with aortic dissection, 2 with acute pericarditis, 3 with myocarditis, 13 with acute heart failure, and 2 with peptic ulcer. Ninety volunteers were served as healthy controls. There was no difference in clinical characteristics including gender and hyperlipidemia between AMI group and non-AMI group. The expressions of plasma miR-1, cTnI and CK-MB were significantly increased in AMI patients as compared with those of the healthy controls [miR-1 (2-ΔΔCt): 4.32±2.60 vs. 1.44±0.75 and 0.98±0.18, cTnI (μg/L): 3.23 (0.63, 10.70) vs. 0.02 (0.00, 0.17) and 0.00 (0.00, 0.00), CK-MB (U/L): 32.40 (14.20, 95.40) vs. 14.40 (11.20, 17.10) and 8.90 (8.28, 9.50), all P < 0.01]. The expression of plasma miR-1 had a significantly positive correlation with cTnI and CK-MB in AMI patients (r1 = 0.395, r2 = 0.490, both P < 0.000). It was demonstrated by ROC curve analysis that the area under ROC curve (AUC) for the diagnostic value of miR-1 on AMI was 0.905 [95% confidence interval (95%CI) = 0.860-0.950, P = 0.000], the sensitivity was 86.6%, and the specificity was 95.4%; the AUC for cTnI was 0.908 (95%CI = 0.870-0.946, P = 0.000), the sensitivity was 81.9%, and the specificity was 95.9%; the AUC for CK-MB was 0.795 (95%CI = 0.736-0.854, P = 0.000), the sensitivity was 63.0%, and the specificity was 92.9%. Conclusions Plasma miR-1 has the capacity in early diagnosis of AMI, superior to CK-MB, and equal to cTnI. It can provide additional diagnostic information beyond cTnI. The diagnostic accuracy for early AMI can be improved with the combination of plasma miR-1 and cTnI.

Objective:To evaluate the diagnostic value of circulating microRNA-1 (miR-1) in early coronary artery plaque rupture in patients with stable coronary artery disease (SCAD).Methods:A prospective cohort study was conducted. Sixty-seven patients with SCAD admitted to the department of cardiology of the Third Affiliated Hospital of Soochow University from January to June in 2019 were enrolled. All patients had completed coronary angiography (CAG), percutaneous coronary intervention (PCI) single stent implantation or only CAG was performed according to the CAG results. Blood samples were collected before (0 hour) and 3 hours after the procedure. The expression of plasma miR-1 was detected by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR), and electrocardiogram was used to detect cardiac troponin I (cTnI) levels. The difference of miR-1 and cTnI levels in PCI or CAG patients before and after procedure were compared, and the value for early diagnosis of coronary artery plaque rupture in SCAD patients was evaluated. The diagnostic efficacy was evaluated by the receiver operating characteristic curve (ROC curve).Results:There were 38 CAG patients and 29 PCI patients. There were no significant differences in gender, age, previous history (without hypertension history) and baseline data of cardiac function between the two groups. The expression of miR-1 after PCI was significantly higher than that before PCI [2 -ΔΔCt: 2.11 (1.56, 2.73) vs. 1.26 (1.07, 1.92), P < 0.01], and there was no significant difference in cTnI level before and after PCI [μg/L: 0.00 (0.00, 0.02) vs. 0.00 (0.00, 0.02), P > 0.05]. There were no significant differences in miR-1 and cTnI levels before and after procedure in the CAG group [miR-1 (2 -ΔΔCt): 1.09 (1.00, 1.40) vs. 1.21 (1.00, 1.71), cTnI (μg/L): 0.00 (0.00, 0.02) vs. 0.00 (0.00, 0.02), both P > 0.05]. ROC curve analysis showed that the area under ROC curve (AUC) and 95% confidence interval (95% CI) of miR-1 in the diagnosis of coronary plaque rupture were 0.794 (0.687-0.900), P < 0.01, the sensitivity was 82.8%, the specificity was 68.4%, and the optimal cut-off value was 1.51. The AUC and 95% CI of the difference of miR-1 before and after operation (ΔmiR-1) were 0.704 (0.567-0.842), P = 0.004, the sensitivity was 62.1%, the specificity was 84.2%, and the optimal cut-off value was 0.39. The efficancy of miR-1 and ΔmiR-1 after procedure to diagnose coronary plaque rupture in patients with SCAD was similar ( Z = 1.287, P = 0.198). However, baseline miR-1 might not predict whether patients with SCAD need PCI or not (AUC = 0.630, P > 0.05). Multivariate binary Logistic regression analysis showed that increased postoperative miR-1 expression was an independent risk factor for coronary plaque rupture in SCAD patients [odds ratios ( OR) = 2.887, 95% CI was 1.044-7.978, P = 0.041]. Conclusion:Circulating miR-1 might have the value for early diagnosis of coronary artery plaque rupture in SCAD patients.

ObjectiveTo investigate the effect and mechanism of Yiqi Wenyang Huwei decoction （YWHD） on airway inflammation in bronchial asthma （BA） rats based on transforming growth factor-β₁ （TGF-β₁）/SMAD family member 3 （Smad3） signaling pathway. MethodSixty male SD rats were randomly divided into a normal group， a model group， a dexamethasone （DEX） group， and low-， medium-， and high-dose YWHD groups， with 10 rats in each group. The BA model was induced by intraperitoneal injection of 1 mL of ovalbumin （OVA）-aluminum hydroxide suspension for sensitization， followed by nebulization with 2% OVA. One hour before daily OVA nebulization， the control group was treated with saline， the DEX group with DEX solution at 0.2 g·L^-1， and the low-， medium-， and high-dose YWHD groups with YWHD at 1， 2， 4 g·mL^-1， respectively. General conditions and lung function were observed. Bronchoalveolar lavage fluid （BALF） and serum were collected to count inflammatory cells in BALF and measure immunoglobulin E （IgE） levels in serum and inflammatory cytokines in BALF using enzyme-linked immunosorbent assay （ELISA）. Pathological changes in lung tissues， collagen deposition， and airway mucus secretion were observed by hematoxylin-eosin （HE）， Masson， and periodic acid-Schiff （PAS） staining. TGF-β₁/Smad3-related mRNA and protein levels in lung tissues were determined by Real-time fluorescent quantitative polymerase chain translation （Real-time PCR） and Western blot analysis. ResultCompared with the normal group， the model group showed increased total airway resistance （RL） and decreased dynamic compliance （Cdyn） （P<0.05， P<0.01）， elevated serum IgE levels， increased inflammatory cell counts， and higher inflammatory cytokine levels in BALF （P<0.01）. Additionally， there was significant inflammatory cell infiltration， collagen deposition， and mucus secretion in lung tissues. The levels of TGF-β₁， α-smooth muscle actin （α-SMA）， and Smad3 phosphorylation in lung tissues were significantly increased （P<0.01）. Compared with the model group， the DEX group and high-dose YWHD group exhibited significantly reduced RL （P<0.01）， improved lung dynamic compliance （P<0.05）， and lower serum IgE levels， inflammatory cell counts， and inflammatory cytokine levels in BALF （P<0.05）. Moreover， these treatments alleviated pathological damage in lung tissues and reduced the levels of TGF-β₁， α-SMA， and Smad3 phosphorylation （P<0.01）. ConclusionYWHD reduces airway inflammation， improves pathological damage， and mitigates airway remodeling in bronchial asthma rats， possibly by downregulating TGF-β₁， α-SMA protein levels， and Smad3 phosphorylation.