Dynamic changes in cardiac morphology, function, and diffuse myocardial fibrosis duration of diabetes in type 1 and type 2 diabetic mice models using 7.0 T CMR and echocardiography.

Background: Diabetes mellitus (DM) is associated with an increased risk of cardiovascular disease (CVD). Hence, early detection of cardiac changes by imaging is crucial to reducing cardiovascular complications. Purpose: Early detection of cardiac changes is crucial to reducing cardiovascular complications. The study aimed to detect the dynamic change in cardiac morphology, function, and diffuse myocardial fibrosis(DMF) associated with T1DM and T2DM mice models. Materials and methods: 4-week-old C57Bl/6J male mice were randomly divided into control (n=30), T1DM (n=30), and T2DM (n=30) groups. A longitudinal study was conducted every 4 weeks using serial 7.0T CMR and echocardiography imaging. Left ventricular ejection fraction (LV EF), tissue tracking parameters, and DMF were measured by cine CMR and extracellular volume fraction (ECV). Global peak circumferential strain (GCPS), peak systolic strain rate (GCPSSR) values were acquired by CMR feature tracking. LV diastolic function parameter (E/E') was acquired by echocardiography. The correlations between the ECV and cardiac function parameters were assessed by Pearson's test. Results: A total of 6 mice were included every 4 weeks in control, T1DM, and T2DM groups for analysis. Compared to control group, an increase was detected in the LV mass and E/E' ratio, while the values of GCPS, GCPSSR decreased mildly in DM. Compared to T2DM group, GCPS and GCPSSR decreased earlier in T1DM(GCPS 12W,P=0.004; GCPSSR 12W,P=0.04). ECV values showed a significant correlation with GCPS and GCPSSR in DM groups. Moreover, ECV values showed a strong positive correlation with E/E'(T1DM,r=0.757,P<0.001;T2DM, r=0.811,P<0.001). Conclusion: The combination of ECV and cardiac mechanical parameters provide imaging biomakers for pathophysiology, early diagnosis of cardiac morphology, function and early intervention in diabetic cardiomyopathy in the future.

Cardiac Computed Tomography to Guide the Selection of Better Display Angle of Cardiac Right Ventricular Pacing Electrode in Radiography.

BACKGROUND: Traditional radiography angles do not adequately reveal the shape and position of the right ventricular pacing electrode. OBJECTIVE: This study aimed to explore better radiography angles with the help of cardiac computed tomography (CT). METHODS: We analyzed the cardiac CT images of consecutive outpatients from 2018 to 2019. The right anterior oblique (RAO) 30° and the left anterior oblique (LAO) 40° were found to sufficiently display the shape and position of the right ventricular pacing electrode. RESULTS: A total of 214 consecutive outpatients were enrolled, whose average age was 55.0 ± 13.0 years, and 151 were male (70.6%). Through analyzing the cardiac CT images, the α angle (33.7° ± 6.1) and the γ angle (38.8° ± 8.0) were determined. Furthermore, we verified these angles in 48 patients after pacemaker implantation. The results showed that the ratio of the length of right ventricular electrode using the RAO α angle (≈30°) to the posterior-anterior position (PA position) was 1.099 ± 0.157 vs. 1.053 ± 0.182 (the ratio using the traditional RAO 45°) (P < 0.001). We observed that the relationship between the right ventricular active electrode and the ventricular septum was better identified using the LAO γ angle (≈40°) than the traditional 60° angle. CONCLUSION: With the help of cardiac CT, we found that RAO 30° could better show the shape and length of the right ventricular pacing electrode, and LAO 40° could better show the positional relationship between the pacing electrode and the ventricular septum.

Overexpression miR-520a-3p inhibits acute myeloid leukemia progression via targeting MUC1.

BACKGROUND: Acute myeloid leukemia (AML) is one of the familiar malignant tumors in the hematological system. miR-520a-3p is reported to be involved in several cancers' progression. However, miR-520a-3p role in AML remains unclear. In this study, we aimed to clarify the role and potential mechanism of miR-520a-3p in AML. METHODS: Cell viability, proliferation, cycle and apoptosis were detected by MTT assay, colony formation assay, flow cytometry, respectively. The levels of PNCA, Bcl-2, Cleaved caspase 3, Cleaved caspase 9 and ß-catenin protein were detected by Western blot. Dual-luciferase reported assay was performed to detect the regulation between miR-520a-3p and MUC1. To verify the effect of miR-520a-3p on tumor proliferation in vivo, a non-homogenous transplant model of tumors was established. RESULTS: miR-520a-3p expression was down-regulated, and MUC1 expression was up-regulated in AML patients. miR-520a-3p overexpression suppressed THP-1 cell proliferation, induced cell cycle G0/G1 inhibition and promoted apoptosis. miR-520a-3p targeted MUC1 and negatively regulated its expression. MUC1 knockdown inhibited THP-1 cell proliferation and promoted apoptosis. miR-520a-3p overexpression inhibited AML tumors growth. CONCLUSION: Overexpression miR-520a-3p inhibited AML cell proliferation, and promoted apoptosis via inhibiting MUC1 expression and repressing Wnt/ß-catenin pathway activation.