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Background: Ventricular tachycardia (VT) is a life-threatening heart condition commonly seen in patients with myocardial infarction (MI). Although personalized computational modeling has been used to understand VT and its treatment noninvasively, this approach can be computationally intensive and time consuming. Therefore, finding a balance between mesh size and computational efficiency is important. This study aimed to find an optimal mesh resolution that minimizes the need for computational resources while maintaining numerical accuracy and to investigate the effect of mesh resolution variation on the simulation results. Methods: We constructed ventricular models from contrast-enhanced magnetic resonance imaging data from six patients with MI. We created seven different models for each patient, with average edge lengths ranging from 315 to 645 µm using commercial software, Mimics. Programmed electrical stimulation was used to assess VT inducibility from 19 sites in each heart model. Results: The simulation results in the slab model with adaptive tetrahedral mesh (same as in the patient-specific model) showed that the absolute and relative differences in conduction velocity (CV) were 6.1 cm/s and 7.8% between average mesh sizes of 142 and 600 µm, respectively. However, the simulation results in the six patient-specific models showed that average mesh sizes with 350 µm yielded over 85% accuracy for clinically relevant VT. Although average mesh sizes of 417 and 478 µm could also achieve approximately 80% accuracy for clinically relevant VT, the percentage of incorrectly predicted VTs increases. When conductivity was modified to match the CV in the model with the finest mesh size, the overall ratio of positively predicted VT increased. Conclusions: The proposed personalized heart model could achieve an optimal balance between simulation time and VT prediction accuracy when discretized with adaptive tetrahedral meshes with an average edge length about 350 µm.

Evaluation of the effects of alirocumab on cardiovascular (CV) events, CV mortality and all-cause mortality. Data search was carried out using the Cochrane Library, PubMed, Web of Science and Embase. The search time is up to November 18, 2020. All randomized clinical trials (AEs) comparing alirocumab with placebo were searched. Meta-analysis was performed by Review Manager version 5.3 (The Cochrane Collaboration, Copenhagen, Denmark), and the heterogeneity between studies was tested by Cochrane’s Q test and measured with I2 statistics. A total of 13 randomized controlled trials with 24,815 participants were included. Alirocumab usage can considerably lower the incidence of CV events when compared to the control group (risk ratio(RR) 0.89, 95% confidence interval(CI) 0.83–0.95). No significant difference in CV mortality between the two groups was observed (RR 0.87, 95% CI 0.74–1.04). Treatment with alirocumab has been associated with a major decrease in all-cause mortality compared to placebo (RR 0.80, 95% CI 0.66–0.96). The incidence of serious adverse events (AEs) was similar in the two groups (RR 0.94, 95% CI 0.90–0.99). Alirocumab can reduce CV events and all-cause mortality. The AEs were mild and tolerable.

Introduction Recent studies have proved the diverse roles of miRs in different cancer-related processes. This study was undertaken to determine the therapeutic implications of miR-325-3p in breast cancer. Material and methods Expression analysis was carried out by qRT-PCR. Transfections were performed by Lipofectamine 2000 reagent. MTT assay was used for cell viability. Transwell assays were used for cell migration and invasion. Western blot analysis was used for protein expression analysis. Results Gene expression analysis revealed miR-325 to be significantly suppressed in breast cancer tissues and cell lines. Nonetheless, ectopic expression of miR-325 resulted in suppression of the growth and colony development potential of the SK-BR-3 and CAMA-1 cells. Transwell assays showed that miR-325 overexpression also resulted in the decline of the migration and invasion of the SK-BR-3 and CAMA-1 cells. Bioinformatic analysis showed that miR-325 targets lipocalin 15 (LNC15) in breast cancer cells. LNC15 was also overexpressed in the breast cancer tissues and cell lines. However, overexpression of miR-325 caused a significant decline in the LNC15 expression in SK-BR-3 cells. Additionally, silencing of LNC15 resulted in inhibition of the growth, migration and invasion of the SK-BR-3 cells. Rescue assay showed that overexpression of LNC15 could promote the growth, migration and invasion of the miR-325 overexpressing effects. Conclusions Taken together, the evidence shows that miR-325 acts as a tumor suppressor in breast cancer and may be used in the treatment of breast cancer.

MiR-30 family plays an important role in the tumorigenesis of human cancers. The aim of the study is to investigate the role of miR-30d in human colon cancer cell lines and explore the molecular mechanism in the proliferation of colon cancer cells. The expression of miR-30d was determined by real-time polymerase chain reaction assay in colon cancer cell lines (HCT15, HCT116, HT-29, DLD-1, and SW480) and the results demonstrated that miR-30d level was significantly decreased in human colon cancer cell lines, compared with normal colon epithelial cell line. Transfection with miR-30d mimics inhibited cell proliferation, and transfection with miR-30d inhibitors significantly promoted cell viability of colon cancer cells. Furthermore, TargetScan analysis predicted that miR-30d interacted with messenger RNA on its 3′ untranslated region of ATG5, phosphoinositide 3-kinase, and Beclin1 to negatively regulate cell autophagy in colon cancer cells. Moreover, transfection with miR-30d induced cell arrest at G2/M phase of HT-29 cells. Overexpression of miR-30d mimics inhibited cell viability probably due to the inhibition of cell autophagy and promotion of cell apoptosis. Thus, MiR-30d inhibited cell autophagy by directly targeting messenger RNA of ATG5, phosphoinositide 3-kinase, and Beclin1 and promoted cell apoptosis of human colon cancer cells. It is helpful to clarify the function of miR-30d in tumorigenesis of human cancers.