DNA adduct formation and reduced EIF4A3expression contributes to benzo[a]pyrene-induced DNA damage in human bronchial epithelial BEAS-2B cells.

Benzo[a]pyrene(B[a]P) is a known human carcinogen. The ability of B[a]P to form stable DNA adducts has been repeatedly demonstrated. However, the relationship between DNA adduct formation and cell damage and its underlying molecular mechanisms are less well understood.

A Bioinformatics Investigation into the Pharmacological Mechanisms of Sodium-Glucose Co-transporter 2 Inhibitors in Diabetes Mellitus and Heart Failure Based on Network Pharmacology.

Purpose: Diabetes mellitus (DM) is a major risk factor for the development of heart failure (HF). Sodium-glucose co-transporter 2 (SGLT2) inhibitors have demonstrated consistent benefits in the reduction of hospitalization for HF in patients with DM. However, the pharmacological mechanism is not clear.

A genome-wide screen for differentially methylated long noncoding RNAs identified that lncAC007255.8 is regulated by promoter DNA methylation in Beas-2B cells malignantly transformed by NNK.

Tobacco exposure is well known to induce genetic and epigenetic changes that contribute to the pathogenesis of lung cancer. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a significant tobacco-specific carcinogen, but the oncogenic mechanisms of NNK have not been thoroughly elucidated. In this study we found that DNA methyltransferase 1 (DNMT1) was overexpressed in malignantly transformed human bronchial epithelial Beas-2B cells induced by NNK (2B-NNK cells), by treatment with NNK (400 μg/mL) for 7 days.

Novel biomarkers for post-contrast acute kidney injury identified from long non-coding RNA expression profiles.

Post-contrast acute kidney injury (PC-AKI) is a severe complication of cardiac catheterization. Emerging evidence indicated that long non-coding RNAs (lncRNAs) could serve as biomarkers for various diseases. However, the lncRNA expression profile and potential biomarkers in PC-AKI remain unclear.

Integrative Analysis of Transcriptome-Wide Association Study and mRNA Expression Profiles Identified Candidate Genes and Pathways Associated With Acute Myocardial Infarction.

Background: Acute myocardial infarction (AMI), characterized by an event of myocardial necrosis, is a common cardiac emergency worldwide. However, the genetic mechanisms of AMI remain largely elusive.

Methods: A genome-wide association study dataset of AMI was obtained from the CARDIoGRAMplusC4D project.

Association of dialysis-requiring acute kidney injury with 90-day prognosis in patients with coronary artery disease and advanced kidney disease after coronary angiography.

Background: Dialysis-requiring acute kidney injury (AKI-D) is a potentially serious complication associated with high in-hospital mortality among patients with coronary artery disease (CAD) after coronary angiography (CAG). Patients with existing advanced kidney disease (AKD) have an increased risk of developing AKI-D. However, few studies have investigated the prognosis of AKI-D in patients with both CAD and AKD.

Fine particulate matter exposure induces DNA damage by downregulating Rad51 expression in human bronchial epithelial Beas-2B cells in vitro.

Although an accumulating body of evidence suggests that fine particulate matter (PM) can cause lung injury and lung cancer, the underlying mechanisms are not yet clear. In this study, multiple endpoints associated with the cellular response to PM exposure, including the cell proliferation rate, cell apoptosis, malondialdehyde (MDA) content and DNA damage, were evaluated in human bronchial epithelial Beas-2B cells. The mRNA expression profile in PM-treated cells was analyzed by transcriptome sequencing.