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Effect of electrochemical topology on detection sensitivity in MEA assay for drug-induced cardiotoxicity screening.
Biosens Bioelectron
March 2025
Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, 21205, United States; Department of Medicine, Johns Hopkins University, Baltimore, MD, 21205, United States; Institute for NanoBio Technology, Johns Hopkins University, Baltimore, MD, 21218, United States; Center for Microphysiological Systems, Johns Hopkins University, Baltimore, MD, 21205, United States. Electronic address:
Cardiotoxicity remains a major challenge in drug development, accounting for 45% of medication withdrawals due to cardiac ischemia and arrhythmogenicity. To overcome the limitations of traditional multielectrode array (MEA)-based cardiotoxicity assays, we developed a Nafion-coated NanoMEA platform with decoupled reference electrodes, offering enhanced sensitivity for electrophysiological measurements. The 'Decoupled' configuration significantly reduced polarization resistance (Rp) from 12.
View Article and Find Full Text PDFBackground: Famotidine is a competitive histamine H-receptor antagonist that reduces the formation of stomach acid and is used to treat gastrointestinal disorders associated with acid reflux, gastroesophageal reflux disease, duodenal ulcer, gastric ulcer, and pathological hypersecretory disorders. This study is designed to investigate the possible neuroprotective effects of the ranolazine scopolamine-induced Alzheimer's disease-like feature in a mouse model.
Methods: Mice were divided equally into five groups (ten mice per group), including control group and induction group.
In vitro to in vivo extrapolation from 3D hiPSC-derived cardiac microtissues and physiologically based pharmacokinetic modeling to inform next-generation arrhythmia risk assessment.
Toxicol Sci
September 2024
Center for Biomedical Engineering, School of Engineering, Brown University, Providence, RI 02912, United States.
Proarrhythmic cardiotoxicity remains a substantial barrier to drug development as well as a major global health challenge. In vitro human pluripotent stem cell-based new approach methodologies have been increasingly proposed and employed as alternatives to existing in vitro and in vivo models that do not accurately recapitulate human cardiac electrophysiology or cardiotoxicity risk. In this study, we expanded the capacity of our previously established 3D human cardiac microtissue model to perform quantitative risk assessment by combining it with a physiologically based pharmacokinetic model, allowing a direct comparison of potentially harmful concentrations predicted in vitro to in vivo therapeutic levels.
View Article and Find Full Text PDFRanolazine ameliorates T1DM-induced testicular dysfunction in rats; role of NF-κB/TXNIP/GSDMD-N/IL-18/Beclin-1 signaling pathway.
Eur J Pharmacol
August 2024
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.
Approximately 90% of diabetic males have varying degrees of testicular dysfunction. The current study investigates the possible beneficial consequences of ranolazine against T1DM-induced testicular dysfunction in rats. Thirty-two male Sprague Dawley rats were assorted into 4 groups; normal, diabetic (single 50 mg/kg STZ, I.
View Article and Find Full Text PDFIbrutinib, a Bruton's tyrosine kinase inhibitor, regulates ventricular electromechanical activities and enhances arrhythmogenesis.
Eur J Pharmacol
August 2024
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Cardiovascular Research Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. Electronic address:
Background: Ibrutinib, a Bruton's tyrosine kinase inhibitor used in cancer therapy, exerts ventricular proarrhythmic effects; however, the underlying mechanisms remain unclear. Excitation-contraction coupling (E-C) disorders are pivotal for the genesis of ventricular arrhythmias (VAs), which arise mainly from the right ventricular outflow tract (RVOT). In this study, we aimed to comprehensively investigate whether ibrutinib regulates the electromechanical activities of the RVOT, leading to enhanced arrhythmogenesis, and explore the underlying mechanisms.
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