Study Objectives: Poor sleep is a prevalent complaint in the population with chronic tinnitus, but the relationship between the two is not well-characterized. The objective of this study was to understand how subjective and objective measures of sleep compare in patients with or without chronic tinnitus.
Methods: This prospective cohort study included consecutive adult patients who presented to a sleep laboratory between January 19, 2017, and January 10, 2020.
Objective: Patients with underlying conditions are predicted to have worse outcomes with COVID-19. A strong association between baseline cardiovascular disease and COVID-19-related mortality has been shown by a number of studies. In the current retrospective study, we aim to identify whether patients with pulmonary hypertension have worse outcomes compared with patients without pulmonary hypertension.
View Article and Find Full Text PDFSunitinib is associated with cardiotoxicity through inhibition of AMP-protein kinase (AMPK) signaling. By contrast, the common antidiabetic agent metformin has demonstrated cardioprotection through indirect AMPK activation. In this study, we investigate the effects of metformin during sunitinib-induced cytotoxicity.
View Article and Find Full Text PDFThe discovery and application of human-induced pluripotent stem cells (hiPSCs) have been instrumental in the investigation of the pathophysiology of cardiovascular diseases. Patient-specific hiPSCs can now be generated, genome-edited, and subsequently differentiated into various cell types and used for regenerative medicine, disease modeling, drug testing, toxicity screening, and 3D tissue generation. Modulation of the retinoic acid signaling pathway has been shown to direct cardiomyocyte differentiation towards an atrial lineage.
View Article and Find Full Text PDFThe cardiac work-loop technique closely mimics the intrinsic in vivo movement and characteristics of cardiac muscle function. In this study, six known inotropes were profiled using the work-loop technique to evaluate the potential of this method to predict inotropy. Papillary muscles from male Sprague-Dawley rats were mounted onto an organ bath perfused with Krebs-Henseleit buffer.
View Article and Find Full Text PDFJ Pharmacol Toxicol Methods
July 2016
Adverse drug effects on the cardiovascular system are a major cause of compound attrition throughout compound discovery and development. There are many ways by which drugs can affect the cardiovascular system, including effects on the electrocardiogram, vascular resistance, heart rate and the force of contraction of the heart (inotropy). Compounds that increase the force of contraction of the heart can be harmful in patients with ischemic heart disease, whilst negative inotropes can induce symptoms of heart failure.
View Article and Find Full Text PDFDoxorubicin is known to cause cardiotoxicity through multiple routes including the build-up of reactive oxygen species and disruption of the calcium homeostasis in cardiac myocytes, but the effect of drug treatment on the associated biomechanics of cardiac injury remains unclear. Detecting and understanding the adverse effects of drugs on cardiac contractility is becoming a priority in non-clinical safety pharmacology assessment. The work-loop technique enables the assessment of force-length work-loop contractions, which mimic those of the pressure-volume work-loops experienced by the heart in vivo.
View Article and Find Full Text PDFDoxorubicin is one of the most effective anti-cancer agents. However, its use is associated with adverse cardiac effects, including cardiomyopathy and progressive heart failure. Given the multiple beneficial effects of the mitochondrial division inhibitor (mdivi-1) in a variety of pathological conditions including heart failure and ischaemia and reperfusion injury, we investigated the effects of mdivi-1 on doxorubicin-induced cardiac dysfunction in naïve and stressed conditions using Langendorff perfused heart models and a model of oxidative stress was used to assess the effects of drug treatments on the mitochondrial depolarisation and hypercontracture of cardiac myocytes.
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