6 research outputs found
ANTI-DUMPING IN AGRICULTURE BETWEEN CANADA AND THE UNITED STATES: TWO CASES OF TOMATOES
International Relations/Trade,
Modified Langendorff technique for mouse heart cannulation: Improved heart quality and decreased risk of ischemia
Oscar Langendorff introduced the first method for isolating a heart with contractile activity in 1895. Since then, the Langendorff method has remained a powerful technique in cardiac research and has led to major advances in medicine. The primary goal of the Langendorff method is to provide an isolated heart with oxygen and metabolites via a cannula inserted into the aorta. The Langendorff heart is a complex in vitro technique used primarily in pharmacological and physiological research that allows the evaluation of multiple cardiac hemodynamic parameters including, but not limited to, contractility and heart rate. This article will first provide a brief background of the Langendorff method as well as details regarding organ isolation. Finally, the article will discuss the benefits of a new technique for hanging the isolated heart aorta and the benefits of this technique over traditional method
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Role of Oxidized Lipids in Pulmonary Arterial Hypertension
Pulmonary arterial hypertension (PAH) is a multifactorial disease characterized by interplay of many cellular, molecular, and genetic events that lead to excessive proliferation of pulmonary cells, including smooth muscle and endothelial cells; inflammation; and extracellular matrix remodeling. Abnormal vascular changes and structural remodeling associated with PAH culminate in vasoconstriction and obstruction of pulmonary arteries, contributing to increased pulmonary vascular resistance, pulmonary hypertension, and right ventricular failure. The complex molecular mechanisms involved in the pathobiology of PAH are the limiting factors in the development of potential therapeutic interventions for PAH. Over the years, our group and others have demonstrated the critical implication of lipids in the pathogenesis of PAH. This review specifically focuses on the current understanding of the role of oxidized lipids, lipid metabolism, peroxidation, and oxidative stress in the progression of PAH. This review also discusses the relevance of apolipoprotein A-I mimetic peptides and microRNA-193, which are known to regulate the levels of oxidized lipids, as potential therapeutics in PAH
Estrogen rescues heart failure through estrogen receptor Beta activation
Abstract Background Recently, we showed that exogenous treatment with estrogen (E2) rescues pre-existing advanced heart failure (HF) in mice. Since most of the biological actions of E2 are mediated through the classical estrogen receptors alpha (ERĪ±) and/or beta (ERĪ²), and both these receptors are present in the heart, we examined the role of ERĪ± and ERĪ² in the rescue action of E2 against HF. Methods Severe HF was induced in male mice by transverse aortic constriction-induced pressure overload. Once the ejection fraction (EF) reached ~ā35%, mice were treated with selective agonists for ERĪ± (PPT, 850Ā Ī¼g/kg/day), ERĪ² (DPN, 850Ā Ī¼g/kg/day), or E2 (30Ā Ī¼g/kg/day) together with an ERĪ²-antagonist (PHTPP, 850Ā Ī¼g/kg/day) for 10Ā days. Results EF of HF mice was significantly improved to 45.3āĀ±ā2.1% with diarylpropionitrile (DPN) treatment, but not with PPT (31.1āĀ±ā2.3%). E2 failed to rescue HF in the presence of PHTPP, as there was no significant improvement in the EF at the end of the 10-day treatment (32.5āĀ±ā5.2%). The improvement of heart function in HF mice treated with ERĪ² agonist DPN was also associated with reduced cardiac fibrosis and increased cardiac angiogenesis, while theĀ ERĪ± agonist PPT had no significant effect on either cardiac fibrosis or angiogenesis. Furthermore, DPN improved hemodynamic parameters in HF mice, whereas PPT had no significant effect. Conclusions E2 treatment rescues pre-existing severe HF mainly through ERĪ². Rescue of HF by ERĪ² activation is also associated with stimulation of cardiac angiogenesis, suppression of fibrosis, and restoration of hemodynamic parameters