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Glycol methacrylate-embedding medium to study morphological alterations of saphenous vein under brief and crescent pressurizations.Increased sarcolemmal permeability as an early event in experimental septic cardiomyopathy: a potential role for oxidative damage to lipids and proteins.Coronary microvascular disease in chronic Chagas cardiomyopathy including an overview on history, pathology, and other proposed pathogenic mechanisms.Aspirin treatment of mice infected with Trypanosoma cruzi and implications for the pathogenesis of Chagas diseaseImmobilization and therapeutic passive stretching generate thickening and increase the expression of laminin and dystrophin in skeletal musclePyridostigmine restores cardiac autonomic balance after small myocardial infarction in miceDisruption of calcium homeostasis in cardiomyocytes underlies cardiac structural and functional changes in severe sepsis.Early neonatal echocardiographic findings in an experimental rabbit model of congenital diaphragmatic hernia.Dantrolene improves in vitro structural changes induced by serum from Trypanosoma cruzi-infected mice.Role of dystrophin in acute Trypanosoma cruzi infection.Micro-positron emission tomography in the evaluation of Trypanosoma cruzi-induced heart disease: Comparison with other modalities.Disruption of sarcolemmal dystrophin and beta-dystroglycan may be a potential mechanism for myocardial dysfunction in severe sepsis.5-lipoxygenase is a key determinant of acute myocardial inflammation and mortality during Trypanosoma cruzi infection.Cardiac mast cell proteases do not contribute to the regulation of the rat coronary vascular responsiveness to arterial delivered angiotensin I and II.Remobilization through stretching improves gait recovery in the rat.Chronic inhibition of nitric oxide synthase induces hypertension and cardiomyocyte mitochondrial and myocardial collagen remodelling in the absence of hypertrophy.Changes in hemodynamic and neurohumoral control cause cardiac damage in one-kidney, one-clip hypertensive mice.Tempol inhibits TGF-β and MMPs upregulation and prevents cardiac hypertensive changes.Isoproterenol induces primary loss of dystrophin in rat hearts: correlation with myocardial injury.Early dystrophin disruption in the pathogenesis of experimental chronic Chagas cardiomyopathy.Turbulent blood flow plays an essential localizing role in the development of atherosclerotic lesions in experimentally induced hypercholesterolaemia in rats.β1-Adrenergic blockers exert antioxidant effects, reduce matrix metalloproteinase activity, and improve renovascular hypertension-induced cardiac hypertrophy.Early dystrophin loss is coincident with the transition of compensated cardiac hypertrophy to heart failure.Increase in parasympathetic tone by pyridostigmine prevents ventricular dysfunction during the onset of heart failure.Acetylcholinesterase Inhibition Attenuates the Development of Hypertension and Inflammation in Spontaneously Hypertensive Rats.Combining two potential causes of metalloproteinase secretion causes abdominal aortic aneurysms in rats: a new experimental model.Temporal changes in cardiac matrix metalloproteinase activity, oxidative stress, and TGF-β in renovascular hypertension-induced cardiac hypertrophy.Circumferential wall tension due to hypertension plays a pivotal role in aorta remodelling.Erectile dysfunction in heart failure rats is associated with increased neurogenic contractions in cavernous tissue and internal pudendal artery.Pyridostigmine prevents haemodynamic alterations but does not affect their nycthemeral oscillations in infarcted miceCalpain-mediated dystrophin disruption may be a potential structural culprit behind chronic doxorubicin-induced cardiomyopathyImbalance between matrix metalloproteinases and tissue inhibitor of metalloproteinases in hypertensive vascular remodelingMatrix Metalloproteinase Inhibition Improves Cardiac Dysfunction and Remodeling in 2-Kidney, 1-Clip HypertensionCardiovascular risk factors: can long-term alcohol withdrawal benefit heavy drinkers?MYOCARDIAL STRUCTURAL CHANGES IN LONG-TERM HUMAN SEVERE SEPSIS/SEPTIC SHOCK MAY BE RESPONSIBLE FOR CARDIAC DYSFUNCTION
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description
onderzoeker
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researcher
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հետազոտող
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name
Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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Cibele M. Prado
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P1053
P-5773-2016
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P1153
7005744924
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P3829
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0000-0003-4321-0879