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Anthracycline-induced cardiotoxicity.
TLDR
Modification of dosage schedule and synthesis of new anthracycline analogues may represent alternative approaches to mitigate anthrACYcline cardiotoxicity while preserving antitumour activity.
Role of reactive oxygen species in ischemic preconditioning of subcellular organelles in the heart.
TLDR
Current knowledge of both ROS-dependent and ROS-independent mechanisms of IPC are focused on, some events, which are related to functional preservation of subcellular organelles, are described for a better understanding of the IPC phenomenon.
Myofibrillar remodeling in cardiac hypertrophy, heart failure and cardiomyopathies.
TLDR
Although myofibrillar remodelling appears to be associated with cardiac dysfunction, alterations in both contractile and regulatory proteins are dependent on the type and stage of heart disease.
Renin–angiotensin blockade attenuates cardiac myofibrillar remodelling in chronic diabetes
TLDR
The results suggest the occurrence of myofibrillar remodelling in diabetic cardiomyopathy and provide evidence that the beneficial effects of RAS blockade in diabetes may be associated with attenuation of my ofibrillsar remodelled in the heart.
β-adrenergic blockade attenuates cardiac dysfunction and myofibrillar remodelling in congestive heart failure
TLDR
The results suggest that improvement of cardiac function by β‐AR blockade in CHF may be associated with attenuation of myofibrillar remodelling.
Molecular defects in cardiac myofibrillar proteins due to thyroid hormone imbalance and diabetes.
TLDR
How myofibrillar proteins are altered in response to thyroid hormone imbalance and lack of insulin or its responsiveness is discussed, and how their structural and functional changes explain the contractile defects in the heart.
Amelioration of Cardiac Remodeling in Congestive Heart Failure by β-Adrenoceptor Blockade is Associated with Depression in Sympathetic Activity
TLDR
The results indicate that the beneficial effects ofβ-AR antagonists on cardiac remodeling and heart dysfunction in CHF may be due to the blockade of β-ARs in the myocardium and a depression in the sympathetic activity.
Cardiac troponin T following repeated administration of pyridoxal isonicotinoyl hydrazone in rabbits.
TLDR
The data concerning cTnT support the opinion that the possible cardiotoxicity of PIH is very low, and the cytosolic and myofibrillar fraction of cTNT in the left ventricular myocardium was analyzed.
Evaluation of cardiac effects of the new antineoplastic drug --dimethoxybenfluron--in the rabbit.
TLDR
The lack of cardiotoxicity of this new antineoplastic drug was supported by the absence of alterations in PEP:LVET ratio, left ventricle dP/dtmax or histological heart examination as well as by the fact that no premature death of animals occurred following repeated administration of dimethoxybenfluron.
Troponins in experimental studies.
TLDR
It is concluded that in rabbits after repeated administration of cardiotoxic or cardioprotective drugs meaningful dependence between cTNT and cTnI was not found and the choice of the most suitable cardiomarker in laboratory animals deserves further studies.
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