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Proton MR spectroscopy in quantitative in vivo determination of fat content in human liver steatosis
TLDR
The results indicate that determination of the fat volume fraction in steatotic liver can be achieved noninvasively with MR spectroscopy. Expand
Levosimendan: molecular mechanisms and clinical implications: consensus of experts on the mechanisms of action of levosimendan.
TLDR
The data indicate that the cardiovascular effects of levosimendan are exerted via more than an isolated drug-receptor interaction, and involve favorable energetic and neurohormonal changes that are unique in comparison to other types of inodilators. Expand
Noninvasive in vivo quantitative assessment of fat content in human liver.
TLDR
It is concluded that the use of test objects allows an accurate and reproducible noninvasive quantitative assessment of hepatic fat infiltration in humans and may prove useful in the evaluation of the natural course and treatment of liver steatosis as well as in the assessment of donor livers prior to transplantation. Expand
A role for the RISK pathway and KATP channels in pre‐ and post‐conditioning induced by levosimendan in the isolated guinea pig heart
TLDR
This work investigated whether the heart could be pre‐ and/or post‐conditioned using levosimendan and whether the prosurvival kinases and/ or the sarcolemmal or mitochondrial KATP channels are involved. Expand
Binding of a new Ca2+ sensitizer, levosimendan, to recombinant human cardiac troponin C. A molecular modelling, fluorescence probe, and proton nuclear magnetic resonance study.
TLDR
The binding of a new calcium sensitizer, levosimendan, to human cardiac troponin C (cTnC) is described, and the role of Asp-88 in the binding of the drug to the NH2-terminal domain of cTNC is revealed. Expand
Binding of Levosimendan, a Calcium Sensitizer, to Cardiac Troponin C*
TLDR
It was shown that levosimendan was in fast exchange on the NMR time scale with a secondary binding site in the C-domain of both cTnCC35S andcTnCA-Cys, where all the cysteine residues are mutated to serine, and the small angle x-ray scattering experiments confirm the binding of levosIMendan to Ca2+-saturated cTNC but show no domain-domain closure. Expand
Levosimendan: current data, clinical use and future development
TLDR
Data from clinical trials indicate that levosimendan improves haemodynamics with no attendant significant increase in cardiac oxygen consumption and relieves symptoms of acute heart failure; these effects are not impaired or attenuated by the concomitant use of beta-blockers. Expand
Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the
TLDR
Several aspects of fibrosis are discussed, including early insidious perturbations such as subclinical hypertension or inflammation may trigger first fibrotic events, while more dramatic triggers such as myocardial infarction are discussed. Expand
Pharmacological mechanisms contributing to the clinical efficacy of levosimendan.
TLDR
Results of preclinical and clinical investigations suggest that the combination of levosimendan-induced cardiac and vascular changes has favorable effects on the coronary, pulmonary and peripheral circulations, which may contribute to stabilization of the circulation and improved life expectancy of patients with chronic heart failure. Expand
Interaction of levosimendan with cardiac troponin C in the presence of cardiac troponin I peptides.
TLDR
The effective binding site of levosimendan on cTnC resulting in the calcium-sensitizing effect is located in the regulatory domain (N-domain), which is relevant for the mechanism of calcium sensitization. Expand
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