Edward G. Lakatta

TL;DR: Age-dependent changes in ICa,L and its modulations are similar to those observed in the enlarged myocytes of the hypertrophied and failing heart and may be an important cause of the age-related decrease in cardiac reserve function.

TL;DR: The data do not support the idea that treating subclinical disorders might help to prevent arterial remodelling or carotid atherosclerosis, and Thyroid hormone is not associated with increased IMT or with the presence ofCarotid artery plaque.

TL;DR: This work investigated the relationship between thyroid function and carotid‐femoral PWV, as an index of arterial stiffness, and found that thyroid dysfunction may accelerate atherosclerosis.

TL;DR: It is demonstrated that PDGF-stimulated smooth muscle cells activate the STAT (signal transducers and activators of transcription) family of proteins in addition to other signaling pathways (e.g., RAS-RAF-MAP Kinase) and hypothesize that signal transduction by p91 plays an important role in VSMC, especially after injury with the release of growth factors such as PDGF.

TL;DR: In intact cells the positive inotropic effect of EMD 53998 is due to specific properties of its enantiomers: the (-)-enantiomer has adenosine 3',5'-cyclic monophosphate-like effects (increase in amplitude and reduction of [Ca2+]i transient and contraction durations), whereas the (+)- enantiomer enhances the myofilament- Ca2+ interaction.