Calcineurin-induced energy wasting in a transgenic mouse model of heart failure.

Overexpression of calcineurin (CLN) in the mouse heart induces severe hypertrophy that progresses to heart failure, providing an opportunity to define the relationship between energetics and contractile performance in the severely failing mouse heart. Contractile performance was studied in isolated hearts at different pacing frequencies and during dobutamine challenge. Energetics were assessed by 31P-NMR spectroscopy as ATP and phosphocreatine concentrations ([ATP] and [PCr]) and free energy of ATP hydrolysis (|Delta G( approximately ATP)|).

Availability of 11-cis retinal and opsins without chromophore as revealed by small bleaches of rhodopsin in excised albino mouse eyes.

Small bleaches were used to study the rhodopsin regeneration process. At bleaches from 5.2% to 24.