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1. Measuring Ca²⁺ sparks in cardiac myocytes.

2. Assessing Ca²⁺-removal pathways in cardiac myocytes.

3. A systematic approach for assessing Ca²⁺ handling in cardiac myocytes.

4. Characterizing the trigger for sarcoplasmic reticulum Ca2+ release in cardiac myocytes.

5. Measuring sarcoplasmic reticulum Ca2+ content, fractional release, and Ca2+ buffering in cardiac myocytes.

6. Basic methods for monitoring intracellular Ca2+ in cardiac myocytes using Fluo-3.

7. T-tubule remodelling and ryanodine receptor organization modulate sodium-calcium exchange.

8. Phospholamban ablation in hearts expressing the high affinity SERCA2b isoform normalizes global Ca²⁺ homeostasis but not Ca²⁺-dependent hypertrophic signaling.

9. Pharmacological inhibition of na/ca exchange results in increased cellular Ca2+ load attributable to the predominance of forward mode block.

10. Remodeling of T-tubules and reduced synchrony of Ca2+ release in myocytes from chronically ischemic myocardium.

11. Window Ca2+ current and its modulation by Ca2+ release in hypertrophied cardiac myocytes from dogs with chronic atrioventricular block.

12. The amiodarone derivative KB130015 [2-methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran] induces an Na+-dependent increase of [Ca2+] in ventricular myocytes.

13. Reduced synchrony of Ca2+ release with loss of T-tubules-a comparison to Ca2+ release in human failing cardiomyocytes.

14. Spatial and temporal inhomogeneities during Ca2+ release from the sarcoplasmic reticulum in pig ventricular myocytes.

15. Early exercise training after myocardial infarction prevents contractile but not electrical remodelling or hypertrophy.

16. Reduced synchrony of Ca2+ release with loss of T-tubules—a comparison to Ca2+ release in human failing cardiomyocytes

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