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David A. Eisner
Researcher at University of Manchester
Publications - 267
Citations - 14383
David A. Eisner is an academic researcher from University of Manchester. The author has contributed to research in topics: Ryanodine receptor & Calcium. The author has an hindex of 69, co-authored 256 publications receiving 13473 citations. Previous affiliations of David A. Eisner include University of Oxford & Research Triangle Park.
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A novel method for absolute calibration of intracellular pH indicators.
TL;DR: These methods are based on the change in intracellular pH following the addition of weak acids and weak bases to the extracellular medium and use a null method which uses a mixture of weak acid and weak base that does not change the fluorescent signal.
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Mechanisms underlying enhanced cardiac excitation contraction coupling observed in the senescent sheep myocardium.
TL;DR: In the ageing ovine myocardium, the amplitude of the systolic Ca(2+) transient is increased and it is suggested that the greater inward L-type Ca( 2+) current provides a more effective trigger for calcium-induced-calcium release from the SR whilst maintaining a stable SR Ca(1+) content.
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The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.
TL;DR: The reasons for this ignorance are discussed before reviewing the basic mechanisms that control diastolic intracellular Ca2+ concentration and how these may result in heart failure with preserved versus reduced ejection fraction.
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Does nitric oxide modulate cardiac ryanodine receptor function? Implications for excitation–contraction coupling
TL;DR: The evidence that NO may modulate the function of the ryanodine receptor Ca(2+) release channel (RyR2) on the cardiac sarcoplasmic reticulum (SR) is discussed and the proposed migration of nNOS from the SR to the sarcolemma in the failing heart may have consequences for the nitrosative vs. oxidative balance at the level of the RyR2.
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The effect of tetracaine on stimulated contractions, sarcoplasmic reticulum Ca2+ content and membrane current in isolated rat ventricular myocytes
TL;DR: It is concluded that the effects of tetracaine can be accounted for by depression of calcium‐induced Ca2+ release (CICR) because the response is transient because the inhibition is compensated for by an increase of SRCa2+ content such that there is no steady‐state effect on the magnitude of the systolic Ca 2+ transient.