R
Robert A. Haworth
Researcher at University of Wisconsin-Madison
Publications - 72
Citations - 5696
Robert A. Haworth is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Calcium & Ouabain. The author has an hindex of 29, co-authored 72 publications receiving 5493 citations. Previous affiliations of Robert A. Haworth include University of Wisconsin Hospital and Clinics.
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Journal ArticleDOI
The Ca2+-induced membrane transition in mitochondria: I. The protective mechanisms
TL;DR: It is concluded that mitochondria have a set of protective mechanisms involving endogenous NADH, ADP, and energization which regulate the rate of the Ca2+-induced transition, and that the transition requires neither electron flow nor energy, but rather the mere accessibility of some internal site to Ca2+.
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The Ca2+-induced membrane transition in mitochondria. II. Nature of the Ca2+ trigger site.
TL;DR: It is concluded that the trigger site (by “trigger site” the authors mean the site of binding of Ca2+ which, whenCa2+ is bound, will allow the transition in permeability to occur) is possibly also the site for high-affinity Ca2-induced uptake.
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Relationship between configuration, function, and permeability in calcium-treated mitochondria.
TL;DR: The results of this work indicate that mitochondria have a built-in mechanism which responds to low levels of calcium, phosphate, and fatty acids, resulting in simultaneous changes, including increased permeability, inducation of ATPase, uncoupling of oxidative phosphorylation, and loss of respiratory control.
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The Ca2+-induced membrane transition in mitochondria. III. Transitional Ca2+ release.
TL;DR: Na2+-induced Ca2+ release was not accompanied by a configurational change; it is concluded that it is not mediated by the Ca2-induced transition.
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Increased late sodium current in myocytes from a canine heart failure model and from failing human heart.
Carmen R. Valdivia,William W. Chu,Jielin Pu,Jason D. Foell,Robert A. Haworth,Mathew R. Wolff,Timothy J. Kamp,Jonathan C. Makielski +7 more
TL;DR: It is concluded that a peak I(Na) is decreased, and non-inactivating late I( Na) is increased in heart failure and this may contribute to action potential prolongation and the generation of arrhythmia.