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Beatrice A. Wittenberg
Researcher at Albert Einstein College of Medicine
Publications - 62
Citations - 5031
Beatrice A. Wittenberg is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Heme & Myoglobin. The author has an hindex of 38, co-authored 62 publications receiving 4910 citations. Previous affiliations of Beatrice A. Wittenberg include Yeshiva University & Marine Biological Laboratory.
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Transport of oxygen in muscle.
TL;DR: This work addresses intracellular events within the myocyte with particular attention to the role of myoglobin, and asks how the massive and variable flow of oxygen to muscle mitochondria is achieved at near-constant low sarcoplasmic oxygen pressure.
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Myoglobin function reassessed.
TL;DR: The heart and those striated muscles that contract for long periods, having available almost limitless oxygen, operate in sustained steady states of low sarcoplasmic oxygen pressure that resist change in response to changing muscle work or oxygen supply.
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Truncated Hemoglobins: A New Family of Hemoglobins Widely Distributed in Bacteria, Unicellular Eukaryotes, and Plants
TL;DR: Crystal structures show that trHb tertiary structure is based on a 2-on-2 -hel-ical sandwich, which represents an unprecedented editing of the highly conserved globin fold, and may provide a path for ligand diffusion to the heme.
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Quantitative determination of adenovirus-mediated gene delivery to rat cardiac myocytes in vitro and in vivo
Alyson Kass-Eisler,Erik Falck-Pedersen,Mauricio Alvira,Johanna Rivera,Peter M. Buttrick,Beatrice A. Wittenberg,Laura Cipriani,Leslie A. Leinwand +7 more
TL;DR: The amount of CAT activity resulting from adenovirus infection of the myocardium was orders of magnitude higher than that seen from DNA injection and was proportional to the amount of input virus.
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Truncated hemoglobin HbN protects Mycobacterium bovis from nitric oxide.
Hugues Ouellet,Yannick Ouellet,Christian Richard,Marie LaBarre,Beatrice A. Wittenberg,Jonathan B. Wittenberg,Michel Guertin +6 more
TL;DR: It is reported that disruption of M. bovis bacillus Calmette–Guérin glbN caused a dramatic reduction in the NO-consuming activity of stationary phase cells, and that activity could be restored fully by complementing knockout cells withglbN, and an NO-metabolizing activity in M. tuberculosis or M.bovis is demonstrated.