L
Leo E. Otterbein
Researcher at Beth Israel Deaconess Medical Center
Publications - 228
Citations - 24913
Leo E. Otterbein is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Heme oxygenase & Heme. The author has an hindex of 79, co-authored 221 publications receiving 22713 citations. Previous affiliations of Leo E. Otterbein include Veterans Health Administration & Johns Hopkins University School of Medicine.
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Journal ArticleDOI
Characterization of a versatile organometallic pro-drug (CORM) for experimental CO based therapeutics
João Seixas,Abhik Mukhopadhyay,Teresa Santos-Silva,Leo E. Otterbein,David Gallo,Sandra Rodrigues,Bruno Guerreiro,Ana M. L. Gonçalves,Nuno Penacho,Ana R. Marques,Ana C. Coelho,Patrícia M. Reis,Maria João Romão,Carlos C. Romão +13 more
TL;DR: The complex fac-[Mo(CO)(3)(histidinate)]Na has been reported to be an effective CO-Releasing Molecule in vivo, eliciting therapeutic effects in several animal models of disease and can readily liberate all of its three CO equivalents under biological conditions.
Journal ArticleDOI
Intraoperative Administration of Inhaled Carbon Monoxide Reduces Delayed Graft Function in Kidney Allografts in Swine
Douglas W. Hanto,T. Maki,M. H. Yoon,Eva Csizmadia,Beek Yoke Chin,D. Gallo,B. Konduru,Kaori Kuramitsu,N. R. Smith,A. Berssenbrugge,Chiara Attanasio,M. Thomas,Barbara Wegiel,Leo E. Otterbein +13 more
TL;DR: It is demonstrated that donor warm ischemia time is a critical determinant of DGF as evidenced by a transient increase in serum creatinine and blood urea nitrogen following transplantation before returning to baseline.
Journal ArticleDOI
Heme as a danger molecule in pathogen recognition.
TL;DR: This review will focus on how sterile and infective stimuli activate the stress response gene heme oxygenase-1 (Hmox1, HO-1), a master gene critical to an appropriate host response that is now recognized as one with enormous therapeutic potential.
Journal ArticleDOI
Low-dose carbon monoxide reduces airway hyperresponsiveness in mice.
Bill T. Ameredes,Leo E. Otterbein,Lauryn Kohut,Amber L. Gligonic,William J. Calhoun,Augustine M.K. Choi +5 more
TL;DR: It is indicated that low-dose CO can effectively reverse AHR in the presence and absence of airway inflammation in mice and a potential role for CO in the modulation of AHR is suggested.
Journal ArticleDOI
Hypoxia activates a Ca2+-permeable cation conductance sensitive to carbon monoxide and to GsMTx-4 in human and mouse sickle erythrocytes.
David H. Vandorpe,David H. Vandorpe,Chang Xu,Chang Xu,Boris E. Shmukler,Boris E. Shmukler,Leo E. Otterbein,Leo E. Otterbein,Marie Trudel,Frederick Sachs,Philip A. Gottlieb,Carlo Brugnara,Carlo Brugnara,Seth L. Alper,Seth L. Alper +14 more
TL;DR: Electrophysiological and fluorimetric data provide compelling evidence in sickle erythrocytes of mouse and human for a deoxygenation-induced, reversible, Ca2+-permeable cation conductance blocked by inhibition of HbSS polymerization and by an inhibitor of strctch-activated cation channels.