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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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Cystatin C Is Downregulated in Prostate Cancer and Modulates Invasion of Prostate Cancer Cells via MAPK/Erk and Androgen Receptor Pathways

TL;DR: A novel role is uncovered for cystatin C and its associated cellular pathways in prostate cancer invasion and metastasis as well as the association with matrix metalloproteinases 2 and androgen receptor (AR) in a tissue microarray comparing benign and malignant specimens.
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Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells.

TL;DR: It is concluded that HO-1 and CO in part are critical for myeloid cell differentiation and may prove to be a novel therapeutic agent to improve functional recovery of bone marrow cells in patients undergoing irradiation, chemotherapy and/or bone marrow transplantation.
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Inhalation of carbon monoxide prevents liver injury and inflammation following hind limb ischemia/reperfusion.

TL;DR: It is suggested that HO‐derived hepatic protection is mediated by CO, and inhalation of low concentrations of CO may represent a novel therapeutic approach to prevent remote organ injury during systemic inflammatory response syndrome, or SIRS.
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Mitochondrial DAMPs Are Released During Cardiopulmonary Bypass Surgery and Are Associated With Postoperative Atrial Fibrillation.

TL;DR: Mitochondrial DNA is released by CPB surgery and is associated with POAF, and may be involved in the pathogenesis of SIRS and related postoperative inflammatory events like POAF and infections.
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Bilirubin suppresses Th17 immunity in colitis by upregulating CD39

TL;DR: It is noted that UCB modulates T helper type 17 (Th17) immune responses, in a manner dependent upon heightened expression of CD39 ectonucleotidase, which might provide therapeutic options to address development of Th17 dysfunction in IBD.