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Deborah Burstein

Researcher at Beth Israel Deaconess Medical Center

Publications -  99
Citations -  11359

Deborah Burstein is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Cartilage & Delayed Gadolinium Enhanced Magnetic Resonance Imaging of Cartilage. The author has an hindex of 52, co-authored 97 publications receiving 10854 citations. Previous affiliations of Deborah Burstein include Massachusetts Institute of Technology & Harvard University.

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Nondestructive imaging of human cartilage glycosaminoglycan concentration by MRI.

TL;DR: In vivo clinical images of T1 in the presence of Gd(DTPA)2‐ (i.e., GAG distribution) correlated well with the validated ex vivo results after total knee replacement surgery, showing that it is feasible to monitor G AG distribution in vivo.
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Gd‐DTPA2− as a measure of cartilage degradation

TL;DR: Equilibration of the tissue in Gd‐DTPA2‐ gives the opportunity to directly image (through T1, weighting) the concentration of GAG, a major and critically important macromolecule in cartilage, suggesting that this technique is clinically feasible.
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Protocol issues for delayed Gd(DTPA)(2-)-enhanced MRI (dGEMRIC) for clinical evaluation of articular cartilage.

TL;DR: The factors that have been found to be important for the practical implementation of the delayed gadolinium‐enhanced MRI technique are described and in some cases of hypointensities in the subchondral patellar bone, decreased penetration of the contrast agent into cartilage from bone was found.
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Glycosaminoglycan in articular cartilage: in vivo assessment with delayed Gd(DTPA)(2-)-enhanced MR imaging.

TL;DR: The data suggest that Gd(DTPA)(2-)-enhanced MR imaging has potential for monitoring glycosaminoglycan content of cartilage in vivo.
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PGC-1α promotes recovery after acute kidney injury during systemic inflammation in mice

TL;DR: It is shown that endotoxemia reduces oxygen delivery to the kidney, without changing tissue oxygen levels, suggesting reduced oxygen consumption by the kidney cells, and that PGC-1α induction may be necessary for recovery from this disorder.