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Denise Drazul-Schrader

Researcher at Children's Hospital of Philadelphia

Publications -  11
Citations -  1038

Denise Drazul-Schrader is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Cholesterol & Efflux. The author has an hindex of 8, co-authored 11 publications receiving 932 citations.

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Journal ArticleDOI

The Ability to Promote Efflux Via ABCA1 Determines the Capacity of Serum Specimens With Similar High-Density Lipoprotein Cholesterol to Remove Cholesterol From Macrophages

TL;DR: It is found that independently of HDL-C, sera with higher efflux capacity had a significant increase in ABCA1-mediated efflux, which was significantly correlated to the concentration of pre&bgr;-1 HDL.

Cell Biology/Signaling The Ability to Promote Efflux Via ABCA1 Determines the Capacity of Serum Specimens With Similar High-Density Lipoprotein Cholesterol to Remove Cholesterol From Macrophages

TL;DR: In this article, the authors measured efflux from macrophages to apolipoprotein B-depleted serum from 263 specimens and found instances in which serum having similar high-density lipoprotein cholesterol (HDL-C) differed in their efflux capacity.
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L-Carnitine intake and high trimethylamine N-oxide plasma levels correlate with low aortic lesions in ApoE(-/-) transgenic mice expressing CETP.

TL;DR: It is suggested that TMAO slows aortic lesion formation in this mouse model and may have a protective effect against atherosclerosis development in humans.
Journal ArticleDOI

Serum albumin acts as a shuttle to enhance cholesterol efflux from cells

TL;DR: Synergistic efflux was obtained when LPDS was incubated with cells and LDL, and a synergistic effect was also obtained when RBC was used as the sink and albumin as shuttle.
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Separation of Lipid Transport Functions by Mutations in the Extracellular Domain of Scavenger Receptor Class B, Type I*

TL;DR: Findings uncover a difference in the SR-BI-mediated efflux pathways for FC transfer to HDL acceptors versus phospholipid vesicles and the loss of the cholesterol oxidase-sensitive FC pool and FC efflux to small unilamellar vesicle acceptors in Class 4 mutants suggests that these activities may be mechanistically related.