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Diana M. Shih

Researcher at University of California, Los Angeles

Publications -  100
Citations -  15202

Diana M. Shih is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: PON1 & Paraoxonase. The author has an hindex of 51, co-authored 100 publications receiving 13802 citations. Previous affiliations of Diana M. Shih include Technion – Israel Institute of Technology & University of California, San Francisco.

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Genome sequence, comparative analysis and haplotype structure of the domestic dog

Kerstin Lindblad-Toh, +241 more
- 08 Dec 2005 - 
TL;DR: A high-quality draft genome sequence of the domestic dog is reported, together with a dense map of single nucleotide polymorphisms (SNPs) across breeds, to shed light on the structure and evolution of genomes and genes.
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Mice lacking serum paraoxonase are susceptible to organophosphate toxicity and atherosclerosis

TL;DR: When fed on a high-fat, high-cholesterol diet, PON1 -null mice were more susceptible to atherosclerosis than their wild-type littermates.
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Trimethylamine-N-Oxide, a Metabolite Associated with Atherosclerosis, Exhibits Complex Genetic and Dietary Regulation

TL;DR: It is demonstrated that two flavin mono-oxygenase family members, FMO1 and FMO3, oxidize trimethylamine (TMA), derived from gut flora metabolism of choline, to TMAO, and it is shown that F MO3 exhibits 10-fold higher specific activity than F MO1.
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The Yin and Yang of Oxidation in the Development of the Fatty Streak: A Review Based on the 1994 George Lyman Duff Memorial Lecture

TL;DR: The hypothesis that the fatty streak develops in response to specific phospholipids contained in LDL that become trapped in the artery wall and become oxidized as a result of exposure to the oxidative waste of the artery Wall cells is supported.
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Trimethylamine N‐Oxide Promotes Vascular Inflammation Through Signaling of Mitogen‐Activated Protein Kinase and Nuclear Factor‐κB

TL;DR: It was shown that activation of nuclear factor‐κB signaling was necessary for TMAO to induce inflammatory gene expression in both of these relevant cell types as well as endothelial cell adhesion of leukocytes, which suggests a likely contributory mechanism for T MAO‐dependent enhancement in atherosclerosis and cardiovascular risks.