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Judy K. Shigenaga

Researcher at University of California, San Francisco

Publications -  70
Citations -  7418

Judy K. Shigenaga is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Tumor necrosis factor alpha & Receptor. The author has an hindex of 43, co-authored 69 publications receiving 6908 citations. Previous affiliations of Judy K. Shigenaga include United States Department of Veterans Affairs & San Francisco General Hospital.

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In vivo and in vitro regulation of sterol 27-hydroxylase in the liver during the acute phase response. potential role of hepatocyte nuclear factor-1.

TL;DR: Data indicate that LPS suppresses both the classic and alternate pathways of bile acid synthesis, as well as investigating the molecular mechanisms of LPS-induced decrease in sterol 27-hydroxylase, in the liver of Syrian hamsters.
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Apolipoproteins A-IV and A-V are acute-phase proteins in mouse HDL.

TL;DR: Significant changes in the protein composition of HDL during infection and inflammation are identified and these changes are likely to alter the functional properties of HDL perhaps increasing the risk of atherosclerosis.
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Downregulation of liver X receptor-α in mouse kidney and HK-2 proximal tubular cells by LPS and cytokines

TL;DR: It is concluded that the APR suppresses the expression of both nuclear receptors LXRalpha/RXRalpha and several LXR alpha coactivators in kidney, which could be a mechanism for coordinately regulating the expressionof multiple LXR target genes that play important roles in lipid metabolism in kidney during the APR.
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Endotoxin increases parathyroid hormone-related protein mRNA levels in mouse spleen. Mediation by tumor necrosis factor.

TL;DR: The increase in P THrP in the spleen during the immune response suggests that PTHrP may play an important role in immune modulation, perhaps by mediating changes in lymphocyte proliferation and/or function.
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Infection and inflammation decrease apolipoprotein M expression

TL;DR: The regulation of apolipoprotein M during the acute phase response is described, consistent with the finding that infections and inflammatory disorders accompanied by systemic inflammation are associated with an increased risk of atherosclerosis.