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Matthew C. Cave

Researcher at Jewish Hospital

Publications -  6
Citations -  738

Matthew C. Cave is an academic researcher from Jewish Hospital. The author has contributed to research in topics: Constitutive androstane receptor & Pregnane X receptor. The author has an hindex of 6, co-authored 6 publications receiving 588 citations. Previous affiliations of Matthew C. Cave include United States Department of Veterans Affairs & University of Louisville.

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Probiotics restore bowel flora and improve liver enzymes in human alcohol-induced liver injury: a pilot study

TL;DR: It is concluded that patients with alcohol-induced liver injury have altered bowel flora compared to healthy controls and short-term oral supplementation with B. bifidum and L. plantarum 8PA3 was associated with restoration of the bowel flora and greater improvement in alcohol- induced liver injury than standard therapy alone.
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Nuclear receptors and nonalcoholic fatty liver disease.

TL;DR: The impact of nuclear receptor crosstalk in NAFLD is likely to be profound, but requires further elucidation and novel strategies currently under development may be required to separate the beneficial effects ofnuclear receptor activation from unwanted metabolic side effects.
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Polychlorinated Biphenyl-Xenobiotic Nuclear Receptor Interactions Regulate Energy Metabolism, Behavior, and Inflammation in Non-alcoholic-Steatohepatitis.

TL;DR: Pxr and Car regulated inflammation, behavior, and energy metabolism in PCB-mediated NASH, and future studies should address the 'off-target' effects of PCBs in steatohepatitis.
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Epidermal Growth Factor Receptor Signaling Disruption by Endocrine and Metabolic Disrupting Chemicals.

TL;DR: Based on NHANES data, EGFR inhibition may be an environmentally relevant mode of action for some PCBs, pesticides, and herbicides.
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Vinyl Chloride Metabolites Potentiate Inflammatory Liver Injury caused by LPS in Mice.

TL;DR: Exposure to VC/metabolites at levels that are not overtly hepatotoxic can potentiate liver injury caused by another hepatot toxicant, serving as proof-of-concept that VC hepatotoxicity may be modified by an additional metabolic stress such as endotoxemia, which commonly occurs in acute and chronic diseases.