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Thus, Xu and Hammock hypothesized that the mechanism underlying the effect of the sEH inhibitor t -AUCB ( 1 ) (Hwang et al., 2007) on epithelial progenitor cells (EPCs) was the EETs-PPAR pathway

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Human studies In a Phase II trial [38] designed to investigate the impact of antibiotics on gut microbiota, 150 stable individuals with HFrEF were divided into three groups, receiving either rifaximin, probiotic yeast (brady yeast), or no treatment at all