Stanley A Hazen

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.

TL;DR: Findings support a key role for free radical-mediated linoleic acid oxidation in human NASH and define a risk score, oxNASH, for noninvasive detection of the presence of NASH.

TL;DR: A method to measure TMAO in biological matrices by stable isotope dilution liquid chromatography tandem mass spectrometry (LC/MS/MS) with lower and upper limits of quantification of 0.05 and >200μM is reported, which should be of value for further studies evaluating T MAO as a risk marker and for examining the effect of dietary, pharmacologic, and environmental factors on TMAo levels.

TL;DR: A potent immunomodulatory role for apoA1 in the tumor microenvironment is revealed, altering tumor-associated macrophages from a pro-tumor M2 to an anti-t tumor M1 phenotype, which may hold benefit as a potential cancer therapeutic.

TL;DR: These findings support the use of mucolytics as a therapeutic strategy for CF and related inflammatory lung diseases and suggest that oxidation arising from airway inflammation or environmental exposure contributes to pathologic mucus gel formation in the lung, which suggests that it can be targeted by thiol-modified carbohydrates.