Publications by authors named "J J Cali"

Background: Adverse drug-drug interactions (DDI) may occur when one drug accelerates or slows a second drug's metabolism by, respectively, inducing or inhibiting a cytochrome P450 (CYP) that metabolizes that second drug. We developed an method employing urinalysis to complement CYP induction and inhibition measurements widely used to predict DDIs.

Research Design And Methods: Focusing on Cyp3a enzymes, the major mammalian drug metabolizers, we applied luciferin-IPA, a selective Cyp3a probe substrate to mice after Cyp3a inducers and inhibitor treatments.

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Article Synopsis
  • All-trans retinoic acid (atRA), derived from vitamin A, acts as a signaling molecule and is regulated by CYP26 enzymes, specifically CYP26A1, during development.
  • This study developed a high-throughput screening assay for identifying inhibitors of CYP26A1, achieving a strong performance indicated by favorable statistical metrics.
  • The assay successfully confirmed known inhibitors and identified new potential inhibitors, highlighting its utility in assessing the developmental toxicity of various chemicals related to atRA signaling.
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Intracellular pathways transduce signals through changes in post-translational modifications (PTMs) of effector proteins. Among the approaches used to monitor PTM changes are immunoassays and overexpression of recombinant reporter genes. Genome editing by CRISPR/Cas9 provides a new means to monitor PTM changes by inserting reporters onto target endogenous genes while preserving native biology.

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The rupture of hepatocellular carcinoma (rHCC) is uncommon but causes sudden life-threatening bleeding. Selective transarterial embolization (STAE) is an effective bleeding-control option. The optimal embolic agent is unknown, and data on the use of cyanoacrylate glue are lacking.

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As a key regulator of the innate immune system, the NLRP3 inflammasome responds to a variety of environmental insults through activation of caspase-1 and release of the proinflammatory cytokines IL-1β and IL-18. Aberrant NLRP3 inflammasome function is implicated in numerous inflammatory diseases, spurring drug discovery efforts at NLRP3 as a therapeutic target. A diverse array of small molecules is undergoing preclinical/clinical evaluation with a reported mode of action involving direct modulation of the NLRP3 pathway.

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