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A direct comparative analysis elucidates how these agents may be positioned rationally as adjunctive or alternative interventions depending on clinical phenotype, biological vulnerability, and therapeutic goals

As recently deciphered, JNK emerges as a key culprit in APAP-induced hepatocellular death and liver damaged caused by a Sab-dependent mechanism that involves inactivation of intramitochondrial Src in the MIM, which in turn inhibits electron transport, increases ROS, and sustains JNK activation (Win et al., 2016)

doi: 10.1055/s-2007-978596

TMAO is expected to become a potential biomarker for the diagnosis and prognosis evaluation of specific diseases

SahasranamanS.HowardD.RoyS.2008Clinical pharmacology and pharmacogenetics of thiopurines.648(August 2008),753767, ISNN 0031-6970 95