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These results all encourage a conclusion that LASSS treatment (at 1:8000 ratio to HGF) may enhance the c-met binding-affinity of HGF without disturbing HGF-c-Met signaling and that this enhancement occurs through a mechanism that is unrelated to prevention of HGF nitration

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Long-term CPT1B inhibition can cause lipotoxicity in the heart under pathological stress, leading to more cardiomyocyte apoptosis and exacerbation of cardiac hypertrophy (He et al., 2012