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The increase in glutaminolysis in PAH also promotes fibrosis by stimulating collagen translation and stability via the -ketoglutarate-mediated mammalian target of rapamycin activation and proline hydroxylation [81], sparking a vicious cycle of arterial stiffening, glutaminolysis, and hyperproliferation
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Both LOD and LOQ were tested and verified experimentally
Why buffering may matter: buffering support is not intended to force blood pH outside its tightly regulated range
Functional characterization of the intermediate isoform of the human prolactin receptor
