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Notably, fructose metabolism synergistically amplifies this metabolic reprogramming by bypassing EMP rate-limiting steps (e.g., phosphofructokinase (PFK)) and enhancing nicotinamide adenine dinucleotide phosphate (NADPH)-mediated redox buffering capacity, thereby exacerbating CRC aggressiveness and positioning ALDOB inhibition as a therapeutic vulnerability [6, 7]

Identifying good surrogates for process monitoring can be challenging, especially if there are gaps in the scientific knowledge about the mechanisms of pathogen reduction in those processes or about the design, operational, or environmental factors that influence pathogen reduction

doi: 10.1016/j.siny.2009.01.002

To assess its safety for therapeutic use, its cytotoxicity was evaluated in RAW264.7 and human leukocytes, including peripheral blood mononuclear (PBMCs) and polymorphonuclear leukocytes (PMNs) cells