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Its core proposed mechanism is the sequestering of G-actin, which influences the cell migration central to tissue repair, alongside preclinical links to angiogenesis and reduced inflammation
Castle noted: (1) gastric achlorhydria precedes the other clinical manifestations of pernicious anemia, and (2) even when the blood of a patient with pernicious anemia is returned to normal with liver feeding, gastric achlorhydria persisted (139)
Multiple groups have studied, characterised, and observed both compounds across in vitro, animal-model, and clinical-research contexts the combined-compound translation is not yet documented in clinical-trial-stage publications
P., Kamimura, A
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