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Such observations raise the question as to why D-2HG only acts as an oncometabolite in specific genetic backgrounds and highlights the need to further study endogenous D-2HG metabolism in both healthy tissues and disease models

Even the very low fluidity membranes incapable for supporting growth retain a robust diffusion barrier function

It is of interest that, like other extraintestinal manifestations, oral lesions may precede the onset of the underlying intestinal inflammatory disorder [3, 7, 8]