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The proposed mechanism involves accumulated effect over the course rather than peak concentrations

One hypothesis for RA pathogenesis is that the disease begins in genetically predisposed individuals at mucosal sites (i.e., oral cavity, lung, gut) as a consequence of the interaction between a dysbiotic microbiota and the mucosal immune system, and then transitions to synovitis [8]

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- Duracin tpica: 412 semanas

Derangement of these interactions could underlie gastrointestinal disease onset and elicit variable degrees of abnormal gut function, pinpointing, perhaps unexpectedly, the ENS as a diligent participant in idiopathic but also in inflammatory and cancerous diseases of the gut

This suggests that formation of niche blood vessels in the developing cerebral cortex regulates the switch from RG expansion to RG differentiation and neurogenesis