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The inflammatory response after TBI involves both the resident microglia and infiltrating inflammatory cells, primarily phagocytic, CD68+/CD163- macrophages apparently stimulated by large quantities of damaged myelin and markedly elevated inflammatory cytokines including IL1, IL-6, IFN and chemokines with degradation of tight junctions (TJs), cytoskeletal rearrangements and protein promoted by adhesion molecules [14]

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This is approximately 1,000 times higher than the concentration of insulin that does not have a binding protein [11]

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