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PET tracers targeting transferrin receptors underperform in diffuse axonal injury, as injury boundaries are unclear and non-specific uptake occurs in perihematomal edema, resulting in signal levels below clinical detection thresholds

These interventions have consistently boosted survival and synaptic incorporation of grafts across different pathological contexts

In that case, the T-cells responsible for those regulations begin to divide rapidly and become pro-inflammatory, leading to a drought of Th1 and Th17 T-cells [4]

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