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Gene expression analysis showed upregulation of survival pathways (Egr1, Akt1, Kras, Src, Foxo, Srf, VEGFR2, NOS1, NOS3) and downregulation of inflammatory mediators (NOS2, NFB)

We further assessed the consequence of increased tonic GABA inhibition by evaluating the spike probability of layer V neurons in the IL cortex by measuring the spike probability upon electrical stimulation of the layer II/III circuit

We show that the heterogeneity in mitochondrial function and signalling observed across CRC samples could explain, and be used to predict, poor clinical responses in patients with locally advanced CRC

These metabolites can simultaneously drive inflammatory processes, such as oxidative stress or excitotoxicity, while activating compensatory anti-inflammatory mechanisms like IL-10 production, reflecting their inherently bidirectional immunomodulatory roles in the brain

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