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This perspective is reinforced by the central gain model of tinnitus, which suggests that tinnitus results from an abnormal compensatory increase in gain (i.e., neural amplification) within the CAS to compensate for a loss of sensory input from the cochlea 9,10,11

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This high demand for glutamine means that supplies of it inside of a tumor are often quite low

however the modifiers adjusted for were limited, only model fit parameters were reported, and given the sparse networks it is unclear if these analyses were appropriate