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  • rees of cerebral oedema in response to the presence of unfiltered circulating toxins, such as ammonia, with subsequent regulatory lowering of mI levels in an effort to maintain astrocyte osmotic equilibrium, as the brain swells.[34] Clearly, this is not the mechanism in our cohort with documented acute HCV infection, who may be up to 30 years away from developing HCV-related end-stage liver diseas
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