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Safety pharmacology investigations, and toxicology studies in rodent and canine neonates, suggest that TRP601 is a lead compound for further drug development to treat ischemic brain damage in human newborns.
One major hurdle to resolving this central debate is the fact that brain damage in human patients typically encompasses large portions of the anteromedial temporal lobe, such that the identification of individual substructures and precise neuroanatomical locus of the functional impairments has been difficult.
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It can cause fatal brain damage in humans, but seldom does.
The work has revealed how individual cells respond to the injury and has helped the researchers suggest a possible therapeutic approach for limiting brain damage in humans.
The treatment restored some cognitive function, which raises the possibility that the brain's own cells could be stimulated to repair brain damage in humans.
Studies on the effects of brain damage in humans have a long pedigree, recently supplemented by transcranial magnetic stimulation studies in normal subjects.
Moreover, there is evidence that increased levels of TNF-α and IL1-β further exacerbate ischemic and excitotoxic brain damage in humans [ 11, 12].
In particular, PrPC is upregulated following ischemic brain damage, in both humans and mice (McLennan et al, 2004; Weise et al, 2004).
It is still controversial that intrapartum exposure to magnesium may or may not reduce brain damage in premature infants in human and animal models.
Phenylketonuria (PKU), a genetic disease leading to irreversible brain damage in children, arises in humans when PAH is defective.
Researchers have developed drugs that diminish the brain damage in animals--but the drugs haven't helped much in humans.
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CEO of Professional Science Editing for Scientists @ prosciediting.com