Exact(7)
In his study, Dharap[28] reported miR-29b (at 3, 6 and 24 h) and miR-137 (at 24 h) to be downregulated in a MCAo adult rat model, while Lei[33] reported the same findings in a TBI adult rat model at 6 h post injury.
Although 400 mg/kg of VPA is useful in a TBI rodent model, this dose is too high for humans.
For example, the cathepsin B inhibitor, CA-074Me, reduced biomarkers of apoptosis, such as Bax, and neuronal cell death, and reduced memory loss in a TBI model.
The 3-year incremental cost associated with psychological distress in a TBI patient was estimated to be $3529 compared to the incremental cost associated with psychological distress in a nonTBI patient of $2769.
In this way, strategies aimed at directly scavenging ROS are restricted due to the extremely short half-life of free radicals and the small therapeutic window in a TBI event.
Studies in a TBI model showed that the protective effect of oxaloacetate was abolished in the presence of excess glutamate in serum or when it was administered in combination with maleate (a GOT inhibitor), which effectively demonstrates its serum glutamate-scavenging action.
Similar(53)
Animal models of TBI have shown that normovolemic anemia results in decreased brain tissue oxygenation in comparison with a TBI without anemia [ 22].
In humans with a TBI, transfusion of RBCs increases brain tissue oxygen [ 10, 23].
However, the clinical literature examining transfusion thresholds in patients with a TBI is weak and results are conflicting [ 18].
Large and well-designed multicenter observational studies and randomized control trials are needed to further elucidate transfusion thresholds for anemia in patients with a TBI.
However, these benefits in patients with a TBI must be weighed against established and potentially harmful effects of RBC transfusion [ 11- 15].
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